Local anesthetic agents by Dr. Deepesh

Local Anesthetic Agents and
Techniques
Dr. Deepesh Mehta
1st Year MDS
Department of Conservative Dentistry and Endodontics
2

Contents
• Introduction
• History
• Desirable Properties of a Local Anesthetic
• Electrochemistry of Nerve Conduction
• Theories of Local Anesthesia
• Mechanism of Action of LA
• Structure of Local Anesthetic
• Classification
• Pharmacology of Local Anesthetics
• Pharmacology of Vasoconstrictors
• Clinical Actions of Specific Agents
• Complications of Local Anesthetics
• Management of Complications
• Techniques of Local Anesthesia
3

Local Anesthesia?
“Local anesthesia 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 the conduction
process in peripheral nerves”.
4

Desired 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.
• It must be effective regardless of whether it is injected into
the tissue 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 yet not so long as to require an
extended recovery.
• It should be relatively free from producing allergic reactions.
• It should be sterile or capable of being sterilized without
deterioration.
6

Electrophysiology of Nerve Conduction:
• Electrical events that occur within a nerve during the
conduction of an impulse:
An initial phase of slow depolarization: The
electrical potential within the nerve becomes slightly
less negative.
When the falling electrical potential reaches a critical
level, an extremely rapid phase of depolarization
results. This is termed threshold potential; or firing
Threshold.
This phase of rapid depolarization results in a
reversal of the electrical potential across the nerve
membrane.
After these steps of depolarization, repolarization
occurs. The electrical potential gradually becomes
more negative inside the nerve cell until the original
resting potential of - 70mV is again achieved.
7
A nerve possesses a resting potential. This is a
negative electrical potential of -70 mV that exists
across the nerve membrane.

Electrochemistry of Nerve Conduction:
The preceding sequence of events depends on two important
factors:
• the concentrations of electrolytes in the axoplasm (interior of
the nerve cell) and extracellular fluids.
• the permeability of the nerve membrane to sodium and
potassium ions.
8

Resting State:
In its resting state, the nerve membrane is
• Slightly permeable to sodium ions (Na+)
• Freely permeable to potassium ions (K+)
• Freely permeable to chloride ions (Cl-)
Potassium remains within the axoplasm, despite its ability to
diffuse freely through the nerve membrane.
Chloride remains outside the nerve membrane instead of
moving along its concentration gradient into the nerve cell.
Sodium migrates inwardly because both the concentration
(greater outside) and the electrostatic gradient (positive ion
attracted by negative intracellular potential) favor such
migration.
9

Membrane Excitation:
Depolarization: Excitation of a nerve segment leads to an
increase in permeability of the cell membrane to sodium ions.
This is accomplished by a transient widening of transmembrane
ion channels sufficient to permit the passage of sodium ions.
The rapid influx of sodium ions to the interior of the nerve cell
causes depolarization of the nerve membrane from its resting
level to its firing threshold of approximately -50 to -60 mV.
This firing threshold is actually the magnitude of the decrease in
negative transmembrane potential that is necessary to initiate
an action potential (impulse).
10

At the end of depolarization (the peak of the action potential),
the electrical potential of the nerve is actually reversed; an
electrical potential of +40 mV exists.
The entire depolarization process requires approximately
0.3msec.
Repolarization:
The action potential is terminated when the membrane
repolarizes. This is caused by the extinction (inactivation) of
increased permeability to sodium ions.
Movement of sodium ions into the cell during depolarization
and subsequent movement of potassium ions out of the cell
during repolarization are passive (not requiring the expenditure
of energy), because each ion moves along its concentration
gradient (higher → lower).
11

After the return of the membrane potential to its original
level (-70 mV), a slight excess of sodium exists within the
nerve cell, along with a slight excess of potassium
extracellularly.
A period of metabolic activity then begins in which active
transfer of sodium ions out of the cell occurs via the sodium
pump. An expenditure of energy is necessary to move sodium
ions out of the nerve cell against their concentration gradient.
The same pumping mechanism is thought to be responsible
for the active transport of potassium ions into the cell against
their concentration gradient.
The process of repolarization requires 0.7msec.
12

