includes all about LA except the techniques

1. GOOD
MORNING
5/21/2018
1

2. LOCAL
ANESTHETICS
Prepared by,
Dr.Sachin Sunny Otta
1st yr MDS
Rajarajeswari Dental
College & Hospital,
Bangalore

3. CONTENTS
1. Introduction
2. History
3. Electrophysiology of nerve conduction
4. Theories of pain
5. Properties of ideal anaesthetics
6. Mode & site of action of LA
7. Theories of LA action
8. Constituents of LA
9. Dissociation of LA
10. Pharmacokinetics of LA
11. Classification of LA
12. Armamentarium
13. Preoperative evaluation of patients before LA
14. Duration of LA
15. Systemic actions of LA
16. Local anaesthetic agents
17. Topical anaesthesia
18. Effect of inflammation on LA administration
19. Complications of LA
20. LA in special patients
21. Recent advances in LA
22. Conclusion
23. Bibliography
5/21/2018
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4. INTRODUCTION
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..
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5. HISTORICAL
BACKGROUND
• COCAINE -first local anesthetic agent isolated by
NIEMAN in 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 & diethyl amino ethanol
• Its anesthetic properties were identified by
BIBERFIELD and the agent was introduced
into clinical practice by BRAUN.
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6. • LIDOCAINE- LOFGREN in 1948.
• The discovery of its anesthetic properties was
followed in 1949 by its clinical use by T.GORDH.
series of potent anesthetic
with a wide spectrum of
soon
clinical
• Thereafter,
followed
properties.5/21/2018
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7. ELECTROPHYSIOLOGY OF
NERVE CONDUCTION
• At rest: Na+& K+ channels closed. -70mV
outside
inside
Resting potential of neuron = -70mV
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8. • Fibre stimulated: Na+channel opens, Na+ enters
cell. Potential rising
Slow depolarisation
Rapid depolarisation
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9. • 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
Repolarisation
• Depolarization takes 0.3 msec
• Repolarization takes 0.7 msec
• The entire process require 1 msec5/21/2018
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10. 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.
Conduction rate of myelinated fibers is 120m/sec.5/21/2018
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11. THEORIES OF PAIN
Specific Theory (Descartes in 1644)
Proposed that pain transmission is through sensory
fibers. Vany Prey – developed the concept of specific
receptors for sensation of touch, heat, cold and pain. Free
nerve endings were implicated as pain receptors
Pattern Theory
Particular patterns of nerve impulses that evoke pain are
produced by the summation of sensory input within the
dorsal horn of the spinal column. Pain result when the
total output of the cells exceeds a critical level.
Gate Control Theory (Melzakc and Wall in 1965)
Information about the presence of injury is transmitted to
the CNS by small peripheral nerves
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12. 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
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13. MECHANISM OF ACTION OF LOCAL
ANESTHETICS
THEORIES
The nerve membrane is the site as which LA exert their
pharmacological action.
There are many theories explaining the mechanism of
action of LA. They include:
1. Acetyl choline theory
2. Calcium displacement theory
3. Surface charge repulsion theory
4. Membrane expansion theory
5. Specific receptor theory
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14. 1.Acetyl Choline theory
Acetyl choline theory started that acetyl
choline was involved in nerve conduction to its role in
neurotransmitters nerve synapses. But there is no
evidence that acetyl choline is involved in neural
transmission
2.Calcium Displacement Theory
This theory stated that LA nerve block was
produced by displacement of calcium from same
membrane site in a controlled permeability to sodium.
Evidences that varying the concentration of calcium
ions bathing a nerve does not affect LA potency has
diminished the credibility of this theory.
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15. 3.Surface Charge (Repulsion) Theory
Proposed that LA acted by binding to the nerve
membrane and changing the electrical potential at the
nerve membrane.
Current evidence indicates that the resting membrane
potential is unaltered. Theory also fails to explain
action of uncharged anesthetic molecules.
4.Specific Receptor Theory
LA acts by binding to specific receptors on the
sodium channel. The action of drug is direct, not
mediated by some change in the general properties of
the cell membrane.Once LA has gained access to the
receptor,permeability to Na is decreased or eliminated
and nerve conduction is interpreted.
