The document discusses local anesthesia, outlining its historical development, definitions, mechanisms of action, and pharmacology. It describes key local anesthetic agents, their properties, methods of induction, and the physiological processes involved in nerve conduction and pain sensation. Additionally, it highlights the effects of local anesthetics on blood vessels and factors influencing their absorption and effectiveness in clinical applications.

1. Local Anesthesia
Dr. Rinisha Sinha
MDS Part I

2. Contents
Introduction
Historical Background
Definition
Neurophysiology of Local Anesthetics
Mechanism of Action
Theories of mechanism of action of Local Anesthetics
Classification of Local Anesthetics
Composition of Local Anesthetics
Pharmacology of Local Anesthetics
Pharmacology of Vasoconstrictors
Vasoconstrictors Classification
Calculation of Maximum Doses
Lidocaine HCl and Bupivacaine HCl

3. Introduction
•What is Pain ???
An unpleasant emotional experience usually initiated by
a noxious stimulus and transmitted over a specialized
neural network to the central nervous system where it is
interpreted as such.
An unpleasant sensory and emotional experience
associated with actual or potential tissue damage, or
described in terms of such damage.
Reference : Monheims’s Local Anesthesia and Pain Control in Dental Practice – 7th edition
Reference : Bonica JJ. The need of taxonomy. Pain - 1979

4. PAIN THEORIES
Specificity Theory
Descartes in 1644
Intensive/Summation /
Intensity Theory
Erb in 1874
Reference : Kenins 1988; Perl 2007; Rey 1995

5. Gate Control Theory
Melzack and Wall, 1965

6. Historical Background
•Cocaine
 1st local anesthetic agent
 Isolated by ALBERT NEIMAN, 1860 from the leaves of the coca
tree.
 Anesthetic action was demonstrated by Karl Koller, 1884
 Because of high toxicity and addictive effects of cocaine, a
safer local aesthetic was sought.

7. •Prococaine
 An ester derivative of cocaine
 Produced by Einhorn in 1905
 Anesthetic properties were identified
by Biberfield
 Introduced into clinical practice by
Braun
 Brand name : Novocaine ( New
Cocaine )

8. •LIDOCAINE
 During the 2nd world war Swedish scientist
Nils Lofgren made this amide compound in
1948
 Anaesthetic property discovered by T. Gordh
in 1949
 Worked faster and more effectively than
cocaine and is not addictive
•Articaine
Introduced in 1970
Lidocaine and Articaine is now the most commonly used local
anesthetic agents in dentistry.

9. DEFINITION
•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.
•It is defined as transient regional loss of sensation to a
painful or potentially painful stimulus resulting from a
reversible interruption of a peripheral conduction
along a specific neural pathway to its central
integration & perception in the brain.
Reference : Covino BG, Vassallo HG. Local Anesthetics: Mechanisms of Action and Clinical Use. Grune & Stratton;
1976
• Important feature of local anesthesia
– it produces this loss of sensation without inducing
loss of consciousness
Reference : Daniel Laskin

10. Methods to induce Local
Anesthesia
Mechanical trauma
(compression of tissues)
Low temperature
Anoxia
Chemical irritants
Neurolytic agents such as
alcohol and phenol
Chemical agents such as local
anesthetics

11. Desirable Properties of Local
Anesthetics
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 tissue
or is applied topically 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.

12. An IDEAL local anesthetic
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
deterioration.
Reference : Bennett CR. Monheim’s Local Anesthesia and Pain Control in Dental Practice. 1974

13. Fundamentals of Impulse Generation
and Transmission
Concept – prevents Generation + Conduction of a Nerve Impulse
IMPULSE IMPULSE

14. THE NEURON

15. THE AXON

16. PHYSIOLOGY OF
PERIPHERAL NERVES
•Function of a nerve  to carry messages from
one part of the body to another
•IMPULSES – Messages in the form of electrical
action potential.
•Action potentials are transient depolarizations
of the membrane that result
from a brief increase in the permeability of the
membrane to sodium,
usually also from a delayed increase in its
permeability to potassium.
Thermal
Chemical
Electrical
Impulse conduction is like the active progress of a spark along a fuse of gunpowder
Reference : de Jong RH. Local Anesthetics. 2nd ed - 1977
Reference :
Heavner JE.
Molecular action
of local
anesthetics. 1991

17. ELECTROPHYSIOLOGY OF NERVE CONDUCTION

19. • 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.
• The FIRING THRESHOLD is the magnitude of the decrease in
negative transmembrane potential that is necessary to initiate an
action potential (impulse).
ELECTROCHEMISTRY OF NERVE CONDUCTION

20. Immediately after a stimulus has initiated an action
potential, a nerve is unable, for a time, to respond to
another stimulus regardless of its strength.
It lasts for about the duration of the main part of the
action potential.
The absolute refractory period is followed by a relative
refractory period, during which a new impulse can be
initiated but only by a stronger than-normal stimulus.
Absolute Refractory Period
Relative Refractory Period

21. MODE AND SITE OF ACTION
Local anesthetics can interfere with the excitation process in a
nerve membrane in one or more of the following ways:
Altering the
basic resting
potential of
the nerve
membrane
Altering the
threshold
potential
(firing level)
Decreasing the
rate of
depolarization
Prolonging the
rate of
repolarization
Primary effects of Local Anaesthesia occur during the
Depolarization Phase of Action Potential
Reference : de Jong RH, Wagman IH. Physiological mechanisms of peripheral nerve block by local anesthetics. 1963

22. Proposed Mechanism of Action
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 !!!

23. MECHANISM OF ACTION
•ACETYLCHOLINE THEORY
Acetylcholine was involved in nerve conduction in addition to its
role as a neurotransmitter at nerve synapses.
No evidence exists indicating that acetylcholine is involved in
neural transmission along the body of the neuron.
• CALCIUM DISPLACEMENT THEORY
Local anesthetic nerve block was produced by the displacement of
calcium from some membrane site that controlled permeability
to sodium.
Evidence that varying the concentration of calcium ions bathing a
nerve does not affect local anesthetic potency has diminished the
credibility of this theory.
Reference : Dettbarn WD. The acetylcholine system in peripheral nerve. 1967
Reference : Goldman DE, Blaustein MP. Ions, drugs and the axon membrane. 1966

24. •SURFACE CHARGE (REPULSION) THEORY
Local anesthetics acted by binding to the nerve membrane and
changing the electrical potential at the membrane surface.
Cationic (RNH+) drug molecules are aligned at the membrane-
water interface, and some of the local anesthetic molecules carry a
net positive charge, they make the electrical potential at the
membrane surface more positive, thus decreasing the excitability
of the nerve by increasing the threshold potential.
The resting potential of the nerve membrane is unaltered by local
anesthetics (they do not become hyperpolarized), and that
conventional local anesthetics act within membrane channels
rather than at the membrane surface.
The surface charge theory cannot explain the activity of
uncharged anesthetic molecules in blocking nerve impulses (e.g.,
benzocaine).
Reference : Wei LY. Role of surface dipoles on axon membrane. 1969

25. MEMBRANE EXPANSION THEORY
Reference : Lee AG. Model for action of local anesthetics. 1976; Seeman P. The membrane actions of anesthetics
and tranquilizers. 1972
Local anesthetic molecules (highly lipid soluble)
diffuse to hydrophobic regions of excitable
membranes
Producing a general disturbance (change in
configuration) of the cell membrane structure
(lipoprotein matrix of the nerve membrane)
Expanding critical regions in the membrane
Decreased diameter of sodium channels thus,
Preventing an increase in the permeability to
sodium ions
Inhibition of both sodium conductance and neural
excitation

26. SPECIFIC RECEPTOR THOERY
Local anesthetics act by binding to specific receptors on the sodium
channel
Direct action; not mediated by some change in the general
properties of the cell membrane.
Both biochemical and electrophysiological studies have indicated
that a specific receptor site for local anaesthetic agents exists in the
sodium channel either on its external surface or on the internal
axoplasmic surface.
Once the local anaesthetic has gained access to the receptors,
permeability to sodium ions is decreased or eliminated and nerve
conduction is interrupted.
References : Strichartz GR, Ritchie JM. The action of local anesthetics on ion channels of excitable tissues. 1987.
Scholz A. Mechanisms of (local) anaesthetics on voltage-gated sodium and other ion channels. 2002
References : Butterworth JFIV, Strichartz GR. Molecular mechanisms of local anesthesia: a review. 1990; Ritchie
JM. Mechanisms of action of local anesthetic agents and biotoxins. 1975

27. CLASSIFICATION
Injectable
anesthetic
Low potency, short duration - Procaine
Chloroprocaine
Intermediate potency and duration -
Lidocaine (Lignocaine) Prilocaine
High potency, long duration -
Tetracaine (Amethocaine) Bupivacaine
Ropivacaine Dibucaine (Cinchocaine)
Surface
anesthetic
Soluble - Cocaine Lidocaine,
Tetracaine, Benoxinate
Insoluble - Benzocaine,
Butylaminobenzoate
(Butamben), Oxethazaine

28. CHEMISTRY
Weak bases with
amphiphilic property.
A hydrophilic secondary
or tertiary amine on
one side and a lipophilic
aromatic residue on the
other are joined by an
alkyl chain through an
ester or amide linkage.