Theories of Local Anesthesia:
1. Acetylcholine Theory
2. Calcium Displacement Theory
3. Surface Charge Theory
4. Membrane Expansion Theory
5. Specific Receptor Theory
Proposes that local anesthetics act by binding to specific
receptors on the sodium channel.
Studies have indicated that a specific receptor site for local
anesthetics exists in the sodium channel either on its external
surface or on the internal axoplasmic surface. Once the local
anesthetic has gained access to the receptors, permeability to
sodium ions is decreased or eliminated, and nerve conduction is
interrupted.
Most
Favored
13

How Local AnestheticsWork?
• The primary action of local anesthetics in producing a
conduction block is to decrease the permeability of ion
channels to sodium ions (Na+).
• Local anesthetics selectively inhibit the peak permeability of
sodium, whose value is normally about five to six times
greater than the minimum necessary for impulse conduction
(e.g., there is a safety factor for conduction of 5x to 6x).
• Local anesthetics reduce this safety factor, decreasing both
the rate of rise of the action potential and its conduction
velocity.
• When the safety factor falls below unity, conduction fails and
nerve block occurs. 14

The following sequence is a proposed mechanism of action of
local anesthetics:
• Displacement of calcium ions from the sodium channel
receptor site, which permits…
• Binding of the local anesthetic molecule to this receptor site,
which produces ...
• Blockade of the sodium channel, and a ...
• Decrease in sodium conductance, which leads to …
• Depression of the rate of electrical depolarization, and ...
• Failure to achieve the threshold potential level, along with ...
• Lack of development of propagated action potentials, which is
called ...
• “Conduction blockade”.
15

Structure of Local Anesthetic:
Most injectable local anesthetics are tertiary amines. Only a few (e.g.,
prilocaine, hexylcaine) are secondary amines.
Largest Part
Benzoic
acid,
Aniline,
or
Thiophene
Amino
derivative of
Ethyl
Alcohol or
Acetic Acid
The anesthetic structure is completed by an intermediate hydrocarbon chain
containing an ester or an amide linkage.
16

• It is well known that the pH of a local anesthetic solution (as
well as the pH of the tissue into which it is injected) greatly
influences its nerve-blocking action.
• Acidification of tissue decreases local anesthetic effectiveness.
• The pH of normal tissue is 7.4; the pH of an inflamed area is 5
to 6.
• The pH of solutions without epinephrine is about 6.5;
epinephrine-containing solutions have a pH of about 3.5.
• Elevating the pH (alkalinization) of a local anesthetic solution
speeds its onset of action, increases its clinical effectiveness,
and makes its injection more comfortable. 17

Dissociation of Local Anesthesia:
• Local anesthetics are available as acid salts (usually
hydrochloride) for clinical use.
• The local anesthetic salt, both water soluble and stable, is
dissolved in sterile water or saline.
• In this solution, it exists simultaneously as uncharged
molecules (RN), also called the base, and as positively charged
molecules (RNH+),called the cation.
RNH+ ↔ RN + H+
18

• In the presence of a high concentration of hydrogen ions (low
pH), the equilibrium shifts to the left, and most of the
anesthetic solution exists in cationic form:
RNH+ > RN + H+
• As hydrogen ion concentration decreases(higher pH), the
equilibrium shifts toward the free base form
RNH+ < RN + H+
19

Classification of Local Anesthetics:
20

Based on Mode of Administration:
I. INJECTABLE:
a. Low potency, short duration:
- procaine, chloroprocaine
b. Intermediate potency and duration:
- lidocaine, prilocaine
c. High potency, long duration:
- tetracaine, bupivacaine, ropivacaine, dibucaine
II. SURFACE ANESTHETIC:
a. Soluble
- cocaine, lidocaine, tetracaine
b. Insoluble
- benzocaine, butylaminobenzoate, oxyethazine
22

Pharmacology of Local Anesthetics:
23

Distribution of Local Anesthetics:
• Local anesthetics, once absorbed into the blood are
distributed throughout the body to all tissues.
• Highly perfused organs (and areas), such as the brain, head,
liver, kidneys, lungs, and spleen, initially will have higher
anesthetic blood levels than less highly perfused organs.
24

• The blood level of the local anesthetic is influenced by the
following factors:
1. Rate at which the drug is absorbed into the cardiovascular
system.
2. Rate of distribution of the drug from the vascular compartment
to the tissues.
3. Elimination of the drug through metabolic or excretory
pathways.
• The rate at which a local anesthetic is removed from the blood
is described as its elimination half-life. Simply stated, the
elimination half-life is the time necessary for a 50% reduction
in the blood level.
• All local anesthetics readily cross the blood-brain barrier.
• They also readily cross the placenta and enter the circulatory
system of the developing fetus. 25

