local anesthesia

2. Local anesthesia
N.Nitya krishna
1st year post graduate
Department of Public Health Dentistry
2

3. CONTENTS
 Introduction
 History
 Definition
 Properties of local anesthesia
 Classification of local anesthesia
 Composition of local anesthesia
 Theories of local anesthesia
 Mechanism of action of local anesthesia
 Techniques of maxillary anesthesia
 Techniques of mandibular anesthesia
 Future trends of local anesthesia
 Indication and contraindications of local anesthesia
 Advantages and disadvantages of local anesthesia
 Conclusion
 References
3

4. INTRODUCTION
 The word anesthesia is derived from the
greek language.
 The words "an", means without; and
"aisthetos" means sensation.
 This was coined by Oliver Wendell
Holmes in 1846.
 He, at the time of discovery of ether,
wrote to Morton, and said that the state
should be called "anesthesia“, the
adjective will be anesthetic. Thus, he said,
"state of anesthesia" or "the anesthetic
state".

5. HISTORY
1844
• Dr. Horace Wells-for the first time used nitrous oxide in
dentistry to reduce pain during surgery.
1846
• William.T.G.Mortan- used ether as an anesthetic agent.
1855
• Friedrich Gaedcke- first person to isolate cocaine alkaloid and
named it as erythroxyline .
1860
• Albert Niemann- isolated pure cocaine from the coca leaves.
• Cocaine is the only naturally occuring anesthetic that is used in
medical practice.

6. 1884
• Karl koller –quickly appreciated that the anesthetizing
properties of cocaine had great practical importance
and soon introduced cocaine into ophthamology as
local anesthesia
1884
• William S Halsted and R.J.Hall- utilized this knowledge
to block nferior alveolar nerve to remove mandibular
teeth..
1905
• Einhorn- produced first effective synthetic local
anesthetic agent procaine obtained from benzoic acid
diethyl amino ethanol
1948
• Lofgren- introduced lidocaine for clinical use.

7. DEFINITION
local anesthesia has been defined as the loss of
sensation in circumscribed area of the body caused
by depression of excitation in nerve endings or an
inhibition of the conduction process in the peripheral
nerve.

8. PROPERTIES
8
 it should not be irritating to the tissue.
 It should not cause any permanent alteration of
nerve structure.
 Its systemic toxicity should be low.
 The time of onset of anesthesia - short.
 It must be effective.
 The duration of action must be long.

9. CLASSIFICATION

10. ON THE BASIS OF OCCURRENCE IN
NATURE
1. Naturally occurring, e.g. cocaine
2. Synthetic compounds
 a. Nitrogenous compounds
 i. Derivatives of para-aminobenzoic acid (PABA)
o Freely soluble, e.g. procaine
o Poorly soluble, e.g. benzocaine
 ii. Derivatives of acetanilide, e.g. lignocaine (lidocaine, xylocaine)
 iii. Derivatives of quinolone, e.g. cinchocaine (nupercaine)
 iv. Derivatives of acridine, e.g. bucricaine (centbucridine,
centoblock)
 b. Non-nitrogenous compounds, e.g. benzyl alcohol, and
propanediol
3. Miscellaneous drugs with local anesthetic action, e.g. clove oil,
phenol,chlorpromazine, certain antihistaminics such as
diphenhydramine.

11. BASED ON CHEMICAL STRUCTURE
11
 ESTER GROUP
 Benzoic acid esters
 Benzocaine, Cocaine, Butacaine, Tetracaine,
Hexylcaine, Piperocaine
 Para amino benzoic acid esters
 Procaine, Chloroprocaine, Propoxycaine
 AMIDE GROUP
 Lignocaine, Bupivacaine, Mepivacaine, Prilocaine,
Articaine, Dibucaine, Etidocaine, Ropivacaine
 QUINOLONE
 Centbucridine

12. BASED ON DURATION OF
ACTION
12
SHORT
DURATION(pulpal
anesthesia
approximately 30
minutes)
INTERMEDIATE
ANESTHESIA(pulpal
anesthesia
appproximately 60
minutes)
LONG
DURATION(pulpal
anesthesia
approximately 90 +
miniutes)
•.Lidocaine HCL 2%
•Mepivacaine HCL 3%
•Prilocaine HCL 4%(by
infiltration)
•Articaine HCL 4% +
Epinephrine 1:100,000
•Articaine HCL 4% +
Epinephrine 1:200,000
•Lidocaine HCL 2% +
Epinephrine 1:50,000
•Lidocaine HCL 2% +
Epinephrine 1:100,000
•Mepivacine HCL 2%+
Epinephrine 1:100,000
•Prilocaine HCL 4%+
Epinephrine1:200,000
Bupivacine HCL 0.5% +
Epinephrine