29. DISSOCIATION OF LOCAL
ANAESTHESIA
• Local anesthetics are available as acid salt (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+
• In case of low pH , the equilibrium shifts to the left.
RNH+ > RN + H+
• In case of higher pH, the equilibrium shifts towards the right.
RNH+ < RN + H+
• The relative proportion of ionic forms also depends on the dissociation
constant (pKa).
When Ph has same value as pKa of local anesthetic,
exactly 50% of the drug exists in RNH+ form and 50% in the RN form

30. Henderson-Hasselbalch
equation
• To determine the percentage of drug existing in either form
( cationic form or as base )
pH = pKa + log [cationic base]
[acid]

31. INDUCTION OF LOCAL
ANESTHETICS
• Following administration of a local anesthetic into the soft tissues
near a nerve, molecules of the local anesthetic traverse the
distance from one site to another according to their concentration
gradient.
• During induction phase of anesthesia, local anesthetic moves from
its extra neural site of deposition towards the nerve.
• This process is termed as DIFFUSION.
• It is the unhindered migration of molecules or ions through a fluid
medium under the influence of the concentration gradient.
• Penetration of an anatomic barrier to diffusion occurs when a drug
passes through a tissue that tends to restrict free molecular
movement
Greatest barrier to penetration of local anesthetics : PERINEURIUM

32. Composition of nerve fibers and bundles within a peripheral nerve
Most significant factor governing the rate of diffusion
CONCENTRATION GRADIENT
The greater the initial concentration of the local anesthetic, the faster the
diffusion of its molecules and the more rapid its onset of action
Fasciculi located near
the surface of the
nerve.
The first ones reached
by the local anesthetic.
Hence, are exposed to a
higher concentration of
LA.
Usually blocked
completely shortly after
injection of a local
anesthetic
Mantle Bundles
Fasciculi found closer to
the center of the nerve.
Contacted by local
anesthetic after much
delay.
Hence, are exposed to a
lower concentration of
LA.
Core Bundles

33. It is defined as the period from deposition of the
anesthetic solution to complete conduction
blockade.
INDUCTION TIME
Several factors control
induction time of a given
drug
Under operator’s control
the concentration of the drug
the Ph of local anesthetic molecule
Not under clinician’s control
Diffusion Constant of the anesthetic drug
The Anatomic Diffusion barriers of the nerve

34. Some of the
drug is
absorbed by
nonneural
tissues (e.g.,
muscle, fat)
Some is diluted
by interstitial
fluid
Some is
removed by
capillaries and
lymphatics
from the
injection site
Ester-type
anesthetics are
hydrolyzed by
plasma
cholinesterase
The solution diffuses three-dimensionally
according to prevailing concentration gradients
BLOCKING PROCESS
Sum total effect : Decrease the local anesthetic concentration outside the nerve
however, the concentration of local anesthetic within the nerve continues to rise as
diffusion progresses.
These processes continue until an equilibrium results between intraneural and extra
neural concentrations of anesthetic solution.

35. Recovery From Local Anesthetic
Block
• Follows the Same Diffusion Patterns as induction, BUT in the
Reverse Order.
• Extra neural concentration of local anesthetic is continually
depleted by
• Intraneural concentration of local anesthetic remains relatively
stable.
VASCULAR
UPTAKE
DISPERSIONDIFFUSION
Once the concentration gradient has been reversed with the intraneural
concentration exceeding the extra neural concentration
Anesthetic molecules begin to diffuse out of the nerve.

36. Recurrence of Immediate
Profound Anesthesia
• Concentration of Local Anesthesia
• Core fibers < Mantle fibers
• After deposition of a new high
concentration
• Increased concentration in the
core fibers
Difficulty Re-achieving
Profound Anesthesia
• Effective control of pain does not
develop.
• Tachyphylaxis
• Increasing tolerance to a drug that
is administered repeatedly
• If nerve function returns before
reinjection
Re-administration of Local
Anesthetic
• Occasionally a dental procedure lasts longer than the duration of clinically
effective pain control, and a repeated injection is required.
• This repeated injection results in the immediate return of profound
anesthesia.
Rapid onset of profound anesthesia =
Residual local anesthetic (in the nerve) + the
newly deposited local anesthetic
Reference : Cohen EN, Levine DA, Colliss JE, Gunther RE. The role of pH in the development of tachyphylaxis to
local anesthetic agents. Anesthesiology. 1968; Scott DB. Tachyphylaxis and local anesthetics. 1986.
Edema, localized hemorrhage, clot
formation, transudation, hypernatremia,
and decreased pH of tissues

37. COMPOSITION OF LOCAL
ANESTHETIC

38. Balanced Chemical
Characteristics
LIPOPHILIC HYDROPHILIC
Ability to diffuse into lipid
rich nerves is DIMINISHED
Little Clinical Importance;
Since it is INSOLUBLE in water
and unable to diffuse through
interstitial tissue

39. • When injected into soft tissues, local anesthetics exert
pharmacologic action on blood vessels in the area
• All local anesthetics possess a degree of vasoactivity, producing
dilation of the vascular bed into which they are deposited
Procaine, the most potent vasodilator among local anesthetics, is
injected occasionally to induce vasodilation when peripheral flow
has been compromised.
Tetracaine, chloroprocaine and propoxycaine also possess
vasodilating properties to varying degrees.
Cocaine is the only local anesthetic that consistently produces
vasoconstriction. The initial action of cocaine is vasodilation
followed by an intense and prolonged vasoconstriction.
PHARMACOLOGY OF LOCAL
ANESTHETICS
Ester local anesthetics are potent vasodilating drugs
Reference : Benowitz NL. Clinical pharmacology and toxicology of cocaine. 1993

40. ORAL ROUTE
• Local anesthetics are
absorbed poorly
(Cocaine)
• Most local anesthetics
(especially lidocaine)
undergo a significant
hepatic first-pass effect.
• Fraction of the drug dose
is carried to the liver,
where approximately
72% of the dose is bio
transformed into
inactive metabolites.
• Hampered the use of
lidocaine as an oral
antidysrhythmic drug.
TOPICAL ROUTE
• Different rate of
absorption after
application to mucous
membrane
• In the TRACHEAL
MUCOSA : as rapid as
with intravenous (IV)
administration -
epinephrine, lidocaine,
atropine, naloxone, and
flumazenil
• In the PHARYNGEAL
MUCOSA : Slower
Absorption
• In the ESOPHAGEAL /
BLADDER MUCOSA :
Even Slower Uptake
INJECTION
• Rate of uptake
(absorption) of local
anesthetics
(subcutaneous,
intramuscular, or IV) is
related to both
• the vascularity of the
injection site
• the vasoactivity of the
drug
• Most rapid elevation
of blood levels and is
used clinically in the
primary management
of ventricular
dysrhythmias
In 1984,
Astra Pharmaceuticals and
Merck Sharp & Dohme
introduced an analogue of
lidocaine, tocainide
hydrochloride : effective orally
A eutectic mixture of local
anesthetics lidocaine and
prilocaine (EMLA) developed
capable of providing surface
anesthesia of intact skin
Reference : Soliman IE, Broadman
LM, Hannallah RS, McGill WA. 1988
An aid before venipuncture in
needle-phobic patients
Reference : Schreiber S, Ronfani L,
Chiaffoni GP, et al. 2013
Reference : Otto CW. 2013:
Rapid IV administration 
high local anesthetic blood
levels  induce serious
adverse reactions

41. 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
• It is used primarily before painful procedures
such as venipuncture and other needle
insertions
• Because intact skin is a barrier to drug diffusion ,
EMLA is applied 1 hour before the procedure
• Satisfactory numbing of the skin
 occurs 1 hour after application
 reaches a maximum at 2 to 3 hours
 lasts for 1 to 2 hours after removal

42. PATTERNS OF DISTRIBUTION
Once absorbed into the blood, local anesthetics are distributed
throughout the body to all tissues

43. Rate at which the drug is absorbed into the CVS
Rate of distribution of the drug from the vascular compartment to the
tissues (more rapid in healthy patients than in those who are medically
compromised [e.g., congestive heart failure], thus leading to lower
blood levels in healthier patients)
Elimination of the drug through metabolic or excretory pathways
The Blood Level of the local anesthetic is influenced by
Decreasetheblood
levelofthelocal
anesthetic
Elimination half-life : Rate at which a local anesthetic is removed from the blood
time necessary for a 50% reduction in the blood level
One half-life = 50% reduction; two half-lives = 75% reduction;
three half-lives = 87.5% reduction; four half-lives = 94% reduction;
five half-lives = 97% reduction; six half-lives = 98.5% reduction

