Local anaesthesia - Basics in dentistry, conventional local anesthesia techniques and complications

1. DR.K.PRASHANT
III YEAR MDS

2.  Introduction
 Historical background
 Definition
 Ideal properties
 Electrophysiology of nerve
conduction & Impulse propagation
 Theories of mechanism of action of
local anesthesia
 Classification of LA
 Dissociation of local anesthesia 2
CONTENTS

3. 3
 Local Anesthetic agent
 Types of Local Anesthetics
 Biokinetics
 Metabolism
 MRD
 Armamentarium
 Injection techniques
 Local & Systemic complications
 References

4.  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
HISTORICAL BACKGROUND
•LIDOCAINE- Lofgren in 1948.
•The discovery of its anesthetic properties
was followed in 1949 by its clinical use by
T. Gordh

5. 5
DEFINITION:
Local anesthesia is defined as a reversible 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.
LOSS OF SENSATION WITHOUT INDUCING LOSS OF
CONSCIOUSNESS..

6. 6
METHODS OF INDUCING LOCAL
ANESTHESIA:
Low temperature
Mechanical trauma
Anoxia
Neurolytic agents such as alcohol & phenol
Chemical agents such as local anesthetics

7. 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
7
PROPERTIES OF LOCAL ANESTHESIA

8. 8
inside
outside
Resting potential of neuron = -70mV
+
-
+
-
+
-
+
-
+
-
ELETROPHYSIOLOGY OF
NERVE CONDUCTION

9. 9
DEPOLARIZATION
DEPOLARIZATION:
REPOLARIZATION:
0.3 msec
•0.7 msecResult is a voltage gradient along
axon, causing a current i.e
sequential configurational
change in Na-channels in the
next segmentCONDUCTION.

10. Local anesthetic agent achieves interference 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.
10
MECHANISM OF ACTION OF LOCAL
ANESTHETICS

11. ACETYLECHOLINE THEORY:
There is no evidence that acetylcholine is
involved in neural transmission.
11
THEORIES MECHANISM OF
ACTION OF LOCAL ANESTHETICS

12. CALCIUM DISPLACEMENT THEORY:
.
12
SURFACE CHARGE (REPULSION) THEORY:

13. 13
MEMBRANE EXPANSION THEORY
 Lipid soluble LA can easily penetrate the lipid portion of cell
membrane decreasing the diameter of sodium channel.

14. The most favored today, proposed that local
anesthetics act by binding to specific receptors on
sodium channel ;the action of the drug is direct,
14
SPECIFIC RECEPTOR THEORY:

15.  Local anesthetics are available as salts (usually
hydrochlorides) for clinical use.
 In this solution it exists simultaneously as unchanged
molecule (RN), also called base and positively charged
molecules (RNH
+
) called cations.
RNH+
==== RN+ H+
15
DISSOCIATION OF LOCAL
ANESTHETICS

16.  In the presence of high concentration of hydrogen ion
(low pH) the equilibrium shifts to left 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
+
16

17.  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 hasselbach equation which determines how much of a
local anesthetic will be in a non-ionized vs ionized form . Based on
tissue pH and anesthetic Pka .
Log base/acid = pH - pKa
17

18. 18
LOCAL
ANESTHETIC
AGENT

19. 19
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 (distilled water, NaCl)

20.  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
20
REDUCING AGENT

21.  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.
21
PRESERVATIVE

22.  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.
22
FUNGICIDE

23.  The anesthetic agent and the additives referred to above
are dissolved in distilled water & sodium chloride.
 This isotonic solution minimizes discomfort during
injection.
23
VEHICLE

24.  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.
 Max dose of vasoconstrictors
- Healthy patient approximately 0.2mg
- Patient with significant cardiovascular history:
0.04mg
24
VASOCONSTRICTORS

25. The local anesthetics used in dentistry are divided
into two groups:
ESTER GROUP
AMIDE GROUP
25
LOCAL ANESTHETIC AGENT

26. 26
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

27. 27
CLASSIFICATION OF LOCAL
ANESTHETICS
ESTERS
Esters of benzoic acid
 Butacaine
 Cocaine
 Benzocaine
 Hexylcaine
 Piperocaine
 Tetracaine
Esters of Para-amino
benzoic acid
 Chloroprocain
 Procaine
 Propoxycaine

28. 28
AMIDES
 Articaine
 Bupivacaine
 Dibucaine
 Etidocaine
 Lidocaine
 Mepivacaine
 Prilocaine
 Ropivacaine
QUINOLINE
 Centbucridine
ABCDE LMPR

29.  NATUAL
 SYNTHETIC
 OTHERS
BASED ON MODE OF APPLICATION
• INJECTABLE
• TOPICAL
BASED ON DURATION OF ACTION
• ULTRA SHORT( < 30min)
• SHORT( 45-75min)
• MEDIUM( 90- 150min)
• LONG( 180 min)
29
BASED ON THE SOURCE BASED ON ONSET OFACTION
 SHORT
 INTERMEDIATE
 LONG
CLASSIFICATIONS:

