LOCAL ANAESTHESIA

ASWATHI S NAIR
IInd year MDS
DEPARTMENT OF PERIODONTOLOGY
CONTENTS
 Introduction
 Historical background
 Definition
 Desirable properties of L.A
 Pharmacology of L.A (CLASSIFICATION)
 Theories of local anesthesia
 Mechanism of action of local anaesthetics
 Composition
 Pharmocokinetics
 Vasoconstrictors
 Factors in selection of a L.A for a patient
 Common questions to ask patient
 Stress reduction protocol
 Local anaesthetic used in medically compromised patients
 Techniques of local anaesthesia
 Local and systemic complications
 Recent Advances and future trends in pain control
 Conclusion
 References
INTRODUCTION
 Local anesthesia is a widely used and accepted method of pain control during
operative dental procedure.

 The development and acceptance of dental treatment can be credited to local

anesthesia which offers freedom from pain.

 Helps dentist to achieve the primary goal of their profession i.e. painless treatment &
more comfort to the patient.

 Local anesthetics have also got acceptance during operative procedures under general
anesthesia.
 Local anesthetics must traverse several tissue barriers to reach their
site of action on neuronal membranes. In particular, the perineurium
is a major rate-limiting step.

 Adjuncts available to block sensory nerves are there, but these

typically also prolong motor block.

 Their clinical introduction profoundly changed perioperative

medicine.
Today,in parallel with advances in neurosciences, our understanding
of LA has become much more detailed.
HISTORICAL BACKGROUND
 1842 Ether used as anesthetic by Dr. Crawford W. Long
 1850’s Cocaine isolated, hypodermic needle developed
 1853 Chloroform used as anesthetic by Dr. John Snow

Chloroform being used as anesthesia

 The 1st chemical local anaesthetic came with discovery of
cocaine in 1860 by Albert Nieman from the leaves of the coca
tree.
 Its anesthetic action was demonstrated by KARL KOLLER
in1884.
 William Halsted Steward carried out the 1st recorded inferior
dental nerve block using cocaine in 1884.
 First effective and widely used synthetic local anesthetic -
PROCAINE -produced by EINHORN in 1905 by esterification
of the base alcohol ,diethyl amino ethanol with benzoic acid.
 Its anesthetic properties were identified by BIBERFIELD and
the agent was introduced into clinical practice by BRAUN.
 LIDOCAINE- Lofgren succeeded in synthesizing Lidocaine from a
series of aniline derivatives in 1948.

 The discovery of its anesthetic properties was followed in 1949 by its

clinical use by T. GORDH.

 Thereafter, series of potent anesthetic soon followed with a wide

spectrum of clinical properties.

 Bupivacaine became the longest acting amide LA in 1980’s to be

followed by Rupivacaine in mid 1990.
PAIN
It is defined as an unpleasant emotional experience usually
initiated by a noxious stimulus and transmitted over a specific
neural pathway to the central nervous system where it is
interpreted as such.

International Association for the Study of Pain (IASP, 1973)

LOCAL ANAESTHESIA:DEFINITION
 Local anesthesia is defined as a loss of sensation in a circumscribed area of the body
caused by depression of excitation in nerve endings or an inhibition of the conduction
process in peripheral nerves.
- STANLEY F.MALAMED, 1980
(Malamed SF. Handbook of local anesthesia. 5th ed. Elsevier Mosby, St Louis 2004.)

Important feature of L.A-

 Produces loss of sensation without inducing a loss of consciousness (STANLEY
F.MALAMED)
 In this one major area, local anesthesia differs dramatically from general anesthesia.
 Are drugs which upon topical application or local injection cause reversible loss of
sensory perception, especially of pain in a localized area of the body. 
 No structural damage to the neurons.
Many methods are used 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.
DESIRABLE PROPERTIES OF L.A

 It should not be irritating to the tissue to which it is applied.

 It should not cause any permanent alteration of nerve
structure.
 systemic toxicity should be low.
 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.

Ref: Malamed SF. Handbook of local anesthesia. seventh ed. Elsevier Mosby, St Louis 2004.
In addition to these qualities, Bennett lists other desirable properties of 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.
Indications

 Minor Surgeries
 Diagnostic & therapeutic purpose
 Control of post-op pain
 Blood less field (as an adjunct).
SPECIFIC INDICATIONS IN DENTISTRY

 Extraction of teeth.  Removal of residual infection, small

neoplastic growths and salivary stones
 Alveoloplasty and alveolectomy. etc.
 Incision and drainage of abcesses.  Sore spots as a result of denture get
relieved.
 Cavity preparation especially in deep
 Treatment of trismus and trigeminal
painful cavities.
neuralgia
 Pulp procedures like pulpotomy and  In patients who shows gagging especially
pulpectomy. during placement of film.
 Periodontal surgeiy and gingival surgery.  For anesthesia of oral cavity and jaw
bones for routine surgical procedures like
 Cyst enucleation or marsupializatioin. treatment of fractures etc

Bali RK. Exodontia and local anaesthesia in dental practice. 1st ed. A 2008.
Howe GL. Local anaesthesia in dentistry. 3rd ed Wright, London.
Contraindications

Absolute:
 Allergic to all forms of local anesthetic

Relative:
 Local infection
 Uncooperative patient - Mental Deficiency
- Fear / Apprehension
 Fearful and apprehensive patients who refuse for injection.
 Mentally retarded and unco-operative chi1dren or very young
children.
 Anatomic anomalies.
 Hyperthyroidism- may precipitate thyroid crisis.
 Liver disorders, Renal disorders.
 Diabetes mellitus
 Cardiac Problems: Heart block,second or third degree (without pacemaker),
Severe sinoatrial block(without pacemaker)
 Internal hemorrhage.
 Concurrent treatment with quinidine,flecainide,disopyramide,procainamide(Class
1 antiarrhythmic agents.)
 Major oral surgical procedure.
 Advantages

 Patient remains awake and cooperative & well  Less pulmonary complications
oriented.  Aspiration of gastric contents unlikely.
 Non inflammable.  Less nausea and vomiting.
 Postoperative analgesia.
 Excellent muscle relaxant effect.
 There is reduction surgical stress.
 Maintains his own airway.  Earlier discharge for outpatients.
 Very low incidence of morbidity.  Local anesthesia is useful for ambulatory patients
 Can leave the dental office unescorted. having minor procedures.
 Ideal for procedures in which it is desirable to
 Little distortion of normal physiology have the patient awake and cooperative.
 Techniques are not difficult to master.  Less bleeding.
  Need not omit the previous meal.
No additional trained personal is necessary.
 Failures are very less.
 No additional expense to the patient.
DISADVANTAGES

 There are individual variations in response to local anesthetic drugs.

 Rapid absorption of the drug into the bloodstream can cause severe, potentially fatal
reactions.
 Apprehension may be increased by the patient's ability to see and hear. Some patients prefer
to be unconscious and unaware.
 Direct damage of nerve.
 Post-dural headache from CSF leak.
 Hypotension and bradycardia through blockade of the sympathetic nervous system.
 Not suitable for extremes of ages.
 Multiple needle pricks may be needed.
 NEUROPHYSIOLOGY
Fundamentals of Impulse Generation and
Transmission

 Concept behind the actions of local anesthetics →

prevent both the generation and the conduction of a
nerve impulse.
 Set up a chemical roadblock between the source of the
impulse (e.g., the scalpel incision in soft tissues) and
the brain.
 The aborted impulse, prevented from reaching the
brain, cannot be interpreted by the patient as pain.
NEURON

 Structural unit of the nervous system

 Transmit message between CNS and all parts of
the body

The neuron is the structural unit of the nerve

 Two types of neurons
 1) Sensory afferent (toward the CNS)
 2) Motor efferent (away from the CNS)
Sensory neurons capable of transmitting the sensation of pain consist of three major portions.
1.The peripheral process (Dendritic Zone) - free nerve endings; most distal portion of the
neuron
 These free nerve endings respond to stimulation produced in the tissues in which they lie,
provoking an impulse that is transmitted centrally along the axon.

2. AXON -
 long cylinder of neural cytoplasm [axoplasm] encased in a thin sheath ,the nerve
membrane or axolemma(the giant squid axon has been measured at 100 to 200cm.
 At its mesial or central end is an arborization similar to that seen in the peripheral process.
 synapses with the CNS to transmit input to the brain.
3.The cell body is the third part of the neuron.
 In the sensory neuron , the cell body is located at a distance from the axon, the main pathway
of impulse transmission in this nerve.
 The cell body of the sensory nerve therefore is not involved in the process of impulse
transmission, its primary function being to provide vital metabolic support for the entire
neuron
MOTOR NEURON

 Nerve cells that conduct impulses from the CNS

toward the periphery are termed motor neurons
 In motor neuron, cell body is interposed between the
axon and dendrites.
 In motor neurons the cell body not only is an
integral component of the impulse transmission
system but also provides metabolic support for the
cell.
 Near its termination, the axon branches, with each
branch ending as a bulbous axon terminal (or bouton).
Axon terminals synapse with muscle cells.
 Both sensory nerve excitability and conduction are attributable to
changes that develop within the nerve membrane.

 The cell body and the axoplasm are not essential for nerve conduction.

 They are important however, for the metabolic support of the nerve
membrane is probably derived from the axoplasm.
 NERVE CELL MEMBRANE

 Every neuron has a separation of

electrical charge across its cell
membrane.
 Maintained because the lipid bilayer
acts as a barrier to the diffusion of ions.
 The membrane is described as a flexible
nonstretchable structure consisting of
two layers of lipid molecules (bilipid
layer of phospholipids) and associated
proteins, lipids, and carbohydrates.
 Nerve cell membrane is ~75 Angstroms thick
 All cell membranes are organized to block the
diffusion of water soluble molecules
 Selectively permeable via specialized pores
 Transduce information by protein receptors
responsive to chemical or physical stimulation by
neurotransmitters, hormones, light, vibrations.
The cell membrane is a bilipid layer of
phospholipids

 hydrophilic (polar) ends facing the outer surface

and
 hydrophobic (nonpolar) ends projecting to the
middle of the membrane

CONFIGURATION OF THE
NERVE MEMBRANE
Selective Permeability of Membranes
 Some ions permitted to cross more
easily than others.
 Neuronal membranes contain ion
channels.
 Nongated- stay open all the
time.
 Gated - Open on the
occasion of an action
potential, causing a change
in the permeability of the
membrane (Voltage- gated
& Ligand- gated)
 Channel proteins are thought to be continuous pores
through the membrane, allowing some ions (Na+, K+,
Ca2+) to flow passively, whereas other channels are
gated, permitting ion flow only when the gate is open.

 The nerve membrane lies at the interface between

extracellular fluid and axoplasm. It separates highly
diverse ionic concentrations within the axon from those
outside.
 The resting nerve membrane has an electrical
resistance about 50 times greater than that of the
extra/intracellular fluids, thus preventing the passage
of Na, K and Cl ions down their concentration
gradients .
 when a nerve impulse passes, electrical conductivity
of the nerve membrane increases 100-fold
 increased conductivity allows the passage of Na and
K ions down their concentration gradient through the
nerve membrane
Regular interval constrictions are called
 Movement of these ions provides the energy for Nodes of Ranvier which form gaps
impulse conduction along the nerve between two adjoining Schwann cells
 some nerve fibers are covered in myelin, specialized
Schwann cells.
Physiology of the Peripheral Nerves

 The function of a nerve is to carry messages from one part of the body to another.
 These messages, in the form of electrical action potentials, are called impulses.
 Action potentials are transient depolarizations of the membrane that result from a
brief increase in the permeability of the membrane to sodium, and usually also from a
delayed increase in its permeability to potassium.
 Impulses are initiated by chemical, thermal, mechanical, or electrical stimuli.
 Once an impulse has been initiated by a stimulus in any particular nerve fiber, the
amplitude and shape of that impulse remain constant, regardless of changes in the quality
of the stimulus or in its strength.

 This is because the energy used for its propagation is derived from energy that is released
by the nerve fiber along its length and not solely from the initial stimulus.

 De Jong has described impulse conduction as being like the active progress of a spark
along a fuse of gunpowder.

