Local anesthesia in endodontics

LOCAL
ANESTHESIA
Dr.Hema M
1st year PG
Department of Conservative dentistry and Endodontics
04-07-2021 LocalAnesthesia 1

CONTENTS
■ Definition
■ Historical Background
■ Methods of Inducing Local Anesthesia
■ Ideal Properties of local Anesthetics
■ Classification of Local Anesthetics
■ Classification of Peripheral Nerves
■ Physiology of Nerve Conduction
■ Mode & Site of Action of Local Anesthetics
■ Theories of Mechanism of Action of Local Anesthetics
■ Dissociation of Local Anesthetics

■ Composition of Local Anesthetics
■ Clinical Action of Various Local Anesthetics
■ Factors in Selection of Local Anesthetics for a Patient
■ Pharmacokinetics of Local Anesthesia
■ Vasoconstrictors
■ Classification of Vasoconstrictors
■ Pharmacology of Specific Vasoconstrictors
■ The Armamentarium
■ Local Complications
■ Systemic Complications
■ Conclusions
■ References

DEFINITION
■ Local Anaesthesia has been defined as loss of sensation in a
circumscribed area of the body caused by depression of excitation in
nerve endings or inhibition of conduction process in peripheral nerves.
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Historical background
■ Cocaine – first local anesthetic agent , isolated by Nieman in 1860 from
the leaves of the cocoa tree.
■ It's 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.
■ It's anesthetic properties were identified by Biberfield and the agent was
introduced into clinical practice by Braun.
■ Lidocaine – was discovered by Lofgren in 1948.
■ The anesthetic properties were discovered by T.Gordh in 1949.

Methods of inducing local anaesthesia
■ Low temperature
■ Mechanical trauma
■ Anoxia
■ Neurolytic agents such as alcohol and phenol
■ Chemical agents such as local anaesthetics

Ideal properties of local anesthesia
■ It should not be irritating to the tissue to which it is applied.
■ It should not cause any permanent alteration of nerve structure.
■ Its systemic toxicity should be low.
■ It must be effective regardless of whether it is injected into the tissues or
is applied locally to mucous membranes.
■ The time of onset of anesthesia should be as short as possible.
■ The duration of action must be long enough to permit completion of the
procedure but not so long as to require an extended recovery.

■ It should have potency sufficient to give complete anesthesia without the use of
harmful concentrated solutions.
■ It should be relatively free from producing allergic reactions.
■ It should be stable in solution and should readily undergo biotransformation in
the body.
■ It should be sterile or capable of being sterilized by heat without detoriation.

Classification of local anesthetics
1. Based on the source
I. Natural
II. Synthetic
III. Others
2. Based on mode of application
I. Injectable
II. Topical

3. BASED ON DURATION OF ACTION
i. Ultra Short
ii. Short
iii. Medium
iv. Long
4. BASED ON ONSET OF ACTION
i. Short
ii. Intermediate
iii. Long

5. Based on biological site and mode of action
Sl. No. Classification Definition Chemical Substance
i. Class A Agents acting at receptor sites on
external surface of the nerve membrane.
Biotoxins ( e.g tetrodotoxins, saxitoxin )
ii. Class B Agents acting at receptor sites on
internal surface of the nerve membrane.
Quaternary ammonium analogs of
Lidocaine , Scorpion venom
iii. Class C Agents acting by a receptor-independent
physico-chemical mechanism.
Benzocaine
iv. Class D Agents acting by combination of receptor
and receptor-independent mechanisms.
Local anesthetic agents ( e.g articaine,
lidocaine, prilocaine, mepivacaine )

6. Based on chemical nature
ESTERS AMIDES QUINOLONE
BENZOIC ACID
ESTERS
PABA ESTERS Prilocaine Centbucridine
Cocaine Procaine Lignocaine
Benzocaine Chlorprocaine Bupivacaine
Tetracaine Propoxycaine Ropivacaine
Articaine
Dibucaine

Physiology of nerve conduction
■ Impulses are the messages, in the form of electrical action potentials,
carried from one part of the body to another.
■ Electrical action potentials are transient depolarizations of the membrane
due to increase in the permeability of the membrane to sodium and
delayed increase potassium.
■ Impulse can be initiated by chemical, thermal, mechanical or electrical
stimuli.
■ Once an impulse is initiated, the amplitude and shape remains constant.

Mode & site of action of local anaesthetics
Local anaesthetics interfere with the excitation process in a nerve membrane
in one or more of the following ways:
a. altering the basic resting potential of the nerve membrane.
b. altering the threshold potential (firing level).
c. decreasing the rate of depolarisation.
d. prolonging the rate of repolarization.

