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LOCAL 
ANESTHESIA 
DR.PRIYANKA SHARMA 
II YEAR MDS 
PUBLIC HEALTH DENTISTRY 
JSSDCH
CONTENTS 
 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 
2
3 
Mode and site of action of local 
anesthesia 
Classification of local anesthetic 
according to biological site and 
mode of action 
Mechanism of action of local 
anesthesia 
Local anesthetics description 
Armamentarium 
Injection techniques 
Local & Systemic complications 
 Special care groups 
Recent advancements 
Conclusion 
References
Historical background 
• 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. 
4
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
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..
7 
METHODS OF INDUCING LOCAL 
ANESTHESIA: 
 
Low temperature 
 
Mechanical trauma 
 
Anoxia 
 
Neurolytic agents such as alcohol & phenol 
 
Chemical agents such as local anesthetics
PROPERTIES OF LOCAL 
ANESTHESIA 
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 
8
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.
ELETROPHYSIOLOGY OF 
NERVE CONDUCTION 
• 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. 10
outside 
inside 
11 
+ 
- 
+ 
- 
+ 
- 
+ 
- 
+ 
- 
Resting potential of neuron = -70mV
Action Potentials 
• 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 
12
13
SLOW DEPOLARIRIZATION 
RAPID DEPOLARIZATION: 
The interior of nerve is POSITIVE in relation to 
exterior. 
14
REPOLARIZATION: 
. 
SODIUM PUMP 
energy comes from the oxidative 
metabolism of ATP 
• Depolarization takes 0.3 msec 
• Repolarization takes 0.7 msec 
• The entire process require 1 msec 
15
IMPULSE PROPOGATION 
DEPOLARIZED SEGMENT ADJACENT RESTING 
AREA 
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
MYLINATED NERVES: 
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. 
17
18
MODE AND SITE OF ACTION OF 
LOCAL ANESTHETICS 
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 
19
THEORIES MECHANISM OF 
ACTION OF LOCAL 
ANESTHETICS 
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. 
20
CALCIUM DISPLACEMENT 
THEORY: 
States that local anesthetic nerve block was 
produced by displacement of calcium from 
some membrane site that controlled 
permeability of sodium. 
21
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. 22
MEMBRANE EXPANSION THEORY 
• 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. 23
MEMBRANE EXPANSION 
THEORY 
24
SPECIFIC RECEPTOR THEORY: 
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. 25
CLASSIFICATION OF LOCAL 
ANESTHETIC SUBSTANCES 
ACCORDING TO BIOLOGICAL SITE 
AND MODE OF ACTION 
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 
26
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) 
27
BASED ON THE SOURCE 
• NATUAL 
• SYNTHETIC 
• OTHERS 
BASED ON MODE OF 
APPLICATION 
• INJECTABLE 
• TOPICAL 
• BASED ON DURATION OF 
ACTION 
• ULTRA SHORT 
• SHORT 
• MEDIEM 
• LONG 28
BASED ON ONSET OF ACTION 
• SHORT 
• INTERMEDIATE 
• LONG 
29
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+ 
30
• 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+ 
31
• 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 
32
• 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. 
33
• 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. 34
MECHANISM OF ACTION OF LOCAL 
ANESTHETICS 
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 
35
 
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… 
36
37 
Na + Na +
LOCAL 
ANESTHETIC 
AGENT 
38
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)
40
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. 
• SHELF LIFE INCRESES 
41
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. 
42
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. 
43
VEHICLE 
• The anesthetic agent and the additives referred to 
above are dissolved in distilled water & sodium 
chloride. 
• This isotonic solution minimizes discomfort 
during injection. 
44
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.
LOCAL ANESTHETIC AGENT 
The local anesthetics used in dentistry are 
divided into two groups: 
 