Metabolism:
• Metabolism (or biotransformation or detoxification) of local
anesthetics is important because the overall toxicity of a drug
depends upon it.
• Ester Local Anesthetics. Ester local anesthetics are hydrolyzed
in the plasma by the enzyme pseudocholinesterase.
• Approximately 1 of every 2800 persons has an atypical form of
pseudocholinesterase, which causes an inability to hydrolyze
ester local anesthetics.
26

• Amide Local Anesthetics:
• The primary site of biotransformation of amide local
anesthetics is the liver.
• Virtually the entire metabolic process occurs in the liver for
lidocaine, mepivacaine, etidocaine, and bupivacaine.
• Prilocaine undergoes primary metabolism in the liver, with
some also possibly occurring in the lung.
27

Excretion:
• The kidneys are the primary excretory organ for both the local
anesthetic and its metabolites.
• A percentage of a given dose of local anesthetic is excreted
unchanged in the urine.
• Esters appear only in very small concentrations as the parent
compound in the urine because they are hydrolyzed almost
completely in the plasma.
• Amides usually are present in the urine as the parent
compound in a greater percentage than the esters, primarily
because of their more complex process of biotransformation. 28

SystemicActionsof LocalAnesthesia:
• Local anesthetics are chemicals that reversibly block action
potentials in all excitable membranes.
• The central nervous system(CNS) and the cardiovascular
system(CVS) therefore are especially susceptible to their
actions.
Central Nervous System(CNS):
• Their pharmacologic action on the CNS is seen as depression.
• At higher (toxic, overdose) levels, the primary clinical
manifestation is a generalized tonic-clonic convulsion.
• Between these two extremes exists a spectrum of other
clinical signs and symptoms.
29

• Local anesthetics possess a second action in relation to the
CNS. Administered intravenously, they increase the pain
reaction threshold and also produce a degree of analgesia.
• Cocaine has long been used for its euphoria-inducing and
fatigue-lessening actions.
• Cardiovascular System(CVS):
• Local anesthetics have a direct action on the myocardium and
peripheral vasculature.
• Local anesthetics produce a myocardial depression; decreases
electrical excitability, conduction rate and force of contraction.
31

• All local anesthetics, except cocaine, produce a peripheral
vasodilation through relaxation of smooth muscle in the walls
of blood vessels.
• The primary effect of local anesthetics on blood pressure is
hypotension.
• In summary, negative effects on the cardiovascular system are
not noted until significantly elevated local anesthetic blood
levels are reached.
32

Respiratory System:
• Local anesthetics exert a dual effect on respiration.
• At non-overdose levels, they have a direct relaxant action on
bronchial smooth muscle, whereas at overdose levels, they
may produce respiratory arrest as a result of generalized CNS
depression.
Local Tissue Toxicity:
• Skeletal muscle appears to be more sensitive than other
tissues to the local irritant properties of local anesthetics.
• The changes that occur in skeletal muscle are reversible, with
muscle regeneration being complete within 2 weeks after
local anesthetic administration. 33

Pharmacology of Vasoconstrictors:
• All clinically effective injectable local anesthetics are
vasodilators.
• Vasoconstrictors are drugs that constrict blood vessels and
thereby control tissue perfusion.
• They are important additions to a local anesthetic solution for
the following reasons:
1. By constricting blood vessels, vasoconstrictors decrease blood
flow (perfusion) to the site of drug administration.
2. Absorption of the local anesthetic into the cardiovascular
system is slowed, resulting in lower anesthetic blood levels.
3. Vasoconstrictors decrease bleeding at the site of
administration; therefore they are useful when increased
bleeding is anticipated (e.g., during a surgical procedure). 34

• The vasoconstrictors commonly used in conjunction with
injected local anesthetics are chemically identical or similar to
the sympathetic nervous system mediators epinephrine and
norepinephrine.
35

Epinephrine:
• Proprietary Name: Adrenalin
• Systemic Actions:
• Epinephrine stimulates β1 receptors of the myocardium.
There is a positive inotropic (force of contraction) and a
positive chronotropic (rate of contraction) effect.
• Both cardiac output and heart rate are increased.
• Systolic blood pressure is increased; Diastolic pressure is
decreased when small doses are administered because of the
greater sensitivity to epinephrine of β2 receptors compared
with α receptors.
36