Theories of action of local anesthesia
a) Calcium Displacement Theory
b) Acetyl Choline Theory
c) Surface Charge Theory
d) Membrane Expansion Theory
e) Specific Receptor Theory

a. Calcium Displacement Theory
■ Goldman in 1966.
■ According to this theory, local anesthetic nerve
block was due to the displacement of calcium
from the membrane sites that control
permeability to sodium.
■ But, evidences suggest that varying the
concentration of calcium ions bathing a nerve
has no effect on the potency of local anesthesia.
Hence , the theory was discarded.

b. Acetylcholine Theory
■ It was proposed by Dett barn in 1967.
■ This theory suggested that acetyl choline,
a neurotransmitter at nerve synapses,
was involved in nerve conduction as
well.
■ But, lack of evidences failed to support
this theory.

c. Surface Charge Theory (Repulsion Theory)
■ Wei in 1969.
■ The theory suggested, that local anesthetics
act by binding to the nerve membrane and
changing the electrical potential at the
membrane surface.
But some local anesthetic molecules carried net
positive charge, that made the electrical potential
at the membrane surface more positive, thus
decreasing the excitability of the nerve and
hence increasing the threshold potential.
This theory fails to explain the activity of
uncharged anesthetic molecules in blocking the
nerve impulses such as benzocaine.

d. Membrane Expansion theory
■ Lee in 1976.
■ The local anesthetic molecules
diffuse to hydrophobic regions of
excitable membrane structure,
expanding some critical regions in
the membrane and preventing an
increase in permeability to sodium
ions.
■ Local anaesthetics that are highly
lipid soluble can penetrate the lipid
portion of the cell membrane,
producing a change in the
configuration of the lipoprotein
matrix of the nerve membrane..

■ This results in a decreased diameter of the sodium channels and hence inhibits
sodium conductance and neural excitation
■ Thus, this theory explains the local anesthetic activity of drugs such as
benzocaine that do not exist in cationic form, yet exhibit potent topical anesthetic
activity. Nerve membranes, when subjected to local anesthetics, do expand but
then become more fluid. Hence, no direct evidence supports this theory.

e. Specific Receptor Theory:
■ Strichartz in 1987.
■ According to this theory, the specific
receptor sites for local anesthetics exist in
sodium channel either on its external surface
or on the internal axoplasmic surface.
■ Local anesthetics can alter nerve conduction
in at least four sites within the sodium
channel:
i. within the sodium channel(tertiary amine
local anesthetics)

ii. at the outer surface of the sodium channel (tetrodotoxin, saxitoxin).
iii. and iv. at the activation or the inactivation gate(scorpion venom).
This is the most favoured theory. Once LA has gained access to the receptors,
permeability to sodium ions is decreased or eliminated and nerve conduction is
interrupted.
Dissociation of LA can be stated as:
RNHOH + HCL = RNHCL + H2O
(weak base) (strong acid) (acid salt)
RNHCL RNH+ + CL-
RNH+ RN + H+
(cation) (base)

The proposed mechanism of action of local anesthetics is:
a. displacement of calcium ions from the sodium channel receptor site, which
permits
b. binding of the local anesthetic molecule to this receptor site, which produces
c. blockade of sodium channels, and a
d. decrease in sodium conductance, which leads to
e. depression of the rate of electrical depolarization, and
f. failure to achieve the threshold potential level, along with
g. lack of development of propagated action potentials, which is called
h. conduction blockade.

Composition of local anesthetics
1. Local anesthetic agent: Lignocaine Hydrochloride 2%
2. Reducing agent: Sodium metabisulphite(0.5 mg)
3. Preservative: Methylparaben 0.1% (1mg)
4. Diluting agent: Distilled water
5. Fungicide: Thymol
6. Isotonic solution: Sodium chloride
7. Vehicle: Ringerʹs solution(6mg)
8. Vasoconstrictor: Adrenaline-1:80,000(0.012mg)
9. To adjust PH- Sodium Hydroxide
10. Nitrogen bubble

■ Role of individual components
1. Local anesthetic agent – lignocaine HCl 2%- anesthesia.
2. Reducing agent – Sodium Metabisulphite(0.5mg) competes for the
available oxygen and prevents oxidation of the vasoconstrictor in presence of
sunlight.
3. Preservative – Methyl Paraben(0.1%) is to increase the shelf life. Modern
local anesthetic solutions are very stable and often have a shelf life of 2 years
or more and their sterility is maintained by the inclusion of small amount of a
preservative such as capryl hydrocupreinotoxin. Some preservative such as
methyl paraben have shown allergic reaction in sensitized subjects.

4. Distilled water acts as a vehicle.
5. Isotonic solution – Sodium Chloride minimizes discomfort during
injection.
6. Vasoconstrictor - decreases blood flow to the site of injection, prevents
absorption of local anesthetic into the cardiovascular system, decrease the
risk of local toxicity, increases the duration of action and decrease bleeding
at the site of administration.
7. Nitrogen bubble(2mm) in diameter prevents oxygen from being trapped
in the cartridge and potentially destroying the vasoconstrictor.

