LOCAL
ANESTHESIA
DR.PRIYANKA SHARMA
II YEAR MDS
PUBLIC HEALTH DENTISTRY
JSSDCH

CONTENTS
 Introduction
 Historical background
 Definition
 Methods of inducing local anesthesia
 Desirable properties
 Electrophysiology of nerve conduction
 Impulse propagation and spread
 Theories of mechanism of action of local
anesthesia
 Dissociation of local anesthesia
2

3
Mode and site of action of local
anesthesia
Classification of local anesthetic
according to biological site and
mode of action
Mechanism of action of local
anesthesia
Local anesthetics description
Armamentarium
Injection techniques
Local & Systemic complications
 Special care groups
Recent advancements
Conclusion
References

Historical background
• COCAINE -first local anesthetic agent-isolated
by Nieman -1860 -from the leaves of the coca
tree.
• Its anesthetic action was demonstrated by Karl
Koller in 1884.
• First effective and widely used synthetic local
anesthetic -PROCAINE -produced by Einhorn in
1905 from benzoic acid and diethyl amino
ethanol.
4

5
•It anesthetic properties were identified by Biberfield
and the agent was introduced into clinical practice by
Braun.
•LIDOCAINE- Lofgren in 1948.
•The discovery of its anesthetic properties was
followed in 1949 by its clinical use by T. Gordh

6
DEFINITION:
Local anesthesia is defined as a loss of sensation in a
circumscribed area of the body caused by depression
of excitation in nerve endings or an inhibition of the
conduction process in peripheral nerves.
An important feature of local anesthesia is that it
produces:
LOSS OF SENSATION WITHOUT
INDUCING LOSS OF CONSCIOUSNESS..

7
METHODS OF INDUCING LOCAL
ANESTHESIA:

Low temperature

Mechanical trauma

Anoxia

Neurolytic agents such as alcohol & phenol

Chemical agents such as local anesthetics

PROPERTIES OF LOCAL
ANESTHESIA
I==It should not be irritating to tissue to which it is
applied
N==It should not cause any permanent alteration of
nerve structure
S==Its systemic toxicity should be low
T==Time of onset of anesthesia should be short
E== It should be effective regardless of whether it is
injected into the tissue or applied locally to
mucous membranes
D==The duration of action should be long enough
to permit the completion of procedure
8

9

It should have the potency sufficient to give
complete anesthesia with out the use of harmful
concentration solutions

It should be free from producing allergic
reactions

It should be free in solution and relatively
undergo biotransformation in the body

It should be either sterile or be capable of being
sterilized by heat with out deterioration.

ELETROPHYSIOLOGY OF
NERVE CONDUCTION
• There is an electrical charge across the membrane.
• This is the membrane potential.
• The resting potential (when the cell is not firing)
is a negative electrical potential of -70mv that
exists across the nerve membrane, produced by
different concentrations of either side of the
membrane.
• The interior of nerve is NEGATIVE in relation to
exterior. 10

outside
inside
11
+
-
+
-
+
-
+
-
+
-
Resting potential of neuron = -70mV

Action Potentials
• At rest: Na+& K+ channels closed. -70mV
• Fibre stimulated: Na+channel opens, Na+ enters
cell. Potential rising
• Cell depolarised, Na+ channel closes. +20mV
• K+ channel opens, K+ exits cell, potential falling
• Fibre repolarised, Na+& K+ channels closed.
Na/K pump restores balance. -70mV
• Result is a voltage gradient along axon, causing
a current. This causes configurational change in
Na-channels in the next segmentconduction
12

13

SLOW DEPOLARIRIZATION
RAPID DEPOLARIZATION:
The interior of nerve is POSITIVE in relation to
exterior.
14

REPOLARIZATION:
.
SODIUM PUMP
energy comes from the oxidative
metabolism of ATP
• Depolarization takes 0.3 msec
• Repolarization takes 0.7 msec
• The entire process require 1 msec
15

IMPULSE PROPOGATION
DEPOLARIZED SEGMENT ADJACENT RESTING
AREA
IMPULSE SPREAD
The propagated impulse travels along the nerve
membrane towards CNS. The spread of impulse
differs in myelinated and unmyelinated nerve
fibers.
UNMYELINATED NERVES: The high
resistance cell membrane and extra cellular media
produce a rapid decrease in density of current with
in a short distance of depolarized segment.
The spread of the impulse is characterized as a
slow forward-creeping process.
Conduction rate is 1.2m/sec