• Epinephrine is a potent dilator (β2 effect) of bronchiole
smooth muscle. It is an important drug for management of
more refractory episodes of bronchospasm (e.g., status
asthmaticus).
• Epinephrine increases oxygen consumption in all tissues.
Side Effects and Overdose:
• The clinical manifestations of epinephrine overdose relate to
CNS stimulation and include increasing fear and anxiety,
tension, restlessness, throbbing headache, tremor, weakness,
dizziness, pallor, respiratory difficulty, and palpitation.
37

Clinical Applications:
• Management of acute allergic reactions.
• Management of refractory bronchospasm (status
asthmaticus).
• Management of cardiac arrest.
• As a vasoconstrictor, for hemostasis.
• As a vasoconstrictor in local anesthetics, to decrease
absorption into the cardiovascular system; to increase depth
of anesthesia; to increase duration of anesthesia.
• To produce mydriasis. 38

Availability in Dentistry:
• Epinephrine is the most potent and widely used
vasoconstrictor in dentistry. It is available in the following
dilutions and drugs:
39

• Other vasoconstrictors: Norepinephrine, Phenylephrine,
Felypressin are no longer used in dentistry.
40

Selection of a Local Anesthetic:
• With the availability of the local anesthetics, in various
combinations with and without vasoconstrictors, it is possible
for a doctor to select a local anesthetic solution that possesses
the specific pain controlling properties necessary for the
patient for any given dental procedure.
• Several concepts are required for the selection of a specific
local anesthetic. These include the duration of action of the
drug and determination of the maximum recommended
dose.
41

Duration of local Anesthetic:
• Many factors affect both the depth and the duration of a
drug's anesthetic action, prolonging or (much more
commonly) decreasing it.
• These factors include:
1. Individual response to the drug
2. Accuracy in deposition of the local anesthetic
3. Status of tissues at the site of drug deposition (vascularity, pH)
4. Anatomic variation
5. Type of injection administered (supraperiosteal ["infiltration"]
or nerve block)
42

Maximum Doses of a Local Anesthetic:
• Maximum doses are unlikely to be reached in most dental
patients, especially adults of normal body weight, for most
dental procedures.
• The maximum recommended dose calculated should always
be decreased in a medically compromised, debilitated, or
elderly person.
44

Clinical Actions of Specific Agents:
Procaine HCl:
• Metabolism: Hydrolyzed rapidly in plasma by plasma
pseudocholinesterase.
• Excretion: More than 2% unchanged in the urine.
• Vasodilating Properties: Produces the greatest vasodilation of
all currently used local anesthetics.
• Onset of Action: 6 to 10 minutes.
• Effective Dental Concentration: 2% to 4%.
• Anesthetic Half-Life: 0.1 hour (6 minutes).
46

Propoxycaine HCl:
• Metabolism: Hydrolyzed in both plasma and the liver.
• Excretion: Via the kidneys; almost entirely hydrolyzed.
• Vasodilating Properties: Yes, but not as profound as those of
procaine.
• Onset of Action: Rapid (2 to 3 minutes).
• Effective Dental Concentration: 0.4%.
• Propoxycaine was not available alone because its higher
toxicity (seven to eight times that of procaine) limited its
usefulness as a sole agent.
47

Lidocaine HCl:
• Metabolism: In the liver.
• Excretion: Via the kidneys; less than 10% unchanged, more than
80% various metabolites.
• Vasodilating Properties: Considerably less than those of procaine;
however, greater than those of prilocaine or mepivacaine.
• Effective Dental Concentration: 2%.
• Anesthetic Half-Life: 1.6hours (=90 minutes).
• Compared with procaine, lidocaine possesses a significantly more
rapid onset of action (3 to 5 minutes vs. 6 to 10 minutes), produces
more profound anesthesia, has a longer duration of action, and has
greater potency.
48

Mepivacaine HCl:
• Metabolism: In the liver.
• Excretion: Via the kidneys; approximately 1% to 16% of anesthetic
dose is excreted unchanged.
• Vasodilating Properties: Mepivacaine produces only slight
vasodilation. The duration of pulpal anesthesia with mepivacaine
without a vasoconstrictor is 20 to 40 minutes (lidocaine without a
vasoconstrictor is about 5 to 10 minutes; procaine without a
vasoconstrictor may produce effects up to 2 minutes).
• Effective Dental Concentration: 3% without a vasoconstrictor; 2%
with a vasoconstrictor.
• Anesthetic Half-Life: 1.9 hours
49

