Local anesthesia 2

 Introduction
 Historical background
Definition
Methods of inducing local anesthesia
Desirable properties
Electrophysiology of nerve conduction
Impulse propagation and spread
Theories of mechanism of action of
local anesthesia
Dissociation of local anesthesia
2Dr. Firas Kassab

3
Classification of local anesthetic
according to biological site and
mode of action
Mode and site of action of local
anesthesia
Mechanism of action of local
anesthesia
Local anesthetics description
Armamentarium
Injection techniques
Local & Systemic complications
 Special care groups
Recent advancements
Conclusion
References
Dr. Firas Kassab

• COCAINE -first local anesthetic agent-isolated by Nieman
-1860 -from the leaves of the coca tree.
• Its anesthetic action was demonstrated by Karl Koller in
1884.
• First effective and widely used synthetic local anesthetic -
PROCAINE -produced by Einhorn in 1905 from benzoic
acid and diethyl amino ethanol.
4Dr. Firas Kassab

5
•It anesthetic properties were identified by Biberfield
and the agent was introduced into clinical practice by
Braun.
•LIDOCAINE- Lofgren in 1948.
•The discovery of its anesthetic properties was
followed in 1949 by its clinical use by T. Gordh
Dr. Firas Kassab

6
DEFINITION:
Local anesthesia is defined as a loss of sensation in a circumscribed
area of the body caused by depression of excitation in nerve endings
or an inhibition of the conduction process in peripheral nerves.
An important feature of local anesthesia is that it produces:
LOSS OF SENSATION WITHOUT INDUCING LOSS
OF CONSCIOUSNESS..
Dr. Firas Kassab

7
METHODS OF INDUCING LOCAL ANESTHESIA:
Low temperature
Mechanical trauma
Anoxia
Neurolytic agents such as alcohol & phenol
Chemical agents such as local anesthetics
Dr. Firas Kassab

I==It should not be irritating to tissue to which it is
applied
N==It should not cause any permanent alteration of nerve
structure
S==Its systemic toxicity should be low
T==Time of onset of anesthesia should be short
E== It should be effective regardless of whether it is
injected into the tissue or applied locally to mucous
membranes
D==The duration of action should be long enough to
permit the completion of procedure
8Dr. Firas Kassab

9
It should have the potency sufficient to give complete anesthesia
with out the use of harmful concentration solutions
It should be free from producing allergic reactions
It should be free in solution and relatively undergo
biotransformation in the body
It should be either sterile or be capable of being sterilized by heat
with out deterioration.
Dr. Firas Kassab

• There is an electrical charge across the membrane.
• This is the membrane potential.
• The resting potential (when the cell is not firing) is a
negative electrical potential of -70mv that exists across the
nerve membrane, produced by different concentrations of
either side of the membrane.
• The interior of nerve is NEGATIVE in relation to exterior
10Dr. Firas Kassab

11
inside
outside
Resting potential of neuron = -70mV
+
-
+
-
+
-
+
-
+
-
Dr. Firas Kassab

• At rest: Na+& K+ channels closed. -70mV
• Fibre stimulated: Na+channel opens, Na+ enters cell.
Potential rising
• Cell depolarised, Na+ channel closes. +20mV
• K+ channel opens, K+ exits cell, potential falling
• Fibre repolarised, Na+& K+ channels closed. Na/K pump
restores balance. -70mV
• Result is a voltage gradient along axon, causing a current.
This causes configurational change in Na-channels in the
next segmentconduction
12Dr. Firas Kassab

SLOW DEPOLARIRIZATION
14
RAPID DEPOLARIZATION:
The interior of nerve is POSITIVE in relation to exterior.
Dr. Firas Kassab

REPOLARIZATION:
.
15
• Depolarization takes 0.3 msec
• Repolarization takes 0.7 msec
SODIUM PUMP
energy comes from the oxidative metabolism of ATP
• The entire process require 1 msec
Dr. Firas Kassab

• 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: The high resistance cell
membrane and extra cellular media produce a rapid
decrease in density of current with in a short distance of
depolarized segment.
• The spread of the impulse is characterized as a slow
forward-creeping process.
• Conduction rate is 1.2m/sec
DEPOLARIZED SEGMENT ADJACENT RESTING AREA
Dr. Firas Kassab 16