MYLINATED NERVES:
Impulse conduction in myelinated nerves occurs by
means of current leaps from nodes to node this
process is called as SALTATORY
CONDUCTION.
It is more rapid in thicker nerves because of increase in
thickness of myelin sheath and increase in distance
between adjacent nodes of ranvier.
If conduction of impulse is blocked at one node the
local current will skip over that node and prove
adequate to raise that membrane potential at next
node to its firing potential and produce
depolarization.
Conduction rate of myelinated fibers is 120m/sec.
17

18

MODE AND SITE OF ACTION OF
LOCAL ANESTHETICS
Local anesthetic agent interferes with excitation
process in a nerve membrane in one of the
following ways:

Altering the basic resting potential of nerve
membrane

Altering the threshold potential

Decreasing the rate of depolarization

Prolonging the rate of repolarization
19

THEORIES MECHANISM OF
ACTION OF LOCAL
ANESTHETICS
Many theories have been promulgated over
the years to explain the mechanism of
action of local anesthetics.
ACETYLECHOLINE THEORY: Stated
that acetylcholine was involved in nerve
conduction in addition to its role as a
neurotransmitter at nerve synapses. There
is no evidence that acetylcholine is
involved in neural transmission.
20

CALCIUM DISPLACEMENT
THEORY:
States that local anesthetic nerve block was
produced by displacement of calcium from
some membrane site that controlled
permeability of sodium.
21

SURFACE CHARGE (REPULSION)
THEORY:
Proposed that local anesthetic acted by binding to nerve
membrane and changing the electrical potential at
the membrane surface. Cationic drug molecule were
aligned at the membrane water interface, and since
some of the local anesthetic molecule carried a net
positive charge, they made the electrical potential at
the membrane surface more positive, thus
decreasing the excitability of nerve by increasing
the threshold potential. Current evidence indicate
that resting potential of nerve membrane is unaltered
by local anesthetic. 22

MEMBRANE EXPANSION THEORY
• It states that local anesthetic molecule diffuse to
hydrophobic regions of excitable membranes,
producing a general disturbance of bulk membrane
structure, expanding membrane, and thus preventing
an increase in permeability to sodium ions. Lipid
soluble LA can easily penetrate the lipid portion of
cell membrane changing the configuration of
lipoprotein matrix of nerve membrane. This results
in decreased diameter of sodium channel, which
leads to inhibition of sodium conduction and neural
excitation. 23

MEMBRANE EXPANSION
THEORY
24

SPECIFIC RECEPTOR THEORY:
The most favored today, proposed that local anesthetics
act by binding to specific receptors on sodium
channel the action of the drug is direct, not mediated
by some change in general properties of cell
membrane. Biochemical and electrophysiological
studies have indicated that specific receptor sites for
local anesthetic agents exists in sodium channel
either on its external surface or on internal
axoplasmic surface. Once the LA has gained access
to receptors, permeability to sodium ion is decreased
or eliminated and nerve conduction is interrupted. 25

CLASSIFICATION OF LOCAL
ANESTHETIC SUBSTANCES
ACCORDING TO BIOLOGICAL SITE
AND MODE OF ACTION
CLASS A: Agents acting at receptor site on external
surface of nerve membrane
Chemical substance: Biotoxins (e.g., tetrodotoxin and
saxitoxin)
CLASS B: Agents acting on receptor sites on internal
surface of nerve membrane
Chemical substance: Quaternary ammonium analogues
of lidocaine, scorpion venom
26

CLASS C: Agents acting by receptor
independent of physiochemical mechanism
Chemical substance: Benzocaine
CLASS D: Agents acting by combination of
receptors and receptor independent
mechanisms
Chemical substance: most clinically useful
anesthetic agents (e.g., lidocaine,
mepivacaine, prilocaine)
27

BASED ON THE SOURCE
• NATUAL
• SYNTHETIC
• OTHERS
BASED ON MODE OF
APPLICATION
• INJECTABLE
• TOPICAL
• BASED ON DURATION OF
ACTION
• ULTRA SHORT
• SHORT
• MEDIEM
• LONG 28