Prilocaine HCl:
• Metabolism: The metabolism of prilocaine differs significantly from
that of lidocaine and mepivacaine. Because it is a secondary amine,
prilocaine is hydrolyzed straight forwardly by hepatic amidases.
• Excretion: Prilocaine and its metabolites are excreted primarily via
the kidneys. Renal clearance of prilocaine is faster than for other
amides, resulting in its faster removal from the circulation.
• Vasodilating Properties: Prilocaine is a vasodilator. It produces
greater vasodilation than is produced by mepivacaine but less than
lidocaine and significantly less than procaine.
• Onset of Action: Slightly slower than that of lidocaine (3 to 5
minutes).
• Effective Dental Concentration: 4%.
• Anesthetic Half-Life: 1.6hours
50

Articaine HCl:
• Metabolism: Because Articaine HCl is the only widely used
amide-type local anesthetic that contains an ester group,
biotransformation of Articaine HCl occurs in both plasma and
liver.
• Excretion: Via the kidneys; approximately 5% to 10%
unchanged, approximately 90% metabolites.
• Vasodilating Properties: Articaine has a vasodilating effect
equal to that of lidocaine.
• Effective Dental Concentration: 4% with 1: 100,000 or
1:200,000 epinephrine.
• Anesthetic Half-Life: 0.5 hours (27 minutes)
51

Bupivacaine HCl:
• Metabolism: Metabolized in the liver by amidases.
• Excretion: Via the kidney; 16% unchanged bupivacaine has
been recovered from human urine.
• Vasodilating Properties: Relatively significant: greater than
those of lidocaine, prilocaine, and mepivacaine, yet
considerably less than those of procaine.
• Onset of Action: Slower onset time than other commonly
used local anesthetics (e.g., 6 to 10 minutes).
• Effective Dental Concentration: 0.5%.
• Anesthetic Half-Life: 2.7 hours.
52

Benzocaine:
Benzocaine (ethyl p-aminobenzoate) is an ester local anesthetic:
• Poor solubility in water.
• Poor absorption into the cardiovascular system.
• Systemic toxic (overdose) reactions virtually unknown.
• Remains at the site of application for long, providing a
prolonged duration of action.
• Not suitable for injection.
• Localized allergic reactions may occur after prolonged or
repeated use.
• Availability: Benzocaine is available in the following
formulations in numerous dosages: aerosol, gel, ointment,
and solution.
53

EMLA (Eutectic Mixture of Local Anesthetics):
• EMLA cream (composed of lidocaine 2.5% and prilocaine
2.5%) is an emulsion in which the oil phase is a eutectic
mixture of lidocaine and prilocaine in a ratio of 1:1 by weight.
• It was designed as a topical anesthetic able to provide surface
anesthesia for intact skin and as such is used primarily before
painful procedures such as venipuncture and other needle
insertions.
• EMLA has gained popularity among needle-phobic adults and
persons having other superficial, but painful, procedures
performed (e.g., hair removal).
54

• Because intact skin is a barrier to drug diffusion, EMLA must
be applied 1 hour before the procedure.
• Satisfactory numbness of the skin occurs 1hour after
application, reaches a maximum at 2 to 3 hours, and lasts for 1
to 2 hours after removal.
• The use of EMLA could eliminate to some extent use of the
needle in procedures performed in pediatric dentistry.
55

Local Anesthetic Agents and
Techniques(Part 2)
56
• Complications of Local Anesthetics
• Management of Complications
• Techniques of Local Anesthesia

Complications of Local Anesthetics:
• Needle breakage
• Prolonged anesthesia or paresthesia
• Facial nerve paralysis
• Trismus
• Soft tissue injury
• Hematoma
• Pain on injection
• Burning on injection
• Infection
• Edema
57

NeedleBreakage:
• Since the introduction of non-reusable, stainless steel dental
local anesthetic needles, needle breakage has become an
extremely rare complication of dental local anesthetic
injections.
• Although rare, dental needle breakage can, and does, occur.
Prevention:
• Do not use short needles for inferior alveolar nerve block in
adults or larger children.
• Do not bend needles when inserting them into soft tissue.
• Observe extra caution when inserting needles in younger
children or in extremely phobic adult. 58