Impulse conduction in myelinated nerves occurs by means of
current leaps from nodes to node this process is called as
SALTATORY CONDUCTION.
It is more rapid in thicker nerves because of increase in
thickness of myelin sheath and increase in distance
between adjacent nodes of ranvier.
If conduction of impulse is blocked at one node the local
current will skip over that node and prove adequate to raise
that membrane potential at next node to its firing potential
and produce depolarization.
Conduction rate of myelinated fibers is 120m/sec.
17Dr. Firas Kassab

Local anesthetic agent interferes with excitation process in
a nerve membrane in one of the following ways:
Altering the basic resting potential of nerve membrane
Altering the threshold potential
Decreasing the rate of depolarization
Prolonging the rate of repolarization
19Dr. Firas Kassab

Many theories have been promulgated over the
years to explain the mechanism of action of local
anesthetics.
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.
20Dr. Firas Kassab

CALCIUM DISPLACEMENT THEORY:
States that local anesthetic nerve block
was produced by displacement of calcium
from some membrane site that controlled
permeability of sodium.
21Dr. Firas Kassab

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.
22Dr. Firas Kassab

• 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.
23Dr. Firas Kassab

The most favored today, proposed that local anesthetics act by
binding to specific receptors on sodium channel the action of the
drug is direct, not mediated by some change in general properties
of cell membrane. Biochemical and electrophysiological studies have
indicated that specific receptor sites for local anesthetic agents
exists in sodium channel either on its external surface or on internal
axoplasmic surface. Once the LA has gained access to receptors,
permeability to sodium ion is decreased or eliminated and nerve
conduction is interrupted.
25Dr. Firas Kassab

CLASS A: Agents acting at receptor site on external surface of
nerve membrane
Chemical substance: Biotoxins (e.g., tetrodotoxin and saxitoxin)
CLASS B: Agents acting on receptor sites on internal surface
of nerve membrane
Chemical substance: Quaternary ammonium analogues of
lidocaine, scorpion venom
26Dr. Firas Kassab

CLASS C: Agents acting by receptor independent of
physiochemical mechanism
Chemical substance: Benzocaine
CLASS D: Agents acting by combination of receptors
and receptor independent mechanisms
Chemical substance: most clinically useful anesthetic
agents (e.g., lidocaine, mepivacaine, prilocaine)
27Dr. Firas Kassab

• NATUAL
• SYNTHETIC
• OTHERS
BASED ON MODE OF APPLICATION
• INJECTABLE
• TOPICAL
• BASED ON DURATION OF ACTION
• ULTRA SHORT
• SHORT
• MEDIEM
• LONG
28Dr. Firas Kassab

• SHORT
• INTERMEDIATE
• LONG
29Dr. Firas Kassab

• 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
+
30
Dr. Firas Kassab

• 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
+
31Dr. Firas Kassab

• The relative proportion of ionic form also depends on pKa or
DISSOCIATION CONSTANT, of the specific local anesthetic.
• The pKa is a measure of molecules affinity for H
+
ions.
• When the pH of the solution has the same value as pKa of
the local anesthetic, exactly half the drug will exists in the
RNH
+
form and exactly half in RN form.
• The percentage of drug existing in either form can be
determined by Henderson Hasselbalch equation
Log base/acid = pH - pKa
32Dr. Firas Kassab

• 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.
33Dr. Firas Kassab

• Hence if the tissue is infected, the pH is lower (more
acidic) and according to the HH equation; there will be less
of the non-ionized form of the drug to cross into the nerve
(rendering the LA less effective)
• Once some of the drug does cross; the pH in the nerve will
be normal and therefore the LA re-equilibrates to both the
ionized and nonionized forms; but there are fewer cations
which may cause incomplete anesthesia.
34Dr. Firas Kassab

The following sequence is proposed mechanism of
action of LA:
Displacement of calcium ions from the sodium
channel receptor site
Binding of local anesthetic molecule to this
receptor site
Blockade of sodium channel
35Dr. Firas Kassab

Decrease in sodium conductance
Depression of rate of electrical depolarization
Failure to achieve the threshold potential level
Lack of development of propagated action potential
Conduction blockade…
36Dr. Firas Kassab

39
COMERCIALLY PREPARED LOCAL
ANESTHESIA CONSISTS OF:
Local anesthetic agent (xylocaine, lignocaine 2%)
Vasoconstrictor (adrenaline 1: 80,000)
Reducing agent (sodium metabisulphite)
Preservative (methylparaben,capryl
hydrocuprienotoxin)
Fungicide (thymol)
Vehicle (distillde water,NaCl)
Dr. Firas Kassab