■ The various local anesthetic agents discussed here are:
1. Procaine
2. Propoxycaine
3. Lidocaine
4. Mepivacaine
5. Prilocaine
6. Bupivacaine
7. Articaine
8. Centbucridine
9. Topical Anesthetic Agents

1. PROCAINE HCL
Classification : ester
Chemical formula: 2-diethylaminoethyl 4-
aminobenzoate hydrochloride
Metabolism : hydrolysed rapidly in plasma by
plasma pseudocholinesterase.
Excretion : more than 2% unchanged in urine
( 90% as PABA, 8% as diethylaminoethanol).
Vasodilating properties : maximum
vasodilation.
MRD – 1000mg

pKa : 9.1
pH of plain solution : 5 to 6.5
pH of vasoconstrictor containing
solution : 3.5 to 5.5
Onset of action : 6 to 10 minutes
Effective dental concentration : 2% to
4%
Anesthetic half life : 0.1 hour
Duration of action : no pulpal
anesthesia, soft tissue anesthesia for 15-
20 minutes.
Topical anesthetic action : not in
clinically acceptable concentration.

2. PROPOXYCAINE HCL
Classification : Ester
Chemical Formula: 2-
Diethylaminoethyl-4-amino-2-
propoxybenzoate hydrochloride
Toxicity : 7 to 8
Metabolism : Hydrolyzed in both plasma
and the liver.
Excretion : via kidneys; almost entirely
hydrolysed.
Vasodilating properties : not so profound
as that of procaine.

Onset of action : Rapid (2 to 3 minutes )
Effective Dental Concentration : 0.4%
Topical Anesthetic Action : not in clinically acceptable concentrations.
Due to high level of toxicity, propoxycaine is no longer in use.
Maximum recommended dose was 6.6mg/kg of body weight.

3. Lidocaine HCL
Classification : Amide
Chemical Formula: 2-diethylamino-2`,6-
acetoxylidide hydrochloride
Metabolism : in liver, by microsomal
fixed function oxidases, to
monoethylglyceine and xylidide.
Xylidide is potentially toxic.
Excretion : via kidneys; less than 10% is
unchanged, more than 80% various
metabolites.

Vasodilating properties: Considerably
less than that of procaine; however more
than those of prilocaine or mepivacaine.
pka : 7.9
pH of plain solution : 6.5
pH with vasoconstrictor : 5.0 - 5.5
Onset of action : 2 to 3 minutes
Effective dental concentration :2%
Anesthetic half life : 1.6 hours
Topical anesthetic action : acceptable
concentration 5%

Maximum recommended dose :
with adrenaline 7.0 mg/kg body weight
not to exceed 500mg,
without adrenaline 4.4 mg/kg not to
exceed 300 mg.
Lidocaine is available in three
formulations:
- 2% without vasoconstrictor
- 2% with epinephrine 1:50,000
- 2% with epinephrine 1:1,00,000

4. Mepivacaine HCL
Chemical Formula: 1-methyl 2ʹ6ʹ
-pipecoloxylidide hydrochloride
Metabolism : in the liver by
microsomal fixed function oxidases.
Excretion : via kidneys approx. 1% to
16% of anesthetic dose is excreted
unchanged.
Vasodilating properties : produces
slight vasodilation.

pKa: 7.6
pH of plain solution : 4.5
pH with vasoconstrictor : 3.0 – 3.5
Onset of action : 1.5 to 2minutes
Duration of pulpal anesthesia without vasoconstrictor is 20 to 40 minutes and 2 to 3
hours of soft tissue anesthesia.
Anesthetic half life : 1.9hours
Maximum recommended dose : with adrenaline 6.6 mg /kg body weight not to
exceed 400mg.

5. Prilocaine HCL
Chemical Formula: 2-propylamino-
o-propionotoluidide hydrochloride
Other chemical name :
Propitocaine
Toxicity : 1 (40% less toxic than
lidocaine
Metabolism : Since, it is a secondary
amine, it is hydrolysed directly by
hepatic amidases into orthotoluidine
and N-propylamine.

CO₂ is the major end product.
Orthotoluidine induces methemoglobinemia, if large doses are administered.
As compared to benzocaine and lidocaine, it consistently reduces the bloodʹs oxygen
carrying capacity and can even lead to cyanosis.
To avoid cyanosis, FDA recommends the dosage to 600mg.
Methemoglobin blood levels than 20%, rarely produces any clinical signs and
symptoms.
Biotransformation is more rapid and complete than lidocaine.
Plasma levels decrease more rapidly than lidocaine.
Systemically, it is less toxic as compared to other local anesthetic amides.

Excretion : chiefly excreted through kidneys.
Vasodilating properties : Prilocaine is a potent vasodilator, less than lidocaine.
pKa : 7.9
pH of plain solution : 6.0 – 6.5
pH of vasoconstrictor containing solution : 4.0
Onset of action : slightly slower than that of lidocaine( 3-5 minutes)
Effective dental concentration : 4%
Maximum recommended dose is 8.0 mg/kg to a maximum of 600mg.

Topical Anesthetic Action :
In uncharged base form, prilocaine
forms an integral part of
EMLA(eutectic mixtures of local
anesthetics lidocaine and prilocaine).
This formulation permits anesthetics
to penetrate the imposing anatomic
barrier of intact skin, and is useful in
case of venipuncture.