Management:
• Locating the retained fragment through panoramic and
computed tomographic (CT) scanning.
• Immediate referral of the patient to an appropriate specialist.
59

Prolongedanesthesiaor paresthesia:
• Paresthesia is defined as persistent anesthesia well beyond
the expected duration.
Causes:
• Trauma to any nerve.
• Hemorrhage into or around the neural sheath.
• Injection of a local anesthetic solution contaminated by
alcohol or sterilizing solution.
Prevention:
• Strict adherence to injection protocol and proper care.
60

Management:
• Most paresthesias resolve within approximately 8 weeks
without treatment.
• Explain the patient that paresthesia is not uncommon after
local anesthetic administration.
• Observation is the recommended treatment, although surgery
might be considered as an option.
61

FacialNerveParalysis:
• This may occur when anesthetic is introduced into the deep
lobe of the parotid gland, through which terminal portions of
the facial nerve extend.
Causes:
• Transient facial nerve paralysis is commonly caused by the
introduction of local anesthetic into the capsule of the parotid
gland.
• Directing the needle posteriorly during an IANB.
• Overinserting during a Vazirani-Akinosi nerve block.
62

63
Prevention:
• Adhering to protocol with the inferior alveolar and Vazirani-
Akinosi nerve blocks.
• Avoiding overinsertion of the needle during Vazirani-Akinosi
nerve blocks.
Management:
• Reassure the patient. Explain that the situation is transient.
• Contact lenses should be removed until muscular movement
returns.
• An eye patch should be applied to the affected eye until
muscle tone returns.
• Advise the patient to manually close the affected eyelid
periodically to keep the cornea lubricated.

Trismus:
• Defined as a prolonged, tetanic spasm of the jaw muscles by
which the normal opening of the mouth is restricted (locked
jaw).
Causes:
• Trauma to muscles or blood vessels in the infratemporal fossa.
• Excessive volumes of local anesthetic solution deposited into a
restricted area.
Prevention:
• Properly care for and handle dental local anesthetic cartridges.
• Use aseptic technique.
• Practice atraumatic insertion and injection technique.
• Avoid repeat injections and multiple insertions. 64

Management:
• Prescribe heat therapy, warm saline rinses, analgesics, and, if
necessary, muscle relaxants.
• Advise to initiate physiotherapy consisting of opening and
closing the mouth.
• Chewing gum (sugarless) is yet another means of providing
lateral movement of the TMJ.
• Surgical intervention to correct chronic dysfunction maybe
indicated in some instances.
65

SoftTissueInjury:
• Self-inflicted trauma to the lips and tongue is frequently
caused by the patient inadvertently biting or chewing these
tissues while still anesthetized.
Causes:
• The primary reason is the fact that dental patients receiving
local anesthetic during their treatment usually are dismissed
from the dental office with residual soft tissue numbness.
Prevention:
• A cotton roll can be placed between the lips and the teeth if
they are still anesthetized at the time of discharge.
• Warn the patient and the guardian against eating, drinking hot
fluids, and biting on the lips or tongue.
66

Management:
• Analgesics for pain, as necessary.
• Petroleum jelly or other lubricant to cover a lip lesion and
minimize irritation.
• Lukewarm saline rinses to aid in decreasing any swelling that
may be present.
67
Traumatized lip

Hematoma:
• The effusion of blood into extravascular spaces can be caused
by inadvertent nicking of a blood vessel (artery or vein) during
administration of a local anesthetic.
Causes:
• Hematoma may result from arterial or venous puncture after a
posterior superior alveolar or inferior alveolar nerve block.
Prevention:
• Knowledge of the normal anatomy involved in the proposed
injection is important.
• Use a short needle for the PSA nerve block to decrease the
risk of hematoma. 68

Management:
• Immediate: When swelling becomes evident during or
immediately after a local anesthetic injection, direct pressure
should be applied to the site of bleeding.
• Subsequent: The patient may be discharged once bleeding
stops. Advise the patient about possible soreness and
limitation of movement (trismus).
• Discoloration will likely occur as a result of extravascular blood
elements; it is gradually resorbed over 7 to 14 days.
• Do not apply heat to the area for at least 4 to 6 hours after the
incident.
• Ice maybe applied to the region immediately on recognition of
a developing hematoma.
69