• 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.
• SHELF LIFE INCRESES
41Dr. Firas Kassab

• 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.
42Dr. Firas Kassab

• 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.
43Dr. Firas Kassab

• The anesthetic agent and the additives referred to above
are dissolved in distilled water & sodium chloride.
• This isotonic solution minimizes discomfort during
injection.
44Dr. Firas Kassab

45
. 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.
Dr. Firas Kassab

The local anesthetics used in dentistry are divided
into two groups:
ESTER GROUP
AMIDE GROUP
46Dr. Firas Kassab

47
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
Dr. Firas Kassab

48
CLASSIFICATION OF LOCALANESTHETICS
ESTERS
Esters of benzoic acid
Butacaine
Cocaine
Benzocaine
Hexylcaine
Piperocaine
Tetracaine
Esters of Para-amino
benzoic acid
Chloroprocain
Procaine
Propoxycaine
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49
AMIDES
Articaine
Bupivacaine
Dibucaine
Etidocaine
Lidocaine
Mepivacaine
Prilocaine
Ropivacaine
QUINOLINE
Centbucridine
ABCDE LMPR
Dr. Firas Kassab

UPTAKE:
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.
Vasodilation is due to increase in the rate of absorption of
the local anesthetic into the blood, thus decreasing the
duration of pain control while increasing the anesthetic
blood level and potential for over dose.
50Dr. Firas Kassab

ORAL ROUTE:
Except cocaine, local anesthetics are poorly absorbed from
GIT
Most local anesthetics undergo hepatic first-pass effect
following oral administration.
72% of dose is biotransformed into inactive metabolites
TOCAINIDE HYDROCHLORIDE an analogue of lidocaine is
effective orally
51Dr. Firas Kassab

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.
52Dr. Firas Kassab

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.
RATES AT WHICH LOCAL ANESTHETICS ARE ABSORBED AND REACH THEIR PEAK
BLOOD LEVEL
ROUTE TIME TO PEAK
LEVEL (MIN)
INTRAVENOUS 1
TOPICAL 5
INTRAMUSCULA
R
5-10
SUBCUTANEOUS 30 - 90
53Dr. Firas Kassab

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.
54Dr. Firas Kassab

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.
55Dr. Firas Kassab

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.
56Dr. Firas Kassab

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.
57Dr. Firas Kassab

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.
58Dr. Firas Kassab

• Constrict vessels and decrease blood flow to the site of
injection.
• Absorption of LA into bloodstream is slowed, producing
lower levels in the blood.
• Lower blood levels lead to decreased risk of overdose
(toxic) reaction.
• Higher LA concentration remains around the nerve
increasing the LA's duration of action.
60Dr. Firas Kassab

• Minimize bleeding at the site of administration.
• Naturally Occurring Vasoconstrictors:
- Epinephrine
- Norepinephrine
• 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.
61Dr. Firas Kassab

• 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
• Levonordefrin - One fifth as active as epinephrine
• Vasoconstrictors - Unstable in Solution Sodium
metabisulfite added Known allergen
62Dr. Firas Kassab

• Max dose of vasoconstrictors
- Healthy patient approximately 0.2mg
- Patient with significant cardiovascular history: 0.04mg
• Max Dose for Vasoconstrictors (CV patient) 1 carpule =
1.8cc 1:100,000=.01mg/cc
0.01 X 1.8cc= 0.018mg 0.04/0.018=2.22 carpules
• In a healthy adult patient 0.2/0.018=11.1 carpules
63Dr. Firas Kassab

1.) The Syringe
2.) The Needle
3.) The Cartridge
4.) Other Armamentarium
- Topical Anesthetic (strongly recommended) -
ointments, gels, pastes, sprays
- Applicator sticks
- Cotton gauze
64Dr. Firas Kassab

Syringe Components
1.) Needle adapter
2.) Piston with harpoon
3.) Syringe barrel
4.) Finger grip
5.) Thumb ring
67Dr. Firas Kassab

• American Dental Association (ADA) criteria for
acceptance of LA syringes:
1-Durable and re-sterilzable or packaged in a sterile container (if
disposable).
2-Accept a wide variety of cartridges and needles of different
manufactures (universal use)
3-Inexpensive, light weight, and simple to use with one hand.
4-Provide effective aspiration and the blood be easily observed in
the cartridge. The incidence of positive aspiration may be as high
as 10%-15% in some injection techniques.
68Dr. Firas Kassab