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16. 5.Membrane Expansion
This theory states that LA Molecules diffuse to
hydrophobic regions of excitable membranes,
producing a general disturbance of bulk membrane
structure, expanding some critical regions in
membranes and preventing an increase in permeability
to Na+ ions
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17. MECHANISM OF ACTION OF
LOCAL ANESTHETICS
Displacement of calcium ions from the sodium
channel receptor site
Binding of local anesthetic molecule to this
receptor site
 Blockade of sodium channel
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…
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18. PROPERTIES OF IDEAL ANESTHETIC
• Action should be reversible
• Non irritating to tissues & will not produce
secondary local reactions
• Low systemic toxicity
• Rapid onset of action and sufficient duration.
• Sufficient potency to give complete anesthesia
without use of harmful concentrated solution
• Sufficient penetrating property to be effective as a
topical anesthetic.
• No allergic reaction.
• Stable in solution and have ready biotransformation
in body.
• Sterile or capable of being sterilized by heat without
deterioration
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19. CONSTITUENTS OF LOCAL
ANESTHETICS
1. Local anesthetic drug: It prevents impulse
propagation.
2. Vasopressin or vasoconstrictive drug
3. Preservative for vasopressor
sodiumbisulphite or sodium meta bisulphate
[prevent oxidation of the vasopressor]
4. NaCl or Ringer solution
To make the solution isotonic
5. Distilled water
Diluents to provide volume to the solution
6. General preservative
To increase the shelf life
e.g:Methylparaben - Bacteriostatic agent
Thymol-Antiseptic,fungistatic and antihelminthic.
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20. VASOCONTRICTORS
These are chemical agents or adjuvants added to the
local anesthetic solution:
• To oppose vasodilatations caused by these
agents
• To achieve haemostasis
Mode of action:-
• Decrease blood flow to the site of injection by
vasoconstriction
• Decrease the rate of absorption of Local anesthetics
into CVS
• Increased amount of local anesthetics remain in and
around the nerve for longer period , thus increasing
the duration of action
• Decreased bleeding at the site of administration
• Decreased plasma level of local anesthetics –
decreased risk of systemic toxicity5/21/2018
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21. Categories:-
• Direct acting – exert direct action on adrenergic
receptors. e.g.:- epinephrine, nor- epinephrine,
dopamine
• Indirect acting – act by releasing nor –
epinephrine from adrenergic nerve terminals e.g.:-
amphetamine
• Mixed acting – both direct and indirect action
Dilution of vasoconstrictors:-
Commonly referred to as RATIO.
Eg; 1:1000
1gm drug in 1000ml solution ie; 1000mg in 1000 ml or
1mg/ml
Usual doses:
1:80000 ie; 0.0125mg/dl
1:100000 ie; 0.01mg/dl
1:200000 ie;0.005mg/dl5/21/2018
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22. Systemic action:-
Myocardium- Stimulate beta-1 receptors-increased force & rate of
contraction leading to increased cardiac output and heart rate
Pacemaker cell- increased irritability leads to dysrhythmia
Coronary artery: dilatation – increased coronary blood flow
Blood pressure- systolic BP increases
diastolic BP – small doses decreases , large doses
increases
CVS- Increased heart rate , cardiac output and stroke volume
Blood vessel : Alpha receptors – vasoconstriction
Beta receptors - vasodilatation
Rebound phenomenon – at high concentrations alpha
effect exists i.e.: vasoconstriction and thus achieving haemostasis.
During biotransformation, reuptake occurs leading to decreased
tissue level and beta receptors are stimulated – vasodilatation and
bleeding5/21/2018
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23. Respiratory system- Alpha 2 receptors potent
vasodilator – useful in bronchospasm
CNS- Excessive dose - stimulation
Contraindications Of Vasoconstrictors In LA:-
1. CVS diseases
2. Hyperthyroidism, diabetes mellitus
3. Patients taking monoamino-oxidase inhibitors,
beta blockers, tricyclic anti depressants etc
4. Patients with sulphite sensitivity
5. Pregnancy
6. Patient undergoing general anesthesia with
halogenated agents
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24. Maximum 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
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25. 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+
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26. • 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+
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27. • 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
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28. 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.