13. BASED ON BIOLOGICAL SITE AND MODE
OF ACTION
13
Classification Definition Chemical substance
Class-A Agents acting at receptor site on
external surface of nerve membrane
Biotoxins
(e.g.,tetrodoxin and
saxitoxin)
Class-B Agents acting at receptor sites on
internal surface of nerve membrane
Quarternary
ammonium analogues
of lidocaine
Scorpion venom
Class-C Agents acting by a receptor-
independent physico - chemical
mechanism
benzocaine
Class-D Agents acting by combination of
receptor and receptor-independent
mechanisms
Most clinically useful
local anesthetic
agents(e.g., articaine,
lidocaine,
mepivacaine,
prilocaine

14. COMPOSITION OF LOCAL
ANESTHESIA
 Local anesthetic agent
 Vasoconstrictor
 Preservative
 Reducing agent
 Fungicide
 Sodium chloride and distilled water

15. Local Anesthetic Agent
•Majority of local anesthetics are
tertiary amines (except Prilocaine)
•All local anesthetics are amphipathic
(lipophilic/hydrophilic)
•Three main parts of the local
anesthetic molecule:
1) Lipophilic Part (aromatic ring)
2) Intermediate Chain (amide or ester)
3) Hydrophilic Part (ethyl alcohol/acetic
acid)

16. Ester vs Amides
Ester Amides
Short acting Long acting
Metabolized in plasma and tissue
fluids
Metabolized in liver
Unstable in solution Stable in solution
Produces allergic reactions Allergic reactions occur very rarely
Cannot be stored for a long time Can be stored for a long time
Ester linkage is more easily
broken
Linkage is not broken easily

17. Chemical
agent
Lidocaine
(Xylocaine)
Mepivacaine
(Carbocaine)
Prilocaine
(Citanest)
Chemical
formula
Nature 1st amide to be
used in dentistry
as L.A.
Is an amide L.A. drug Amide L.A. drug
Vasodilating
properties
Less than
procaine & more
than prilocaine
and mepivacaine
Gives slight
vasodilatation
More than mepivacaine
and less than lidocaine
and procaine
Onset of
action
Rapid onset of
action (2-3 min)
Rapid onset of
action(1.5-2 mint.)
Its onset of action is
slightly slower than
lidocaine(2-4 mint.)

18. Chemical
agent
lidocaine Mepivacaine Prilocaine
Dental
concentration
-2%- 3%
- Both conc. Can be
used with or without
vasoconstrictor.
-vasoconstrictor used is
epinephrine 1:50,000
or 1:100,000
3% without vasoconstrictor
2% with vasoconstrictor.
Two Vaoconstrictors-
levonordephrine
(1:20,000)& epinephrine
(1:100,000) are available
with mepivacaine
-4% with or without
vasoconstrictor.
- V.asoconstrictor used
with it is epinephrine
1:200,000
Maximum
dose
-without vaoconstrictor
-4.4 mg/kg body
weight- adults and
children
-with vasoconstrictor -
6.6mg/kg body weight
-adults
-4.4 mg/kg body wt. for
adults or children
- 6 mg/kg body wt. for
adults
Topical
anesthetic
action
In concentration 5% Not in clinically acceptable
concentration
Prilocaine in its
uncharged base form , is
an integral part of EMLA
cream used to provide
topical anesthesia of skin

19. Item Lidocaine Mepivacaine Prilocaine
Notes - 2% lidocaine with
epinephrine 1:50,000
can be used safely with
max. epinephrine dose
(0.2mg) for healthy pt.
-For cardiac or
hyperthyroid pt. max.
safe dose is 0.04mg(1
cartridge)
-2 % lidocaine with
epinephrine 1:100,000
,2 catridges can be used
for cardiac or
hyperthyroid pt..
-For hemostasis, 2%
lidocaine + epinephrine
1:50,000 is
recommended
-For duration & depth of
pain control, 2%
lidocaine with 1:100,000
or 1:50,000 epinephrine
is recommended.
-It is the least
vasodilating
L.A. , so best
for short
procedures
-It has the least
concentrated epinephrine
dilution 1:200,000
-Therefore cardiac or
hyperthyroid pt. may
receive up to 4 cartridges
in one appointment.
-It’s relatively
contraindicated in pt. with
idiopathic or congenital
methemoglobinemia,
sickel cell anemia,
cardiac or respiratory
failure because
methemoglobine level is
elevated.