6. Bupivacaine HCL
Chemical Formula: 1-Butyl-2ʹ
6ʹ-pipecoloxylidide hydrochloride
Metabolism : in the liver by amidases.
Excretion : via kidneys 16% of
anesthetic dose is excreted unchanged.
Vasodilating properties : greater than
lidocaine, prilocaine and mepivacaine,
less than procaine.
pKa : 8.1
pH of plain solution : 4.5 - 6

pH with vasoconstrictor : 3.0 - 4.5
Onset of action : 6 – 10 minutes
Effective dental concentration : 0.5%
Duration with vasoconstrictor pulpal anesthesia is 90 – 180minutes and soft tissue is
240 -540minutes.
Topical anesthetic action : not in clinically acceptable concentration.
Maximum recommended dose : 1.3 mg/kg body weight not to exceed 90 mg.

Bupivacaine HCL (0.5%) without
vasoconstrictor
Bupivacaine HCL (0.5%) with
vasoconstrictor

7. Articaine HCL
Classification : classified as an amide,
but possesses both amide and ester
characterstics.
Prepared by H. Rusching et al,1969.
FDA approved : April 2000 (United
States)
Introduced : 1976 in Germany and
Switzerland, 1983 in Canada, 2000 in
United States.

Chemical Formula: 3-N-Propylamino-propionylamino-2-carbomethoxy-4-
methylthiophene hydrochloride
Potency : 1.5 times that of lidocaine; 1.9 times that of procaine.
Toxicity : similar to lidocaine and procaine.
Metabolism : Articaine is the only amide type of local anesthetic that
contains a thiophene group.
It is the only amide type of local anesthetic that contains
an ester group as well.
Biotransformation occurs in plasma (by plasma esterase)
and in liver (hepatic microsomal enzymes).
Degradation of articaine HCL is initiated by hydrolysis of
carboxylic acid ester group to obtain free carboxylic
acid.

The primary metabolite, articainic acid is pharmacologically inactive.
It undergoes additional biotransformation to form articainic acid glucuronide.
Excretion : via kidneys
Vasodilating properties : equal to that of lidocaine, but less than
procaine.
pKa : 7.8
pH of vasoconstrictor containing solution: 3.5-4.0

Onset of action: articaine (1:2,00,000) – infiltration 1-2 minutes
- mandibular block 2-3 minutes
articaine (1:1,00,000) – infiltration is 1-2 minutes
- mandibular block is 2-2.5 minutes
Effective dental concentration – 4% with 1:1,00,000 or
1:2,00,000epinephrine
Anesthetic half-life – 0.5 hours
Maximum recommended dose : 7.0 mg/kg

Articaine HCL 4% with
Articaine HCL 4% with

8. Centbucridine :
It is a quinolone derivative with local anesthetic action.
It has intrinsic vasoconstricting and antihistaminic properties.
In a concentration of 0.5%, it is used for infiltration, nerve blocks and spinal
anesthesia with an anesthetic potency 4-5 times greater than that of 2% lignocaine.

Anaesthetics for topical application
a) Benzocaine – used as gel, gel patch, ointment and solution.

b) Butamben and Tetracaine HCL
They are used as aerosol, gel, ointment and solution.
c) Cocaine hydrochloride
It is used in topical application.
d) Dyclonine hydrochloride
It is a ketone derivative and is used in patients with known allergy to ester
or amide group of local anesthetics.
e) Eutectic Mixture of Local Anesthetics
It is a mixture of lignocaine and prilocaine bases, which forms an oil phase
in the cream and passes through the intact skin.

f) Dentipatch
A patch that contains 10-20% lignocaine and is placed on dry mucosa for 15
minutes to achieve topical anesthesia for maxilla and mandible.

■ PHENTOLAMINE MESYLATE
It is a drug used for the reversal of local anesthetic solution.
It is non-selective alpha adrenergic blocking agent.
It reverses the effects of epinephrine or nor-epinephrine on tissues containing alpha1
and alpha2 adrenergic receptors.
Alpha receptor blockade causes vasodilation, that results in rapid distribution of
local anesthetic solution away from the injection site.
Peak concentration is achieved after 20 minutes.
Elimination half life is 2-3 hours.
Adverse reactions include diarrhoea, facial swelling, oral pain, swelling and
vomiting.

■ It should be used with caution in
patients with cardiovascular
diseases.

Factors in selection of a local anesthetic for a patient
1. Length of time for which pain control is necessary
2. Potential need for post treatment pain control
3. Possibility of self mutilation in the post operative period
4. Requirement for hemostasis
5. Presence of any contraindication(absolute or relative) to the local anesthetic
solution selected for administration

Pharmacokinetics of local anesthesia
It can be described in following
stages:
1. Uptake
2. Distribution
3. Biotransformation
4. Excretion

1. Uptake:
Oral route – except cocaine, all local anesthetics are poorly absorbed from
GIT.
Topical route- In tracheal mucosa, uptake is quiet rapid.
In pharyngeal mucosa and bladder mucosa, uptake
is quiet slow.
EMLA has been developed to provide surface
anesthesia for skin.
Injection-The rate of uptake depends on vascularity of the
injection site and vasoactivity of the drug.
IV administration provides the most rapid elevation
of the drug.

2. Distribution
Highly perfused organs such as brain,
liver, head, kidney and lungs have
higher blood levels of anesthetic than
do less higher perfused organs.
3. Biotransformation
Esters are hydrolysed in plasma by
pseudocholinesterase.
Amides are metabolised in liver by
microsomal enzymes.