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29. • 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)
RNH+
> RN+
+ H+
• 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 non ionized
forms; but there are fewer cations which may cause
incomplete anesthesia.
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30. PHARMACOKINETICS OF LA
• When injected into soft tissue LA exert a
pharmacological action on the blood vessels in
that area. They produce various degree of
vasoactivity mostly producing dilation of
vascular bed.
• Cocaine is the only LA consistently producing
vasoconstriction. It first produced vasodilatation
and then it produces intense and prolonged
vasoconstriction.
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31. ORAL ROUTE
• With exception of cocaine, LA is absorbed poorly.
Most undergo hepatic first pass metabolism in liver.
• TOCAINIDE HYDROCHLORIDE an analogue of
lidocaine is effective orally
TOPICAL ROUTE
• In tracheal mucosa the absorption is rapid when
comparable to IV. In pharyngeal mucosa absorption
is slower and is still slower in esophageal or
bladder mucosa.
• Eutectic mixture of local anesthesia (EMLA) has
been developed to provide surface anesthesia for
intact skin.
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32. INJECTION
• Rate of uptake of LA is defined on vascularity.
Sudden LA administration through IV route can
induce serious toxic reactions
DISTRIBUTION
• Once absorbed into the nerve, LA is distributed
throughout the body to all tissues. The blood level
of LA are influenced by the following factors:
1. Rate at which the drug is absorbed into CVS.
2. Elimination of drug through metabolic/ excretory
pathways.
• All local anesthetic agents readily cross the blood-
brain barrier, they also readily cross the placenta
METABOLISM
• There is a significant difference between the
metabolism of two major groups of LA.5/21/2018
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33. Ester Local Anesthetics
Ester local anesthetic are hydrolyzed in the plasma by
the enzyme pseudo – cholinesterase.
Amide Local Anesthetics
The biotransformation of amide local anesthetics is
more complex than that of the ester. The primary site
of biotransformation of amide drug in the liver.
EXCRETION
• The kidneys - primary excretory organ for both the
local anesthetic and its metabolites. A percentage of
a given dose of local anesthetic is excreted
unchanged in urine, which varies according to drug.
• Esters appear in only very small concentrations.
• Amides are present in the urine as a parent
compound in a greater percentage than are esters.5/21/2018
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34. CLASSIFICATION OF LA
The local anesthetics used in dentistry are divided into
two groups:
ESTER GROUP
AMIDE GROUP
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35. ESTER GROUP
• An aromatic lipophilic group
• An intermediate chain containing an ester linkage
• A hydrophilic secondary or tertiary amino group
Esters of benzoic acid
Butacaine
Cocaine
Benzocaine
Hexylcaine
Tetracaine
Esters of Para-amino
benzoic acid
Chloroprocain
Procaine
Propoxycaine
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36. AMIDE GROUP
• An aromatic, lipophilic group
• An intermediate chain containing amide linkage
• A hydrophilic secondary or tertiary amino group
AMIDES
Articaine
Bupivacaine
Dibucaine
Etidocaine
Lidocaine
Mepivacaine
Prilocaine
Ropivacaine
QUINOLINE:
Centbucridine
ABCDE LMPR
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37. Based on Biological site and mode of action:
CLASSIFICATION DEFINITION CHEMICAL SUBSTANCE
Class A Agents acting at the
receptor site on
external surface of
nerve membrane
Biotoxins. [e.g.:-
tetradotoxins,
saxitoxin]
Class B Acting on the internal
surface
Quaternary
ammonium analogues
of lidocaine
Class C Receptor independent
– act via
physiochemical
mechanism
Benzocaine
Class D Combination of
receptor and receptor
independent
mechanism
Most clinically useful
local anesthetics
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38. Based on mode of administration:
Injectable
• Low potency short duration – Procaine,
Chloroprocaine
• Intermediate potency and duration –
Lignocaine, Prolocaine
• High potency long duration – Tetracaine,
bupivacaine
Surface agents
• Soluble – Cocaine, lignocaine, tetracaine
• Insoluble – benzocaine, butylaminobenzoate
Local anesthesia can be produced by cooling as well.