BASED ON ONSET OF ACTION
• SHORT
• INTERMEDIATE
• LONG
29

DISSOCIATION OF LOCAL
ANESTHETICS
• Local anesthetics are available as salts (usually
hydrochlorides) for clinical use.
• The salts, both water soluble and stable, is
dissolved in either sterile water or saline.
• In this solution it exists simultaneously as
unchanged molecule (RN), also called base and
positively charged molecules (RNH+) called
cations.
RNH+ ==== RN+ H+
30

• The relative concentration of each ionic form in the
solution varies in the pH of the solution or
surrounding tissue.
• In the presence of high concentration of hydrogen
ion (low pH) the equilibrium shifts to left and most
of the anesthetic solution exists in cationic form.
RNH+ > RN+ + H+
• As hydrogen ion concentration decreases (higher
pH) the equilibrium shifts towards the free base
form.
RNH+ < RN + H+
31

• The relative proportion of ionic form also depends
on pKa or DISSOCIATION CONSTANT, of the
specific local anesthetic.
• The pKa is a measure of molecules affinity for H+
ions.
• When the pH of the solution has the same value as
pKa of the local anesthetic, exactly half the drug will
exists in the RNH+ form and exactly half in RN
form.
• The percentage of drug existing in either form can be
determined by Henderson Hasselbalch equation
Log base/acid = pH - pKa
32

• Henderson hasselbach equation
Determines how much of a local
anesthetic will be in a non-ionized
vs ionized form . Based on tissue pH
and anesthetic Pka .
• Injectable local anesthetics are weak
bases (pka=7.5-9.5) When a local
anesthetic is injected into tissue it is
neutralized and part of the ionized
form is converted to non-ionized
The non-ionized base is what
diffuses into the nerve.
33

• Hence if the tissue is infected, the
pH is lower (more acidic) and
according to the HH equation; there
will be less of the non-ionized form
of the drug to cross into the nerve
(rendering the LA less effective)
• Once some of the drug does cross;
the pH in the nerve will be normal
and therefore the LA re-equilibrates
to both the ionized and nonionized
forms; but there are fewer cations
which may cause incomplete
anesthesia. 34

MECHANISM OF ACTION OF LOCAL
ANESTHETICS
The following sequence is proposed
mechanism of action of LA:

Displacement of calcium ions from the
sodium channel receptor site

Binding of local anesthetic molecule to
this receptor site

Blockade of sodium channel
35


Decrease in sodium conductance

Depression of rate of electrical
depolarization

Failure to achieve the threshold potential
level

Lack of development of propagated action
potential

Conduction blockade…
36

37
Na + Na +

LOCAL
ANESTHETIC
AGENT
38

39
COMERCIALLY PREPARED
LOCAL ANESTHESIA
CONSISTS OF:
Local anesthetic agent (xylocaine,
lignocaine 2%)
Vasoconstrictor (adrenaline 1:
80,000)
Reducing agent (sodium
metabisulphite)
Preservative
(methylparaben,capryl
hydrocuprienotoxin)
Fungicide (thymol)
Vehicle (distillde water,NaCl)

40

REDUCING AGENT
• Vasoconstrictors are unstable in solution and
may oxidize especially on prolong exposure to
sunlight this results in turning of the solution
brown and this discoloration is an indication that
such a solution must be discarded.
• To overcome this problem a small quantity of
sodium metabisulphite is added - competes for
the available oxygen.
• SHELF LIFE INCRESES
41

PRESERVATIVE
• Modern local anesthetic solution are very stable
and often have a shelf of two years or more.
Their sterility is maintained by the inclusion of
small amount of a preservative such as capryl
hydrocuprienotoxin.
• Some preservative such as methylparaben have
been shown to allergic reaction in sensitized
subjects.
42

FUNGICIDE
• In the past some solutions tended to become
cloudy due to the proliferation of minute fungi.
• In several modern solutions a small quantity of
thymol is added to serve as fungicide and
prevent this occurrence.
43

VEHICLE
• The anesthetic agent and the additives referred to
above are dissolved in distilled water & sodium
chloride.
• This isotonic solution minimizes discomfort
during injection.
44

45
. The chemical characteristics are so balanced that
they have both lipophilic and hydrophilic properties.
If hydrophilic group predominates, the ability to
diffuse into lipid rich nerves is diminished. If the
molecule is too lipophilic it is of little clinical value as
an injectable anesthetic, since it is insoluble in water
and unable to diffuse through interstitial tissue.