• The Needle Gauge: the larger the gauge the smaller the
internal diameter of the needle Usual dental needle
gauges are 25,27, & 30 Length:
1-Long(approximately 40 mm "32-40 mm"), for NB.
2-Short(20-25 mm).
3-Extra-short(approximately 15 mm), for PDL.
69Dr. Firas Kassab

• The Cartridge Components:
- Cylinder, plunger, diaphragm
- Types: Standard – Self aspirating, plastic, Glass
- Contents: LA, VC, Vehicle, preservative.
- Volume: 1.8, 2.00 & 2.2 ML.
71Dr. Firas Kassab

• The Cartridge:
- Should not be autoclaved Stored at room temperature
(21°C to 22°C (70°F to 72°F)
- Should not soak in alcohol
- Should not be exposed to direct sunlight
72Dr. Firas Kassab

• MAXILLARY :
1) Supraperiosteal
2) PDL
3) Intraseptal Injection
4) Intracrestal Injection
5) Intraosseous Injection
6) PSA Nerve Block
7) MSA Nerve Block
8) ASA Nerve Block
9) Maxillary Nerve Block
10) Greater Palatine Nerve Block
11) Nasopalatine Nerve Block
12) AMSA Nerve Block
13) P-ASA Nerve Block
73Dr. Firas Kassab

• Greater palatine nerve block • Naso-palatine nerve block
77Dr. Firas Kassab

• MANDIBULAR INJECTION TECHNIQUES:
1) IANB Nerve block
2) Buccal Nerve Block
3) Mandibular nerve block techniques:
- Gow Gates technique
- Vazirani Akinosi closed mouth mandibular block
4) Mental Nerve block
5) Incisive nerve block
78Dr. Firas Kassab

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.
85Dr. Firas Kassab

2) 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.
86Dr. Firas Kassab

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.
87Dr. Firas Kassab

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
88Dr. Firas Kassab

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.
89Dr. Firas Kassab

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.
90Dr. Firas Kassab

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
91Dr. Firas Kassab

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
92Dr. Firas Kassab

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.
93Dr. Firas Kassab

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.
94Dr. Firas Kassab

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
95Dr. Firas Kassab

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).
96Dr. Firas Kassab

 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
97Dr. Firas Kassab

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
98Dr. Firas Kassab

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
Dr. Firas Kassab

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
100Dr. Firas Kassab

• 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.
101Dr. Firas Kassab

• 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
102Dr. Firas Kassab

• 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.
103Dr. Firas Kassab

• 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.
104Dr. Firas Kassab

• 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
105Dr. Firas Kassab

• 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
106Dr. Firas Kassab

Recent developments in local anesthesia and oral sedation.
2003 Journal of anesthesia
• Yagiela JA.
Abstract
• 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.
109Dr. Firas Kassab

110
surface anesthesia for intact skin.
Dr. Firas Kassab

• DentiPatch (lidocaine transoral delivery system)
Preinjection – 10-15 minutes exposure prior to injection -
Root scaling/planing – apply 5-10 minutes prior to
beginning procedure.
111Dr. Firas Kassab

• PRESSURE SYRINGE :
Used in IL injection techniques, especially in mandibular
teeth (types: pistol-grip, pen-grip).
112Dr. Firas Kassab

• 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 user
117Dr. Firas Kassab

• Handbook of local anesthesia – Stanley F Malamed – 6th
edition
• Essentials of Local Anesthetic Pharmacology : Daniel E
Becker : Anesth Prog. 2006 Fall; 53(3): 98–109.
• Vasoconstrictors in local anesthesia for dentistry: A. L.
Sisk; Anesth Prog. 1992; 39(6): 187–193.
118Dr. Firas Kassab

• Local anesthetic failure associated with inflammation:
verification of the acidosis mechanism and the hypothetic
participation of inflammatory peroxynitrite : Takahiro Ueno
et al ; Journal of Inflammation Research; November
2008 Volume 2008:1 Pages 41 - 48
• Advanced techniques and armamentarium for dental local
anesthesia; Clark TM; Dent Clin North Am. 2010
Oct;54(4):757-68
• Advances in dental local anesthesia techniques and
devices: An update ; Payal Saxena et al: National Journal of
Maxillofacial Surgery | Vol 4 | Issue 1 | Jan-Jun 2013
119Dr. Firas Kassab

THANK YOU!
Dr. Firas Kassab 120

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