Eg;- application of ice, carbondioxide snow, ethyl
chloride spray
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39. Based on
duration of
action
Ultra short Short Medium Long
Pulpal = < 10 min
Soft tissue = 30 –
45 min
•Chlorprocaine
•Procaine
Pulpal = 5-10 min
Soft tissue = 60 –
120 min
•Lidocaine
•Prilocaine
Soft tissue = 120 –
240 min
•Mepivacaine
•Artricaine
Pulpal = 45 – 90 min Pulpal = 90 –180
min
Soft tissue = 240
– 540 min
•Bupivacaine
•Etidocaine
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40. Based on
potency
LOW INTERMEDIATE HIGH
•Procaine
•Chlorprocaine
•Lidocaine
•Mepivacaine
•Tetracaine
•Bupivacaine
•Dibucaine
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41. ARMAMENTARIUM
1. The Syringe
2. The Needle
3. The Cartridge
4. Other Armamentarium
- Topical Anesthetic (strongly recommended) -
ointments, gels, pastes, sprays
- Applicator sticks
- Cotton gauze
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42. SYRINGE
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43. Plastic disposable syringe: Commonly used
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44. Syringe components:-
1.) Needle adapter
2.) Piston with harpoon
3.) Syringe barrel
4.) Finger grip
5.) Thumb ring
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45. 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.
Components of needle:-
5/21/2018
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46. CATRIDGE
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.
• 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
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47. FACTORS DETERMINING
SELECTION OF LA FOR A
PATIENT
1. Length of time of pain control is necessary.
2. Potential need for post treatment pain control
3. Possibility of self-mutilation in the
postoperative period
4. Requirement for haemostasis
5. Presence of any contraindication to theLA
solution selected for administration
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48. COMMON QUESTIONS TO ASK
THE PATIENT
• Allergic to any medications?
• Have you ever had a reaction to local
anesthesia?
• If yes, describe what happened
• Was treatment given? If so, what?
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49. PREPARATION OF THE
PATIENT
• Careful preoperative assessment
• History
• A clear explanation of what to expect
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50. PREOPERATIVE ASSESSMENT
1. Baseline vital signs: 1.blood pressure
2.laboratory
values
3.Results of ECG
monitoring
4.any other tests.
2. Weight, height, and age:
 Dosage of some drugs is calculated on the
basis of body weight in kilograms (mg/kg).
 Some drugs are contraindicated for age extremes
(i.e., pediatric or geriatric patients).
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51. 3. Current medical problem(s) past history of
medical events, including a history of substance
abuse.
4. Current medications or drug therapy, such as
insulin for diabetes or hypertensive drugs.
5. Allergy, or hypersensitivity reactions to previous
anesthetics or other drugs.
6. Mental status including emotional state and
level of consciousness.
7. Communication ability A patient with hearing
impairment or language barrier may be unable
to understand verbal instructions during the
procedure or to respond appropriately
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52. DURATION OF LOCAL
ANESTHETIC ACTION
Examples
• Local Infiltration
Lidocaine
30-60 min
Bupivacaine
120-240
• Minor Nerve Block 60-120 180-360
• Major Nerve Block 120-240 360-720
• Epidural 30-90 180-300
• Addition Of Epi improved improved
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53. SYSTEMIC ACTIONS OF LA
LA reversibly block action potentials in all
membranes. The CNS and CVS therefore are
especially susceptible to their actions.
CENTRAL NERVOUS SYSTEM
LA readily cross blood brain barrier. Their
pharmacological action is CNS depression. At low
blood level there is no CNS effects. At high levels
there will be tonic – clonic convulsions.
1.Anti Convulsant properties
• Depressant action on CNS
• Decreasing the excitability of neurons, thereby
preventing or terminating seizures.
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54. 2.Analgesic
• Increase pain reaction threshold and also
produce a degree of analgesia
3.Mood Elevation
• Mood elevation and rejuvenation.
• Cocaine has been used for its euphoric inducing
and fatigue lessening action.