 Once lit, the fuse burns steadily along its length, with one burning segment provid ing the
energy necessary to ignite its neighbor. Such is the
situation with impulse propagation along a nerve.
Electrophysiology of Nerve Conduction
 Nerve resting potential is -70 mV; this is produced by differing concentrations of ions on
either side of the nerve membrane
 Interior of the nerve is negative compared to the exterior before a stimulus excites the
nerve

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−)
 STEP 1 - Stimulus excites nerve which leads to:

1) Slow Depolarization- inside of nerve becomes less negative

2) Threshold Potential- extremely rapid depolarization occurs from the falling

electrical potential

3) Rapid Depolarization- interior is electrically positive +40 mV and the outside

is negative (-70 mv)
RESTING TO THREASHOLD POTENTIAL
THRESHOLD POTENTIAL TO RAPID DEPOLARISATION
Malamed SF. Handbook of local anesthesia. seventh ed. Elsevier
Mosby, St Louis 2004.
 STEP 2 - after depolarization,
repolarization occurs
 Repolarization- electric potential
inside the cell gradually becomes
more negative until the interior is
again restored to –70 Mv
 Entire process require 1milli sec
Depolarization- 0.3msec,
repolarization 0.7msec
MEMBRANE EXCITATION

Depolarization

 excitation leads to increase in permeability of the cell

membrane to sodium ions

 transient widening of transmembrane ion channels allow

passage of the sodium ions

 rapid influx of sodium ions into the interior of the nerve

cell causes depolarization of the cell membrane from
resting to firing threshold which is -50 to -60 mV
FIRING THRESHOLD
 Magnitude of the decrease in negative trans-
membrane potential that is necessary to initiate an
action potential (impulse); getting more positive with
more influx of Na+
 Decrease in negative transmembrane potential of +15
mV; from –70 mV to –55 mV is necessary to reach
the firing threshold;
 voltage differences of less than +15 mV will not
induce firing
 exposure of a nerve with local anesthetic raises its
firing threshold -elevating the firing threshold means
that more sodium must pass through the membrane to
decrease the negative transmembrane potential to a
level where depolarization occurs.
 When the firing threshold is reached,
sodium rapidly enters the axoplasm due
to increased membrane permeability
 -depolarization lasts ~ .3 msec

 REPOLARISATION
 The action potential is terminated when
the membrane repolarizes; this is caused
by the inactivation of increased
permeability to sodium Repolarisation
 The movement of Na+ and K+ during
depolarization is passive
 After the membrane potential returns to –70 mV there is still a slight
amount of excess sodium within the nerve cell and a slight excess of
potassium extracellularly.

 Sodium is moved out of the cell using ATP and the sodium pump .

 Repolarization requires ~ .7 msec

 REFRACTORY PERIOD
 Absolute Refractory Period 
 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. This is termed the absolute refractory
period.
 lasts for about the duration of the main part of the action
potential.

 Relative Refractory Period 

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.
 The relative refractory period continues to decrease until the
normal level of excitability returns, at which point the nerve is
said to be repolarized.
 MEMBRANE CHANNELS
 Sodium channels line the excitable nerve membrane which are
lipoglycoproteins situated firmly in the membranes .
 Sodium passes through the channels 12 times easier than
potassium .
 Sodium ions are “thinner” than potassium or chloride ions and
should therefore move easily down the concentration gradients
through membrane channels into the nerve cell.
 However, sodium ions are hydrated at rest and increase in size to 3.4
Angstroms; they are too large to pass through the sodium channels
when the nerve is at rest.
 Potassium and chloride can pass through these gated channels .
 During depolarization the gated transmembrane sodium channels
change their configuration to allow the sodium ions to enter the cell.
 IMPULSE PROPAGATION
Activation of an action potential by a stimulus

Disruption of the resting nerve membrane potential

Interior of the cell goes from negative (–70 mV) to positive (+40 mV)

Exterior of the cell changes from positive to negative

Local currents begin flowing between the depolarized segment and the adjacent resting area

Local currents flow from positive to negative extending for several mm along the nerve membrane

As a result, the interior of adjacent areas become less negative and the exterior becomes less
positive
 Transmembrane potential decreases approaching firing threshold for
depolarization .
 When transmembrane potential decreases by 15mV from resting potential, firing
threshold is reached and rapid depolarization occurs.
 The newly depolarized segment sets up local currents and it all starts over again.
 Newly depolarized segments return to resting state after absolute and relative
refractory periods.
 Waves of depolarization can move in only one direction due to the absolute and
relative refractory periods, thus retrograde (backward) movement is prevented.
IMPULSE SPREAD
 The propagated impulse travels along the nerve membrane towards CNS. The spread of
impulse differs in myelinated and unmyelinated nerve fibers.

Unmyelinated Nerves
 high electrical resistance cell membrane
 slow forward “creeping” spread of
impulses
 conduction of unmyelinated C fibers is1.2
m/sec
 2.Myelinated Nerves
 Insulating myelin separates the extra/intracellular charges.
 current leaps from node to node -saltatory conduction
 if conduction of an impulse is blocked at one node, the
local current skips that node and continues to the next
node to its firing potential and produce depolarization.
 Conduction rate of myelinated fibers is 120m/sec.
 It is more rapid in thicker nerves because of increase in
thickness of myelin sheath and increase in distance
between adjacent nodes of ranvier.
 A minimum of 8 to 10 mm of nerve must be covered by
anesthetic solution to ensure adequate block of impulse
spread.
ORDER OF BLOCKADE 

 AUTONOMIC 
 PAIN 
 TEMPERATURE 
 TOUCH 
 DEEP PRESSURE 
 MOTOR
 Recovery in reverse order
MODE AND SITE OF ACTION OF L.A

LA interfere with the excitation process in nerve membrane, by one

of the following mechanism:

• Altering the basic resting potential of the nerve membrane.

• Altering the threshold potential
• Decreasing the rate of depolarization
• Prolonging the rate of repolarization
Theories of Action of L.A

ACETYLECHOLINE THEORY:
• Stated that acetylcholine was involved in nerve conduction in addition to its
role as a neurotransmitter at nerve synapses.
• There is no evidence that acetylcholine is involved in neural transmission.
[Disapproved]

CALCIUM DISPLACEMENT THEORY:

• States that local anesthetic nerve block was produced by displacement of

calcium from some membrane site that controlled permeability of sodium.
[Disapproved]
Surface charge (repulsion) theory

 Proposed that local anesthetic acted by binding to nerve membrane and changing the
electrical potential at the membrane surface.
 Cationic drug molecule were aligned at the membrane water interface, and since some of
the local anesthetic molecule carried a net positive charge, they made the electrical
potential at the membrane surface more positive, thus decreasing the excitability of nerve
by increasing the threshold potential.
 Current evidence indicate that resting potential of nerve membrane is unaltered by local
anesthetic.
 Also, the surface charge theory cannot explain the activity of uncharged anesthetic
molecules in blocking nerve impulses (e.g., benzocaine).
Membrane expansion theory

• Drug molecule penetrates the lipid portion of membrane & brings

about a change in the configuration of lipoprotein matrix, leading to
inhibition of Na2+ conductance hence inhibiting neural excitation.
• It states that local anesthetic molecule diffuse to hydrophobic regions
of excitable membranes, producing a general disturbance of bulk
membrane structure, expanding membrane, and thus preventing an
increase in permeability to sodium ions
• Lipid soluble LA can easily penetrate the lipid portion of cell
membrane changing the configuration of lipoprotein matrix of nerve
membrane. This results in decreased diameter of sodium channel,
which leads to inhibition of sodium conduction and neural excitation.
Membrane Expansion Theory
Specific receptor theory
 The most favored today, proposed that local anesthetics act by binding to specific
receptors present on the external or internal axoplasmic surface of sodium
channels .
 The actionof the drug is direct, not mediated by some change in the general
properties of the cell membrane.
 Binding to specific receptors on sodium channel the action of the drug is direct,
Both biochemical and electrophysiologic 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.
 Tertiary amine local anesthetics inhibit
the influx of sodium during nerve
conduction by binding to a receptor
within the sodium channel (R-LA).
 This blocks the normal activation
mechanism (O gate configuration,
depolarization) and also promotes
movement of the activation and
inactivation gates (m and h) to a position
resembling that in the inactivated state
(I).
 Biotoxins (R-T) block the influx of
sodium at an outer surface receptor;
various venoms do it by altering the
activity of the activation and inactivation
gates; and benzocaine (R-B) does it by
expanding the membrane. C, Channel in
the closed configuration. (Redrawn from
Pallasch TJ: Dent Drug Serv Newsl 4:25,
1983.)
Active Forms of Local Anesthetics
Local Anesthetic Molecules
 Majority of local anesthetics are tertiary amines (except
Prilocaine)
 All local anesthetics are amphipathic
(lipophilic/hydrophilic)

Three main parts of the local anesthetic molecule:

1) Lipophilic Part (aromatic ring) - largest portion of the
molecule
2) Intermediate Chain (amide or ester)
3) Hydrophilic Part (ethyl alcohol/acetic)-Local anesthetics
without a hydrophilic portion are not suitable for injection but
are good topical anesthetics, i.e., Benzocaine a)TYPICAL LOCAL ANAESTHETIC
B)AMINO ESTER
C)AMINO AMIDE
Hypothesized Mechanism Of Action Of
Local Anesthetics
 LA agents are available as acid salts of weak bases

 The LA weak base (BNHOH) must be combined with a strong

acid (HCI) in order to make acid salt (BNHCL) that is soluble in
solution
BNHOHWEAK BASE +HCLSTRONG ACID = BNHCL + HOH

 For this solution to act as an LA it must dissociate into a freebase

(BH)
DISSOCIATION OF LOCAL
ANESTHETICS
 Local anesthetics are available as salts (usually hydrochlorides) for
clinical use.
 The salts, both water soluble and stable, is dissolved in either sterile
water or saline.
 In this solution it exists simultaneously as unchanged molecule
(RN), also called base and positively charged molecules (RNH+)
called cations.
RNH+ ==== RN + H+
The relative concentration of each ionic form in the solution varies in the
pH of the solution or surrounding tissue.
 In the presence of high concentration of hydrogen ion (low pH) the
equilibrium shifts to left and most of the anesthetic solution exists in
cationic form.
RNH+ > RN + H+
 As hydrogen ion concentration decreases (higher pH) the equilibrium
shifts towards the free base form.

RNH+ < RN + H+
 The relative proportion of ionic form also
depends on pKa or DISSOCIATION
CONSTANT, of the specific local
anesthetic.
 The pKa is a measure of molecules
affinity for H+ ions.
 When the pH of the solution has the
same value as pKa of the local anesthetic,
Henderson Hasselbalch equation
exactly half the drug will exists in the
RNH+ form and exactly half in RN form.
 The percentage of drug existing in either
form can be determined by Henderson
Hasselbalch equation
 Henderson hasselbach equation
 Determines how much of a local anesthetic will be in a non-ionized
vs ionized form .
 Based on tissue pH and anesthetic Pka .
 Injectable local anesthetics are weak bases (pka=7.5-9.5). When a
local anesthetic is injected into tissue it is neutralized and part of the
ionized form is converted to non-ionized .
 The non-ionized base is what diffuses into the nerve.
 Once some of the drug dose cross; the pH in the nerve will be
normal and therefore the LA re-equilibrates to both the ionized and
nonionized forms; but there are fewer cations which may cause
incomplete anesthesia.
 In an infected tissue, the pH is lower (more acidic) and according to the HH equation; there
will be less of the non-ionized form of the drug to cross into the nerve (rendering the LA
less effective)

EFFECT OF DECREASED TISSUE PH ON THE

ACTIONS OF A LOCAL ANAESTHETIC

Malamed SF. Handbook of local anesthesia. seventh ed.

Elsevier Mosby, St Louis 2004.
DISSOCIATION CONSTANTS(PKA OF LOCAL
ANAESTHETICS)

A local anesthetic with a lower pKa

(e.g., lidocaine, pKa7.7) has a greater
number of lipophilic free base
molecules available to diffuse through
the nerve sheath;
however, the anesthetic action of this
drug is inadequate because at an
intracellular pH of 7.4 only a very
small number of base molecules
dissociate back to the cationic form
necessary for binding at the receptor
site.
Factors Are Involved In The Action of a Local Anesthetic:

The two factors involved in the action of a local anesthetic

are
(1) Diffusion of the drug through the nerve sheath
(2) Binding at the receptor site in the ion channel.