44. Hydrolyzed in the plasma by the
enzyme Pseudocholinesterase
Chloroprocaine : most rapidly
hydrolyzed; least toxic
Tetracaine : hydrolyzed 16 times
slower than chloroprocaine;
greatest potential toxicity.
Procaine : hydrolysis to p-
aminobenzoic acid (PABA); excreted
unchanged in urine
More complex
Primary site of biotransformation :
the liver
lidocaine, mepivacaine, etidocaine,
and bupivacaine
Prilocaine undergoes primary
metabolism in the liver, with some
occurring in the lung
Articaine, a hybrid molecule,
undergoes metabolism in both the
blood (primarily) and the liver.
METABOLISM
(BIOTRANSFORMATION, DETOXIFICATION)
The body biologically transforms the active drug into one that is
pharmacologically inactive.
Reference : Kalow W. 1952
An absolute contraindication implies that under no circumstance should
the drug in question be administered to the patient as the possibility of
potentially toxic or lethal reactions is increased.
A relative contraindication means that the drug in question may be
administered to the patient after careful weighing of the risk associated
with use of the drug versus the potential benefit to be gained, and if an
acceptable alternative drug is not available.
Reference : Gutenberg LL,
Chen JW, Trapp L. 2013;
Arthur GR. 1981
Reference : Oertel R, Berndt
A, Kirch W. 1996; Oertel R,
Rahn R, Kirch W. 1997

45. • The Kidneys are the primary excretory organ for both the local
anesthetic and its metabolites.
• A proportion 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.
• Procaine appears in the urine as PABA (90%) with 2%
unchanged.
• 10 percent of a Cocaine dose is found in the urine unchanged.
• Amides : usually present in the urine as the parent compound in
a greater percentage than the esters, because of their more
complex process of biotransformation.
• % OF PARENT DRUG FOUND IN URINE = less than 3% lidocaine,
1% mepivacaine, and 1% etidocaine is found unchanged in the
urine.
EXCRETION

46. SYSTEMIC ACTIONS OF LA
• 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.
• Centbucridine (a quinoline derivative) : 5 – 8 times as potent a local
anesthetic as lidocaine, with an equally rapid onset of action and an
equivalent duration
• Local anesthetics are absorbed from their site of administration into
the circulatory system, which effectively dilutes them and carries them
to all cells of the body.
• The resulting blood level of the local anesthetic depends on its
rate of uptake from the site of administration into the circulatory
system (increasing the blood level)
rates of distribution in tissue and biotransformation (in the liver),
processes that remove the drug from the blood (decreasing the blood
level)
Central
Nervous
System
Cardiovascular
System
Respiratory
System
Local Tissue
Toxicity

47. ACTIONS ON CNS
• Local anesthetics readily crosses blood brain barrier
• Pharmacological action : DEPRESSION
• At low blood levels (therapeutic / non-toxic) : No CNS Effect
• At higher levels, the primary clinical manifestation : Generalized tonic-
clonic convulsion Some local anesthetics (e.g. procaine,
lidocaine, mepivacaine, prilocaine,
even cocaine) have demonstrated
anticonvulsant properties
When administered intravenously, local
anesthetics increase the pain reaction
threshold and produce a degree of
analgesia
Cocaine used for its euphoria-inducing
and fatigue-lessening actions
Procaine used as a rejuvenating drug
Procaine, mepivacaine, and lidocaine :
terminate or decrease the duration of
grand mal and petit mal seizures
Bernhard CG, Bohm E. 1956
Lidocaine appeared to be the most promising anticonvulsant
Berry CA, Sanner JH, Keasling HH; 1961
De Jong RH. 1994

48. ACTIONS ON CVS
• Local anesthetics have direct action on the myocardium and peripheral
vasculature.
• They produce a myocardial depression that is related to the local anesthetic
blood level.
• Therapeutic blood levels of lidocaine for antidysrhythmic activity ranges from
1.8 to 6 microgram/ml.
• Lidocaine is used clinically primarily in the management of ventricular
tachycardia.
• It is also used as a drug in advanced cardiovascular life support and in
management of cardiac arrest caused by ventricular fibrillation.
• Direct cardiac actions of local anesthetics at blood levels greater than
therapeutic level include a decrease in myocardial contractility and decreased
cardiac output, both of which lead to circulatory collapse.
Decrease the electrical excitability of the myocardium
Decrease the conduction rate
Decrease the force of contraction

49. • Cocaine produces vasoconstriction at commonly employed
dosages.
• Ropivacaine causes cutaneous vasoconstriction.
• All other local anesthetics produce
A peripheral vasodilation through relaxation of
smooth muscle in the walls of blood vessels
Increased blood flow to and from the site of
local anesthetic deposition
Increases the rate of drug absorption
Decreased depth and duration of local
anesthetic action
Increased bleeding in the treatment area and
Increased local anesthetic blood levels

50. RESPIRATORY ACTION
• Local anesthetics exert a dual effect
on respiration
• At non-overdose levels,
they have a direct relaxant action on
bronchial smooth muscles
• At overdose levels,
they may produce respiratory arrest
as a result of generalized CNS
depression
• Respiratory function is unaffected by
local anesthetics until near-overdose
levels are achieved

51. LOCAL TISSUE TOXICITY
• Skeletal muscles appears to be more sensitive than other
tissues to the local irritant properties of local anesthetics.
• Intramuscular and intraoral injection of articaine, lidocaine,
mepivacaine, prilocaine, bupivacaine and etidocaine can
produce skeletal muscle alterations.
• It appears that LONGER – ACTING local anesthetics causes
MORE localized skeletal muscle damage than shorter – acting
drugs
• The changes that occur in skeletal muscle are reversible, with
muscle regeneration being complete within 2 weeks after local
anesthetic administration.
Reference : Zink W, Graf BM, Sinner B, Martin E, Fink RH, Kunst G. 2002; Hinton RJ, Dechow PC, Carlson DS. 1986

52. MISCELLANEOUS ACTIONS
Drug Interactions
• CNS depressants (e.g.,
opioids, antianxiety drugs,
phenothiazines, barbiturates)
+ local anesthetics =
Potentiation of the CNS
depressant actions
• Ester local anesthetics +
succinylcholine (depolarizing
muscle relaxant) require
plasma pseudocholinesterase
for hydrolysis = Prolonged
apnea may result from
concomitant use of these
drugs
Malignant Hyperthermia
• Pharmacogenic disorder in which
a genetic variant in an individual
alters that person’s response to
certain drugs
• Acute clinical manifestations :
tachycardia, tachypnea, unstable
blood pressure, cyanosis,
respiratory and metabolic
acidosis, fever (temperature as
high as 42°C [108°F], muscle
rigidity, and death.
• Mortality rates of 80% in the 1980s
have been decreased to less than 5%
(2006)
Reference : Bevan DR, Donati F. Succinylcholine apnoea:
attempted reversal with anticholinesterases. 1983
Reference : Rosenberg H, Pollock N, Schiemann A, Bulger
T, Stowell K. Malignant hyperthermia: a review. 2015

53. • Vasoconstrictors are drugs that constrict blood vessels and thereby
control tissue perfusion.
• They are added to local anesthetic solutions to oppose the inherent
vasodilatory actions of the local anesthetics
PHARMACOLOGY OF
VASOCONSTRICTORS
Vasoconstrictors decrease blood flow (perfusion) to the site of drug administration
Absorption of the local anesthetic into the cardiovascular system is slowed, resulting in
lower anesthetic blood levels
Decreasing the risk of local anesthetic toxicity from over administration of the drug
More local anesthetic diffuses into the nerve, where it remains longer, thereby
increasing the duration of action of most local anesthetics.
Decrease bleeding at the site of administration

54. VASOCONSTRICTORS
CLASSIFICATION
CATECHOLAMINES
• Epinephrine
• Norepinephrine
• Dopamine
• Levonordefrin
• Isoproterenol
NON -
CATECHOLAMINES
• Amphetamine
• Methamphetamine
• Hydroxy-
amphetamine
• Ephedrine
• Mephetermine

55. LOCAL ANESTHETICS - FORMULATION
• Biologically active substance are frequently administered as very
dilute solutions which can be expressed as
Parts of Active Drug per 100 parts of solution
(grams percent)
E.g. 2 % solution = 2 grams = 2000 mg = 20 mg
100 cc’s 100 cc’s 1 cc’s
• Maximum recommended doses of Local Anesthetics = milligram of
drug per unit body weight

57. LIDOCAINE HCL
• Classification: Amide
• Chemical formula: 2-diethylamino-2’,6-
acetoxylidide hydrochloride
• Prepared by: Nils Lofgren 1943
• FDA approved: November 1948
• Potency: TWICE (compared with
procaine)
• Toxicity: TWICE (compared to procaine)
• Metabolism: In the liver, by the
microsomal fixed-function oxidases, to
monoethylglyceine and xylidide
• Excretion: Via the kidneys; less than 10%
unchanged, more than 80% various
metabolites
• Vasodilating properties:
 Considerably less than those of procaine
 Greater than those of prilocaine or
mepivacaine
• pKa = 7.9
• pH of plain solution = 6.5
• pH of vasoconstrictor - containing
solution = 3.5
• Onset of action: Rapid (3 to 5 minutes)
• Effective dental concentration: 2%
• Anesthetic half-life: 1.6 hours (~90
minutes)
• Topical anesthetic action: Yes
• Maximum recommended dose:
The maximum recommended dose by the
FDA of lidocaine with or without
epinephrine
 Adults = 3.2mg/lb of body weight
 Pediatric patient = 7.0 mg/kg of body
weight
 An absolute maximum dose of 500
mg

58. BUPIVACAINE HCL
• Classification: Amide
• Chemical formula: 1-Butyl-2’,6’-
pipecoloxylidide hydrochloride
• Prepared by: A.F. Ekenstam in 1957
• FDA approved: October 1972
• Potency: Four times that of
lidocaine, mepivacaine and
prilocaine
• Toxicity: Less than four times that
of lidocaine and mepivacaine
• Metabolism: Metabolized in the
liver by amidases
• Excretion: Via the kidney
• Vasodilating properties: Relatively
significant
• pKa = 8.1
• pH of plain solution = 4.5 to 6.0
• pH of vasoconstrictor-containing
solution = 3.0 to 4.5
• Onset of action: Slower onset
time than other commonly used
local anesthetics (e.g. 6 to 10
minutes)
• Anesthetic half-life = 2.7 hrs
• Maximum recommended dose:
The FDA maximum recommended
dose of bupivacaine is 90 mg.