CARDIOVASCULAR SYSTEM
LA’s have directed action on the myocardium and
peripheral vasculature.
Direct Action In Myocardium:
• LAs modify electrophysiological events in
myocardium.
• Various phases of myocardial depolarization is
reduced.
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55. • There is no change in resting membrane potential
and no significant prolongation of phases of
repolarisation.
Direct Action On Peripheral Vasculture:
• The primary effect of LA on blood pressure is
hypotension
• Cocaine is the only drugs that consistently
produce vasoconstriction at commonly employed
doses. Ropivacaine produces cutaneous
vasoconstriction & all other LA produce
peripheral vasodilatation.
RESPIRATORY SYSTEM
• LA produced dual effect on respiration.
• At non overdose levels - direct relaxant action on
bronchial smooth muscle
• At over dose levels - respiratory arrest due to
CNS depression5/21/2018
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56. NEUROMUSCULAR BLOCKADE
• Inhibition of sodium diffusion through a blockade
of Na channels in cell membrane.
• This may lead to abnormally prolonged period of
muscle paralysis
• LA decrease electrical excitability of
myocardium, decrease the conduction rate &
decrease the force of contraction.
• Increased blood level greater than therapeutic
level reads to circulatory collapse.
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57. LOCAL ANESTHETICS
Non – ester derivatives
LIDOCAINE
• First non ester type LA to be used in dentistry
• Synthesized in 1943 by LofGren.
• It represents the GOLD STANDARD DRUG, to
which all new compounds are compared.
• Potency & toxicity - twice that of procaine
• Metabolism – in liver by microsomal fixed function
oxidases to monoethaneglycine & xylidide.
• Excretion – via kidney (< 10% unchanged & >80%
as various metabolites)
• Vasodilating property <Procaine but >Prilocaine or
Mepivacaine.
• pH of
* plain solution = 6.5
* vasoconstrictor containing solution = 5 – 5.55/21/2018
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58. • Onset of action – rapid [ 2 – 3 mts]
• Effective dental concentration = 2%
• Maximum acceptable dose = 4.4mg/kg
• Anesthetic half life = 90mts
• Topical anesthetic action in clinically acceptable
concentration = 5%
• Pregnancy classification = B
• Safe during lactation
• Anti arrhythmic
• 2% lignocaine with 1: 50000 epi. – hemostasis
• 2% lignocaine with 1: 100000 or 1:
200000 epi.– local anesthesia
• Major clinical advantage over ester type is that
allergy is virtually non existent for them.
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59. MEPIVACAINE
• 2 times as potent & toxic as procaine.
• Moderately long duration of action.
• Its action within the body is similar to Lignocaine.
PRILOCAINE
• Similar to lidocaine in some respect, but its
absorption from injection site is less rapid than
lidocaine
• Lesser degree of toxicity to CNS than lidocaine
• Disadvantage – its metabolite orthotoluidine produce
methemoglobinemia, so contraindicated in patients
with congenital or idiopathic methemoglobinemia
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60. BUPIVACAINE
• It has 35 fold increase in oil water partition
coefficient (a factor that greatly increases fat
solubility + a significant increase in protein
binding qualities)
• 4 fold increase in intrinsic anesthetic activity &
significant prolongation of duration
ETIDOCAINE
• Structural modification of lidocaine
• 50 fold increase in oil water partition coefficient
• 2 times protein binding characteristic
• Faster onset & longer duration
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61. Ester derivatives
PROCAINE
• Useful in immediate management of inadvertent intra-
arterial injection of drugs, its vasodilation property is
used to aid in breaking arteriospasm.
• Rarely used now, due to risk of allergy.
TETRACAINE
• Compatible with sulfonamides & can be combined
with all vasoconstrictors.
• Popular for spinal anesthesia.
• In dentistry it is limited to topical application.
PROPOXYCAINE
• Rapid onset of action.
• Potency & toxicity similar to tetracaine.
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62. 2-CHLOROPROCAINE
• More potent & less toxic than procaine.
• Hydrolysed 4-5 times faster than procaine. So it
has got a favorable therapeutic index.
• Useful in dentistry only when anesthesia of very
short duration needed.