The uncharged, lipid-soluble, free base form (RN) of the anesthetic is

responsible for diffusion through the nerve sheath.
 The ability of a local anesthetic to diffuse through the tissues surrounding a nerve is of
critical significance, because in clinical situations the local anesthetic cannot be
applied directly to the nerve membrane as it can in a laboratory setting.
 Local anesthetic solutions better able to diffuse through soft tissue provide an
advantage in clincal practice
 A local anesthetic with a high pKa has very few molecules available in the RN form at
a tissue pH of 7.4.
 The onset of anesthesia of this drug is slow because too few base molecules are
available to diffuse through the nerve membrane (e.g., procaine, with a pKa of 9.1).
 The rate of onset of anesthesia is related to the pKa of the local anaesthetic.
FACTORS AFFECTING LOCAL ANESTHETIC ACTION
Factor Action affected Description
pKa Onset Lower pKa = more rapid onset of action, more RN molecules
present to diffuse through nerve sheath, thus onset time is
decreased
Lipid solubility Anesthetic potency Increased lipid solubility = increased potency
(example:procaine = 1, etidocaine = 140)
Etidocaine produces conduction blockade at very low
concentrations whereas procaine poorly suppresses nerve
conduction, event at higher concentrations

Protein binding Duration Increased protein binding allows anesthetic cations (RNH +) to
be more firmly attached to protein located at receptor sites, thus
duration of action is increased

Non-nervous tissue Onset Increased diffusibility = decreased time of onset

diffusibility

Vasodilator activity Anesthetic potency Greater vasodilator activity = increased blood flow to region =
and duration rapid removal of anesthetic molecules from injection site, thus
decreased anesthetic potency and decreased duration
FACTORS AFFECTING DURATION OF ANESTHESIA

 Accuracy in deposition of LA ( deposition of drug closer to nerve provides greater

anesthesia)

 Status of tissue (infection and Vascularity of region .)

 Anesthetic duration is increased in areas of decreased vascularity (e.g., Gow Gates
mandibular nerve block vs. inferior alveolar nerve block), and the addition of a vasopressor
decreases tissue perfusion to a local area, thus increasing the duration of the block.

 Anatomical variation ( e.g., dense alveolar bone )

 Type of injection Administered ( supraperiosteal or nerve block )

CHEMICAL STRUCTURE,PHYSICOCHEMICAL PROPERTIES AND PHARMACOLOGIC
PROPERTIES OF LA AGENTS

Malamed SF. Handbook of local anesthesia. seventh ed. Elsevier Mosby, St Louis 2004.
How Local Anesthetics Work to Block Nerve Conduction

Displacement of calcium ions from the sodium channel receptor site.

Binding of the local anesthetic molecule to this receptor site.

Blockade of the sodium channel. Decrease in sodium conductance

Depression of the rate of electrical depolarization

Failure to achieve the threshold potential level (firing level)

Lack of development of propagated action potentials

Conduction blockade
Classification of LA
 (1) Esters: They possess an ester linkage
between the benzene ring and the intermediate
chain.

 (2) Amide: They possess an ainide linkage

between the benzene ring & intermediate
chain.

 (3)Quinolones
 Based on structure

 Amides
Esters
Esters of benzoic acid
Butacaine
Cocaine
Ethyl aminobenzoate (benzocaine)
Hexylcaine
Piperocaine
Tetracaine

Articaine
Esters of p-aminobenzoic acid
Chloroprocaine
Procaine
Propoxycaine

Bupivacaine
Dibucaine
Etidocaine
Lidocaine
Mepivacaine
Prilocaine
Ropivacaine

 Quinoline
Centbucridine
2.Based on duration of action
 Ultra short acting < 30 min 2 % Lignocaine without a vasoconstrictor &

4% Prilocaine without vasoconstrictor

 Short acting- 45-75 min Procaine HCL 4%,

2 % Lignocaine with 1:1,00,000 Epinephrine

 Medium acting=90-150 min Mepivacaine, Prilocaine, 2 %

Lignocaine with 1:2,00,000 Epinephrine

 Long acting≥ 180 min Bupivacaine (400-450 min),

Etidocaine, 5 % Lignocaine with 1:2,00,000 epinephrine
 Based on potency and duration

lnjectable:
 A) Low potency, short duration : Procaine, Chloroprocaine
 B) Intermediate potency & duration : Lidocaine, Prilocaine.
 C) High poteiicy & long duration: Bupivacaine, Tetracaine.

Surface anesthetic:
 Soluble: Cocaine, Tetracaine. Beiioxinate, Ligiio- caine.
 Insoluble: Benzocaine, Oxethazine
 Classification of Local Anesthetic Substances
According to Biological Site and Mode of Action
Class Definition Chemical Substance

A Agents acting at receptor site on Biotoxins (e.g.,

external surface of nerve membrane tetrodotoxin,
saxitoxin)
B Agents acting by a receptor Quaternary
independent physicochemicalmechanism ammonium analogues of lidocaine, Scorpion
venom.
Agents acting by a receptor-independent
C physicochemical mechanism Benzocaine

D Agents acting by combination of receptor and Most clinically useful

receptor-independent mechanisms local anesthetic
agents (e.g., articaine, bupivacaine,
lidocaine, mepivacaine, prilocaine)

Modified from Covino BG, Vassallo HG: Local anesthetics: mechanisms

of action and clinical use, New York, 1976, Grune & Stratton.
COMPOSITION
 Local anesthetic agent: LIdocaine Hcl 2%
 Vasoconstrictor: adrenaline 1:80000
 Reducing agent: sodium metabisulphite 0.5 mg .[as an antioxidant , to prevent
oxidation of L.A solution
 Preservative:methyparaben0.1%,capryl hydrocuprienotoxin
 Isotonic solution: sodium chloride 6mg
 Fungacide:thymol
 Vehicle: ringer's solution-minimize discomfort during injection
 Diluting agent:distilled water
 To adjust ph:sodium hydroxide
 Nitrogen bubble:1-2mm in diameter and is present to prevent o2 from being trapped
cartridge and potentially destroying the vasopressor or vasoconstrictor
 REDUCING AGENT

 Vasoconstrictors are unstable in solution and may oxidize especially on prolong

exposure to sunlight this results in turning of the solution brown and this
discoloration is an indication that such a solution must be discarded.
 To overcome this problem a small quantity of sodium metabisulphite is added -
competes for the available oxygen.

 PRESERVATIVE

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

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

VEHICLE

 The anesthetic agent and the additives referred to above are dissolved in distilled water
& sodium chloride.
 This isotonic solution minimizes discomfort during injection.
The chemical characteristics are so balanced that they have both lipophilic and hydrophilic
properties. If hydrophilic group predominates, the ability to diffuse into lipid rich nerves is
diminished. If the molecule is too lipophilic it is of little clinical value as an injectable
anesthetic, since it is insoluble in water and unable to diffuse through interstitial tissue.
PHARMACOLOGY OF LOCAL ANAESTHETICS
The local anesthetics used in dentistry are divided into two groups: 
 ESTER GROUP 
 AMIDE GROUP
ESTER GROUP:
 It is composed of the following
 An aromatic lipophilic group
 An intermediate chain containing an ester linkage
 A hydrophilic secondary or tertiary amino group
AMIDE GROUP:
 It is composed of the following
 An aromatic, lipophilic group
 An intermediate chain containing amide linkage
 A hydrophilic secondary or tertiary amino group
COMPARISON OF ESTERS AND AMIDES
PHARMACOKINETICS
UPTAKE
• Most local anesthetics have vasodilating properties .
• Procaine= most vasodilating
• A significant clinical effect of vasodilation is an increase in the rate of absorption
of the local anesthetic into the blood, thus decreasing the duration and quality (e.g.,
depth) of pain control, while increasing the anesthetic blood (or plasma)
concentration and its potential for overdose (toxic reaction). When injected into
soft tissue most local anesthetics produce dilation of vascular bed.
• Cocaine is the only local anesthetic that produces vasoconstriction, initially it
produces vasodilation which is followed by prolonged vasoconstriction.
• The rates at which local anesthetics are absorbed into the bloodstream and reach
their peak blood level vary according to the route of administration
RELATIVE VASODILATING VALUES OF
AMIDE TYPE LA

Malamed SF. Handbook of local anesthesia. seventh ed. Elsevier Mosby, St Louis 2004.
 ORAL ROUTE

 With the exception of cocaine, local anesthetics are absorbed

poorly, if at all, from the gastrointestinal tract after oral
administration.
 Undergo a significant hepatic first-pass effect after oral
administration.
 After absorption of lidocaine from the gastrointestinal tract
into the enterohepatic
circulation, a fraction of the drug dose is carried to the liver,
where approximately 72% of the dose is biotransformed into
inactive metabolites.This has seriously hampered the use of
lidocaine as an oral antidysrhythmic drug.
 In 1984 Astra Pharmaceuticals and Merck Sharp & Dohme
introduced an analogue of lidocaine, tocainide
hydrochloride,
that is effective orally.
TOPICAL ROUTE
 Local anesthetics are absorbed at different rates after application to mucous
membranes, in the tracheal mucosa uptake is as rapid as with intravenous
administration. In pharyngeal mucosa uptake is slow In bladder mucosa uptake is even
slower
 Eutectic mixture of local anesthesia (EMLA) has been developed to provide surface
anesthesia for intact skin.

INJECTION
 The rate of uptake of local anesthetics after injection is related to both the vascularity of
the injection site and the vasoactivity of the drug.
 IV administration of local anesthetics provide the most rapid elevation of blood levels
and is used for primary treatment of ventricular dysrhythmias.
TIME TO ACHIEVE PEAK LEVEL
DISTRIBUTION
 Once absorbed in the blood stream local anesthetics are distributed through out
the body to all tissues. 
 Highly perfused organs such as brain, head, liver, kidney, lungs have higher blood
levels of anesthetic than do less higher perfused organs.

The blood level is influenced by the following factors: 

 Rate of absorption into the blood stream. 
 Rate of distribution of the agent from the vascular compartment to the tissues. 
 Elimination of drug through metabolic and/or excretory pathways.
 All local anesthetic agents readily cross the blood-brain barrier, they also readily
cross the placenta.
METABOLISM (BIOTRANSFORMATION)

ESTER LOCAL ANESTHETICS:

 Ester local anesthetics are hydrolyzed in the plasma by the enzyme pseudocholinesterase.
 Chloroprocaine the most rapidly hydrolyzed, is the least toxic.
 Tertracaine hydrolyzed 16 times more slowly than Chloroprocaine ,hence it has the
greatest potential toxicity.

AMIDE LOCAL ANESTHETICS

 The metabolism of amide local anesthetics is more complicated then esters.
 The primary site of biotransformation of amide drugs is liver.
 Entire metabolic process occurs in the liver for lidocaine, articaine, etidocaine, and
bupivacaine.
 Prilocaine undergoes more rapid biotransformation then the other amides.
EXCRETION
 Kidneys are the primary excretory organs for both the local anesthetic and its metabolites .
 A percentage of given dose of local anesthetic drug is excreted unchanged in the urine.
 Esters appear in only very small concentration as the parent compound in urine.
 Procaine appears in the urine as PABA (90%) and 2% unchanged.
 10% of cocaine dose is found in the urine unchanged.
 Amides are present in the urine as a parent compound in a greater percentage then are
esters.
MAXIMUM RECOMMENDED DOSE
 Doses of local anesthetic drugs are presented in terms of milligrams of drug per unit of
body weight—as milligrams per kilogram (mg/kg) or as milligrams per pound (mg/lb).