4. Excretion
Kidneys are the primary excretory
organs for the local anesthetics.
Amides are present in urine as a
parent compound in a greater
percentage as compared to esters.
Renal impairment leads to
accumulation of the drug and hence,
toxicity.

Vasoconstrictors
• These are the drugs that constrict blood vessels and there by control tissue
perfusion. They are added to local anesthetic solutions to oppose the
inherent vasodilatory actions of the local anesthetics.
• Vasoconstrictors are added to local anesthetics due to following reasons:
a) by constricting blood vessels, vasoconstrictors decrease blood flow
(perfusion) to the site of drug administration.
b) absorption of the local anesthetic into the cardiovascular system is
slowed, resulting in lower anesthetic blood levels.

c) Since local anesthetic blood levels are reduced, risk of local anesthetic toxicity is
reduced.
d) More local anesthetic enters into the nerve, where it remains for longer periods,
thereby increasing the duration of most of the local anesthetics.
e) Vasoconstrictors decrease bleeding at the site of administration; therefore they are
useful when increased bleeding is anticipated.
Vasoconstrictors are classified as sympathomimetic or adrenergic drugs. They are
classified on the basis of chemical structure and mode of action.
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Vasoconstrictors are classified as:
(chemical structure)
Catecholamines Non-catecholamines
Epinenephrine Amphetamine
Norepinephrine Methamphetamine
Levonordefrine Hydroxyamphetamine
Isoproterenol Ephedrine
Dopamine Mephentermine
Metaraminol
Methoxamine
Phenylephrine
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Mode of action.
Direct acting Indirect acting Mixed acting
Epinephrine Tyramine Metaraminol
Norepinephrine Amphetamine Ephedrine
Levonordefrine Methamphetamine
Isoproterenol Hydroxyamphetamine
Dopamine
Methoxamine
Phenylephrine

The armamentarium
■ The Armamentarium can be categorized as :
a. The Syringe
b. The Needle
c. The Cartridge
d. Additional Armamentarium
- Topical Antiseptic
- Topical Anesthetic
- Applicator sticks
- Cotton gauze (2 x 2 inches )
- Hemostat

syring
e
needle
cartridge Cotton gauze
Applicator
sticks

■ According to American Dental Association criteria for acceptance of local
anesthetic syringes include the following:
i. They must be durable and able to withstand repeated sterilization without damage.
(If the unit is disposable, it should be packaged in a sterile container).
ii. They should be capable of accepting a wide variety of cartridges and needles of
different manufacture, and should permit repeated use.
iii. They should be inexpensive, self –contained, lightweight and simple to use with
one hand.
iv. They should provide for effective aspiration and be constructed so that blood
may be easily observed in the cartridge.

a. The Syringe
The following types of syringes available are:
1. Non-disposable syringes
 Breech-loading, metallic, cartridge-type, aspirating
 Breech-loading, plastic, cartridge-type, aspirating
 Breech-loading, metallic, cartridge-type, self-aspirating
 Pressure syringe for periodontal ligament injection
 Jet injector (needleless syringe)
2. Disposable syringes
3. Safety syringes
4. Computer-controlled local anesthetic delivery systems

1. Non-disposable syringes
 Breech-loading, metallic, cartridge-type, aspirating
■ Breech-loading - cartridge is inserted into the syringe from the side of the barrel
of the syringe.
■ The needle is attached to the barrel of the syringe at the needle adaptor.
■ The needle adaptor is also known as the screw hub or convertible tip.
■ A harpoon is attached to the piston. It penetrates the thick silicone rubber stopper
at the opposite end of the cartridge.

■ When negative pressure is applied
on the thumb ring, blood is visible
in the cartridge if the needle tip rests
in the lumen of the blood vessel.
■ When positive pressure is applied
on the thumb ring, it forces the local
anesthetic into the needle lumen and
then into the tissues.
■ They are made of chrome-plated
brass and stainless steel.

 Breech loading, plastic, cartridge-
type aspirating
■ It is autoclavable.
■ It is sterilisable.
■ It can be used for multiple
anesthetic administration.

 Breech Loading, metallic, cartridge-
type, self aspirating
■ It increases the ease of aspiration.
■ The elasticity of the rubber
diaphragm in the anesthetic cartridge
is used to obtain the necessary
negative pressure for aspiration.

■ Pressure acting directly on the
cartridge through the thumb disc or
indirectly through the plunger shaft
distorts the rubber diaphragm and
produces positive pressure.
■ When that pressure is released,
sufficient negative pressure develops
within the cartridge to permit
aspiration.

 Pressure syringes for periodontal
ligament injection
The original pressure devices are:
-Peripress
-Ligmaject
-Wilcox Jewett obtunder

 Jet Injectors
■ Principle- liquids forced through very
small openings, called jets, at very
high pressure can penetrate intact
skin or mucous membrane.
■ Primary purpose- to obtain topical
anesthesia before insertion of needle.
■ Syrijet Mark II and the MadaJet are
the two jet injectors.