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63. TOPICAL ANESTHETICS
• Topical anesthesia is that form of anesthesia
obtained by direct application of drug to abraded
skin or to mucous membrane surface. Effective only
on surface tissues [2 – 3 mm].
• Poorly soluble in water and do not form soluble acid
salts.
• Effective whenever skin is no longer intact or on
mucous membrane.
• Buffering capacity of mucous membrane is low. So
LA used here are in a more concentrated form. [5% -
10% lidocaine] than for injection [as concentration
increases number of base available also increases]
• Easy diffusion through mucous membrane.
• Potent vasodilators and do not contain
vasoconstrictor.
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64. • Benzocaine is the common topical anesthetic agent
1. Unaffected by pH.
2. Poor water solubility; its absorption from the site
of applications is minimal & systemic reactions are
rare.
• Localized irritation & allergic reactions are noted
after prolonged or rapid use.
Benzocaine + Vasopressor used.
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65. EFFECT OF INFLAMMATION ON
LOCAL ANESTHETICS
• Local anesthetic injection is in its acid salt forms
to improve water solubility.
• In tissue it is rapidly neutralized by tissue fluid
buffers & RN [bases] from which it is able to
penetrate neural membrane.
• During infection, tissue pH decreases(pH 5.5).
• Increased acidity increases the ionization of LA
• Lesser penetration of LA into nerves
• Delay the onset of anesthesia and possibly
interfere with nerve blockade.
• It causes unusual dilation of blood vessels – rapid
uptake of anesthetic from site of injection– blood
levels elevated.
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66. 2 primary methods of obtaining anesthesia on this
condition are:-
• Administer LA away from area of inflammation
- undesirable to inject the area of inflammation
- possibility of spreading infection to uninvolved
regions.
- Adequate pain control due to more normal tissue
condition. Regional nerve block anesthesia is a major
factor in pain control for pulpal involved teeth.
• Deposit a large volume of anesthetic into region
providing greater number of unchanged base molecules
able to diffuse through nerve sheath.
Water soluble – Lignocaine hydrochloride
Insoluble – benzocaine
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67. COMPLICATIONS OF LA
LOCAL COMPLICATIONS
1. Needle Breakage
2. Persistent anesthesia or paresthesia
3. Facial nerve paralysis
4. Trismus
5. Soft Tissue injury
6. Hematoma
7. Pain on injection
8. Burning and injection
9. Infection
10. Edema
11. Sloughing of tissues
12. Post anesthetic intra oral lesions
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68. SYSTEMIC COMPLICATIONS
1. Allergic reactions
2. Overdose reactions
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69. 1.NEEDLE BREAKAGE
Causes:
• weakening of the dental needles by bending it
before insertion into patient mouth
• sudden unexpected movement by patient
• smaller needles
Prevention:
• Use larger gauge needless for techniques requiring
penetration of significant depths of soft tissues.
• Do not use 30-gauge short needles for inferior
alveolar nerve block in adults or children
• Do not insert a needle into tissue to its hub.
• Do not redirect a needle once it is inserted into
tissues.
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70. Management:
When needle breaks:
• Remain calm, do not panic
• Instruct patient not to move
• If fragment is visible move with a small hemostat.
If needle is lost:
• Do not proceed with incident or probing
• Locate it though radiographic examination.
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71. 2.PERSISTENT ANESTHESIA / PARESTHESIA
It is defined as present anesthesia or altered sensation
well beyond the excepted duration.
Cause:
• Trauma to any nerve lead to parathesia.
• Injection of a local anesthetic solution contaminated
by alcohol or sterilizing solution
• Hemorrhage into or around the neural sheath.
Problem:
• It can lead to self inflicted injury.
• Hyperesthesia - Increased sensitivity to stimulus
• Dysesthesia - Pain for sensation occurring to
unusually non noxious stimulus.
Prevention:
• Strict adherence to injection protocol
• Proper care and handling of cartridges
• Resolve within approximately 8 weeks
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72. 3.FACIAL NERVE PARALYSIS
Cause:
Transient facial nerve paralysis is commonly caused by
introduction of LA into capsule of parotid gland.