Infection:
• Infection subsequent to local anesthetic administration in
dentistry is an extremely rare occurrence since sterile
disposable needles and glass cartridges have been introduced.
Causes:
• Contamination of the needle before administration of the
anesthetic.
Prevention:
• Use sterile disposable needles.
• Store cartridges aseptically.
• Properly prepare the tissues before penetration.
70

Management:
• Low-grade infection, which is rare, is seldom recognized
immediately.
• Immediate treatment consists of those procedures used to
manage trismus; heat and analgesic if needed, muscle relaxant
if needed, and physiotherapy.
71

Edema:
• Edema related to local anesthetic administration is seldom
intense enough to produce significant problems such as
airway obstruction.
Causes
• Trauma during injection.
• Infection.
• Allergy.
• Hemorrhage.
• Injection of irritating solutions.
72

Prevention:
• Proper care for and handle the local anesthetic
armamentarium.
• Use atraumatic injection technique.
• Complete an adequate medical evaluation of the patient
before drug administration.
Management:
• Reduction of the swelling as quickly as possible.
• 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 is
summoned.
73

Techniques of Local Anesthesia:
• Three major types of local anesthetic injection can be
differentiated: local infiltration, field block, and nerve block.
74
Small terminal nerve
endings in the area
of the dental
treatment are
flooded with local
anesthetic solution.
Local anesthetic is
deposited near the
larger terminal
nerve branches.
Local anesthetic is
deposited close to a
main nerve trunk.

Maxillary Injection Techniques:
Numerous injection techniques are available to provide clinically
adequate anesthesia of the teeth and soft and hard tissues in
the maxilla.
• Posterior Superior Alveolar Nerve Block.
• Middle Superior Alveolar Nerve Block.
• Anterior Superior Alveolar Nerve Block (lnfraorbital Nerve
Block).
Palatal Approach:
• Greater Palatine Nerve Block
• Nasopalatine Nerve Block
75

PosteriorSuperiorAlveolarNerveBlock:
Areas Anesthetized:
• Pulps of the maxillary third, second, and first molars (entire
tooth = 72%; mesiobuccal root of the maxillary first molar not
anesthetized= 28%)
• Buccal periodontium and bone overlying these teeth.
Landmarks:
• Mucobuccal fold
• Maxillary tuberosity
• Zygomatic process of the maxilla
Volume: 0.9 – 1.8mL
76

MiddleSuperiorAlveolarNerveBlock:
Areas Anesthetized:
• Pulps of the maxillary first and second premolars, mesiobuccal
root of the first molar.
• Buccal periodontal tissues and bone over these same teeth
Landmarks:
• Mucobuccal fold over maxillary 2nd premolar.
Volume: 0.9 to 1.2mL
77

AnteriorSuperiorAlveolarNerveBlock(lnfraorbitalNerve
Block)
Areas Anesthetized
• Pulps of the maxillary central incisor through the canine on
the injected side
• In about 72% of patients, pulps of the maxillary Premolars and
mesiobuccal root of the first molar; Buccal(labial)
periodontium and bone of these same teeth
• Lower eyelid, lateral aspect of the nose, upper lip.
Landmarks:
• Mucobuccal fold
• Infraorbital notch
• Infraorbital foramen
Volume: 0.9 to 1.2mL
78

GreaterPalatineNerveBlock:
Areas Anesthetized:
• The posterior portion of the hard palate and its overlying soft
tissues.
Landmarks:
• Greater palatine foramen and junction of the maxillary
alveolar process and palatine bone.
Volume of Anesthesia: 0.45 to 0.6 mL
79

NasopalatineNerveBlock:
Areas Anesthetized:
• Anterior portion of the hard palate (soft and hard tissues)
bilaterally from the mesial of the right first premolar to the
mesial of the left first premolar.
Landmarks:
• Central incisors and incisive papilla.
Volume: 0.3 mL
80

Maxillary(2nd division)NerveBlock:
Areas Anesthetized:
• Pulpal anesthesia of the maxillary teeth on the side of the
block
• Buccal periodontium and bone overlying these teeth
• Soft tissues and bone of the hard palate and part of the soft
palate
• Skin of the lower eyelid, side of the nose, cheek, and upper lip
Landmarks:
• Mucobuccal fold at the distal aspect of the maxillary second
molar
• Zygomatic process of the maxilla
Volume: 1.8ml
81