60. The Armamentarium
Regional Analgesia
Techniques for Injection : BASIC POINTS
Maxillary Anesthesia Techniques
Mandibular Anesthesia Techniques
Anesthetic Complications
Factors in selection of Local Anesthetics for a patient
Management in Special Patients
Recent advances
Conclusion
References
Contents

61. THE SYRINGE THE NEEDLE
THE CARTRIDGE
ADDITIONAL
ARMAMENTARIUM
THE
ARMAMENTARI
UM

62. THE SYRINGE
• It is the vehicle whereby the content of the anesthetic cartridge is
delivered through the needle to the patient.
Non-aspirating syringes are unacceptable as they
increases the risk of inadvertent intravascular drug administration.

63. The American Dental Association criteria for
acceptance of Local Anesthetic Syringes
include
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.)
They should be capable of accepting a wide variety of cartridges and
needles of different manufacture, and should permit repeated use.
They should be inexpensive, self-contained, lightweight, and simple to
use with one hand.
They should provide effective aspiration and be constructed so that blood
may be easily observed in the cartridge.
Reference : Council on Dental Materials and Devices. American National Standards Institute/American Dental
Association specification no. 34 for dental cartridge syringes, ISO 9997:1999, 2016

64. Breech-Loading, Metallic, Cartridge-Type,
Aspirating
The term breech loading implies that the cartridge
is inserted into the syringe from the side of the
barrel of the syringe.
Wiener et al. compared “regular” and “petite” syringes
used by dental and dental hygiene students
62.2% preferred the petite syringe as it gave them better
control during injections and aspiration

65. Breech-Loading, Plastic, Cartridge-Type,
Aspirating
A plastic, reusable, dental aspirating syringe that is both
autoclavable and chemically sterilizable.
With proper care and handling, this syringe may be used for multiple
anesthetic administrations before it is discarded.

66. Breech-Loading, Metallic, Cartridge-Type,
Self-Aspirating
The incidence of positive aspiration may be as high as 10% to 15%
with some injection techniques (e.g., inferior alveolar nerve block).
Reference : Bartlett SZ. Clinical observations on the effects of injections of local anesthetic preceded by aspiration. 1972
An ASPIRATION TEST must be conducted purposefully by the administrator
before or during drug deposition.
introduced into the United States in 1981

67. PRESSURE SYRINGE
Brought about a renewed interest in
the Periodontal Ligament (PDL)
injection (also known as the Intra-
ligamentary injection).
The original pressure devices, Peripress
(Universal Dental Implements, Edison,
New Jersey, United States) and
Ligmaject (IMA Associates,
Bloomington, Indiana, United States),
were modeled after a device that was
available in dentistry in 1905 — the
Wilcox-Jewett obtunder.
These first-generation devices, using a
pistol grip, are larger than the newer,
pen-grip devices.

68. JET INJECTOR
In 1947, Figge and Scherer introduced a new approach to
parenteral injection—the jet or needle-less injection.
The most frequently used jet
injectors in dentistry are the
MadaJet and the Comfort-in
needle-free injection system.
The primary purpose of the jet
injector is to obtain topical
anesthesia before insertion of a
needle. In addition, it may be
used to obtain mucosal
anesthesia of the palate.

69. DISPOSABLE SYRINGES
These syringes contain a Luer-Lok screw-on
needle attachment with no aspirating tip.
Aspiration can be accomplished by pulling back
on the plunger of the syringe before or during
injection.
There is no thumb ring, aspiration with the plastic
disposable syringe requires the use of both
hands.
These syringes do not accept dental cartridges.
Care to avoid contaminating the multiuse vial
during this procedure.
Two-milliliter and 3-mL syringes with 25- or 27-
gauge needles are recommended when the
system is used for intraoral local anesthetic
administration.

70. SAFETY SYRINGES
Safety syringes minimize the risk of
an accidental needlestick injury
occurring to a dental health provider
with a contaminated needle after
administration of a local anesthetic.
These syringes possess a sheath
that “locks” over the needle when
it is removed from the patient’s
tissues, minimizing the risk of
accidental needlestick
Reference : USAF Dental Evaluation and Consultation Service:
1ShotTM Safety Syringe. March 2005. Updated October 2006

71. COMPUTER – CONTROLLED
LOCAL ANESTHETIC DELIVERY
SYSTEM
Advantages:
• Precise control of flow rate & pressure
produces more comfortable injection.
• ↑ tactile feel.
• Automatic Aspiration.
• Light weight hand piece.
Disadvantages :
• Additional Armamentarium.
• Cost.

72. THE NEEDLE
Problems
with Needle
Pain on
Insertion
Breakage
Pain on
withdrawal
Injury to the
Patient /
Administrator
Sterile disposable
needles should be
used.
If multiple injections are to
be administered, needles
should be changed after
three or four insertions in a
single patient.
Needles must never be
used on more than one
patient.
Needles should not be
inserted into tissue to
their hub unless this is
absolutely necessary
for success of the
injection.
The direction of a
needle should not be
changed while it is still
in tissue.
A needle should never
be forced against
resistance.
Needles should remain
capped until used and
should be made safe
immediately when
withdrawn.
Needles should be
discarded and destroyed
after use to prevent injury
or reuse by unauthorized
persons.

73. THE CARTRIDGE
Problems
Bubble
in the
cartridge
Extruded
stopper
Burning
on
injection
Sticky
stopper
Corroded
cap
“Rust”
on the
cap
Leakage
during
injection
Broken
cartridge
Dental cartridges are single-use
items that must never be used
on more than one patient.
Cartridges should be stored at
room temperature.
It is not necessary to warm
cartridges before use.
Cartridges should not be used
beyond their expiration date.
Cartridges should be checked carefully
for cracks, chips, and the integrity of
the stopper and cap before use.

74. ADDITIONAL
ARMAMENTARIUM
Topical
antiseptic
Topical
anesthetic
Applicator sticks
Cotton gauze (2
× 2 inches)
Hemostat
Needle-
recapping device

75. REGIONAL ANALGESIA
= REGIONAL ANESTHESIA = LOCAL ANESTHESIA
NERVE BLOCK
Local anesthetic solution is deposited within close proximity to a
main nerve trunk, at a distance from the site of operative
intervention, preventing afferent impulses from travelling centrally
beyond that point.

76. • FIELD BLOCK
• Local anesthetic
solution is deposited
in proximity to the
larger terminal nerve
branches so the
anesthetized area will
be circumscribed ,
preventing the
passage of afferent
impulses to the
central nervous
system.

77. LOCAL INFILTRATION
• Small terminal nerve
endings in the area of the
dental treatment are flooded
with local anesthetic
solution, rendering them
insensible to pain or
preventing them from
becoming stimulated and
creating an impulse.

78. TOPICAL ANALGESIA
Renders the free nerve endings in accessible structures (intact
mucous membrane, abraded skin, or the cornea of the eye)
incapable of stimulation by the application of a suitable solution
directly to the surface of the area.
INTRALIGAMENTARY TECHNIQUE
Type of INFILTRATION technique
Intended to provide single tooth anesthesia, consists of forcing the
anesthetic solution under pressure into the periodontal membrane
space of maxillary and mandibular teeth.