2% lignocaine means 2g per 100 ml

=2000mg/100ml
=20mg/ml
Maximum doses of LA

 Lidocaine with epinephrine - 7 mg/kg of body weight for

the adult (not to exceed a dose of 500 mg). 
 Lidocaine without epinephrine- 4.4 mg of body weight for
the adult (not to exceed a dose of 300 mg). 
 Same dose for children.
DRUG ,FORMULATION AND MRD OF
VARIOUS DRUGS
Calculation of number of cartridges (for70
kg)
 Lidocaine 2% with epinephrine 
 According to manufacturer – 20 mg/ml i.e. in 1 ml - 20 mg 
 Considering cartridge as 1.8 ml i.e. in 1.8 ml 36mg(1.8×20)
 or in 1 Cartridge - 36 mg 
 Not to exceed a dose of 500 mg
 So total no of cartridges 500/36 = 13.88 cartridges
For Lidocaine without epinephrine
 According to manufacturer – 20 mg/ml i.e. in 1 ml - 20 mg
 Considering cartridge as 1.8 ml i.e. in 1.8 ml 36mg(1.8×20) or in
 1 Cartridge - 36 mg 
 Not to exceed a dose of 300 mg
 So total no of cartridges 300/36 = 8.33 cartridges
HOW TO CALCULATE MRD AND NO OF
CARPULES
Patient: 22 years old, healthy, female, 50 kg
 Local anesthetic: lidocaine hydrochloride + epinephrine
 1:100,000
1 CARTRIDE=1.8 ML
2% MEANS 20mg/ml
 Lidocaine, 2% = 36 mg per cartridge(1.8* 20)
 Lidocaine, 7.0 mg/kg = 350 mg (maximum recommended
dose)50*7
 Number of cartridges 350/36 ≈ 9.75
 IF COMBINATION OF TWO LA IS USED, NO OF CARPULES CAN BE CALCULATED AS
FOLLOWS

Patient: 45-kg female, healthy • The doctor wishes to change to 4% articaine with
epinephrine 1:100,000.
Local anesthetic: mepivacaine, 2%, • How Much Articaine Can This Patient Receive?
with levonordefrin 1:20,000
 Mepivacaine, 2% = 36 mg per • Articaine, 4% = 72 mg percartridge(40*1.8)
• Articaine, 7.0 mg/kg = 315 mg (maximum
cartridge(20*1.8ml) recommended dose)7*45
 Mepivacaine, 6.6 mg/kg = 297 mg • The total dose of both local anesthetics should not
(maximum recommended exceed the lower of the two calculated doses, or 297
mg.
dose)6.6*45 • The patient has received 72 mg(mepivacaine), and
 The patient receives two cartridges thus can still receive 225 mg of articaine.
(72 mg), but anesthesia is • Therefore 225 mg/72 mg per cartridge is equivalent to
3.0
inadequate.
 cartridges of 4% articaine with
epinephrine 1:100,000
Pharmacology of Vasoconstrictors

 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.
 Epinephrine, norepinephrine, and dopamine are the naturally occurring catecholamines of
the sympathetic nervous system.
 Isoproterenol and levonordefrin are synthetic catecholamines.
 Felypressin, a synthetic analogue of the polypeptide vasopressin (antidiuretic hormone), is
available in many countries as a vasoconstrictor.
 Vasoconstrictors should be included unless contraindicated.

Mode of Action -
 Attach to and directly stimulate adrenergic receptors .
 Act indirectly by provoking the release of endogenous catecholamine from intraneuronal
storage sites
CLASSIFICATION

 CATECHOLAMINES  NON CATECHOLAMINES

 – Epinephrine  – Amphetamine
 – Norepinephrine  – Methamphetamine
 – Dopamine  – Hydroxy-amphetamine
 – Levonordefrin  – Ephedrine
 – Isoproterenol  – Mephetermine
Vasoconstrictors are important additions to a local anesthetic
solution for the following reasons:
 By constricting blood vessels, 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.
 Local anesthetic blood levels are lowered, thereby decreasing the risk of local anesthetic
toxicity from overadministration of the drug. (Overdose from rapid intravascular injection
can still occur.)
 More local anesthetic diffuses into the nerve, where it remains longer, thereby increasing
(in some cases significantly, in others minimally) the duration of action of most local
anesthetics.
 Vasoconstrictors decrease bleeding at the site of administration. Their inclusion in the local
anesthetic solution is useful when increased bleeding is anticipated (e.g., during a surgical
procedure)
Selection of a Vasoconstrictor
 Length of the dental procedure (Duration of pulpal and soft tissue anesthesia with 2% lidocaine lasts
for only 10 min; the addition 1:50,000,1:80,000,1:100,000,increases this to 60 min)

 Need for hemostasis during and following the procedure

 Epinephrine is effective in preventing blood loss during surgical procedures, however it also
produces rebound vasodilatory effect.

 Felypressin constricts venous circulation more than arteriolar so minimum value in haemostasis)
 Requirement for postoperative pain control(plain LA produce pulpal anesthesia for short duration )
 Medical status of the patient( Benefits and risk of using LA with vasoconstrictor should be weighed
against benefits and risks of using plain LA in medically compromised patients )
Availability in Dentistry
Epinephrine is the most potent and widely used vasocon_x0002_strictor in
dentistry. It is available in the following dilutions and drugs:

• Concentrations of Vasoconstrictor in
Local Anesthetics -
• 1:50,000 ,1:100,000, 1:200,000 -
0.020mg/ml ,0.010mg/ml, 0.005 mg/ml

• Calculation 1:50,000= 1gram/50,000ml=

1000mg/50,000ml= 1mg/50ml=
0.02mg/ml
Max dose of vasoconstrictors -
 Healthy patient approximately 0.2mg
 Patient with significant cardiovascular history: 0.04mg

NUMBER OF CARPULES CALCULATED AS FOLLOW

In CV patient
1 carpule = 1.8ML
1:100,000=.01mg/ML
(1G IN 100000ML=1000MG IN 1,OOOOO ML=0.01MG/ML)
0.01 X 1.8ML= 0.018mg
0.04/0.018=2.22 carpules
In a healthy adult patient
0.2/0.018=11.1 carpules
CONCENTRATIONS OF CLINICALLY USED
VASOCONSTRICTORS
CONTRAINDICATIONS
Patients with more significant cardiovascular disease (ASA Ш and IV)

Patients with certain non-cardiovascular diseases (e.g., thyroid dysfunction

, and sulfite sensitivity)

Patients receiving Monoamine oxidases inhibitors, Tricyclic antidepressant

, and phenothiazines)

In each cases it is necessary to determine the degree of severity of the

underlying disorder to determine whether a vasoconstrictor may be
included safely
Factors in Selection of a Local
Anesthetic for a Patient
 Length of time pain control is necessary
 2. Potential need for posttreatment pain control
 3. Possibility of self-mutilation in the postoperative period
 4. Requirement for hemostasis
 5. Presence of any contraindications (absolute or relative) to the local anesthetic solution
selected for administration
COMMON QUESTIONS TO ASK THE
PATIENT
 • Allergic to any medications?
 • Have you ever had a reaction to local anesthesia?
 • If yes, describe what happened
 • Was treatment given? If so, what?
PREPARATION OF THE PATIENT
 Careful preoperative assessment
 History
 A clear explanation of what to expect
PREOPERATIVE ASSESSMENT:
 Data to be documented includes:
 1.Baseline vital signs:
1.blood pressure
2.laboratory values
3.Results of ECG monitoring
4.any other tests.
 2. Weight, height, and age: 
 Dosage of some drugs is calculated on the basis of body weight in kilograms (mg/kg).
 Some drugs are contraindicated for age extremes (i.e., pediatric or geriatric patients).
 Current medical problem(s) past history of medical events,
including a history of substance abuse.
 Current medications or drug therapy, such as insulin for diabetes or
hypertensive drugs.
 Allergy, or hypersensitivity reactions to previous anesthetics or
other drugs.
 Mental status, including emotional state and level of consciousness.
 Communication ability: A patient with hearing impairment or
language barrier may be unable to understand verbal instructions
during the procedure or to respond appropriately.
STRESS REDUCTION PROTOCOL

 Morning appointments are usually best. 

 Keep appointments as short as possible. 
 Freely discuss any questions, concerns, or fears that the patient has .
 Establish a honest, supportive relationship with the patient.
 Maintain a calm, quiet, professional environment. 
 Provide clear explanations of what the patient should expect and
feel.
 Premedicate with benzodiazepines if needed. 
 Ensure good pain control through judicious selection of local anesthetic agents appropriate
for treatment. 
 Maintenance of patient comfort throughout the procedure. 
 Use nitrous oxide as needed (avoid hypoxia). 
 Use gradual position changes to avoid postural hypotension. 
 End the appointment if the patient appears overstressed.
LOCAL ANAESTHETICS IN MEDICALLY COMPROMISED
PATIENTS
CLINICAL ACTION OF SPECIFIC AGENTS

 Lignocaine (Xylocaine, Octacaine)-

 Classified – Amide
 Chemical formula -2-diethylamino 2,6 acetoxylidide hcl

 Prepared by : 1943 – Nils Lofgrens

 Introduced in 1948 into dentistry.
 Metabolised- Liver by microsomal fixed function oxidases to monoethyl glycerine and
xylidide
 Excretion -<10% unchanged through kidneys, >80%-metabolized

 Vasodilation Properties -less than Procaine, more than Mepivacaine

 Pka ( dissociation constant )–7.9 ,

 ph(plain)-6.5,

 ph(with Vc) 5 –5.5,

 Onset of action =2-3 min,
 Anesthetic half life = 1.6hrs,
 Effective dental conc. = 2%
 Topical anesthetic =2% in thform of gel
=5% in the form of ointment
=10%- 15% in the form of spray
 Sets on quickly and produces a desired anesthetic effect for several
hours
 Good alternative for those allergic to ester type
 More potent than procaine but about equal toxicity
 It relieves pain during the dental surgeries
 Quicker CNS effects than others
 Anti arrhythmic
 Cause little allergenic reaction; it is hypoallergenic
Recommended dose
With V.C = 7mg/kg not>500mg
Without V.C= 4.4mg/kg not>300mg
 For children with VC= 3.2 mg/kg

 Council for dental therapeutcs- ADA 4.4mg/kg

 It is available in three formulations

Ligno2% with out VC

Ligno2% with VC 1:80,000
Ligno2% with VC 1:100,000
 USE : a) 2% lignocaine with 1: 50000 epi. – hemostasis
 b) 2% lignocaine with 1: 100000 or 1: 200000 – localanesthesia

COMPARISON OF LIDOCAINE WITH PROCAINE

 - More rapid onset of action
 - More profound anesthesia
 - Longer duration of action
 - Greater potency
 Adverse reactions
CVS
 ↓ In electrical excitability of Myocardium
 ↓ in force of contraction
 ↓ in rate of contraction
 ↑dose -Hypo tension & Cardiovascular
collapse
CNS
 Depressing action-lethargy & sleepy
 convulsion
RS
 Small dose- Mild Bronchodialation
 Large dose- RS arrest → CVS arrest
Bupivacaine (marcaine)– A.F.EKENSTAM (1957)

 Classified as - amide

 Potency - 4 times that of lidocaine , prilocaine

 Toxicity - <4 times – Lignocaine, Mepivacaine

 Metabolism - Liver .

 Excretion - by kidney

(16% unchanged)
 Available as 0.5% soln 1:2,00,000 (v/c)

 Indication- Lengthy dental procedure/deep anesthesia-

e.g. Pulpal anesthesia->90- min.

Full mouth reconstruction.

Extensive perio surgery.

Management of post op pain.

 Duration -Pulpal - 90- 180 min

- Soft tissue- 4-12 hrs

 Contra indication- burning sensation at site of injection, in children-anticipating self

trauma .
Procaine (Novocaine) - ALFRED EINHORN (1905)

 Classified under –Esters

 Chemical formula- 2Diethylamino ethyl
4aminobenzoate hcl
 Metabolism- hydrolyzed in Plasma by plasma
pseudocholine esterases
 Excretion >2%unchanged, 90% -PABA,8%
diethyl aminoethanol in urine.
 Pka-9.1,
 Vasodilating property –High
 Onset of action - slow
 increased incidence of allergy,
 Used in breaking arteriospasm
 Toxic effects due to PABA

 1.Nervous system – crosses blood brain barrier

• First stimulation like excitement, tremors, ataxia convulsions.( produced by inhibition
of cortical inhibitory neurons )
• Later CNS depression, analgesia
• Sedation, lethargy in subconvulsive doses

2. CVS
 Locally - Vasodilatation of microcirculation
 Systemically - depresses smooth, cardiac & skeletal
muscle .
 In large doses – hypotension
 Significantly higher doses cardiac collapse (bradycardia or asystole )
Mepivacaine (Carbocaine) by A.F. Ekenstam -

 classified - amide type

 Metabolism - liver.