Mandibular Injection Techniques:
The different injection techniques for mandibular nerve blocks
are:
• INFERIOR ALVEOLAR NERVE BLOCK
• BUCCAL NERVE BLOCK
• MENTAL NERVE BLOCK
• INCISIVE NERVE BLOCK
• THE GOW-GATES TECHNIQUE
• VAZIRANl-AKINOSI CLOSED-MOUTH MANDIBULAR BLOCK
83

InferiorAlveolarNerveBlock:
Areas Anesthetized:
• Mandibular teeth to the midline
• Body of the mandible
• Buccal mucoperiosteum, mucous membrane anterior to the
mental foramen (mental nerve)
• Anterior two thirds of the tongue and floor of the oral cavity
(lingual nerve)
• Lingual soft tissues and periosteum (lingual nerve)
Landmarks:
• Coronoid notch (greatest concavity on the anterior border of
the ramus)
• Pterygomandibular raphe (vertical portion)
• Occlusal plane of the mandibular posterior teeth
Volume: 1.5ml
84

BuccalNerveBlock:
Area Anesthetized:
• Soft tissues and buccal periosteum to the mandibular molar
teeth.
Landmarks:
• Mandibular molars, mucobuccal fold.
Volume: 0.3ml
85

MandibularNerveBlock:Gow-GatesTechnique:
Areas Anesthetized:
• Buccal mucoperiosteum and mucous membranes on the side
of injection
• Lingual soft tissues and periosteum
• Body of the mandible, inferior portion of the ramus
• Skin over the zygoma, posterior portion of the cheek, and
temporal regions
86

Landmarks:
• Extraoral
• Lower border of the tragus (intertragic notch).
• Corner of the mouth
• Intraoral
• Height of injection established by placement of the needle tip
just below the mesiolingual (mesiopalatal) cusp of the
maxillary second molar.
• Penetration of soft tissues just distal to the maxillary second
molar at the height established in the preceding step.
Volume: 1.8-3ml
87

Vazirani-AkinosiClosedMouth Mandibular
Block:
Areas Anesthetized:
• Body of the mandible and inferior portion of the ramus
• Buccal mucoperiosteum and mucous membrane anterior to
the mental foramen
(lingual nerve)
• Lingual soft tissues and periosteum (lingual nerve)
Landmarks:
• Mucogingival junction of the maxillary third (or second) molar
• Coronoid notch on the mandibular ramus
Volume: 1.5-1.8ml
88

MENTALNERVEBLOCK:
Areas Anesthetized:
• Buccal mucous membranes anterior to the mental foramen
(around the second premolar) to the midline and skin of the
lower lip and chin.
Landmarks:
• Mandibular premolars
• Mucobuccal fold
Volume: 0.6ml
89

INCISIVENERVEBLOCK:
Areas Anesthetized:
• Buccal mucous membrane anterior to the mental foramen,
usually from the second premolar to the midline.
• Lower lip and skin of the chin.
• Pulpal nerve fibers to the premolars, canine, and incisors.
Landmarks:
• Mandibular premolars
• Mucobuccal fold
Volume: 0.6ml
90

Methods of AchievingAnesthesiain
Endodontics:
Local Infiltration:
• Local infiltration is commonly used to provide pulpal
anesthesia in maxillary teeth.
• It is usually effective in endodontic procedures when severe
inflammation or infection is not present.
Regional Nerve Block:
• Regional nerve block anesthesia is recommended in cases
where infiltration anesthesia may be ineffective or
contraindicated.
92

lntraosseous Injection:
• IO injections can provide anesthesia profound enough to allow
painless access into the pulp chamber for removal of pulpal
tissue.
lntraseptal Injection:
• This is a variation of IO and periodontal ligament (PDL)
injections and may be used as an alternative to these
techniques.
93

Periodontal Ligament Injection:
• The PDL injection maybe an effective method of providing
anesthesia in pulpally involved teeth if infection and severe
inflammation are not present.
lntrapulpal Injection:
• This technique may be used once the pulp chamber is exposed
surgically or pathologically.
94

References:
• Handbook of Local Anesthesia- Stanley F. Malamed(6th Edition)
• Essentials of Medical Pharmacology- KD Tripathi(7th Edition)
95

Local anesthetic agents by Dr. Deepesh

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