79. Techniques for injection
Basic Points
Use a Sterile Sharp Needle
Check The flow of Solution
Determine Whether to Warm soln before
use or not.
Position the patient
Dry the tissue/ wipe once.
Apply topical anesthetic
Topical antiseptic /optional
Communicate with patient apply firm
hand rest
Inject few drops of soln, communicate
with patient,
Advance to the target slowly ,aspirate ,
inject
Withdraw the needle slowly
Observe the patient & check for anesthetic
symptoms

80. MAXILLARY ANESTHESIA

81. SUPRAPERIOSTEAL INJECTION
• Anaesthetize buccal soft tissue
& hard tissue
• Nerves anaesthetized – large
terminal branches
• Indication : 1 or 2 teeth need to
be anaesthetized small area
• Contra-indication :
Infection, Dense bone covering
• Target area :
• Behind apices of tooth
• Landmarks :
• Muco-buccal fold
• Crown & root length
Signs and Symptoms
1. Subjective: feeling of
numbness in the area of
administration
2. Objective: use of a “freezing
spray” (e.g., Endo-Ice) or an
electric pulp tester (EPT) with
no response from the tooth
with maximal EPT output
(80/80)
3. Absence of pain during
treatment

82. INFRAORBITAL BLOCK
• Infraorbital Nerves
• Anterior Superior Alveolar Nerves
• Middle Superior Alveolar Nerves
• Inferior Palpebral Nerves
• Lateral Nasal Nerves
• Superior Labial Nerves
Nerves
Anesthetized
• Incisors
• Cuspids
• Bicuspids
• Mesiobuccal root of the First Molar on the
injected side
• Upper Lip
• Lower Eyelid
• A portion of the nose on the same side
Areas
Anesthetized
Anterior Superior Alveolar Nerve Block + Middle Superior Alveolar Nerve Block

83. • Infraorbital Ridge
• Infraorbital Depression
• Supraorbital Notch
• Infraorbital Notch
• Anterior teeth
• Pupils of the Eye
Anatomical
Landmarks
Involving more than two maxillary anterior teeth (incisors
through premolars) and their overlying buccal tissues.
In cases of inflammation or infection (which contraindicates
supraperiosteal injection)
When supraperiosteal injection is ineffective because of dense
cortical bone.
Discrete treatment areas (one or two teeth only;
supraperiosteal injection preferred).
Hemostasis of localized areas, when desirable,
cannot be adequately achieved with this injection;
local infiltration into the treatment area is
indicated.

84. Comparatively SIMPLE
Comparatively SAFER;
minimizes the volume of
solution used and the
number of needle
punctures necessary to
achieve anesthesia
Psychological:
a. Administrator: An Initial
fear of injury to the patient’s
eye (with experience
confidence in the technique is
achieved).
b. Patient: Extraoral technique
may prove disturbing;
however, intraoral techniques
are rarely a problem.
Anatomic: Difficulty
defining landmarks (rare).
Positive Aspiration = Negligible (0.7%)
SUBJECTIVE SIGNS AND SYMPTOMS
• Tingling and numbness of the lower eyelid, side of the nose, and upper lip
indicate anesthesia of the infraorbital nerve
• Numbness in the teeth and soft tissues along the distribution of the ASA and
MSA nerves (developing within 3 to 5 minutes if pressure is maintained over
the injection site).

87. MIDDLE SUPERIOR ALVEOLAR
NERVE BLOCK
• Middle Superior Alveolar Nerve
• Its terminal branches
Nerves
Anesthetized
• Pulps of the maxillary first and second
premolars, mesiobuccal root of the first
molar
• Buccal periodontal tissues and bone over
these same teeth
Areas
Anesthetized

88. Minimizes
the number of
injections and
the volume of
solution
None
Positive Aspiration = Negligible (<3%)
When Anterior Superior Alveolar nerve block fails to provide pulpal
anesthesia distal to the maxillary canine.
Dental procedures involving both maxillary premolars only.
Inflammation or infection at the injection site.
Where the Middle Superior Alveolar nerve is absent,
innervation is through the Anterior Superior Alveolar nerve.
SUBJECTIVE SIGNS AND SYMPTOMS
Numbness of the Upper Lip

90. POSTERIOR SUPERIOR
ALVEOLAR NERVE BLOCK
• Posterior Superior Alveolar
Nerve
Nerves
Anesthetized
• Maxillary Molars, exception of the
mesiobuccal root of the first molar
• Buccal Alveolar Process of the
Maxillary Molars, including the
Overlying structures – Periosteum,
Connective Tissue and Mucous
Membrane
Areas
Anesthetized
Tuberosity block, zygomatic block

91. • Mucobuccal fold and its concavity
• Zygomatic process of the maxilla
• Infratemporal surface of the maxilla
• Anterior border and coronoid process of the
ramus of the mandible
• Tuberosity of the maxilla
Anatomical
Landmarks
When involves two or more maxillary molars
When supraperiosteal injection is contraindicated
(e.g., with infection or acute inflammation)
Ineffective supraperiosteal injection
When the risk of hemorrhage is too great
(as with a hemophiliac; patients taking drugs
that can increase bleeding such as coumadin
or clopidogrel (Plavix)), in which case a
supraperiosteal or PDL injection is
recommended.

92. Atraumatic
High success rate (>95%)
Minimum number of
necessary injections:
1 injection ≈ 3 infiltrations.
Minimizes the total
volume of local anesthetic
solution administered
Risk of HEMATOMA, which is
usually diffuse and also
discomfiting and visually
embarrassing to the patient
Technique somewhat
arbitrary: no bony
landmarks during insertion
Second injection necessary
for treatment of the first
molar (mesiobuccal root) in
28% of patients
Positive Aspiration = Approximately 3.1%
SUBJECTIVE SIGNS AND SYMPTOMS
Usually, NONE
COMPLICATION
• Hematoma
• Mandibular Anesthesia

94. PALATAL ANESTHESIA

95. GREATER PALATINE NERVE
BLOCK
• Anterior Palatine Nerve
• As it leaves the greater palatine foramen
Nerves
Anesthetized
• Posterior portion of the Hard Palate and
overlying structures
Areas
Anesthetized
• Second and third maxillary molars
• Palatal gingival margin of second and third
maxillary molars
• Midline of the palate
• A line approximately 1 cm from the palatal
gingival margin toward the midline of the
palate
Anatomical
Landmarks
Anterior Palatine Nerve Block

96. When palatal soft tissue anesthesia is necessary for therapy on more
than two teeth
For pain control during periodontal or oral surgical procedures involving the
palatal soft and hard tissues
Inflammation or infection at the injection site
Smaller area of therapy (one or two teeth)
Minimizes needle
penetrations and
volume of solution
Minimizes patient
discomfort
No hemostasis except
in the immediate area
of injection
Potentially traumatic
Positive Aspiration = Less than 1%
SUBJECTIVE SIGNS AND SYMPTOMS
Numbness in Posterior Palate

98. NASOPALATINE NERVE BLOCK
• Nasopalatine Nerve
• As it emerges from the Anterior Palatine
Foramen
Nerves
Anesthetized
• Anterior portion of the Hard Palate and
overlying structures, back to the bicuspid
area
Areas
Anesthetized
Incisive Canal Injection
• Central Incisor Teeth
• Incisive Papilla in the middle of the Palate
Anatomical
Landmarks
When palatal soft tissue anesthesia is necessary for treatment on
more than two teeth
Inflammation or infection at the injection site
Smaller area of therapy (one or two teeth)

99. Minimizes needle
penetrations and volume
of solution
Minimal patient
discomfort from multiple
needle penetrations
No hemostasis except in
the immediate area of
injection.
Potentially the most
traumatic intraoral
injection; however, the
protocol for an atraumatic
injection or use of a C-CLAD
system or a buffered local
anesthetic solution can
minimize or entirely eliminate
discomfort
Positive Aspiration = Less than 1%
SUBJECTIVE SIGNS AND SYMPTOMS
Numbness in Anterior Palate

100. Technique: Single Needle Penetration

101. Technique: Multiple Needle
Penetrations
SUBJECTIVE SIGNS AND SYMPTOMS
Numbness of the upper lip (in the midline) and the anterior portion of the palate

102. MAXILLARY NERVE BLOCK
• Entire Maxillary Nerve and its subdivisions
peripheral to the site of injection
Nerves
Anesthetized
• Maxillary teeth on the affected site
• Alveolar bone and overlying structures
• Hard palate and portions of soft palate
• Upper lip, cheek, side of the nose, lower eyelid
Areas
Anesthetized
• Differs according to the technique
Anatomical
Landmarks
Second division nerve block, V2 nerve block
HIGH TUBEROSITY TECHNIQUE
Same as Posterior Superior
Alveolar Nerve Block
GREATER PALATINE CANAL
TECHNIQUE
Same as Greater Palatine Nerve
Block

103. Pain control before extensive oral surgical, periodontal, or restorative
procedures requiring anesthesia of the entire maxillary division
When tissue inflammation or infection precludes the use of
other regional nerve blocks (e.g., PSA, ASA, AMSA, P-ASA nerve
blocks) or supraperiosteal injection
Diagnostic or therapeutic procedures for neuralgias or tics of
the second division of the trigeminal nerve
Inexperienced administrator.
Pediatric patients.
a. More difficult because of smaller anatomic dimensions.
b. A cooperative patient is needed.
c. Usually unnecessary in children because of the high success rate
of other regional block techniques.
Uncooperative patients.
Inflammation or infection of tissues overlying the injection site.
When hemorrhage is risky (e.g., in a person with hemophilia or
patient on anticoagulant drugs).
In the greater palatine canal approach: inability to gain access
to the canal; bony obstructions may be present in 5% to 15% of
canals.