Problem:
• Loss of motor function of facial expression produced
by LA is transitory. During this time the patient has
unilateral paralysis.
• Patient is unable to voluntarily close one eye.
Prevention:
• A needle tip in contact with bone before depositing
local anesthetic solution virtually produces the
possibility the anesthetic will be deposited into the
parotid gland.
• Contact lenses should be removed until muscular
movement returns.
• An eye patch should be applied to the affected
eye until muscle tone returns5/21/2018
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73. 4.TRISMUS
It is defined as a prolonged tetanic spasm of jaw
muscles by which normal opening of the mouth is
restricted.
Causes:
• Trauma to muscles or blood vessels in the infra
temporal tissue
• Hemorrhage
• A low grade infection after injection.
• Excessive volume of LA solution deposited into a
restricted area produce distension of tissues which
lead to past injection trismus.
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74. Prevention :
• Use sharp, sterile, disposable needle.
• Properly care for handle of dental LA cartridges.
• Use aseptic technique
• Avoid multiple injection into same area.
• Prescribe heat therapy, warm saline rinses,
analgesics (Aspirin 325 mg)
• If necessary, advice 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
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75. 5.SOFT TISSUE INJURY
Cause:
• Occur in children and physically disabled (soft tissue
anesthesia lasts significantly longer)
Prevention:
• LA of appropriate duration should be selected if
dental appointments are brief.
• A cotton roll can be place between lips and teeth if
they are still anesthetized at time of discharge.
• Warn the patient.
• Analgesics, antibiotics, lukewarm saline rinse,
petroleum jelly
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76. 6.HEMATOMA
The effusion of blood into extra vascular spaces can
result from nicking a blood vessel during the injection of
LA.
Cause:
• Hematoma may result from either arterial or venous
puncture after a nerve block.
• Possible complications include trismus and pain
Prevention:
• Direct pressure should be applied to the site of
bleeding(not less than 2 minutes).
• Ice may be applied to the region immediately on
recognition of a developing hematoma.
• Knowledge of normal anatomy.
• Use short needle for PSA nerve block.
• Minimize the number of needle penetration into
tissue.
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77. 7.PAIN ON INJECTION
Causes:
• Careless injection technique.
• A needle can become dull from multiple injections.
• Rapid deposition of LA solution may cause tissue
damage.
• Needles with barbs may produces pain when they are
withdrawn from tissue.
Prevention:
• Adhere to proper techniques of injection both
anatomical and psychological
• Use sharp needles
• Use topical anesthetic properly before injection.
• Use sterile local solutions with pH 7.4
• Inject LA slowly.
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78. 8.BURNING ON INJECTION
Causes:
• pH of the solution.
• Rapid injection of LA especially in the denser & more
adherent tissues of palate.
• Contamination of LA cartridges.
• Solution warmed to normal body temperature usually
are considered ‘Too hot” by the patient.
Prevention:
• Slowing the injection (ideal 1ml/Min)
• The cartridge of LA should be stored in room
temperature
• Buffering the local anesthetic solution to a pH of
approximately 7.4 immediately before injection
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79. 9.INFECTIONS
Causes:
• Contamination of needle before infection
• Injecting LA solution to an area of injection.
Prevention:
• Sterile disposable needles.
• Proper care and handling of needle
• Properly prepare the tissue before penetration
• Prescribe Penicillin V (250-mg tablets).
• Erythromycin may be substituted if the patient is
allergic to penicillin
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80. 10.EDEMA
Cause:
• Trauma during injection
• Infection
• Allergy
• Hemorrhage
• Injection of irritating solutions
Management:
• P-A-B-C-D
• 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.
• Complete and adequate medical evaluation of patient
before drug administration.
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81. 11.SLOUGHING OF TISSUES
Prolonged irritation or ischemia of gingival soft tissues
may lead to a number of unpleasant complications.
Cause:
Epithelial Desquamation
• Application of a topical anesthetic to gingival tissues
for a prolonged period.
• Heightened sensitivity of tissues to LA
• Reaction in area where a topical LA has been applied.
Sterile abscess
Secondary to prolonged ischemia resulting from the use
of LA with vasoconstriction.