ESTER GROUP 
 
AMIDE GROUP 
46
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
48 
CLASSIFICATION OF LOCAL 
ANESTHETICS 
ESTERS 
Esters of benzoic acid 
Butacaine 
Cocaine 
Benzocaine 
Hexylcaine 
Piperocaine 
Tetracaine 
Esters of Para-amino 
benzoic acid 
Chloroprocain 
Procaine 
Propoxycaine
49 
AMIDES 
Articaine 
Bupivacaine 
Dibucaine 
Etidocaine 
Lidocaine 
Mepivacaine 
Prilocaine 
Ropivacaine 
QUINOLINE 
Centbucridine 
ABCDE LMPR
PHARMACOKINETICS OF LOCAL 
ANESTHETICS 
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. 
50
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 
51
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. 
52
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 
53
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. 
54
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. 
55
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. 
56
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. 
57
EXCREATION 
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. 
58
MRD 
59
VASOCONSTRICTORS 
• 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. 60
• 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. 
61
• 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 
62
• 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 63
Local Anesthesia 
Armanterium 
1.) The Syringe 
2.) The Needle 
3.) The Cartridge 
4.) Other Armamentarium 
- Topical Anesthetic (strongly 
recommended) -ointments, gels, pastes, 
sprays 
- Applicator sticks 
- Cotton gauze 
64
TYPES OF SYRINGES 
65
Plastic disposable syringe 
66
Syringe Components 
1.) Needle adapter 
2.) Piston with harpoon 
3.) Syringe barrel 
4.) Finger grip 
5.) Thumb ring 
67
• 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. 68
Needle 
• 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. 69
Components of needle 
70
Cartridge 
• 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. 
71
• 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 
72
INJECTION 
TECHNIQUES 
• 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 73
Supraperiosteal injection 
74
Posterior superior 
alveolar nerve block 
75
Anterior superior alveolar 
nerve block 
76
Palatal Anasthesia 
• Greater palatine 
nerve block 
• Nasopalatine 
nerve block 
77
• 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 
78
Inferior alveolar nerve 
block 
79
Buccal nerve block 
80
Gow gates technique 
81
Vazirani-Akinosi 
technique 
82
Mental nerve block 
83 
INCISIVE NERVE BLOCK
84
Local 
Complications 
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. 
85
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. 
86
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
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
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. 
90
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
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 
92
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
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. 
94
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
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). 
96
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 97
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
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 
99
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 
100
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
• 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 
102
• 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. 
103
PREGNANCY 
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.
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 
106
DRUG-DRUG 
INTERACTION 
107
RECENT 
ADVANCEMENTS 
108
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. 
109
Eutectic mixture of local anesthesia 
(EMLA) 
110 
surface anesthesia for intact skin.
• DentiPatch (lidocaine transoral 
delivery system) Preinjection – 10- 
15 minutes exposure prior to 
injection - Root scaling/planing – 
apply 5-10 minutes prior to 
beginning procedure. 
111
• PRESSURE SYRINGE : 
Used in IL injection techniques, 
especially in mandibular teeth 
(types: pistol-grip, pen-grip). 
112
113
114
115
116
CONCLUSION 
• 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 
117
References 
• 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. 
118
• 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 
119
• 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. 
120
THANK YOU! 
121

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Local Anesthesia in Dentistry