 Maximum dose - 4.4 mg/kg , absolute max dose-300mg.

 Excretion -1-10% unchanged urine.

 Pka -7.6

 Anesthetic half life -90min,

 Mild vasodilator 3% mepivacaine is used in patients in whom

a vasoconstrictor is not indicated.

 Low reported cases-allergy.

ANAESTHETICS FOR TOPICAL APPLICATION

 Component of atraumatic intra oral administration.

 Conventional applied anesthetics – unable to
penetrate intact skin.
 Topically applied LA lack vasoconstrictor- greater
absorption – greater level in blood
 Effective only on the surface (2-3mm)
 Available as mouth washes, ointments, sprays,
emulsions and strips, aerosol , gels.
 Insoluble in water; soluble in vehicle such as alcohol,
polyethylene glycol, propylene glycol, or carboxymethyl
cellulose -make them amenable to surface application

Advantage:
 1. By incorporating the anesthetic into a viscous liquid, a gel,
or an ointment, they remain in contact with the area for a
longer period, thereby increasing the duration of action.
 2. poorly absorbed into the circulation
 Benzocaine:
 Poor solubility in water
 Poor absorption into CVS
 Remains longer at the site of application
 Prolonged use – localized allergic reaction
 Systemic Toxic reaction unkown
 Availability as: Aerosol, Gel, Gel patch,
Ointment , Solution

 Lidocaine Base :
 Available as flavored gels, ointments,, aerosol
spray
Produce anesthesia within 15 sec,
duration of action = 30 min
Cocaine Hydrochloride:
 Absorbed rapidly, eliminated slowly
 Duration of action =2hrs
 Cause Habituation, so use as topical anesthetic in
dentistry not recommended
Lidocaine Hydrochloride :
 Used in a 2% or 4% concentration. penetrate tissue better than
lidocaine base.
 Maximum recommended dose is 200 mg.
 Lidocaine ( 2% )is a flavored syrup that may be used as an oral
rinse or gargle or swallowed ;it is particularly useful in those
patients who tend to gag during dental procedures.
EMLA (Eutectic Mixture Of Local Anesthetics)

 Cream (Lidocaine 2.5% +Prilocaine 2.5%)

 Emulsion in which oil phase is eutectic mix of lidocaine

and prilocaine in a ratio of 1:1 by wt

 Supplied as 5g or 30 gm tube or as an EMLA disc.

 Can be used to provide surface anesthesia on intact skin.

 Contraindicated: pts with congenital idiopathic

methemoglobulinemia, infants under age of 12 months
Local Anesthesia -Armanterium
MAJOR COMPONENTS
1.) The Syringe
2.) The Needle
3.) The Cartridge
Other Armamentarium -
 Topical Anesthetic (strongly recommended)
 -ointments, gels, pastes, sprays
 - Applicator sticks
- Cotton gauze
SYRINGE
 It is the vehicle whereby the content of the anesthetic cartridge is delivered through
the needle to the patient.
 The American Dental Association criteria for acceptance of local anesthetic syringes
include
1. 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.)
2. They should be capable of accepting a wide variety of cartridges and needles of
different manufacture, and should permit repeated use.
3. They should be inexpensive, self-contained, lightweight, and simple to use with one
hand.
4. They should provide effective aspiration and be constructed so that blood may be easily
observed in the cartridge.
Syringe Types Available in Dentistry
Nondisposable syringes:
a. Breech-loading, metallic, cartridge-type, aspirating
b. Breech-loading, plastic, cartridge-type, aspirating
c. Breech-loading, metallic, cartridge-type, self aspirating
d. Pressure syringe for periodontal ligament injection
e. Jet injector (“needle-less” syringe)

2. Disposable syringes

3. “Safety” syringes

4. Computer-controlled local anesthetic delivery systems

Advantages and Disadvantages of the
Metallic, Breech-Loading, Aspirating Syringe
ADVANTAGES DISADVANTAGES
 Visible cartridge  Weight (heavier than plastic
 Aspiration with one hand  syringe)
 Autoclavable  Syringe may be too big for
 Rust resistant  small operators
 Long lasting with proper  Possibility of infection with
 maintenance  improper care
Advantages and Disadvantages of the
Plastic, Reusable, Aspirating Syringe
 ADVANTAGES  DISADVANTAGES
 Plastic eliminates metallic,  Size (may be too big for
 clinical look  small operators)
 Lightweight: provides bet_x0002_ter “feel”  Possibility of infection with
during injection
  improper care
Cartridge is visible
 Aspiration with one hand  Deterioration of plastic with
 Rust resistant  repeated autoclaving
 Long lasting with proper
 maintenance
 Lower cost
Advantages and Disadvantages of the
Metallic, Self-Aspirating Syringe
ADVANTAGES DISADVANTAGES
 Cartridge visible  Weight
 Aspiration is easier with small hands  Feeling of “insecurity” for doctors
 accustomed to harpoon-type syringe.
Autoclavable
 Finger must be moved from thumb ring
 Rust resistant
to thumb disk to aspirate blood.
 Long lasting with proper  Possibility of infection withimproper
 maintenance care.
 Piston is scored (indicates
 volume of local anes_x0002_thetic
administered)
PRESSURE SYRINGES

• ADVANTAGES
• Measured dose
• Overcomes tissue resistance
• Nonthreatening (new devices)
• Cartridges protected
• Easy to inject anesthetic too rapidly
JET INJECTOR
ADVANTAGES
• Does not require use of a needle (recommended
for persons with needle phobia)
• Delivers very small volumes of local anesthetic
(0.01–0.2 mL)
• Used in place of topical anesthetic.

DISADVANTAGES
• Inadequate for pulpal anesthesia or for regional
block
• Some patients are disturbed
• by the jolt of the injection.
• Cost
• May damage periodontal
• tissues
PLASTIC DISPOSABLE SYRINGES

ADVANTAGES
• Disposable, single use
• Sterile until opened
• Lightweight (may feel awkward
• to the first-time user; tactile
• sensation better)

DISADVANTAGES
• Does not accept prefilled
• dental cartridges
• Aspiration difficult
• (requires two hands)
SAFETY SYRINGE

ADVANTAGES

• Disposable, single use

• Sterile until opened
• Lightweight (better tactile sensation)

DISADVANTAGES

• Requires additional training

• May feel awkward to a first-time
• user
COMPUTER CONTROLLED
ANAESTHETIC DEVICE(C-CLAD)
system(1997)
 The Wand was designed to improve on the ergonomics and precision of the dental
syringe .
 This system enabled a dentist or hygienist to precisely manipulate needle placement
with fingertip accuracy and deliver the local anesthetic with a foot-activated control.
 A lightweight handpiece held in a pen-like grasp, provides increased tactile sensation
and control compared with the traditional syringe. The flow rate of local anesthetic
delivery is computer controlled and thus remains consistent from one injection to the
next.
 Fukayama et al. conducted a controlled clinical trial to evaluate pain perception with a
C-CLAD device. Seventeen of 20 participants reported a slight- or no-pain rating on a
visual analog scale (VAS) for palatal injections adminitered with C-CLAD systems
Wand STA system

 Introduced in 2007, The Wand STA system is a third generation C-CLAD instrument
representing a new and meaningful innovation for subcutaneous injections performed
both in dentistry and in medicine
 The technological advancement is related to the development of what is called dynamic
pressure-sensing technology (DPS technology).
 DPS technology enables the precise monitoring and control of fluid pressure at the
needle tip when a subcutaneous injection is performed.
 The Wand STA system audibly and visually “guides” placement of the needle tip into the
anatomic entrance of the PDL space through DPS technology. Important to the success of
the PDL injection is proper needle placement into the PDL space.
 This transforms the PDL injection technique into a “guided” technique that can be more
easily and accurately performed.
ADVANTAGES
 Dynamic pressure-sensing technology provides continuous real-time feedback when
an injection is performed, resulting in a more predictable injection site location
 Allows the periodontal ligament injection to be used as a predictable primary injection
 Can be used for all traditional injection techniques
 Recommended device for newer injection techniques such as anterior middle superior
alveolar nerve block, palatal anterior superior alveolar nerve block, and STA
periodontal ligament injection
 Reduces pain-disruptive behavior in children and adults
 Reduces stress for patient
 Reduces stress for operator
DISADVANTAGES

 Requires additional armamentarium

 Requires additional training
NEEDLE

 The needle is the vehicle that permits local

anesthetic solution to travel from the dental
cartridge into the tissues surrounding the needle
tip.

 Length:
 1-Long (approximately 40 mm "32-40 mm"),
for NB.
 2-Short(20-25 mm).
 3-Extra-short(approximately 15 mm), for PDL
 NEEDLE GAUGE
 Gauge refers to the diameter of the lumen of
the needle:
 the smaller the number, the greater the
diameter of the lumen.
 Usual dental needle gauges are 25,27, & 30
 A 30-gauge needle has a smaller internal
diameter than a 25-gauge needle. In the United
States, needles are color coded by gauge.
Advantages of Larger-Gauge Needles
Over Smaller-Gauge Needles

1. Less deflection as the needle advances through tissues

2. Greater accuracy of injection
3. Less chance of needle breakage
4. Easier aspiration
5. No perceptual difference in patient comfort
Minimizing Needle Deflection: Birotational
Insertion Technique

 A new approach to reducing needle deflection has

been described.
 Rotational insertion (described as birotational
insertion technique [BRIT]), a technique in which
the operator rotates the handpiece or needle in a
back-and-forth rotational movement while
advancing the needle through soft tissue, is
similar to techniques used for acupuncture or
endodontic instrumentation.
CATRIDGE
 The dental cartridge is a glass cylinder containing the
local anesthetic drug, among other ingredients.
Types:
 Standard ,Self aspirating, plastic, Glass
Contents: LA, VC, Vehicle, preservative.
 Components
 The prefilled 1.8-mL dental cartridge consists of four parts
 1. cylindrical glass tube
 2. stopper (plunger, bung)
 3. aluminum cap
 4. diaphragm
RECOMMENDATIONS

 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.

COLOUR CODING OF LA
CARTRIDGES AS PER AMERICAL
DENTAL ASSOCIATION
additional armamentarium

 1. topical antiseptic
 2. topical anesthetic
 3. applicator sticks
 4. cotton gauze (2 × 2 inches)
 5. hemostat
 6. needle-recapping device
CONCLUSION
 Adapting local anaesthetic technique can overcome difficulties in
access and limit soft tissue anaesthesia .
 Local anesthesia remains the backbone of pain control in dentistry.
 Research has been continued in both medicine and dentistry to seek
new and better means of managing pain associated with many surgical
treatments.
 Painful experiences and poor or prominent surgical scars are the two
most memorable aspects of a surgical procedure for a patient.
 If one can provide a nearly painless surgical procedure without the use
of general anesthesia then you have won half the battle.
Please Remember !!!
 Principle 1- No drug ever exerts a single action .
 -Principle 2- No clinically useful drug is entirely devoid of toxicity .
 Principle 3- The potential toxicity of a drug rests in the hands of the us
REFERENCES
 Handbook of local anesthesia – Stanley F Malamed – 7th edition 
 Local analgesia in dentistry – by d .h.roberts& j. h.sowray 
 Monehim”s local anesthesia and pain control, Benett 
 Practical pearls for nearly painless local anesthesia JOHN K. GEISSE.
 Principles of anesthesiology, 3rd edition, vol- 2, Vincent J. Collins 
 Local anesthesia- mechanism of action and clinical use- Benjamin G Cohino.
 Paincontrol in dental practice by Richard bennet7th edition. 
 Essentials of Local Anesthetic Pharmacology : Daniel E Becker 
 Advanced techniques and armamentarium for dental local anesthesia; Clark TM; Dent Clin North
Am. 
 Vasoconstrictors in local anesthesia for dentistry: A. L. Sisk; Anesth Prog. 
 Practical Local Anaesthesia for Special Needs Patients-John meechan 
 Current trends in pain research and therapy, Vol 4, chronic pain reactions, mechanism and modes of
therapy
LOCAL ANAESTHESIA COMPLICATIONS