20. Item Atricaine
(Ultracaine)
Bupivacaine
(Marcaine)
Etidocaine
Chemical
formula
Nature It is amide L.A.
agent
-It ‘s amide L.A. agent
- it’s structurally related to
mepivacaine
-- It’s long acting L.A. drug
-It is amide and long
acting L.A. drug
Vasodilatin
g
properties
Equal to lidocaine More than lidocaine,
mepivacaine, prilocaine and
less than procaine
As bupivacaine
Onset of
action
Rapid onset equal
to lidocaine
Similar to that of lidocaine,
mepivacaine, prilocaine(6-
10 mint.)
-Less than etidocaine
Rapid onset equal to
lidocaine(1.5-3 mint.)
and more than
bupivacaine

21. Chemical agent Atricaine Bupivacaine Etidocaine
Topical
anesthetic action
Not in clinically
acceptable
concentration
Not in clinically
acceptable
concentration
Not in clinically
acceptable
concentration
Dental
concentration
- 4% conc. With
1:200,000 or
1:100,000 epinephrine
not available in plain
solution
-0.25%-0.5% conc.
With 1:200,000
epinephrine
- 1.5% conc. With
1:200,000
epinephrine
Maximum dose -7 mg/kg body wt. for
adults
- 5 mg/kg body wt. for
children between 4-12
years
- 1.3 mg/kg body wt.
for adults
- 8 mg/kg body wt.
for adults
Notes -It is the only
anesthetic agent of
amide type contain
thiophene ring as its
lipophilic portion
- It cause
methmoglobinemia if
given in large doses
Not recommended for
younger pt. or in those
postoperative soft
tissue injury caused by
self-mutilation is
increased

22. Item Articaine Bupivacaine Etidocaine
Notes -Should not be
used in pt. with
para -group
(sulfur containing
drug) allergy,
because it
contains hydroxyl
gp. In para
position
- Articaine is able
to diffuse through
soft and hard
tissues more
reliably than
other local
anesthetics. So
in max. buccal
infiltration can
provide palatal
indicated for :
1- lengthy dental
procedures for
which deep
anesthesia in
excess of 90
mint. is
necessary.
2- management
of postoperative
pain following
oral surgical
procedure giving
pain free period
up to 12 hours
(long acting L.A.)
As bupivacaine,
is long acting
local anesthetic
agent with same
clinical
indications of
bupivacaine. But
only different in
onset of action
and duration for
infiltration
anesthesia.

23. Chemical agent procaine propoxycaine
Nature Ester ester
Potency Weak anesthetic agent 7-8 times more potent than procaine
Vasodilating
properties
produce the greatest
vasodilation of all currently
used L.A.
not as profound as those of procaine.
Onset of action 6 – 10 minutes rapid (2-3 minutes)
Dental
concentration
2% or 4%
-2% solution gives - 12-15 min
of anesthesia
-Addition of 1:100,000
adrenaline -30-45 min
-0.4%
-Propoxycaine is not available alone
due to its high toxicity (7-8 times that
of procaine).
Maximum
rexommended dose
-1000mg 6.6 mg/kg of body weight for
adults. For children a dose of 3.0
mg/Ib

24. VASOCONSTRICTOR
 Vasoconstrictors are the chemical agents or
adjuncts added to local anesthetic solutions
(a) to oppose vasodilatation caused by the local
anesthetic agents and
(b) to achieve hemostasis.
Advantages of vasoconstrictor in combination
with local anesthesia:
1. Reduces blood flow thus reduces bleeding.
2. Reduce local anesthetic absorption and toxicity.
3. Increase duration and depth of anesthesia.

25. CLASSIFICATION
 Based on mode of action
1. Direct acting drugs:
a. Epinephrine,
b. Norepinephrine,
c. Dopamine,
d. Levonordefrine
e. isoproterenol, etc.
2. Indirect acting drugs:.
a. Tyramine,
b. Amphetamine,
c. Methamphetamine,
d. Hydroxyamphetamine.
3. Mixed acting drugs:
a. Metaraminol
b. ephedrine.