104. Atraumatic injection via the high-
tuberosity approach.
High success rate (>95%).
Positive aspiration is less than 1%
(greater palatine canal approach).
Minimizes the number of needle
penetrations necessary for successful
anesthesia of the hemimaxilla (minimum
of four via PSA, ASA, infraorbital, greater
palatine, and nasopalatine nerve blocks).
Minimizes total volume of local
anesthetic solution injected to 1.8 mL
versus 2.7 mL.
Not traumatic.
Risk of hematoma, primarily with the
high-tuberosity approach.
The high-tuberosity approach is
relatively arbitrary. Over insertion is
possible because of the absence of
bony landmarks if proper technique
is not followed.
Lack of hemostasis. If necessary, this
necessitates infiltration of small
volumes of vasoconstrictor-containing
local anesthetic at the surgical site.
Pain: the greater palatine canal
approach is potentially (although not
usually) traumatic.
SUBJECTIVE SIGNS AND SYMPTOMS
• Pressure behind the upper jaw on the side being injected; this usually subsides
rapidly, progressing to tingling and numbness of the lower eyelid, side of the
nose, and upper lip
• Sensation of numbness in the teeth and buccal and palatal soft tissues on the
side of injection

106. MANDIBULAR ANESTHESIA

107. INFERIOR ALVEOLAR NERVE BLOCK
• Inferior Alveolar Nerve and its subdivisions
• Mental Nerve
• Incisive Nerve
• Occasionally, the Lingual and Buccinator
Nerves (Branches of the Mandibular Nerve)
Nerves
Anesthetized
• Body of the Mandible and an Inferior
portion of the Ramus
• Mandibular teeth
• Mucous membrane and underlying tissues
anterior to the first mandibular molar
Areas
Anesthetized
Mandibular Nerve Block

108. • Mucobuccal fold
• Anterior border of the ramus of the
Mandible
• External Oblique Ridge
• Retromolar Triangle
• Interior Oblique Ridge
• Pterygomandibular Ligament
• Buccal sucking pad
• Pterygomandibular pace
Anatomical
Landmarks
Procedures on multiple mandibular teeth in one quadrant
When buccal soft tissue anesthesia (anterior to the mental
foramen) is necessary
When lingual soft tissue anesthesia is necessary
Infection or acute inflammation in the area of
injection (rare)
Patients who are more likely to bite their lip or
tongue (e.g., a very young child or a physically or
mentally handicapped adult or child)

109. One injection provides a wide
area of anesthesia (useful for
quadrant dentistry).
Not indicated for localized
procedures
Rate of inadequate anesthesia
(31% to 81%)
Intraoral landmarks not reliable
Positive aspiration
Lingual and lower-lip anesthesia,
discomfiting to many patients and
possibly dangerous (self-inflicted
soft tissue trauma) for certain
individuals
Partial anesthesia possible where a
bifid IAN and bifid mandibular canals
are present; cross-innervation in
lower anterior region
Positive Aspiration = Ranges from 10% to 15%

110. POSITION OF THE
ADMINISTRATOR

111. POSITION OF NEEDLE

113. Vazirani-Akinosi Closed-Mouth
Mandibular Block
• Inferior Alveolar and its subdivision
• Mental and Incisive Nerves
• Lingual and Buccinator Nerves
Nerves
Anesthetized
• All Mandibular hard and soft tissue
to the midline,
• Floor of the mouth
• Anterior two-thirds of the tongue
Areas
Anesthetized
Akinosi Technique, Closed-mouth Mandibular Nerve Block,
Tuberosity Technique

114. • Occlusal plane of Occluding teeth
• Mucogingival junction of the maxillary molar
teeth
• Anterior border of the ramus
Anatomical
Landmarks
Limited mandibular opening
Multiple procedures on mandibular teeth
Inability to visualize landmarks for Inferior Alveolar
Nerve Block (e.g., because of large tongue)
Infection or acute inflammation in the area
of injection (rare)
Patients who might bite their lip or their
tongue, such as young children and
physically or mentally handicapped adults
Inability to visualize or gain access to the
lingual aspect of the ramus

115. Relatively atraumatic
Patient need not be able to
open the mouth.
Fewer postoperative
complications (e.g., trismus)
Lower aspiration rate (<10%)
than with the IANB
Provides successful
anesthesia where a bifid IAN
and bifid mandibular canals are
present
Difficult to visualize the
path of the needle and the
depth of insertion
No bony contact; depth of
penetration arbitrary
Potentially traumatic if the
needle is too close to the
periosteum
Positive Aspiration = < 10 %

118. Mandibular Nerve Block : The
Gow-Gate Technique
• Mandibular Nerve and its subdivision
• Inferior Alveolar Nerves
• Lingual and Buccinator Nerves
• Incisive, Mental, Mylohyoid,
Auriculotemporal Nerves
Nerves
Anesthetized
• All Mandibular,
• Hard and Soft tissue to the midline
• Floor of the mouth
• Anterior two-thirds of the tongue
• Lingual soft tissue and periosteum
• Skin over Zygoma, Posterior Cheek
• Temporal region,portion of External Ear
Areas
Anesthetized
Gow-Gates technique, third division nerve block, V3 nerve block

119. • Anterior border of the Ramus
• Tendon of Temporal muscle
• Corner of the mouth
• Intertragic notch of the Ear
• External Ear
Anatomical
Landmarks
Multiple procedures on mandibular teeth
When buccal soft tissue anesthesia, from the third molar
to the midline, is necessary
When lingual soft tissue anesthesia is necessary
When a conventional IANB is unsuccessful
Infection or acute inflammation in the area
of injection (rare)
Patients who might bite their lip or their
tongue, such as young children and
physically or mentally handicapped adults
Patients who are unable to open their
mouth wide (e.g., trismus)

120. Requires only one injection; a
buccal nerve block is usually
unnecessary (accessory
innervation has been blocked)
High success rate (>95%)
Minimum aspiration rate
Few post injection complications
(e.g., trismus)
Provides successful anesthesia
where a bifid IAN and bifid
mandibular canals are present
Lingual and lower-lip anesthesia is
uncomfortable for many patients and
is possibly dangerous for certain
individuals.
The time to onset of anesthesia is
longer than with an IANB, because of
the size of the nerve trunk being
anesthetized and the distance of the
nerve trunk from the deposition site
(approximately 5 to 10 mm).
A learning curve with the Gow-Gates
mandibular nerve block technique.
Clinical experience is necessary to
truly learn the technique and to fully
take advantage of its greater success
rate.
Positive Aspiration = 2 %

124. LINGUAL NERVE BLOCK
• Lingual Nerve
Nerves
Anesthetized
• Anterior two – third of the tongue
• Floor of the Oral Cavity
• Mucosa and Mucoperiosteum on the lingual
side of the Mandible
Areas
Anesthetized
• Same as Inferior Alveolar Nerve Block
Anatomical
Landmarks
Procedures of the anterior two-thirds of the tongue, floor
of the oral cavity, and mucous membrane on the lingual
side of the mandible
Can be achieved by 3 methods
1. By blocking the lingual nerve at the same time as an intraoral inferior
dental injection
2. The submucosal infiltration of 0.5ml of anesthetic a few mm below
and behind the region of the lower third molar on its lingual aspect.
3. The infiltration of LA solution immediately lingual to the gingival of
mucosa to be treated.

125. BUCCAL NERVE BLOCK
• Buccinator Nerve
Nerves
Anesthetized
• Buccal mucous membrane
• Mucoperiosteum of the mandibular molar
area
Areas
Anesthetized
• External Oblique Ridge
• Retromolar Triangle
Anatomical
Landmarks
Long buccal nerve block, Buccinator nerve block

126. When buccal soft tissue anesthesia is necessary for
dental procedures in the mandibular molar region
Infection or acute inflammation in the area of injection
High success
rate
Technically,easy
Potential for
pain if the
needle contacts
the periosteum
during injection
Positive Aspiration = 0.7 %

127. MENTAL NERVE BLOCK
• Mental Nerve
Nerves
Anesthetized
• Lower Lip
• Mucous membrane in the mucolabial fold
anterior to the mental foramen
Areas
Anesthetized
• Mandibular bicuspids
• Since the mental foramen lies at the apex
and just anterior to the second bicuspid root
Anatomical
Landmarks
When buccal soft tissue anesthesia is necessary for procedures
in the mandible anterior to the mental foramen, such as:
1. soft tissue biopsies
2. suturing of soft tissues

128. High success
rate
Technically easy
Usually entirely
atraumatic
Hematoma
Positive Aspiration = Approximately 5.7 %

129. INCISIVE NERVE BLOCK
• Incisive Nerve
• Mental Nerve
Nerves
Anesthetized
• Mandible and overlying labial structures
anterior to the mental foramen
• Bicuspids, cuspids and incisors + Lower Lip
on the affected side
Areas
Anesthetized
• Same as Mental Nerve Block
Anatomical
Landmarks
Dental procedures requiring pulpal anesthesia of
mandibular teeth anterior to the mental foramen
When IANB is not indicated, i.e. when 6, 8, or 10 anterior
teeth (e.g., canine to canine or premolar to premolar) are
treated, the incisive nerve block is recommended in place of
bilateral IANBs