 LOCAL
LOCAL

 • needle breakage
 • prolonged anesthesia (paresthesia)
 • facial nerve paralysis
 • ocular complications
 • trismus
 • soft tissue injury
 • hematoma
 • pain on injection
 • burning on injection
 • infection
 • edema
 • sloughing of tissues
 • postanesthetic intraoral lesions
SYSTEMATIC
Toxicity caused by direct extension of the usual pharmacologic effects of the drug:
 1. side effects
 2. overdose reactions
 3. local toxic effects
Toxicity caused by alteration in the recipient of the drug:
 1. a disease process (hepatic dysfunction, heart failure, renal
 dysfunction)
 2. emotional disturbances
 3. genetic aberrations (atypical plasma cholinesterase, malignant hyperthermia)
 4. idiosyncrasy
Signs & Symptoms of Local Anesthetic Overdose
Minimal to Moderate Overdose Levels

 Sweating
Signs  Vomiting
 Talkativeness
 Failure to follow commands or be
 Apprehension
reasoned with
 Excitability
  Elevated blood pressure
Slurred speech
 Generalized stutter, leading to muscular  Elevated heart rate
twitching and  Elevated respiratory rate
 tremor in the face and distal extremities
 Euphoria
 Dysarthria
 Nystagmus
Moderate to High Overdose Levels

SIGNS SYMPTOMS
 Lightheadedness and dizziness
 Tonic-clonic seizure activity followed by
 Restlessness
 Generalized central nervous system
 Nervousness
depression
 Sensation of twitching before actual twitching
 Depressed blood pressure, heart rate, and is observed
respiratory rate  (see “Generalized stutter” under “Signs”)
 Metallic taste
 Visual disturbances (inability to focus)
 Auditory disturbances (tinnitus)
 Drowsiness and disorientation
 Loss of consciousness
ALLERGIC REACTIONS TO LOCAL ANESTHETIC
AGENTS

 Hypersensitive state as a result of

exposure to an allergen • Re-exposure
can heighten the initial reaction •
Incidents of allergy are low • Often
allergic reaction is to one of the
ingredients within the cartridge, not the
local anesthesia itself
 CLINICAL MANIFESTATIONS OF AN
ALLERGY • Fever • Angioedema •
Urticaria • Dermatitis • Depression of
blood-forming organs • Photosensitivity
• Anaphylaxis
 56.
TOXICITY FROM LOCAL ANAESTHETIC
DRUGS
 When excessive blood levels occur.
Usually due to: 1. Accidental rapid
intravenous injection. 2. Rapid
absorption from mucous membranes. 3.
Absolute overdose if the dose used is
excessive.
SIGNS AND SYMPTOMS OF LA TOXICITY

 It involves the CNS and CVS.  CNS is more sensitive to LA than the CVS. 
 CNS manifestations tend to occur earlier. 
 Brain excitatory effects occur before the depressant effects.
CVS SIGNS & SYMPTOMS

 Early or mild toxicity:

 If LA with Adrenaline :Tachycardia with Hypertension
 If no Adrenaline : Bradycardia with Hypotension

 Severe toxicity:  CV Collapse is due to the depressant effect of the LA acting directly
on the myocardium (e.g. Bupivacaine) 
 Severe and intractable arrhythmias can occur with accidental iv injection.
 PRECAUTIONS:  Secure intravenous
access before injection of any dose .
  Always have adequate equipment and
drugs available before starting to inject
ESSENTIAL PRECAUTIONS AND
TREATMENT
 TREATMENT OF LOCAL
ANESTHETIC TOXICITY Apparent
allergy • Steroids • Histamine (H1)
blockers • With severe reactions –
Intravenous fluid – Epinephrine
 CNS toxicity • Don’t treat minor
reactions • Seizures: maintain airway,
provide O2 – Terminate seizure with
thiopental, midazolam, or propofol –
Intubate patients with full stomach
 6162.
 . TREATMENT OF CV TOXICITY 
Substitute: amiodarone for lidocaine
vasopressin for epinephrine  Consider
cardiopulmonary bypass or lipid infusion
if standard drugs fail
UNIVERSAL SAFETY GUIDELINES FOR
ADMINISTRATION OF LA TO ALL PATIENTS:

 Aspirate carefully before injecting 

To reduce the risk of unintentional intravascular injection
 Inject slowly:A maximum rate of 1 min/ capsule
 Monitor the patient both during and after the injection for unusual reactions
 Select the anesthetic agent with or without a vasoconstrictor based upon the duration of
anesthesia appropriate for the planned procedure
 Use the minimum amount of anesthetic solution 
To achieve an adequate level of anesthesia 
To keep the patient comfortable throughout the dental procedure.
 Adherence to these simple guidelines will reduce the risk of adverse reactions to the local
anesthetic agents themselves or to the vasoconstrictors contained in local anesthetics.
Adverse effect of local anesthesia (13-18)

 1. Caused by anesthetic solutioii.

 2. Caused by vasoconstrictor drugs

 3. Local reactions

 4. Complications attributed to needle insertion

 1. Caused by Anesthetic Solution

 Sign and symptoms

 Neutral Nervous System: All LA produces a se- quence of stimulation followed by depressioii.
 Lido- caine toxicity may commence at conceiitratious >5 pg/mL, but coiivelsive seizures
generally requireconcentrations >8 pg/mL.

 Cardiovascular Reactions: These are cardiac depres- sants but mo significant effects are seem
at conven- tional doses. Bupivacaiiie is relatively more car- diotoxic & can produce ventricular
tachycardia. Li- docaine has little effect oii contractility & conduc- tivity & is used as an
antiairylhinic ageiit.
 Blood vessels: Cause fall iii blood pressure. This is primarily due to sympathetic blockade,
but high doses do cause direct relaxatioii of arteriolar smooth muscles.
 Methemoglobinemia: A metabohte of prilocaine, o- toluidine, can oxidize the iroii in
hemoglobin from feiToiis (Fe2+) to ferric (Fe3+). Altered Heine do not bind oxygen and
normal hemes on the same hemoglobin molecule do not readily release their oxygeii. This
form of hemoglobin is called metlie- moglobin and when >1% of total hemoglobin is so
altered, the condition is called metliemoglobineinia. Typical symptoms
include cyanosis, dyspnea,
 emesis & headache. To reduce the risk clinician
 should take care to refraiii from giving excessive dosages of local anesthetics.
 PeripheralNerve Parestliesia: Articaine is associated with fivefold higher incidence of
parestliesia com- pared with lidocaiiie. as it can cause damage to inferior nerve or liiigtial
nerve.
 Allergic Reaction: The amide local anesthetics ap- pear to have an extremely little
iminunogeuic and therefore low rate of allergic reactions.
 Reaction to Anesthetic Formulations coiitaning a Sulfite Antioxidant: Allergic reactions
like ui4icaria, bronchospasm & anaphylaxis. The use of local anes- thetic without
vasocoustrictors is a possible alterna- tive with these patients.
 should take care to refraiii from giving excessive dosages of local anesthetics.
 PeripheralNerve Parestliesia: Articaine is associated with fivefold higher incidence of
parestliesia com- pared with lidocaiiie. as it can cause damage to inferior nerve or liiigtial
nerve.
 Allergic Reaction: The amide local anesthetics ap- pear to have an extremely little
iminunogeuic and therefore low rate of allergic reactions.
 Reaction to Anesthetic Formulations coiitaning a Sulfite Antioxidant: Allergic reactions
like ui4icaria, bronchospasm & anaphylaxis. The use of local anes- thetic without
vasocoustrictors is a possible alterna- tive with these patients.
 2. Caused by Vasoconstrictor Drug
 For proloiig action of local anesthetic solutioii and to reduce its toxicity, vasocoustrictors
have beeii added but its addition lead to coiitraindication oflocalanes- thetic solution in
various patieiits like in cardiac pa- tients especially those suffering from refractory dys-
rhytbmias, angina pectoris, postmyocardial infarc- tioi(6moiiths) and uncontrolled
hypertension. Other contraindicatious to vasoconstrictors are endocrine disorders such as
hyperthyroidisin, hyperfunction of the medullaiy adreual (pheocliromocytoma) and
iuicoiitrolled diabetes mellitus.

 Symptoms: Palpitation, Tachycardia, Headache, Apprehensioii

 Treatment: Brief duration reaction, so stop drug administratioii and reassiue the patient.
 3. Caused by local reactions
 Infectious caused by contaminated solutions are rare because of high standard of asepsis
practiced by maiiufacturers.

 Prevention: Use LA cartridges only once. Store cartridges as aseptically as possible. Before
inserting needle into the cartridge, rubber diaphragm should be wiped with sterile
disposable alcohol sponge.
4. Caused by Needle Insertion
 (A)Syncope: Most frequent complication. It is a form of neurogenic shock caused by cerebral is- chemia secondary to
vasodilatation.
 Sign and Symptoms
 Pallor, Nausea, Vomiting, Patient may feel straiige or differeiit, Uiicousciousness, Bradycardia and Hy- potension
 Treatment :Stop the deiital procedure.
 • Lower the chair back and elevate the legs of the patient.
 • If patient is conscious, instinct him to take deep breath.
 • Check patients BP, pulse rate arid color.
 • Ensure adequate oxygeuation and CVS stabil- ity.

 (B)Muscle Trismus
 Common and mainly occurs after inferior alveolar nerve block.
 Causes: Trauma to muscle during insertion, Infection (local), HemoiTliage.
 Treatment
 Mild: Slight exercises coupled with application of moist warm compresses for 15-20 min. /h, Mild analgesics, Physiotherapy
consist of opening closing and side to side movement for 5-10 min. after eveiy 3-4 hrs.
 Severe: Add centrally acting muscle relaxant
 embedded in tissue, Do not rise needle of too fine a gauge, Do not use resterilized needle
& Inform the patieiit before inserting the needle
 (E) Hematoma
 It is associated with posterior superior alveolar iierve block and infraorbitalnerve block.
Occurs because of improper technique.
 Treatment
 Immediate: Direct pressure to the bleeding site for at least 2 minutes.
 Subsequeiit: Do not apply heat to the area for 6 to 8 hours after the incident. Apphcation of
ice to the region immediately and reassure the patient.
 (C) Pain or ilyperesthesia
 Most commonly occur due to carelessness of deiitist.
 Preventioii: Use Sharp needle, No multiple traumas, Needle insertion should be Atraiimatic
and slow, LA should be forced into the tissue slowly.
 (D) Broken Needle
 Most aniioying and depressing coinphcation of anes- thesia.
 Preveiition : Do not force needle against resistance, Do not change the direction of the
needle while
complications