LOCAL ANESTHETIC AGENT
The local anesthetics used in dentistry are
divided into two groups:

ESTER GROUP

AMIDE GROUP
46

47
ESTER GROUP:
It is composed of the following
An aromatic lipophilic group
An intermediate chain containing
an ester linkage
A hydrophilic secondary or tertiary
amino group
AMIDE GROUP:
It is composed of the following
An aromatic, lipophilic group
An intermediate chain containing
amide linkage
A hydrophilic secondary or tertiary
amino group

48
CLASSIFICATION OF LOCAL
ANESTHETICS
ESTERS
Esters of benzoic acid
Butacaine
Cocaine
Benzocaine
Hexylcaine
Piperocaine
Tetracaine
Esters of Para-amino
benzoic acid
Chloroprocain
Procaine
Propoxycaine

49
AMIDES
Articaine
Bupivacaine
Dibucaine
Etidocaine
Lidocaine
Mepivacaine
Prilocaine
Ropivacaine
QUINOLINE
Centbucridine
ABCDE LMPR

PHARMACOKINETICS OF LOCAL
ANESTHETICS
UPTAKE:
When injected into soft tissue most local anesthetics
produce dilation of vascular bed.
 Cocaine is the only local anesthetic that produces
vasoconstriction, initially it produces vasodilation
which is followed by prolonged vasoconstriction.
 Vasodilation is due to increase in the rate of
absorption of the local anesthetic into the blood, thus
decreasing the duration of pain control while
increasing the anesthetic blood level and potential for
over dose.
50

ORAL ROUTE:
Except cocaine, local anesthetics are poorly absorbed
from GIT
Most local anesthetics undergo hepatic first-pass effect
following oral administration.
72% of dose is biotransformed into inactive metabolites
TOCAINIDE HYDROCHLORIDE an analogue of
lidocaine is effective orally
51

TOPICAL ROUTE:
Local anesthetics are absorbed at different rates after
application to mucous membranes, in the tracheal
mucosa uptake is as rapid as with intravenous
administration.
In pharyngeal mucosa uptake is slow
In bladder mucosa uptake is even slower
Eutectic mixture of local anesthesia (EMLA) has been
developed to provide surface anesthesia for intact
skin.
52

INJECTION:
The rate of uptake of local anesthetics after injection is related to both the
vascularity of the injection site and the vasoactivity of the drug.
IV administration of local anesthetics provide the most rapid elevation
of blood levels and is used for primary treatment of ventricular
dysrhythmias.
RATES AT WHICH LOCAL ANESTHETICS ARE ABSORBED AND
REACH THEIR PEAK BLOOD LEVEL
ROUTE TIME TO PEAK
LEVEL (MIN)
INTRAVENOUS 1
TOPICAL 5
INTRAMUSCULA
R
5-10
SUBCUTANEOUS 30 - 90
53

DISTRIBUTION
 Once absorbed in the blood stream local anesthetics
are distributed through out the body to all tissues.
 Highly perfused organs such as brain, head, liver,
kidney, lungs have higher blood levels of anesthetic
than do less higher perfused organs.
54

The blood level is influenced by the following
factors:
Rate of absorption into the blood stream.
Rate of distribution of the agent from the
vascular compartment to the tissues.
Elimination of drug through metabolic and/or
excretory pathways.
All local anesthetic agents readily cross the
blood-brain barrier, they also readily cross the
placenta.
55

METABOLISM
(BIOTRANSFORMATION)
ESTER LOCAL ANESTHETICS:
• Ester local anesthetics are hydrolyzed in
the plasma by the enzyme
pseudocholinesterase.
• Chloroprocaine the most rapidly
hydrolyzed, is the least toxic.
• Tertracaine hydrolyzed 16 times more
slowly than Chloroprocaine ,hence it has
the greatest potential toxicity.
56

AMIDE LOCAL ANESTHETICS
The metabolism of amide local anesthetics is more
complicated then esters. The primary site of
biotransformation of amide drugs is liver.
Entire metabolic process occurs in the liver for
lidocaine, articaine, etidocaine, and bupivacaine.
Prilocaine undergoes more rapid biotransformation
then the other amides.
57