130. Provides pulpal and
osseous anesthesia
without lingual
anesthesia ; useful in
place of bilateral IANBs
High success rate
Does not provide
lingual anesthesia.
Partial anesthesia
may develop at the
midline because of
nerve fiber overlap
with the opposite side
(extremely rare)
Positive Aspiration = Approximately 5.7 %

131. ANESTHETIC COMPLICATIONS
Definition
Any deviation from the normally expected pattern during or after the
securing of regional analgesia. Reference : C. Richard Bennett - Monheims
COMPLICATIONS
Primary or
Secondary
Mild or Severe
Transient or
Permanent
COMPLICATIONS
Attributed to the
Solutions
Attributed to the
Insertion of the Needle
Syncope
Muscle Trismus
Pain or Hyperalgesia
Edema
Infections
Broken Needles
Prolonged anesthesia
Hematoma
Sloughing
Bizzare neurological symptoms
Toxicity
Idiosyncrasy
Allergy
Anaphylactoid reactions
Infections caused by contaminated
solutions
Local irritations or Tissue Reactions

132. LOCALCOMPLICATION Needle breakage
Prolonged anesthesia
(paresthesia)
Facial nerve paralysis
Ocular complications
Trismus
Soft tissue injury
LOCALCOMPLICATION
Hematoma
Pain on injection
Burning on
injection
Infection
Edema
Sloughing of
tissues
Postanesthetic
intraoral lesions

133. NEEDLE BREAKAGE
• RARE because of use of Disposable Needles
• CAUSES :
• Bending of the Needle
• Sudden Unexpected Movement of the Patient
• Entire Length of the Needle inserted into the soft tissue
• Use of Smaller Needle
• PREVENTION :
• Use Large Gauze Needle (especially for IANB and PSA Nerve Block)
• Use Large Needles
• Do not insert the Needle into the tissues until the HUB
• Do not Redirect the Needle once it is inserted into the tissue
• MANAGEMENT
Stay Calm
Instruct the patient
not to move and keep
his mouth open
Remove it with
Hemostats or a
Magill Intubation
Forcep
Calmly inform
the patient
Take a Radiograph
If Superficial,
remove it.
If not, leave it and
Follow - up
WHEN VISIBLE WHEN INVISIBLE

134. Known as Altered Sensation beyond Expected duration of anesthesia.
• Causes
• Direct trauma to nerve sheath – bevel of needle
• Contaminated LA solution; containing neurotoxic substance – alcohol or
sterilizing solution
• Insertion of a needle inside a foramen
• Hemorrhage into or around the neural sheath
• Prevention
• Careful injection technique : Proper Care and Handling
• Management
• Usually resolve in 8 weeks
• Reassuring the patient
• Periodic recall & check up of patients
• Is still Persistent more than a year – consult Neurosurgeon
• Recall patient every 2 months for check up
PARASTHESIA / PERSISTENT
ANESTHESIA

135. • Occur when anesthesia is introduced into Deep Lobe of the Parotid
Gland
• CAUSE
• Local Anesthesia solution into capsule of the parotid gland,located
at the posterior border of the mandibular ramus – usually while
giving Inferior Alveolar Nerve Block or Vazirani-Akinosi Nerve Block
• PROBLEM
• Ipsilateral loss of motor control- face appears lopsided
• Inability to raise the corner of Mouth, close Eye lid
• PREVENTION
• Proper care and handling
• Needle tip should contact bone. If tip is not contacting redirect the
needle only after complete withdrawal from tissues.
FACIAL NERVE PARALYSIS

136. • AMAUROSIS : Temporary Blindness
• MYDRIASIS : Pupillary Dilation
• PTOSIS : Droopy Eyelid
• DIPLOPIA : Double Vision
• CAUSES
• Inadvertent Arterial Injection with retrograde blood flow
• Inadvertent into the ORBIT through the Inferior Orbital Fissure
• PREVENTION
• ASPIRATE before actual injection
• Inject SLOWLY
• TREATMENT
OCULAR COMPLICATIONS
Reassure the patient that it is TRANSIENT
Cover the affected eye with gauze dressing
Refer to an OPTHALMOLOGIST, if lasts more than 6 hours
Regular Follow-up

137. “Prolonged, Tetanic Spasm of Jaw Muscles by Restricted Normal
Mouth Opening”
• CAUSES
• Trauma – muscle / blood vessel (infratemporal fossa)
• Contaminated Local Anesthetic Solution (alcohol/sterilizing agent)
• Hemorrhage (large volume of extravascular blood producing tissue
irritation leading to muscle dysfunction)
• Low – grade Infection
• Multiple needle punctures
• Local Anesthesia have been known to have slight myotoxicity
• PROBLEMS
• Pain and Difficulty in Opening (seen mostly after 1-6 days of LA
administration)
• Muscle spasm
• Hypomobility
• Reduced mouth opening(5-23 mm opening)
TRISMUS

138. • PREVENTION
 Use a sharp, sterile, disposable needle.
 Avoid repeated and multiple injections at same area through knowledge
of anatomy and proper technique as atraumatically as possible
 Use effective volumes of Local Anesthesia
• MANAGEMENT
- prescribe warm saline rinses, heat therapy, analgesics and if necessary
muscle relaxants
• Heat therapy
• Hot moist towels for 20 min every hour.
• Warm saline rinse with salt.
• Analgesics
• Aspirin(325mg), Codeine (30-60mg), muscle relaxants (diazepam
10mg bid)
• Initial physiotherapy
• Thrice a day for 5 min every 3-4 hours.
• Antibiotic regime
• Possibility of infection; for 7 days
Improvement starts within 2- 3 days
Recovery range = 4 – 20 weeks
Surgical Intervention, in some cases

139. • CAUSES
• Trauma to the lip or the tongue - occurs frequently mentally / physically
challenged children
• Primary cause – significantly longer duration of action of Local Anesthetic
• PROBLEM
• Pain & swelling
• Infection of soft tissue
• PREVENTION
• Cotton roll between lip & teeth
• Patient – guarded against eating / drinking, bitting on lips
• Warning sticker-”watch me, my lips and cheecks are numb” can be given to
children till the effect of Local Anesthetic is present
• MANAGEMENT
Treatment of patient with self inflicted soft tissue injury secondary to lip or
tongue biting is symptomatic.
- Lukewarm saline rinses (decrease swelling if present)
- Antibiotics (for infection if present)
- Petroleum jelly to cover a lip lesion and minimize irritation
SOFT TISSUE INJURY

140. “Effusion of blood into extra-vascular spaces resulting from inadvertently
nicking a blood vessel during injection”
• CAUSES
• Arterial & venous puncture – common in Posterior Superior Alveolar &
Inferior Alveolar Nerve Block
• PROBLEM
• Bruise – may / may not be visible extra-orally
• Complications – pain & trismus
• Swelling & discoloration (subsides within 7-14 days)
• PREVENTION
• Knowledge of normal anatomy – proper technique
• Shorter needle – Posterior Superior Alveolar Nerve Block, minimize the
number of penetration
• Discard defective needles - barbed needles
HEMATOMA

141. • MANAGEMENT
• Immediate – apply firm pressure  5-10minutes
• Inferior Alveolar Nerve block – medial aspect of ramus
• Infra orbital, Mental, Incisive block – directly over foramen
• Posterior Superior Alveolar Block – pressure on soft tissue with
finger as distally as tolerated by patient – medial superior
direction.
• Ice should be applied
• Patient to be reviewed after 24 hours, advice analgesics, cold
application upto 4-6 hours, warm- pack application next day

142. • CAUSES
• Careless techniques
• Rapid deposition of solution (can cause tissue damage)
• Multiple used needles
• PROBLEMS
- Pain increases due to patient anxiety causing unexpected
movements by patient
• PREVENTION
• Careful technique
• Sharp needles
• Topical anesthetic before injection
• Slow injections
• MANAGEMENT
• Not necessary.
• Care should be taken to avoid recurrance
PAIN ON INJECTION

143. • CAUSES
• Due to pH of solution (3-5 pH)
• Rapid injection (especially in palate)
• Contaminated cartridges (if stored in alcohol can lead to diffusion of soln in
cartridge)
• Warm solution (patient considers it too hot)
• PROBLEMS
• If caused by pH  disappears upon LA action – no residual effect
• Contaminated solution or rapid injection can cause other complications –
edema, paresthesia
• PREVENTION
- Slow injection. (1ml per min)
- Cartridge should be stored at room temperature without alcohol or any
sterilizing agent.
• MANAGEMENT
- As burning on injection is a transient type of complication and do not lead any
tissue involvement, formal treatment is not usually indicated.
BURNING ON INJECTION