26. PHRAMACOLOGY OF SPECIFIC
AGENTS
 Epinephrine remains the most
commonly used and the most effective
vasoconstrictor used in medicine and
dentistry.
 The other vasoconstrictors used are
norepinephrine, phenylephrine,
levonordefrine, and octapressin

27. Agents Epinephrine Nor-
epinephrine
Levonordefrin Phenylephrine Felypressin
Propriotary
name
Adrenaline Levarterenol Neo-cobefrin Neo-
synephrine
octapressin
Source Synthetic, and
also 80%
obtained from
adrenal
medulla of the
animals
Synthetis and
natural(20%
adrenal
medulla)
forms
Synthetic Synthetic synthetic
Mode of
action
α and β
receptors, β
effects
predominates
α receptor-
90%,
β receptor -
10%
α receptor- 75%
β receptor -25%
α receptor- 95% Direct
stimulant of
vaso-
constrictor

28. agents Epinephrine norepinephrine Levonordefri
n
Phenylephrine felypressin
Availabity
in dentistry
1:1000
(alone) -
control of
bleeding.
1:80000 and
1:100000
commonly
used
concentratio
n
1:200000 -
medically
compromised
patient
No longer used
in dentistry.
In the past
it was included
with
propoxycaine
and procaine
in 1:30,000
conentration.
Can be
obtained with
mepivacine
in 1:20,000
No longer
available( was
used with 4%
procaine in a
1: 2500
0.03 IU/ml
with 3%
prilocaine in
japan,
germany and
other
countries.
Not available
in US.
Maximum
recommend
ed dose
0.2mg or
200ug per
appointment,
0.34mg; 4ml of
1:30,000
solution
1 mg ; 20ml
of a 1;20,000
solution
4mg ;10ml of
1;2500
solution
Not
recommende
d for use

29. agents epinephrine norepinephrin
e
Levonordefrine phenylephrine felypressin
Side
effects
and
overdose
•CNS
stimulation
•Increase fear
and anxiety
•Headache
•Tremor
•throbing
•Weakness
diszziness
•Increased
levels of
epinephrine –
cardiac
dysarrythimia
s
•CNS
stimulation
•Elevates
systolic and
diastolic
blood
pressure
•Episodes of
angina in
patients with
cardiac
dysarrythimia.
Same as
epinephrine but
to a lesser
extent
Tachyphylaxis
Ventricualr
dysarrythmia
minimal

30. CONTENTS FUNCTION EXAMPLE
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.
Sodium
metabisulphite-
0.05% to 0.1%,
Sodium bisulfite
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.
Methyl paraben,
Capryl
hydrocuprienotoxin
fungicide Due to the repeated usage, there is a
constant exposure of the solution to air, so
the solution becomes cloudy and there is
proliferation of minute fungi.
Thymol – 4mg/ml
vehicle The anesthetic agent and the additives
referred to above are dissolved in distilled
water & sodium chloride.
This isotonic solution minimizes discomfort
during injection.
Sodium chloride –
6mg/ml
30

31. THEORIES OF LOCAL
ANESTHESIA
 Acetylcholine theory
 Calcium displacement theory
 Surface charge repulsion theory
 Specific receptor theory
 Membrane expansion theory
31

32.  Acetylcholine theory
It is involved in nerve conduction in addition to its role as
nerve synapse.
32

33.  Calcium displacement theory
displacement of calcium from some membrane site alters
permeability of sodium. Evidence varying the concentration of
calcium ion bathing a nerve does not affect local anesthetic
potency has diminished the credibility of this theory.
 Surface charge repulsion theory
Proposed that local anesthetics acted by binding to the nerve
membrane and changing the electrical potential at the membrane
surface.
33

34.  Specifc receptor theory
34

35.  Membrane expansion theory
35

36. Mechanism of action
Displacement of calcium ions from sodium channel receptor site, which
permits
Binding of the L.A molecules to the receptor site, which thus produce
Blockade of the sodium channel
Decrease in sodium conductance which leads to
Depression of the rate of electrical depolarization

37. Failure to receive the threshold potential level,
along with
Lack of development of propogated action
potentials which is called
Conduction blockade
37

39. Techniques of local anesthesia
39

40. Maxillary anesthetic
techniques
 Anterior superior alveolar nerve block
 Posterior superior alveolar nerve block
 Middle superior alveolar nerve block
 Greater palatine nerve block
 Nasopalatine nerve block
40

41. Anterior superior alveolar nerve block
41

42. Posterior superior alveolar nerve block
42

43. Middle Superior Alveolar Nerve Block
43

44. Greater palatine nerve block
44

45. Nasopalatine nerve block
45
Single needle penetration at
incisive papilla

46.  Technique-2 (multiple preparation)
46

47. TECHNIQUES OF
MANDIBULAR ANESTHESIA
 Inferior alveolar nerve block
 Long buccal nerve block
 Mental nerve block
 Incisive nerve block
 Gow gates technique-open mouth technique
 Vazironi akinosi technique-closed mouth technique
47