EXCREATION
Kidneys are the primary excretory organs for both the
local anesthetic and its metabolites
A percentage of given dose of local anesthetic drug is
excreted unchanged in the urine.
Esters appear in only very small concentration as the
parent compound in urine.
Procaine appears in the urine as PABA (90%) and 2%
unchanged.
10% of cocaine dose is found in the urine unchanged.
Amides are present in the urine as a parent compound
in a greater percentage then are esters.
58

MRD
59

VASOCONSTRICTORS
• Constrict vessels and decrease blood
flow to the site of injection.
• Absorption of LA into bloodstream
is slowed, producing lower levels in
the blood.
• Lower blood levels lead to
decreased risk of overdose (toxic)
reaction.
• Higher LA concentration remains
around the nerve increasing the LA's
duration of action. 60

• Minimize bleeding at the site of
administration.
• Naturally Occurring Vasoconstrictors:
- Epinephrine
- Norepinephrine
• Vasoconstrictors should be included
unless contraindicated.
• Mode of Action - Attach to and directly
stimulate adrenergic receptors . Act
indirectly by provoking the release of
endogenous catecholamine from
intraneuronal storage sites.
61

• Concentrations of Vasoconstrictor in
Local Anesthetics - 1:50,000 ,1:100,000,
1:200,000 - 0.020mg/ml ,0.010mg/ml,
0.005 mg/ml
• Calculation 1:50,000= 1gram/50,000ml=
1000mg/50,000ml= 1mg/50ml=
0.02mg/ml
• Levonordefrin - One fifth as active as
epinephrine
• Vasoconstrictors - Unstable in Solution
Sodium metabisulfite added Known
allergen
62

• Max dose of vasoconstrictors
- Healthy patient approximately
0.2mg
- Patient with significant
cardiovascular history: 0.04mg
• Max Dose for Vasoconstrictors (CV
patient) 1 carpule = 1.8cc
1:100,000=.01mg/cc
0.01 X 1.8cc= 0.018mg
0.04/0.018=2.22 carpules
• In a healthy adult patient
0.2/0.018=11.1 carpules 63

Local Anesthesia
Armanterium
1.) The Syringe
2.) The Needle
3.) The Cartridge
4.) Other Armamentarium
- Topical Anesthetic (strongly
recommended) -ointments, gels, pastes,
sprays
- Applicator sticks
- Cotton gauze
64

TYPES OF SYRINGES
65

Plastic disposable syringe
66

Syringe Components
1.) Needle adapter
2.) Piston with harpoon
3.) Syringe barrel
4.) Finger grip
5.) Thumb ring
67

• American Dental Association (ADA) criteria
for acceptance of LA syringes:
1-Durable and re-sterilzable or packaged in a
sterile container (if disposable).
2-Accept a wide variety of cartridges and needles
of different manufactures (universal use)
3-Inexpensive, light weight, and simple to use with
one hand.
4-Provide effective aspiration and the blood be
easily observed in the cartridge. The incidence of
positive aspiration may be as high as 10%-15%
in some injection techniques. 68

Needle
• The Needle Gauge: the larger the
gauge the smaller the internal
diameter of the needle Usual dental
needle gauges are 25,27, & 30
Length:
1-Long(approximately 40 mm "32-40
mm"), for NB.
2-Short(20-25 mm).
3-Extra-short(approximately 15 mm),
for PDL. 69

Components of needle
70

Cartridge
• The Cartridge Components:
- Cylinder, plunger, diaphragm
- Types: Standard – Self aspirating,
plastic, Glass
- Contents: LA, VC, Vehicle,
preservative.
- Volume: 1.8, 2.00 & 2.2 ML.
71

• The Cartridge:
- Should not be autoclaved Stored at
room temperature (21°C to 22°C
(70°F to 72°F)
- Should not soak in alcohol
- Should not be exposed to direct
sunlight
72

INJECTION
TECHNIQUES
• MAXILLARY :
1) Supraperiosteal
2) PDL
3) Intraseptal Injection
4) Intracrestal Injection
5) Intraosseous Injection
6) PSA Nerve Block
7) MSA Nerve Block
8) ASA Nerve Block
9) Maxillary Nerve Block
10) Greater Palatine Nerve Block
11) Nasopalatine Nerve Block
12) AMSA Nerve Block
13) P-ASA Nerve Block 73