Prevention:
• Use topical LA as recommended & when using
vasoconstrictors, never use concentrated solutions.
• 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 days5/21/2018
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82. 12.POST ANESTHETIC INTRA ORAL LESIONS
• Patients occasionally reports that approximately 2
days after injection of LA, reactions developed in
mouth, primarily around sites of injections.
• Reccurent aphthous ulcers
• The cause is unknown.
Prevention:
• 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 tannic acid preparation (Zilactin) can be applied
topically to the lesions extraorally
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83. 5/21/2018
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84. 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 Drug5/21/2018
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85. 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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86. MODERATE TO HIGH BLOOD LEVELS:
 Generalized tonic clonic seizure
 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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87. LA ADMINISTRATION FOR
SPECIAL PATIENTS
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
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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88. 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 hrs, 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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89. Pregnancy
• 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
Liver Disorders
• Avoid LA metabolized in liver: Amides
(Lidocaine, Mepicaine)
• Esters should be used
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90. LOCAL ANESTHETIC USE IN
MEDICALLY COMPROMISED
PATIENTS
2000 JOURNAL OF THE CALIFORNIA DENTAL ASSOCIATION5/21/2018
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91. • Centbucridine
• Ropivacaine
• EMLA
• TENS ( Transcuteneous Electrical Nerve
Stimulation)
• Hyaluronidase
• Ultra –long acting local anesthetics
• Sprays
• Topical gels
• Intraoral lignocaine patch (Dentipatch)
• Iantophoresis
• Jet injection
• Computer controlled system
• Comfort control syringe
• Vibro tactile device
• Ph alteration
• Intra osseous anesthesia
RECENT ADVANCES
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92. RECENT ADVANCES
EUTECTIC MIXTURE OF LOCAL
ANESTHETICS [EMLA]
• EMLA cream [composed of lidocaine 2.5% &
prilocaine2.5%]
• Emulsion in which oil phase is a eutectic mixture of
lidocaine & prilocaine in a ratio 1:1 by weight
• Provide surface anesthesia of intact skin & hence is
used primarily before painful procedures, such as
venipuncture & other needle insertions.
• EMLA has gained popularity among needle phobic
adults & persons having other superficial but
painful procedures performed. E.g.; hair removal.
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93. • EMLA must be applied 1hr before procedure.
Satisfactory numbing of skin occurs 1hr after
application, reaches maximum at 2-3hrs & lasts
for 1-2hr.
• EMLA is supplied in 5gm or 30gm tube or as an
EMLA anesthetic disc.
• EMLA is contraindicated in patients with
congenital or idiopathic methemoglobinemia,
infants under the age of 12months who are
receiving treatment with methemoglobin inducing
agents or patients with a known sensitivity to
amide type LA or any other component of the
product. The product is being redesigned into
child resistant closure tubes. [CRC].
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94. DENTIPATCH (Lidocaine transoral delivery
system)
• Preinjection: 10 - 15 minutes exposure prior to
injection
PRESSURE SYRINGE
 Used in IL injection techniques, especially in
mandibular teeth (Types: pistol-grip, pen-grip).
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95. JET INJECTORS (NEEDLE LESS)
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Mechanical energy source to create a pressure to push a
dose of solution through small orifice

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97. 5/21/2018
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98. 5/21/2018
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99. CONCLUSION
History of local anesthetics starts with the use of
cocaine. Because of advancements in research
newer drugs with less implications and better action
are obtained. LA’s are the safest and most effect
drugs available in medicine for prevention and
management of pain. New local anesthetic cellular
systems also have improved over the years. The past
decade has seen a significant increase in interest in
computer controlled local anesthetic delivery
(CCLAD) system. CCLAD, have increased ability
of doctors to guarantee the pain free delivery of LA
to their patients.
If one can provide a nearly painless surgical
procedure without the use of general anesthesia
then you have won half the battle.
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100. BIBLIOGRAPHY
• Hand book of local anesthesia by Stanley F N
Malamed
• Monheim’s Local anesthesia and pain control in
dental practice
• Manual of local anesthesia in Dentistry A P Chitra
• 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
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101. T
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