48. Long buccal nerve block
48

49. Long buccal nerve block
49

50. 50

51. Mental nerve block
51

52. Incisive nerve block
52

53. Gow gates technique
53

54. Vazironi akinosi technique
54

55. FUTURE TRENDS IN PAIN
CONTROL
 Centbucridine :
 Quinoline derivative
 Five to eight times the potency of lidocaine
Rapid onset and an equivalent duration of action
 Ropivacaine :
 Long acting amide anesthetic, structurally similar to
mepivacaine and bupivacaine.
 Has demonstrated decreased cardiotoxicity.
 Potential for use in dentistry appears great, but awaits
clinical evaluation.
55

56. Carbonated local anesthesia
 Carbon dioxide enhances diffusion of local anesthetic through
nerve membranes, providing a more rapid onset of nerve block
.
 As CO2 diffuses, intracellular pH is decreased, raising the
intracellular concentration of charged cations (RNH+)
 anesthethesia becomes concentrated within the nerve trunk
(termed “ion trapping”), providing a longer duration of
anesthesia.
Electronic Dental Anesthesia
 A hand held electrode is placed at the needle penetration site,
providing a very localized area of intense anesthesia,
permitting both the painless penetration of intraoral soft tissues
with dental needles and administration of local anesthetics
56

57. Indications of local anesthesia
 Reduce or eliminate pain during dental treatment.
 To prevent gagging caused by the contact of the film
with palatal tissues and posterior part of the oral cavity.
Contra indications
Local
•Patient received
radiotherapy
•Acute infection at injection
site
•Vascular abnormality at
operation site
Systemic
•Uncooperative patient like
child
• Uncontrolled hemorrhagic
patient
•Allergic patient to local
anesthesia

58. ADVANTAGES OF LOCAL
ANESTHESIA
 Simple technique
 Minimal equipment
 Transportable
 Minimal
contraindication
 Hemorrhage could be
controlled by
vasoconstrictor
 No airway impairment
 Minimal postoperative
care
 No need for anesthetist
 Duration could be
controlled
 Co-operative patient
simplify the work

59. DISADVANTAGES OF LOCAL
ANESTHESIA
 Difficult to achieve co-operation
 Mechanical obstruction by large tongue or limited mouth
opening
 Failure due to anatomical variation or incomplete anesthesia
 Prolonged parasthesia
 Spread of acute infection

60. DENTAL CONSIDERATIONS IN LOCAL
ANESTHESIA
 If a patient is allergic to both esters and amide local
anesthesia, alternatives to local anesthesia should be
given.
1. 0.9% sodium chloride solution may be injected
intradermally. This produces short-term anesthesia
probably due to local pressure on the nerve endings.
2. Injectable antihistamines such as diphenhydramine
povidine short-term anesthesia when injected locally.
Angina pectoris and post myocardial infection
If emergency treatment is required, stress-reduction
protocols with antianxiety agents are appropriate.
60

61.  Asthma
avoiding local anesthetic with vasoconstrictors in
corticosteroid-dependent asthma patients on account of a
higher risk of sulfite allergy and the possibility that an
accidental intravascular injection might cause a severe and
immediate asthmatic reaction in the sensitive patient.
 Hypertension
If emergency dental treatment is needed, the clinician
may elect to sedate the patient with valium to reduce the
anxiety and use local anesthetic with a vasoconstrictor.
This dose will have minimal physiologic effect and will
provide prolonged anesthesia.
 Hyperthyroidism
The use of epinephrine or other vasoconstrictors in local
anesthetics should be avoided, or at least minimized, in the
untreated or poorly controlled hyperthyroid patient
 Hypothyroidism
Dosage should be minimum as they exhibit
exaggerated responses. 61

62. CONCLUSION
 Local anesthesia forms the back none of pain
control in dentistry.
 Still research is continuing for better management
for pain associated with surgical procedures.
 In the future other agents, may be added to local
anesthetic solutions to help manage postoperative
pain .
 The advancing field of anesthesia has more
exciting avenues for more acceptable means of
anesthesia.
62

63. REFERENCES
 Malamed.S.F. Handbook Of Local
Anesthesia. 6th Edition. Elsevier
publisher. Pg no.1-90.
 Benett.C.R .Leonard M Monheim’s.
Local Anesthesia And Pain Control In
Dental Practice.7TH Edition. Jaypee
publisher.Pg.no.30-120.
 Chitra Chakravarthy. Textbook of Oral
and Maxillofacial Surgery.2nd Edition.
Paras publisher. Pg no-90-106.
63