Supraperiosteal injection
74

Posterior superior
alveolar nerve block
75

Anterior superior alveolar
nerve block
76

Palatal Anasthesia
• Greater palatine
nerve block
• Nasopalatine
nerve block
77

• MANDIBULAR INJECTION
TECHNIQUES:
1) IANB Nerve block
2) Buccal Nerve Block
3) Mandibular nerve block
techniques:
- Gow Gates technique
- Vazirani Akinosi closed mouth
mandibular block
4) Mental Nerve block
5) Incisive nerve block
78

Inferior alveolar nerve
block
79

Buccal nerve block
80

Gow gates technique
81

Vazirani-Akinosi
technique
82

Mental nerve block
83
INCISIVE NERVE BLOCK

84

Local
Complications
1) Needle breakage :
Prevention
• Do not use short needles for inferior alveolar
nerve block in adults or larger children.
• Do not use 30-gauge needles for inferior
alveolar nerve block in adults or children.
• Do not bend needles when inserting them into
soft tissue.
• Do not insert a needle into soft tissue to its hub,
unless it is absolutely essential for the success of
the injection.
• Observe extra caution when inserting needles in
younger children or in extremely phobic adult or
child patients.
85

2) Prolonged Anesthesia or Paresthesia
• Strict adherence to injection protocol
• Most paresthesias resolve within approximately
8 weeks to 2 months without treatment.
• Determine the degree and extent of paresthesia.
• Explain to the patient that paresthesia
• Record all findings
• Second opinion
• Examination every 2 months
• It would be prudent to contact your liability
insurance carrier should the paresthesia persist
without evident improvement beyond 1 to 2
months.
86

3) Facial Nerve palsy
• Reassure the patient
• Contact lenses should be removed until
muscular movement returns.
• An eye patch should be applied to the
affected eye until muscle tone returns
• Record the incident on the patient's chart.
• Although no contraindication is known to
reanesthetizing the patient to achieve
mandibular anesthesia, it may be prudent
to forego further dental care at this
appointment.
87

4) Trismus
• Prescribe heat therapy, warm saline
rinses, analgesics (Aspirin 325 mg)
• If necessary, muscle relaxants to manage
the initial phase of muscle spasm -
Diazepam (approximately 10 mg bid)
• Initiate physiotherapy
• Antibiotics should be added to the
treatment regimen described and
continued for 7 full days
• Patients report improvement within 48 to
72 hours
88

5) Soft tissues injury
• Analgesics, antibiotics, lukewarn
saline rinse, petroleum jelly
• Cotton roll placed between lips and
teeth, secured with dental floss,
minimizes risk of accidental
mechanical trauma to anesthetized
tissues.
89

6) Hematoma :
• Hematoma is not always preventable. Whenever
a needle is inserted into tissue, the risk of
inadvertent puncturing of a blood vessel is
present.
• When swelling becomes evident during or
immediately after a local anesthetic injection,
direct pressure should be applied to the site of
bleeding.
• For most injections, the blood vessel is located
between the surface of the mucous membrane
and the bone; localized pressure should be
applied for not less than 2 minutes. This
effectively stops the bleeding.
• Ice may be applied to the region immediately on
recognition of a developing hematoma.
90

7) Pain on injection
• Adhere to proper techniques of injection,
both anatomic and psychological.
• Use sharp needles.
• Use topical anesthetic properly before
injection.
• Use sterile local anesthetic solutions.
• Inject local anesthetics slowly.
• Make certain that the temperature of the
solution is correct
• Buffered local anesthetics, at a pH of
approximately 7.4, have been
demonstrated to be more comfortable on
administration 91

8) Burning on Injection
• By buffering the local anesthetic solution
to a pH of approximately 7.4 immediately
before injection, it is possible to eliminate
the burning sensation that some patients
experience during injection of a local
anesthetic solution containing a
vasopressor.
• Slowing the speed of injection also helps
92

9) Infection :
• Use sterile disposable needles.
• Properly care for and handle
needles.
• Properly prepare the tissues before
penetration.
• Prescribe 29 (or 41, if 10 days)
tablets of penicillin V (250-mg
tablets).
• Erythromycin may be substituted if
the patient is allergic to penicillin.
93