 local  systemic
 Needle breakage Prolonged anesthesia
or paresthesia Facial nerve paralysis
Trismus Soft tissue injury
Hematoma Pain on injection
Infection Edema Sloughing of
tissues Postanesthetic intraoral lesions
 1) Needle breakage : Prevention • Do not
use short needles for inferior alveolar
nerve block in adults or larger children. •
Do not use 30-gauge needles for inferior
alveolar nerve block in adults or
children. • Do not bend needles when
inserting them into soft tissue. • Do not
insert a needle into soft tissue to its hub,
unless it is absolutely essential for the
success of the injection. • Observe extra
caution when inserting needles in
younger children or in extremely phobic
adult or child patients.
 Prolonged Anesthesia or Paresthesia •
Strict adherence to injection protocol •
Most paresthesias resolve within
approximately 8 weeks to 2 months
without treatment. • Determine the
degree and extent of paresthesia. •
Explain to the patient that paresthesia •
Record all findings • Second opinion •
Examination every 2 months • It would
be prudent to contact your liability
insurance carrier should the paresthesia
persist without evident improvement
beyond 1 to 2 months.
 3) Facial Nerve palsy • Reassure the patient •
Contact lenses should be removed until muscular
movement returns. • An eye patch should be applied
to the affected eye until muscle tone returns •
Record the incident on the patient's chart. •
Although no contraindication is known to
reanesthetizing the patient to achieve mandibular
anesthesia, it may be prudent to forego further
dental care at this appointment. 87
 88. 4) Trismus • Prescribe heat therapy, warm saline
rinses, analgesics (Aspirin 325 mg) • If necessary,
muscle relaxants to manage the initial phase of
muscle spasm - Diazepam (approximately 10 mg
bid) • Initiate physiotherapy • Antibiotics should be
added to the treatment regimen described and
continued for 7 full days • Patients report
improvement within 48 to 72 hours 88
 5) Soft tissues injury • Analgesics, antibiotics,
lukewarn saline rinse, petroleum jelly • Cotton roll
placed between lips and teeth, secured with dental
floss, minimizes risk of accidental mechanical
trauma to anesthetized tissues. 89
 90. 6) Hematoma : • Hematoma is not always
preventable. Whenever a needle is inserted into
tissue, the risk of inadvertent puncturing of a blood
vessel is present. • When swelling becomes evident
during or immediately after a local anesthetic
injection, direct pressure should be applied to the site
of bleeding. • For most injections, the blood vessel is
located between the surface of the mucous
membrane and the bone; localized pressure should be
applied for not less than 2 minutes. This effectively
stops the bleeding. • Ice may be applied to the region
immediately on recognition of a developing
hematoma.
 7) Pain on injection • Adhere to proper techniques
of injection, both anatomic and psychological. •
Use sharp needles. • Use topical anesthetic
properly before injection. • Use sterile local
anesthetic solutions. • Inject local anesthetics
slowly. • Make certain that the temperature of the
solution is correct • Buffered local anesthetics, at
a pH of approximately 7.4, have been
demonstrated to be more comfortable on
administration 91
 92. 8) Burning on Injection • By buffering the
local anesthetic solution to a pH of approximately
7.4 immediately before injection, it is possible to
eliminate the burning sensation that some patients
experience during injection of a local anesthetic
solution containing a vasopressor. • Slowing the
speed of injection also helps
 9) Infection : • Use sterile disposable needles. • Properly care for
and handle needles. • Properly prepare the tissues before
penetration. • Prescribe 29 (or 41, if 10 days) tablets of penicillin V
(250-mg tablets). • Erythromycin may be substituted if the patient
is allergic to penicillin. 93
 94. 10) Edema If edema occurs in any area where it compromises
breathing, treatment consists of the following: • P (position): if
unconscious, the patient is placed supine. • A-B-C (airway,
breathing, circulation): basic life support is administered, as
needed. • D (definitive treatment): emergency medical services
(e.g., 9-1-1) is summoned. • Epinephrine is administered: 0.3 mg
(0.3 mL of a 1:1000 epinephrine solution) (adult), 0.15 mg (0.15
mL of a 1:1000 epinephrine solution) (child [15 to 30 kg]),
intramuscularly (IM) or 3 mL of a 1:10,000 epinephrine solution
intravenously (IV-adult), every 5 minutes until respiratory distress
resolves. • Histamine blocker is administered IM or IV. •
Corticosteroid is administered IM or IV. • Preparation is made for
cricothyrotomy if total airway obstruction appears to be
developing. This is • extremely rare but is the reason for
summoning emergency medical services early. • The patient's
condition is thoroughly evaluated before his or her next
appointment to determine the cause of the reaction.
 10) Sloughing of tissue • Usually, no formal
management is necessary for epithelial desquamation
or sterile abscess. Be certain to reassure the patient of
this fact. • For pain, analgesics such as aspirin or
other NSAIDs and a topically applied ointment
(Orabase) • The course of a sterile abscess may run 7
to 10 days 95
 96. 11) Postanesthetic Intra-oral lesion: • Primary
management is symptomatic • No management is
necessary if the pain is not severe • Topical anesthetic
solutions (e.g., viscous lidocaine) • A mixture of
equal amounts of diphenhydramine (Benadryl) and
milk of magnesia rinsed in the mouth effectively
coats the ulcerations and provides relief from pain. •
Orabase, a protective paste, without Kenalog can
provide a degree of pain relief. • A tannic acid
preparation (Zilactin) can be applied topically to the
lesions extraorally or intraorally (dry the tissues first).
systemic complications

 Adverse drug reaction

 • Toxicity Caused by Direct Extension of
the Usual Pharmacologic Effects of the
Drug: 1) Side effects
 2) Overdose reactions
 3) Local toxic effects • Toxicity Caused by
Alteration in the Recipient of the Drug: 1) A
disease process (hepatic dysfunction, heart
failure, renal dysfunction) 2) Emotional
disturbances 3) Genetic aberrations
(atypical plasma cholinesterase, malignant
hyperthermia) 4) Idiosyncrasy • Toxicity
Caused by Allergic Responses to the Drug
 CLINICAL MANIFESTATION OF LOCAL
ANESTHETIC OVERDOSE SIGNS: LOW
TO MODERATE OVERDOSE LEVELS: 
Confusion  Talkativeness  Apprehension 
Excitedness  Slurred speech  Generalized
stutter  Muscular twitching, tremor of face
and extremities  Elevated BP, heart rate and
respiratory rate 98
 99. MODERATE TO HIGH BLOOD
LEVELS:  Generalized tonic clonic seizure,
followed by  Generalized CNS depression 
Depressed BP, heart rate and respiratory rate
SYMPTOMS:  Headache  Light
headedness  Auditory distrurbances 
Dizziness  Blurred vision  Numbness of
tongue and perioral tissues  Loss of
consciousness
 Management of systemic complications
1) Basic emergency management : A-B-
C-D approach 2) Allergy : Medical
history questionnaire is important. 3)
Elective dental care 4) Emergency dental
care: - Protocol no.1 : no treatment of an
invasive nature - Protocol no.2 : use
general anesthesia - Protocol no.3:
Histamine blockers - Protocol no.4 :
Electronic dental anesthesia/hypnosis
 LA Management For Special Patients •
Uncooperative child The maximum
safe dose of lidocaine for a child is 4.5
mg/kg per dental appointment. Local
infiltration of anesthesia is sufficient for
all dental treatment procedures in 90%
of cases even in the mandible. 101
 102. • Handicapped Patient • retarded
patients choose a shorter needle and/or
a larger gauge needle which is less likely
to be bent or broken. better to use
general anesthesia
 • Patients receiving anticoagulation or
suffering from bleeding disorders  Oral
procedures must be done at the beginning of
the day & must be performed early in the
week, allowing delayed re-bleeding episodes,
usually occurring after 24-48 h, to be dealt
with during the working weekdays.  Local
anesthetic containing a vasoconstrictor
should be administered by infiltration or by
intraligamentary injection wherever practical.
X Regional nerve blocks should be avoided
when possible.  Local vasoconstriction may
be encouraged by infiltrating a small amount
of local anesthetic containing adrenaline
(epinephrine) close to the site of surgery.
 REGNANCY 104 • Lidocaine + vasoconstrictor:
most common local anesthetic used in dentistry
extensively used in pregnancy with no proven ill
effects, Esters are better to be used. • Accidental
intravascular injections of lidocaine pass through
the placenta but the concentrations are too low to
harm fetus.
 105. GERIATRIC PATIENT – When choosing an
anesthetic, we are largely concerned with the
effect of the anesthetic agent upon the patient's
cardiovascular and respiratory systems. –
increased tissue sensitivity to drugs acting on the
CNS – Decreased hepatic size and blood flow may
reduce hepatic metabolism of drugs – hypertension
is common and can reduce renal function – Same
prevention procedures used with children 105
 LIVER DISORDERS – Advanced liver
diseases include:  Liver cirrhosis -
Jaundice - Potential complications: 1 .
Impaired drug detoxication e.g. sedative,
analgesics, general anesthesia. 2.
Bleeding disorders ( decrease clotting
factors, excess fibrinolysis, impaired
vitamin K absorption). 3. Transmission
of viral hepatitis. Management – Avoid
LA metabolized in liver: Amides
(Lidocaine, Mepicaine), esters should be
used
 • Presence of allergy, patieiit’s size and age, emo- tional or psychological problems.
 • Medications the patient may be taking

 CVS slants. Conditions coiiceined to dentists are Congenital heart disease, Acquired heai4 disease,
Rheiimatic heart disease, Atherosclerotic heart dis- ease, Hypertension, CHF, Valvular heart disease Ar-
rhythmia(conductioisystem defect).
 Precautions
 • Consultation with patient physician taken when indicated.
 • Procedure should be planned to fit the individ- ual patient condition.
 • If patieiit is aiixious, he should be moderately premedicated or sedated during appointmeiit.
 • He should be given short appointment to pre- vent undue tii g.
 • Least possible ainoiint of anesthesia should be used.
 • Vasoconstrictors, although not coiitraindicated, should be kept at a miiiimiim dose or eliminated if
necessary.
 • Patient may be given oxygen by nasal caiiniila during procedure.
 • Prophylaxis with appropriate antibiotics should be giveii if indicated
 Respiratory System. Bronchitis, Bronchiectasis, Emphysema, Asthma
 Precautions
 • Treatment should be given in afternoon.
 • Preoperative medications such as adhesives, hypnotics and narcotics should be
used with extreme caution as they interfere with cough reflex and depress ventilatioii.
 • Bronchodialators, nebulizers and expectorants can be given preoperatively.
 • Choice of local anesthetic or vasoconstrictor is riot of utmost importance provided there are mo other
complicating pathologies.
 • Oxygen can be given by nasal caiinula if re- quired duriiig dental procedure.

 Metabolic diseases
 (1) Diabetes Precautions Severity of diabetes.

 • Evaluate the patient treatment whether di- abetes is controlled by diet/hypoglycemic agents/insiiliii.
 • Patient controlling diabetes by diet pose mo problem.
 • Patient oii insulin should be treated between
 9.00 am — l2pm because as a result of food arid insulin intake, it is dining these horns that they are best able to
tolerate stressful situations.
 (2) Hypothyroidism
 These patients do not inetabolize drug as well as the normal individual therefore doses of vasoconstric-
tors in diug should be kept minimum because of relative CVS conditions.
 (3) Hypeilhyroidism Physician consultation

 • Well premedication/sedation
 • Vasoconstrictor should be reduced.

 Local Anesthesia in Pregnancy & Postpartum (27

 Local anesthetics can be safely used when treatiiig pregnaiit & postpartum patients if careful guidelines
are followed . Because teratogeuic risks are highest in the first trimester, the 2“ trimester is usually the
period chosen for routiiie dental care. Lidocaine is least associated with medical complications.
 LA Consideration in Endodontics
 Effect ofInfiammation on LA k2): Inflammation and infection lowers the tissue pH , altering the
ability of a LA to provide clinically adequate pain coiitrol. There are two methods of obtaining
adequate iierve block are:
 1. Administer LA away from the area of inflamma- tion: It helps in preventing the spread of
infection to iuiinvolved regions. It also provides adequate pain control because of presence of more
iiormal tissue condition. Regional iierve block anesthesia is the major factor in pain control for
pulpally iiivolved teeth.
 2. Deposit a larger volume into the region : It will provide a greater no. of iincharged base
molecule to diffuse through the nerve sheath to give satisfactoiy nerve block. Some patients respoiid
unfavorably to instrumentation of their root canal, even when canals are debrided thoroughly.
 Solution : lufiltratioii, Intrapulpal anesthesia & Top- ical aiiesthesia: Can apply a small amount of
topical anesthetic ointment onto the file or reamer prior to insertiiig it iiito the caiial.
Recent Advances in Local Anesthetics and some Additions in
Lidocaine to Improve its Properties

Centbucridine
 It is quinolone derivativewhich is 5- 8 times potent than Lidocaine. It
does not effect CNS or CVS adversely except when higher doses
administered. (28) Vacharajani et al (1983) proved that efficacy of 5%
of Ceiitbucridine is same as that of 2% Lidocaine.
Oraqix
A recently introduced locally applied anesthetic gel, is a eutectic mixttue
of prilocaine & lido- caine each in a 2.5% conceiitratioii. It was approved
by FDA in 2004.
Eutectic mixture of local anesthesia (EMLA) - surface anesthesia for
intact skin.
 DentiPatch (lidocaine transoral delivery system)
Preinjection – 10- 15 minutes prior to the procedure.
Root scaling/planing – apply 5-10 minutes prior to beginning procedure.