  • 1. LOCAL ANESTHESIA DR.PRIYANKA SHARMA II YEAR MDS PUBLIC HEALTH DENTISTRY JSSDCH
  • 2. CONTENTS  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 2
  • 3. 3 Mode and site of action of local anesthesia Classification of local anesthetic according to biological site and mode of action Mechanism of action of local anesthesia Local anesthetics description Armamentarium Injection techniques Local & Systemic complications  Special care groups Recent advancements Conclusion References
  • 4. Historical background • 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. 4
  • 5. 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
  • 6. 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..
  • 7. 7 METHODS OF INDUCING LOCAL ANESTHESIA:  Low temperature  Mechanical trauma  Anoxia  Neurolytic agents such as alcohol & phenol  Chemical agents such as local anesthetics
  • 8. PROPERTIES OF LOCAL ANESTHESIA 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 8
  • 9. 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.
  • 10. ELETROPHYSIOLOGY OF NERVE CONDUCTION • 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. 10
  • 11. outside inside 11 + - + - + - + - + - Resting potential of neuron = -70mV
  • 12. Action Potentials • 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 12
  • 13. 13
  • 14. SLOW DEPOLARIRIZATION RAPID DEPOLARIZATION: The interior of nerve is POSITIVE in relation to exterior. 14
  • 15. REPOLARIZATION: . SODIUM PUMP energy comes from the oxidative metabolism of ATP • Depolarization takes 0.3 msec • Repolarization takes 0.7 msec • The entire process require 1 msec 15
  • 16. IMPULSE PROPOGATION DEPOLARIZED SEGMENT ADJACENT RESTING AREA 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
  • 17. MYLINATED NERVES: 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. 17
  • 18. 18
  • 19. MODE AND SITE OF ACTION OF LOCAL ANESTHETICS 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 19
  • 20. THEORIES MECHANISM OF ACTION OF LOCAL ANESTHETICS 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. 20
  • 21. CALCIUM DISPLACEMENT THEORY: States that local anesthetic nerve block was produced by displacement of calcium from some membrane site that controlled permeability of sodium. 21
  • 22. 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. 22
  • 23. MEMBRANE EXPANSION THEORY • 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. 23
  • 25. SPECIFIC RECEPTOR THEORY: 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. 25
  • 26. CLASSIFICATION OF LOCAL ANESTHETIC SUBSTANCES ACCORDING TO BIOLOGICAL SITE AND MODE OF ACTION 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 26
  • 27. 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) 27
  • 28. BASED ON THE SOURCE • NATUAL • SYNTHETIC • OTHERS BASED ON MODE OF APPLICATION • INJECTABLE • TOPICAL • BASED ON DURATION OF ACTION • ULTRA SHORT • SHORT • MEDIEM • LONG 28
  • 29. BASED ON ONSET OF ACTION • SHORT • INTERMEDIATE • LONG 29
  • 30. 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+ 30
  • 31. • 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+ 31
  • 32. • 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 32
  • 33. • 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. 33
  • 34. • 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. 34
  • 35. MECHANISM OF ACTION OF LOCAL ANESTHETICS 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 35
  • 36.  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… 36
  • 37. 37 Na + Na +
  • 39. 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)
  • 40. 40
  • 41. 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. • SHELF LIFE INCRESES 41
  • 42. 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. 42
  • 43. 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. 43
  • 44. VEHICLE • The anesthetic agent and the additives referred to above are dissolved in distilled water & sodium chloride. • This isotonic solution minimizes discomfort during injection. 44
  • 45. 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.
  • 46. LOCAL ANESTHETIC AGENT The local anesthetics used in dentistry are divided into two groups:  ESTER GROUP  AMIDE GROUP 46
  • 47. 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
  • 48. 48 CLASSIFICATION OF LOCAL ANESTHETICS ESTERS Esters of benzoic acid Butacaine Cocaine Benzocaine Hexylcaine Piperocaine Tetracaine Esters of Para-amino benzoic acid Chloroprocain Procaine Propoxycaine
  • 49. 49 AMIDES Articaine Bupivacaine Dibucaine Etidocaine Lidocaine Mepivacaine Prilocaine Ropivacaine QUINOLINE Centbucridine ABCDE LMPR
  • 50. PHARMACOKINETICS OF LOCAL ANESTHETICS 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. 50
  • 51. 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 51
  • 52. 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. 52
  • 53. 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 53
  • 54. 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. 54
  • 55. 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. 55
  • 56. 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. 56
  • 57. 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. 57
  • 58. EXCREATION 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. 58
  • 60. VASOCONSTRICTORS • 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. 60
  • 61. • 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. 61
  • 62. • 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 62
  • 63. • 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 63
  • 64. Local Anesthesia Armanterium 1.) The Syringe 2.) The Needle 3.) The Cartridge 4.) Other Armamentarium - Topical Anesthetic (strongly recommended) -ointments, gels, pastes, sprays - Applicator sticks - Cotton gauze 64
  • 67. Syringe Components 1.) Needle adapter 2.) Piston with harpoon 3.) Syringe barrel 4.) Finger grip 5.) Thumb ring 67
  • 68. • 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. 68
  • 69. Needle • 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. 69
  • 71. Cartridge • 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. 71
  • 72. • 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 72
  • 73. INJECTION TECHNIQUES • 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 73
  • 75. Posterior superior alveolar nerve block 75
  • 76. Anterior superior alveolar nerve block 76
  • 77. Palatal Anasthesia • Greater palatine nerve block • Nasopalatine nerve block 77
  • 78. • 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 78
  • 83. Mental nerve block 83 INCISIVE NERVE BLOCK
  • 84. 84
  • 85. Local Complications 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. 85
  • 86. 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. 86
  • 87. 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
  • 89. 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. 90
  • 91. 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 92
  • 93. 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. 94
  • 95. 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). 96
  • 97. 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 97
  • 98. 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 99
  • 100. 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 100
  • 101. 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 102
  • 103. • 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. 103
  • 104. PREGNANCY 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
  • 106. 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 106
  • 109. 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. 109
  • 110. Eutectic mixture of local anesthesia (EMLA) 110 surface anesthesia for intact skin.
  • 111. • DentiPatch (lidocaine transoral delivery system) Preinjection – 10- 15 minutes exposure prior to injection - Root scaling/planing – apply 5-10 minutes prior to beginning procedure. 111
  • 112. • PRESSURE SYRINGE : Used in IL injection techniques, especially in mandibular teeth (types: pistol-grip, pen-grip). 112
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  • 117. CONCLUSION • 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 117
  • 118. References • 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. 118
  • 119. • 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):757-68 119
  • 120. • 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. 120