10) Edema
If edema occurs in any area where it compromises breathing, treatment
consists of the following:
• P (position): if unconscious, the patient is placed supine.
• A-B-C (airway, breathing, circulation): basic life support is administered,
as needed.
• D (definitive treatment): emergency medical services (e.g., 9-1-1) is
summoned.
• Epinephrine is administered: 0.3 mg (0.3 mL of a 1:1000 epinephrine
solution) (adult), 0.15 mg (0.15 mL of a 1:1000 epinephrine solution)
(child [15 to 30 kg]), intramuscularly (IM) or 3 mL of a 1:10,000
epinephrine solution intravenously (IV-adult), every 5 minutes until
respiratory distress resolves.
• Histamine blocker is administered IM or IV.
• Corticosteroid is administered IM or IV.
• Preparation is made for cricothyrotomy if total airway obstruction
appears to be developing. This is
• extremely rare but is the reason for summoning emergency medical
services early.
• The patient's condition is thoroughly evaluated before his or her next
appointment to determine the cause of the reaction.
94

10) Sloughing of tissue
• Usually, no formal management is
necessary for epithelial
desquamation or sterile abscess. Be
certain to reassure the patient of this
fact.
• For pain, analgesics such as aspirin
or other NSAIDs and a topically
applied ointment (Orabase)
• The course of a sterile abscess may
run 7 to 10 days
95

11) Postanesthetic Intra-oral lesion:
• Primary management is symptomatic
• No management is necessary if the pain is not
severe
• Topical anesthetic solutions (e.g., viscous
lidocaine)
• A mixture of equal amounts of diphenhydramine
(Benadryl) and milk of magnesia rinsed in the
mouth effectively coats the ulcerations and
provides relief from pain.
• Orabase, a protective paste, without Kenalog can
provide a degree of pain relief.
• A tannic acid preparation (Zilactin) can be
applied topically to the lesions extraorally or
intraorally (dry the tissues first).
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Systemic complications
 Adverse drug reaction
• Toxicity Caused by Direct Extension of the Usual
Pharmacologic Effects of the Drug:
1) Side effects
2) Overdose reactions
3) Local toxic effects
• Toxicity Caused by Alteration in the Recipient of the
Drug:
1) A disease process (hepatic dysfunction, heart failure,
renal dysfunction)
2) Emotional disturbances
3) Genetic aberrations (atypical plasma cholinesterase,
malignant hyperthermia)
4) Idiosyncrasy
• Toxicity Caused by Allergic Responses to the Drug 97

CLINICAL MANIFESTATION OF
LOCAL ANESTHETIC OVERDOSE
SIGNS:
LOW TO MODERATE OVERDOSE LEVELS:
 Confusion
 Talkativeness
 Apprehension
 Excitedness
 Slurred speech
 Generalized stutter
 Muscular twitching, tremor of face and extremities
 Elevated BP, heart rate and respiratory rate
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MODERATE TO HIGH BLOOD LEVELS:
 Generalized tonic clonic seizure, followed by
 Generalized CNS depression
 Depressed BP, heart rate and respiratory rate
SYMPTOMS:
 Headache
 Light headedness
 Auditory distrurbances
 Dizziness
 Blurred vision
 Numbness of tongue and perioral tissues
 Loss of consciousness
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Management of systemic
complications
1) Basic emergency management : A-B-C-D
approach
2) Allergy : Medical history questionnaire is
important.
3) Elective dental care
4) Emergency dental care:
- Protocol no.1 : no treatment of an invasive
nature
- Protocol no.2 : use general anesthesia
- Protocol no.3: Histamine blockers
- Protocol no.4 : Electronic dental
anesthesia/hypnosis
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LA Management For
Special Patients
• Uncooperative child
The maximum safe dose of lidocaine
for a child is 4.5 mg/kg per dental
appointment.
Local infiltration of anesthesia is
sufficient for all dental treatment
procedures in 90% of cases even in
the mandible.
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• Handicapped Patient
• retarded patients
choose a shorter needle and/or
a larger gauge needle which is
less likely to be bent or broken.
better to use general anesthesia
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• Patients receiving anticoagulation or suffering
from bleeding disorders
 Oral procedures must be done at the beginning of
the day & must be performed early in the week,
allowing delayed re-bleeding episodes, usually
occurring after 24-48 h, to be dealt with during
the working weekdays.
 Local anesthetic containing a vasoconstrictor
should be administered by infiltration or by
intraligamentary injection wherever practical.
X Regional nerve blocks should be avoided when
possible.
 Local vasoconstriction may be encouraged by
infiltrating a small amount of local anesthetic
containing adrenaline (epinephrine) close to the
site of surgery.
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PREGNANCY
104
• Lidocaine + vasoconstrictor: most
common local anesthetic used in
dentistry extensively used in
pregnancy with no proven ill effects,
Esters are better to be used.
• Accidental intravascular injections
of lidocaine pass through the
placenta but the concentrations are
too low to harm fetus.