2. Disposable Syringes
• Plastic disposable syringes are
available in a variety of sizes with an
assortment of needle gauges.
• They are used for intramuscular,
intravenous and intraoral injections.
• Aspiration can be accomplished by
pulling back on the plunger of the
syringe.
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3. Safety Syringes
• They possess a sheath that locks over
the needle when it is removed from the
patient′s tissues.
• The syringe may be made safe with
one hand by gently moving the index
and middle fingers against the front
collar of the guard.
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4. Computer-Controlled Local Anesthetic
Delivery Systems (C-CLAD) Systems
• At present three C-CLADs are available. They are:
i. The Wand/Compudent System
ii. The Wand/STA System
iii. The Comfort Control Syringe
Another similar devices are, the QuickSleeper (marketed in Europe )
and Anaeject marketed in Japan.
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i. The Wand/Compudent System
• Manipulate the needle placement
with fingertip accuracy.
• Deliver the local anesthetic with a
foot activated control.
• A lightweight handpiece is held in a
pen like grasp.
• It provides increased tactile
sensation and control .
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• Flow rate of local anesthetic delivery is computer controlled and remains
consistent from one injection to the next.
• Thus this system had a marked improvement on ergonomics and precision of the
dental syringe.
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ii. The Wand/STA system
• Subcutaneous injection.
• Dynamic pressure-sensing technology
(DPS technology).
• Audible sounds and visual indications.
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• The STA system has two basic
components:
a. STA Wand handpiece
b. STA drive unit
STA Wand handpieces can have a pre
attached needle or needle needs to be
attached at the time of treatment. It can
be available as 30 gauge(0.5 or 0.25
inch) or 27 gauge(0.5 or 0.25 inch).
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The STA drive unit integrates two cap
holders into the base of unit, thus allows
single handed recapping of the needle
from either side of the unit.
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The advantages and disadvantages of the
Wand/STA system are:
• Advantages
i. DPS technology.
ii. It results in more predictable
injection site location.
iii. Allows PDL injection to be used as
a predictable primary injection.
iv. Reduces pain-disruptive behaviour
v. Reduces stress for patient as well
operator.
• Disadvantages
i. Cost
ii. Requires additional
armamentarium.
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iii. Comfort Control Syringe
• This is an electronic, pre-programmed
delivery device.
• It has two stage delivery system:
-Initially, the injection is at a slow rate.
-After 10 seconds, the CCS
automatically increases speed to a pre-
programmed injection rate.
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The advantages and disadvantages of Comfort Control
Syringes are:
• Advantages
i. Familiar syringe type of delivery
systems.
ii. Easy to see exactly how much local
anesthetic solution has been
dispensed.
iii. All controls are at finger tips.
iv. Less costly than other C-CLADS.
v. Allows selection of various rates of
delivery matched to the user
injection technique utilized.
• Disadvantages
i. Requires additional
armamentarium.
ii. More bulky than other C-CLAD
devices.
iii. Vibration may bother some users.
iv. Cost.
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The various problems of Syringes are:
• Leakage during injection
• Broken Cartridge
• Bent harpoon
• Disengagement of the harpoon from the plunger during aspiration
• Surface deposits
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b. The Needle
• The needle is the vehicle that permits
local anesthetic solution to travel from
the dental cartridge into the tissues
surrounding the needle tip.
• The various parts of a needle are:
a. the bevel
b. the shaft
c. the hub
d. the cartridge penetrating end
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• The Gauge
It refers to the diameter of the lumen of the needle.
The preferred gauges are 25, 27 and 30 gauge.
The advantages of larger gauge needles over smaller gauge needles are:
i. Less deflection, as needle advances through tissues.
ii. Greater accuracy of injections.
iii. Less chance of needle breakage.
iv. Easier aspiration.
v. No perceptual difference in patient comfort.
Length:
1) Long (approx. 40mm “32-40mm”), for nerve block
2) Short (20-25 mm)
3) Extra-short (approx. 15mm), for PDL
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The Cartridge
• The dental cartridge is a glass cylinder
containing the local anesthetic drug,
among other ingredients.
• The dental cartridge is, referred to by
dental professionals as a carpule.
• The dental cartridge can be made of :
glass or
plastic
Plastic cartridges are obsolete at present.
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Local Anesthesia 91
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Additional armamentarium include:
i. Topical antiseptic
ii. Topical anesthetic
iii. Applicator sticks
iv. Cotton gauze (2x2 inches)
v. Hemostat
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i. Topical Antiseptic
• It is used to prepare the tissues at the
injection site before initial needle
preparation.
• It leads to transient decrease in the
bacterial population at the injection
site and minimizes any risk of post
injection infection.
• E.g Betadine and merthiolate
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ii. Topical anesthetic
• E.g Benzocaine
Lidocaine as gels, pastes and
sprays.
EMLA cream
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iii. Applicator sticks
• They are wooden sticks with a cotton
swab at one end.
• They are used to apply topical
antiseptic and anesthetic solutions to
mucous membranes.
• Compress tissues during palatal
injections.
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iv. Cotton Gauze
• They are used to wipe the area of
injection before needle penetration.
• Drying the mucous membrane to aid in
soft tissue retraction for increased
visibility.
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v. Haemostat
• Its primary function in local anesthesia
is removal of a needle from the soft
tissues of the mouth in the highly
unlikely event of needle breakage
within tissues.
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Systemic complications of local anesthesia
• Whenever, any drug is administered, it has two types of effect:
-desirable actions: that are clinically beneficial
-undesirable actions: that are not sought
• The three principles that are basically followed are:
i. No drug ever exerts a single action.
ii. No clinically useful drug is entirely devoid of toxicity.
iii. The potential toxicity of a drug rests in the hand of the user.
04-07-2021 Local Anesthesia 98