144. • CAUSES
• Needle contamination
• Improper handling of armamentarium
• Infection at injection site
• Improper handling of tissue
• PREVENTION
• Sterile, Disposable needles
• Proper care of equipment
• Aseptic technique
• MANAGEMENT
• Usual sign is trismus (which resolves in 1-3 day)
• Antibiotics (Penicillin V 250 mg for 3-5 days thrice a day)
INFECTION

145. • CAUSES
• Trauma during injection
• Infection
• Allergy
• Hemorrhage
• Irritating solutions
• PROBLEMS
• Pain & dysfunction
• Airway obstruction
• PREVENTION
• Proper care & handling of armamentarium
• Atraumatic injection technique
• Complete medical evaluation prior to injection
EDEMA
• MANAGEMENT
 Trauma – resolve in few days
without therapy
 Hemorrhage – resolve slowly 7-14
days
 Allergy – life threatening
 Airway impairment – basic life
support, call medical help
Epinephrine – 0.3mg,
Antihistamine,
Corticosteroids
 Total airway obstruction –
Tracheostomy / Cricothyroidectomy

146. • CAUSES
• Epithelial desquamation – application of topical anesthesia for long time,
heightened sensitivity to Local Anesthetic
• Sterile abscess – secondary to prolonged ischemia from use of Vasoconstrictor
in Local Anesthetic (usually in hard palate)
• PROBLEMS
• Pain & infection
• PREVENTION
• Topical – for not more than 1-2 minutes
• Vasoconstrictor – minimal concentration in solution
• MANAGEMENT
Symptomatic – PAIN – analgesia (aspirin or codeine)
• Epithelial desquamation – resolve few days
• Sterile abscess resolve  7-10 days
SLOUGHING OF TISSUE

148. “Signs and symptoms that result from an overly high blood level of
a drug in various target organs and tissues”
• PATIENT’S FACTORS
• Age
• Pregnancy
• Diseases – hepatic & renal dysfunction - ↓ body’s ability to
breakdown and excrete Local Anesthetic – TOXICITY
• Congestive heart failure – ↓ liver perfusion - ↑ half-life of drugs -
↑ risk of toxicity
• Fearful patients – lower seizure threshold for Local Anesthetic
TOXICITY / TOXIC
OVERDOSE
DRUG
FACTORS
Vasoactivity
Concentration
Route of Administration
Rate of injection
Vascularity of injection site
Presence of Vasoconstrictor

149. • CAUSES OF TOXICITY
• Biotransformation usually slow
• Excessive total dose
• Rapid Absorption from injection site
• Accidental intra-vascular injection
• TREATMENT
• Mild overdose reaction – (agitated, talkative)
• Slow onset reaction – 5 to 10 mins –
• PABC… D – administer Oxygen , monitor vital signs, in case of
convulsions – anti-convulsants (diazepam/midazolam)
• Slower onset - >15 mins – same procedure
• Severe overdose reaction – rapid onset 1 min – (unconsciousness with
or without convulsion), patient in supine position,
• Convulsions – Protect hand, leg, tongue, BLS, administer anti-
convulsant
• Post seizure – CNS depression usually present

150. “It is an adverse response that is neither an overdose nor an allergic
reaction”
• COMMON CAUSE
• Underlying pathology/psychological /genetic mechanism
• TREATMENT
• symptomatic … remember ABC’s!
• Psychotherapy may be helpful
IDIOSYNCRACY

151. “Transient loss of consciousness that is caused due to cerebral
ischemia (Neurogenic shock)”
• CAUSES
• Anxiety – increased blood supply to muscles, less pressure – cerebral
arteries
• CLINICALLY
• Light headedness, dizziness, tachycardia & palpitation – may further
lead to Unconsciousness
• TREATMENT
• Discontinue procedure, supine position, deep breathing
• O2 administration if required, BLS if required
SYNCOPE

152. “Hypersensitive state acquired through exposure to a particular allergen
re-exposure to which produces a heightened capacity to react”
• 1 % of all reaction in Local Anesthetic is allergy
• Incidence of allergy reduced since introduction of Amides
• Life threatening allergic response is rare
PREDISPOSING FACTORS
• Hyper sensitivity to ester more common - Procaine
• Most of patients allergic to methyl paraben
• Recently allergy to sodium meta bisulfide is also increasing
PREVENTIONS
• H/o of allergy to be recorded
- itching ,swelling, rashes
• H/o any asthmatic attack to be noted.
• Dialogue history.
• Always better to test the patient for allergy before treatment.
• Consultation and allergy testing
ALLERGY
- Skin test is primary mode of assessing
- Intra cutaneous test most reliable - 0.1ml of soln is injected in forearm

153. classificationTYPE MECHANISM ANTIBODY TIME OF
REACTION
CLINICAL EXAMPLE
I Anaphylactic
(Antigen
induced,Antibody
mediated)
IgE Sec to min • Anaphylaxis
• Angioedema
• Hay fever
II Cytotoxic (Anti
membrane)
IgG, IgM - • Hemolytic anemia
• Transfusion reaction
• Certain drug reaction
III Immune complex IgG 6-8 hours • Serum sickness
• Acute viral hepatitis
IV Cell mediated - 48 hours • Allergic contact
dermatitis
• Tissue graft rejection
• Chronic hepatitis
Classification of Allergic Disease (Gell & Coomb)

154. • SIGNS AND SYMPTOMS
• Dermatological reactions
Urticaria – wheal and smooth elevated patches
Angioedema — localized swelling
• Respiratory reactions–
Bronchospasm – Respiratory distress, dyspnea, wheezing, flushing, tachycardia
Laryngeal edema – type of angioneurotic edema to the larynx
- Edema upper airway – laryngeal edema
- Lower airway affect bronchioles.

155. MANAGEMENT
SKIN REACTIONS
• Delayed
• 60 mins after exposure
• Non life threatening
• Oral histamine blockers-
• 50 mg diphenhidramine / chlorpheniramine 10 mg -6 hourly 3-4days
• Immediate
• with conjunctivitis, rhinitis, urticaria
• 0.3 mg epinephrine IM / SC
• 50 mg diphenhydramine IM
• Medical help summoned.
• Observe the patient for 60 mins
• Oral histamine for 3 days

156. RESPIRATORY REACTION – BRONCHOSPASM (BRONCHIAL CONSTRUCTION)
• Terminate dental treatment
• Patient in comfortable position.
• Administer - Oxygen 5-6 liters/min
• Administer Epinephrine or other bronchodilator via aerosol inhaler or IM/SC
epinephrine 0.3mg
• Observe for 60 min
• Advise Histamine blockers to prevent relapse
LARYNGEAL EDEMA
• Patient position, Oxygen, Broncho-dilator, Epinephrine 0.3mg IM/SC
• If needed anti histamines IV, steroids IV
• If condition not improving Cricothyrotomy - achieve patent air way if necessary
give artificial ventilation.
Patient with confirmed allergy status -
If patient allergic to ester Analgesic - use amide analgesic.
Use histamine blocker like diphenhydramine as anesthetic.
General anesthesia
Alternative method of pain control –
electric anesthesia / hypnosis

157. FACTORS IN SELECTION OF LOCAL
ANESTHETIC FOR A PATIENT
Length of Time for which pain control is necessary
Need for post treatment pain control
Possibility of self mutation in the post operative period
Requirement for hemostasis
Presence of any contraindication to the Local anesthetic solution
administered

158. MANAGEMENT IN SPECIAL PATIENTS
• Maximum Safe Dose of Lidocaine = 4.5 mg/kg
• Local infiltration is sufficient for 90% cases in mthe
mandible
UNCOOPERATIVE
CHILD
• Lidocaine + Vasoconstrictor
• Esters are better to use with no proven ill effects
PREGNANT
FEMALE
• Decide upon patient’s cardiovascular and
Respiratory System Fuction
GERIATRIC
PATIENT
• Avoid Amides as it is metabolized in Liver
• Use EstersLIVER DISORDERS

159. RECENT ADVANCES
CENTBUCRIDINE
ROPIVACAINE
EMLA
TENS (Transcutaneous Electrical Nerve Stimulation)
HYALURONIDASE
ULTRA-LONG ACTING LOCAL ANESTHETICS
TOPICAL GELS
JET INJECTIONS
DENTIPATCH (Intraoral Lignocaine Patch)
COMPUTER CONTROLLED SYSTEM
ELECTRONIC DENTAL ANESTHESIA

160. CONCLUSION
No Drug ever exists a Single
Action
No clinically useful drug is
entirely devoid of Toxicity
The potential toxicity of
anything rests in the hands
of the user

161. REFERENCES
 Carranza’s Clinical
Periodontology :
10th Edition
Local Anesthetics :
Benjamin J Cohino
Local Anelgesia in
Dentistry : D.H.
Roberts and J.H.
Sorway
Principles of
Anesthesiology :
Vincent J Collins
Pain Control in
Dental Practice :
Richard Bennett
Vasoconstrictors in
Local Anesthesia : A.
L. Sisk
 Local Anesthesia :
6th edition – Stanley
F. Malamed
Monheim’s Local
Anesthesia and
Pain Control in
Dental Practice : 7th
Edition