 Ropivacaine :
 It is a long acting ainide having lower arrhytlimogeuic potential than Biipivacaine. It has
low toxicity and available in 0.75%, 0.2% concen- tration.
 Transcutaneous electric nerve stimulation ( TENS)/ electronic dental anaesthesia
 It is a non- pharmacological method which is widely used for the management of acute and chronic pain
in a variety of conditions. Transcutaneous electrical nerve stimulation (TENS ) is the use of electric
current produced by a device to stimulate the nerves for therapeutic purposes. It was in 19 th century, a
physician named Francis first described the use of electricity for the relief of dental pain24. According
to articles, use of transcutaneous nerve stimulation to control chronic pain was introduced by Shealy in
19678. In 1972, food and drug administration also has proved transcutaneous electric nerve stimulation
as a method of pain alleviation25
 .
 Indications:
 1. It can be used successfully in pediatric patient. Since the equipment contains no syringes, it will
impart a
 positive behaviour in children and reduces their fear.
 2. It can be equally useful in adult patients to produce analgesia during rubber dam placement, cavity
preparation,
 pulp capping, endodontic procedures, prosthetic tooth preparations, oral prophylaxis, extractions, and to
reduce
 the discomfort from injection of local anaesthesia.
Articaine hydrochloride
 Articaine hydrochloride has become a very popular local anesthetic in dentistry. It provides the
same depth and duration of pulpal and soft tissue anesthesia as the other intermediate-acting dental
local anesthetics—lidocaine, mepivacaine, and prilocaine.
 Because the elimination half life of articaine is considerably shorter than that of other amide local
anesthetics, it is the preferred drug in special patient populations, including children, pregnant
women, and nursing mothers.
 Because of the greater lipid solubility of articaine, the buccal infiltration of articaine in the adult
mandible has a clinically significant rate of success in providing pulpal anesthesia compared with
other amide local anesthetics.
 Several meta-analyses have concluded that articaine is a preferred dental local anesthetic.
 Regarding paresthesia, there is no scientific basis for stating that articaine is more neurotoxic than
other commonly used dental local anesthetics.
 Meta-analyses comparing articaine with lidocaine have con_x0002_cluded “that articaine as
compared with lignocaine provides a higher rate of anaesthetic success, with comparable safety to
lignocaine when used as infiltration or blocks for routine dental treatments” and “this meta-
analysis thus supports a recommendation for 4% articaine (1:100,000 epineph_x0002_rine) in
routine dental practice over and above 2% lidocaine (1:100,000 epinephrine)
Electronic Dental Anesthesia

 Electronic Dental Anesthesia. Anesthesia (Elec tronic Dental Anesthesia or EDA) which
works by transcutaneous electrical iierve stimulation (TENS) was introduced to the dental
profession.
 One study has favored its use as its efficacy in pt has been described as
comparable to local anaesthesia while at the same time avoiding the possible side effects
associated with commonly used local anaesthetic agents arid the inconvenience of post-
operative anaesthetic effect.
 Another study suggested EDA could be indicated for needle-phobic children; however,
studies that have tested its effec- tiveness in children are few.
 Yagiela JA. Journal of anesthesia 2003
 This article reviews 3 recent developments in anxiety and pain control with significant
potential for altering dental practice. First is the introduction of articaine hydrochloride as
an injectable local anesthetic. Although articaine is an amide, its unique structure allows
the drug to be quickly metabolized, reducing toxicity associated with repeated injections
over time.
 The second development is the formulation of a lidocaine and prilocaine dental gel for
topical anesthesia of the periodontal pocket. This product may significantly reduce the
need for anesthetic injections during scaling and root planing.
 Finally, the use of triazolam as an oral sedative/anxiolytic is reviewed. The recent
administration of triazolam in multiple doses has extended the availability of anxiety
control to many dental patients, but unknowns about the safety of the technique as
practiced by some dentists remains a concern.
Phentolamine Mesylate: The Local
Anesthesia “Off” Switch
 Phentolamine mesylate (OraVerse), a nonselective a-adrenergic blocking drug, is the first therapeutic agent marketed for the reversal of
soft-tissue anaesthesia and the associated functional deficits resulting from an intraoral submucosal injection of a local anaesthetic
containing a vasoconstrictor. In clinical trials, phentolamine injected in doses of 0.2 to 0.8 mg (0.5 to 2 cartridges), as determined by
patient age and volume of local anaesthetic administered, significantly hastened the return of normal soft-tissue sensation in adults and
children 6 years of age and older.

 Phentolamine is a short-acting, competitive antagonist

 at peripheral α-adrenergic receptors. It antagonizes both
 α1 and α2 receptors, thus blocking the actions of the cir_x0002_ culating catecholamines epinephrine and norepinephrine.
 Phentolamine mesylate enables the dentist or dental hygien_x0002_ist to significantly decrease the duration of residual soft
tis_x0002_sue anesthesia in patients where such numbness may prove
 to be potentially injurious (children, geriatric, and special
 needs patients) or may have a negative influence on their
 quality of life (speaking, eating, negative body image).

Yagiela JA. What's new with phentolamine mesylate: a reversal agent for local anaesthesia? SAAD Dig. 2011 Jan;27:3-7.
COMPUTER-CONTROLLED LOCAL ANESTHETIC
DELIVERY SYSTEMS [CCLAD]

 • In 1997, a new delivery system using

computer technology to control the rate
and flow of anesthetic solutions evolved,
and are called as computer controlled
local anesthetic delivery systems. The
first of them is the Wand, followed by
Wand Plus and CompuDent.
 This system enabled  It is likely that greater ergonomic
 a dentist or hygienist to precisely manipulate control coupled with fixed flow
needle placement
 rates is responsible for the improved
 with fingertip accuracy and deliver the local
anesthetic with injection experience dem_x0002_
 a foot-activated control onstrated in many clinical studies
conducted with C-CLAD
 A lightweight hand_x0002_ piece (Fig. 5.12),
held in a pen-like grasp, provides increased  devices in dentistry.
 tactile sensation and control compared with the
traditional
 syringe. The flow rate of local anesthetic
delivery is computer
 controlled and thus remains consistent from one
injection to the next
 The Wand STA
 instrument, thus providing continuous
real-time feedback
 while a dental injection is performed (
 64. • Fukayama et al. conducted a controlled
clinical study evaluating pain perception of a
CCLAD device. • They concluded that “the new
system provides comfortable anesthesia for
patients and can be a good alternative for
conventional manual syringe injection.” • There
are three modes of flow rate available: slow, fast
and turbo mode. In 2001, the Comfort Control
Syringe (Dentsply International, N. York, USA)
was marketed as an alternative to the Wand and
has two components; base unit and syringe and
there is no foot pedal. • The most important
functions of this unit is injection and aspiration
can be controlled directly from the syringe. • Five
different basic injection rate settings for specific
applications, block, infiltration, PDL, IO and
Palatal regions.
The Wand STA System

 The Wand STA local anesthetic delivery system represents a  Exit-pressure information is provided to
 significant advance in C-CLAD technology (see Fig. 5.11).
the clinician
 Introduced in 2007, The Wand STA system is a
third_x0002_generation C-CLAD instrument representing a  on a continuous basis in the form of
new and

spoken and/or audible
meaningful innovation for subcutaneous injections
per_x0002_formed both in dentistry and in medicine.21 The
techno_x0002_logical advancement is related to the
 sounds and visual indicators emitted
development of what from The Wand STA
 is called dynamic pressure-sensing technology (DPS
technol_x0002_ogy).22 DPS technology enables the precise  instrument, thus providing continuous
monitoring and
real-time feedback
 control of fluid pressure at the needle tip when a
subcu_x0002_taneous injection is performed. Fluid exit  while a dental injection is performed (
pressure at the
 needle tip is used to identify a given anatomic location and/
 or a specific tissue type on the basis of this repeatable
find_x0002_ing.2
 In addition, The Wand STA sys_x0002_
tem offers a unique approach for
performing PDL injection
 using DPS technology.25 The
instrument has been designed to
 identify the precise anatomic location
for the PDL injection
 The Wand STA system audibly and
visually “guides” place_x0002_ment of
the needle tip into the anatomic entrance
of the
 PDL space through DPS technology.
 Single-Tooth Anesthesia [STA] In 2006, the
manufacturers of the original CCLAD, the Wand,
introduced a new device, Single Tooth Anesthesia
(STA™) which incorporates dynamic pressure-
sensing (DPS) technology that provides a constant
monitoring of the exit pressure of the local
anesthetic solution in real time during all phases of
the drug’s administration.
 66. JET INJECTORS Jet injection technology is
based on the principle of using a mechanical
energy source to create a pressure sufficient to
push a liquid medication through a very small
orifice, that it can penetrate into the subcutaneous
tissues without a needle. Advantages are painless
injection, less tissue damage, faster injection and
faster rate of drug absorption into the tissues.
Drawbacks are: it cannot be used for nerve blocks,
only infiltration and surface anesthesia are
possible.
 VIBROTACTILE DEVICES These
devices work on the principle of ‘gate
control’ theory thereby reduces pain. It
acts based on the fact that the vibration
message is carried to brain through
insulated nerves and pain message
through smaller uninsulated nerves. The
insulated nerves overrule the smaller
uninsulated nerves. The devices are:
VibraJect, Dental Vibe, Accupal.
 68.
 • VibraJect has a battery operated device
which is attached to the standard
anesthetic syringe, causing the syringe
and needle apparatus to vibrate. Nanitsos
et al and Blair have recommended the
use of VibraJect for painless injection. •
Accupal is a cordless device which
applies both vibration and pressure at the
injection site.
 Dental vibe • Dental Vibe is a cordless
hand held device which gently
stimulates the sensory receptors at the
injection site causing the neural pain
gate to close. • Advantage is, the tissues
are vibrated before the needle penetrates.
• Disadvantage is, it is not directly
attached to the syringe and a separate
unit is required, so both hands are
engaged. • Dentalvibe and syringe micro
vibrator uses micro- vibration to the site
where an injection is being administered.
 SAFETY DENTAL SYRINGES • Aim
of these devices is to prevent from the
risk of accidental needle stick injury
occurring with a contaminated needle
after local anesthesia administration. •
These syringes possess a sheath that
locks over the needle when it is removed
from the patient’s tissues preventing
accidental needle stick injury. • Eg are 1.
Ultra safe syringe, 2. Ultra safety plus
XL syringe, 3.hyposafety syringe,
4.safety wand 5. Rev Vac safety syringe.
 DENTIPATCH [INTRAORAL
LIGNOCAINE PATCH] • Dentipatch
contains 10-20% lidocaine, which is
placed on dried mucosa for 15 minutes. •
Hersh et al (1996) studied the efficacy of
this patch and recommended it for use in
achieving topical anesthesia for
injections in both maxilla and mandible.
• It is not recommended in children.
Disadvantages include central nervous
system and cardiovascular system
complications.
 Comfort Control Syringe • This syringe
(Dentsply) is an electronic pre
programmed anesthesia delivery device
that uses a 2-stage delivery rate. • The rate
of injection varies based on the injection
technique chosen. • It begins with as low
rate; the flow the increases to a pre
programmed technique-specific rate
selected by the dentist. • The operation of
this syringe (initiation and termination of
the injection, controlled aspiration and
flow rate) is controlled by a button on the
handpiece. • A disposable cartridges heath
is required for each patient, but a standard
dental needle and anesthetic cartridge can
be used with this device.
 SUMMARY & CONCLUSION:
 The science of LA is an active research field arid LA will continue to be one of the mainstays of
contemporary perioperative medicine. Anxiety, fear & apprehension should be recogiiized & managed
before administration of a local anesthetic.. Vasoconstrictors should be included in all local anesthetics
P)laITRaCOlO arid toxicity. Deiit Clin N Am unless specifically
contraindicated.
 Local anesthetics have been used clinically for more than a century, but new insights into their
mechanisms of action and their interaction with biological systems continue to surprise researchers and
clinicians alike.

 Partialresistance to LA may be more frequent thaiipreviously thought.


 LA are toxic on many tissues brit clinically apparent nerve damage is very rare and LA-iiiduced
toxicity after peripheral nerve block has a good prognosis overall.