GERIATRIC PATIENT
– When choosing an anesthetic, we are largely
concerned with the effect of the anesthetic
agent upon the patient's cardiovascular and
respiratory systems.
– increased tissue sensitivity to drugs acting on
the CNS
– Decreased hepatic size and blood flow may
reduce hepatic metabolism of drugs
– hypertension is common and can reduce renal
function
– Same prevention procedures used with
children
105

LIVER DISORDERS
– Advanced liver diseases include:
 Liver cirrhosis - Jaundice
- Potential complications:
1 . Impaired drug detoxication e.g. sedative,
analgesics, general anesthesia.
2. Bleeding disorders ( decrease clotting factors,
excess fibrinolysis, impaired vitamin K
absorption).
3. Transmission of viral hepatitis.
Management
– Avoid LA metabolized in liver: Amides
(Lidocaine, Mepicaine), esters should be used
106

DRUG-DRUG
INTERACTION
107

RECENT
ADVANCEMENTS
108

Recent developments in local anesthesia and oral sedation.
2003 Journal of anesthesia
• Yagiela JA.
Abstract
• This article reviews 3 recent developments in anxiety and
pain control with significant potential for altering dental
practice. First is the introduction of articaine
hydrochloride as an injectable local anesthetic.
Although articaine is an amide, its unique structure allows
the drug to be quickly metabolized, reducing toxicity
associated with repeated injections over time. The second
development is the formulation of a lidocaine and
prilocaine dental gel for topical anesthesia of the
periodontal pocket. This product may significantly reduce
the need for anesthetic injections during scaling and root
planing. Finally, the use of triazolam as an oral
sedative/anxiolytic is reviewed. The recent administration
of triazolam in multiple doses has extended the availability
of anxiety control to many dental patients, but unknowns
about the safety of the technique as practiced by some
dentists remains a concern.
109

Eutectic mixture of local anesthesia
(EMLA)
110
surface anesthesia for intact skin.

• DentiPatch (lidocaine transoral
delivery system) Preinjection – 10-
15 minutes exposure prior to
injection - Root scaling/planing –
apply 5-10 minutes prior to
beginning procedure.
111

• PRESSURE SYRINGE :
Used in IL injection techniques,
especially in mandibular teeth
(types: pistol-grip, pen-grip).
112

113

114

115

116

CONCLUSION
• Please Remember !!!
- Principle 1- No drug ever exerts a
single action
- Principle 2- No clinically useful
drug is entirely devoid of toxicity
- Principle 3- The potential toxicity of
a drug rests in the hands of the user
117

References
• Handbook of local anesthesia –
Stanley F Malamed – 6th edition
• Essentials of Local Anesthetic
Pharmacology : Daniel E Becker :
Anesth Prog. 2006 Fall; 53(3): 98–
109.
• Vasoconstrictors in local anesthesia
for dentistry: A. L. Sisk; Anesth
Prog. 1992; 39(6): 187–193.
118

• Local anesthetic failure associated
with inflammation: verification of
the acidosis mechanism and the
hypothetic participation of
inflammatory peroxynitrite :
Takahiro Ueno et al ; Journal of
Inflammation Research; November
2008 Volume 2008:1 Pages 41 - 48
• Advanced techniques and
armamentarium for dental local
anesthesia; Clark TM; Dent Clin
North Am. 2010 Oct;54(4):757-68
119

• Advances in dental local anesthesia
techniques and devices: An update ;
Payal Saxena et al: National Journal
of Maxillofacial Surgery | Vol 4 |
Issue 1 | Jan-Jun 2013.
120

THANK YOU!
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