Principle- 1
No drug exerts a single action: it follows as
Right drug Right dose Right route Right patient
Right time Right reason
This is an ideal clinical situation and is rarely achieved.

Principle- 2
No clinically useful drug is entirely devoid of toxicity.
A drug has 2 effect
- Toxic
- Non-toxic
Extra precautions need to be taken for non-toxic effects.
If not properly handled, they prove to be toxic.

Principle- 3
The potential toxicity of a drug rests in the hands of the user.
It is based on:
- The patient's health or the past medical history.
- Patients vary in their reactions to a drug.
- Hence, physical evaluation and past medical and drug history is mandatory before
administering any drug.

Adverse drug reactions are mainly due to:
• 1. Overdose
• 2. Allergy
• 3. Idiosyncrasy

1. Overdose
• It is a clinical sign and symptom
which is responsible for absolute
or relative over administration of
drug.
• Inadequate dose always leads to
adverse effect.
• This normal state can be altered.

LA overdose : predisposing factors
Patient factors:
• Age
• Sex
• Other drugs
• Weight
• Presence of
disease
• Genetics
• Mental Attitude
Drug Factors:
• Vasoactivity
• Concentration
• Dose
• Route of administration
• Rate of injection
• Vascularity of injection site
• Presence of vasoconstrictors

Patient Factors:
1. Age
Adverse drug reaction can occur at
any age.
The functions like absorption,
distribution and secretion are not so
well carried out in old age.

2. Weight
Greater body weight increases
tolerance power against the overdose.
Maximum recommended doses
can be calculated on the basis of
milligram of drug per kilogram or
pound of body weight.

3. Sex
The major instance of sexual
difference affecting a drug response is
pregnancy.
Renal functions are disturbed.
Impaired excretion of certain drugs,
their accumulation in the blood and
increased risk of overdose.

4. Presence of disease
Disease may affect the ability of the body to transform a drug into inactive product.
Hepatic and renal dysfunction impair the bodyʼs ability to breakdown and excrete
the local anesthetic leading to increased anesthetic blood level.
Congestive heart failure decreases liver perfusion that increases half life of amide
local anesthetics.

5. Genetics
It may alter the patient's response to certain drugs.
A genetic deficiency in this enzyme serum cholinesterase is an important example.
This enzyme produced in liver circulates in blood and is responsible for
biotransformation of the ester local anesthetics.
A deficiency in this enzyme, quantitative or qualitative, can prolong the half life of
an ester local anesthetic and increase its blood level.

6. Mental Attitude and Environment
A patient's psychological attitude influences the ultimate effect of a drug.
It affects the patient's response to various stimuli.
The apprehensive patient who overreacts to stimulation is more likely to receive a
larger dose of local anesthetic.
Local anesthetic seizure threshold is lower in patients who are fearful and
apprehensive than in less or not fearful patients.

Drug Factors
1. Vasoactivity
All the LA have vasodilating properties.
Injection into the soft tissues increases perfusion in the area, so greater absorption
occurs in from the site of injection to CVS.
The undesirable effects are:
-Short duration of clinical LA.
-increased blood level of local anesthetic.

2. Concentration
Greater is the concentration of the local anesthetics administered, greater is the
number of mg/ml of solutions and greater is the circulating blood volume of the
drug in the patient.
3. Dose
Larger volume of local anesthetic greater number of mg injected
higher circulating blood level.
High blood levels of the local anesthetics can be achieved in dental situations
because of the greater vascularity of the intraoral injections or intravascular
injections.

4. Route of administration
LA administered for anti-dysarrhythmic purposes must reach a therapeutic blood
level to be effective.
One factor involved in pain control by LA is diffusion of the drug out of the nerve
tissues, absorb into the CVS and removal from the area of injection.
Absorption of LA by oral mucous membrane is dangerous because of the rate at
which some topically applied anesthetics enter the circulatory system.
e.g- lidocaine, tetracaine

5. Rate of injection
An important factor in the causation or prevention of overdose reactions.
IV injection may or may not produce signs and symptoms of overdose.
This decides, if the effect of the drug will be clinically safe or hazardous.

6. Vascularity of the injection site
Greater is the vascularity of the injection site, more rapid the absorption of the drug
from that area into the circulation.
Oral cavity is highly vascular in entire body.
Some areas within the oral cavity that are less well perfused, these areas are more
recommended than any other more well perfused areas.

7. Presence of vasoconstrictors
The addition of vasoconstrictors to a local anesthetic produces a decrease in the
perfusion of an area and a decreased rate of systemic absorption of the drug.

Causes of toxicity
• Biotransformation of the drug is unusually slow.
• The unbiotransformed drug is too slowly eliminated from the body through the
kidneys.
• Too large a total dose is administered.
• Absorption from the injection site is unusually rapid.
• Inadvertant intravascular administration occurs.

Clinical manifestations of overdose

• Local Anesthetics exert a depressant effect on all excitable membranes.
• It causes reversible depression of peripheral nerve conduction, subsequent actions
on smooth muscles, myocardium and CNS.
• It mainly affects:
-Central Nervous System
-Cardiovascular System

Minimal to moderate
Minimal to moderate- Signs:
Talkativeness
Slurred speech
Stutter
Dysarthria
Muscular twitching / tremors Apprehension
Excitability
Euphoria and Nystagmus

Elevated blood pressure
Elevated heart rate
Elevated respiratory rate
Failure to follow commands
Lack of response to painful stimuli
Sweating
Nausea/ vomiting
Disorientation

• Symptoms:
Restless
Nervous
Numbness
Visual disturbances
Auditory disturbances
Metallic taste
Lightheaded and dizzy
Drowsy and disoriented
Loosing consciousness
Sensation of twitching

Moderate to high
Generalized tonic- clonic seizure activity
Generalized CNS depression
Depressed BP, heart rate
Depressed respiratory rate

Management of overdose (slow onset > 5mins)
• Reassure patient
• Administer Oxygen Monitor the vital
signs
• Consider IV anticonvulsant
• Allow recovery or get medical help
• Get medical consultations especially in
case of metabolic dysfunction.

• Mild reaction – slower onset (> 15 mins)
Reassure the patient
Administer oxygen
Monitor vital signs
Administer an anticonvulsant
Summon medical assistance

Severe reaction – rapid onset (within 1 minute)
Stop all treatment.
Place patient in supine position, feet up.
Establish airway(BLS).
If convulsions, protect the patient.
Anticonvulsant drug.
Post seizure Phase
Vasopressor for hypotension
IV fluids

Severe reaction – Slow onset
• Stop all treatment
• Establish airway (BLS)
• Administer anticonvulsant
• Summon emergency medical help
• Consider vasopressors, iv fluids for hypotension
• Get medical consultation, especially for metabolicVasoconstric or renal
dysfunction.

Vasoconstrictor Overdose
• Clinical manifestations
Fear, anxiety
Tenseness
Restlessness
Tremor
Weakness and palpitations
Throbbing headache and
perspirations
Respiratory difficulty, dizziness and
pallor

Epinephrine Overdose
• Sharply elevated systolic BP
• Increased heart rate
• Cardiac tachyarrhythmias
• Stop dental treatment
• Reassure the patient and administer
oxygen
• Monitor BP and pulse until fully
recovered

2. Allergy
• Types
i. Immediate Hypersensitivity
ii. Ig-G Mediated Cytotoxic Hypersensitivity
iii. Immune Complex Mediated Hypersensitivity
iv. Delayed Hypersensitivity

Predisposing Factors
• Local Anesthetic Agent
• Sodium Metabisulphite
• Methyl Paraben
• Latex Energy

Clinical Manifestations
• Dermatologic Reactions
Urticaria
Pruritis
Angioedema

• Respiratory Reactions
Wheezing
Increased Anxiety
Use of accessory muscles for respiration
Laryngeal Edema
Respiratory distress

• Generalized Anaphylaxis
Skin reactions
Smooth muscle Spasm
Respiratory Distress
Cardiovascular tracts

Management
• Skin Reactions
1. Delayed skin reactions
P-A-B-C
Oral Histamine Blocker- 50mg
Diphenhydramine- 10mg
Chlorpheniramine TDS for 3-4 days

2. Immediate Skin Reaction
P-A-B-C
parentral Histamine Histamine Blocker-
Diphenhydramine- 50 mg
Chlorpheniramine- 10mg
Oral Histamine blocker for 3 days

Respiratory Reactions
• Bronchospasm
P-A-B-C
Oxygen 5-6ml
Epinephrine
After recovery, 50mg
Diphenhydramine or 10 mg
Chlorpheniramine- IM

Laryngeal Oedema
• P-A-B-C
• Epinephrine-0.3mg IM every 5-10
mins until recovery
• Maintain Airway
• Administer oxygen
• Histamine blocker
• Corticosteroid
• Perform cricothyrotomy

Generalized Anaphylaxis
• P-A-B-C
• Epinephrine
• Maintain the airway
• Administer Oxygen
• Histamine blocker
• Corticosteroid

3. Idiosyncrasy
• Any reaction to a local anesthetic or drug that cannot be classified as toxic or
allergic can be defined as idiosyncratic.
• Treatment follows as:
maintain the patientʼs airway and adequate oxygenation
evaluate the circulation and support by drugs and parentral fluids.
protect the patient from injury as a result of convulsive seizures
or loss of consciousness.

References
• Handbook of Local Anesthesia by Malamed
• Monheim’s Local Anesthesia and Pain Control in Dental Practice

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