30. 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)
30
CLASSIFICATIONS:
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

31. 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. 31
PHARMACOKINETICS OF LOCAL
ANESTHETICS

32. 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
32

33. 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.( Lidocaine 2.5% + Prilocaine 2.5%)
33

34. 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.
ROUTE TIME TO
PEAK LEVEL
(MIN)
INTRAVENOUS 1
TOPICAL 5
INTRAMUSCUL
AR
5-10
SUBCUTANEOU
S
30 - 90
34
RATES AT WHICH LOCAL ANESTHETICS ARE
ABSORBED AND REACH THEIR PEAK BLOOD
LEVEL

35. 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.
35

36. 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.
36
METABOLISM
(BIOTRANSFORMATION)

37. 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.
37

38. 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.
Amides are present in the urine as a parent
compound in a greater percentage then are esters.
38
EXCRETION

39. 39
MRD

40. 40

41. 1.) The Syringe
2.) The Needle
3.) The Cartridge
4.) Other Armamentarium
- Topical Anesthetic (strongly recommended) -
ointments, gels, pastes, sprays
- Applicator sticks
- Cotton gauze
41
LOCAL ANESTHESIA
ARMANTERIUM

42. 42
TYPES OF SYRINGES

43. 43
PLASTIC DISPOSABLE SYRINGE

44.  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.
44
NEEDLE

45. 45
COMPONENTS OF NEEDLE

46. 1) Supraperiosteal
2) PDL injection
3) Intraseptal Injection
4) Intracrestal Injection
5) Intraosseous Injection
6) PSA Nerve Block
7) MSA Nerve Block
8) ASA Nerve Block
9) Infra-Orbital Nerve
Block
10) MaxillaryNerve Block 46
INJECTION TECHNIQUES
11) Infra-Alveolar Nerve
Block
12) Greater Palatine Nerve
Block
13) Nasopalatine Nerve Block
14) Inferior Alveolar Nerve
Block
15) Mental Nerve Block
16) LingualNerve Block
17) Incisive Nerve Block
18) Gow Gates Nerve Block
19) Vzrani-Akinosi Nerve
Block

47. 47

48. 48
TYPES OF BLOCKS

49. 49
SUPRAPERIOSTEAL INJECTION

50. 50
POSTERIOR SUPERIOR ALVEOLAR
NERVE BLOCK

51. 51
POSTERIOR SUPERIOR ALVEOLAR
NERVE BLOCK

52. 52
ANTERIOR SUPERIOR ALVEOLAR
NERVE BLOCK

53. 53
MIDDLE SUPERIOR ALVEOLAR
NERVE BLOCK

54. 54
INFRA- ORBITAL NERVE BLOCK

55. Greater
palatine nerve
block
Nasopalatine
nerve block
55
PALATAL ANASTHESIA

56. 56
OTHER MAXILLARY ANASTHESIA
High Tuberosity
technique
Greater palatine
Canal Technique

57.  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
57

58. 58
INFERIOR ALVEOLAR
NERVE BLOCK

59. 59
INFERIOR ALVEOLAR NERVE
BLOCK

60. 60
BUCCAL NERVE BLOCK

61. 61
GOW GATES TECHNIQUE

62. 62
VAZIRANI-AKINOSI TECHNIQUE

63. 63
MENTAL NERVE BLOCK
INCISIVE NERVE BLOCK

64. 64

65. 1) Needle breakage :
Prevention
 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.
65
LOCAL COMPLICATIONS

66. 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.
 Examination every 2 months
66

67. 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.
67

68. 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
68

69. 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.
69

70. 6) Hematoma :
 When swelling becomes evident during or
immediately after a local anesthetic
injection, direct pressure should be applied
to the site of bleeding.
 Ice may be applied to the region
immediately on recognition of a
developing hematoma.
70

71. 7) Pain on injection
 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
71

72. 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
72

73. 9) Infection :
 Use sterile disposable needles.
 Use sterile local anesthetic solutions.
73

74. 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., 108) is summoned.
74

75.  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)
 Histamine blocker is administered IM or IV.
 Corticosteroid is administered IM or IV.
75

76. 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
76

77. 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)
 Orabase, a protective paste can provide a
degree of pain relief.
77

78.  Overdose reactions:
 Allergic reaction:
 More common with ester based local
anesthetics
 Most allergies are to preservatives in pre- made
local anesthetic carpules
 Methylparaben
 Sodium bisulfite
 metabisulfite
78
SYSTEMIC COMPLICATIONS

79. 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
79
CLINICAL MANIFESTATION OF LOCAL
ANESTHETIC OVERDOSE

80. 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

81. 81

82.  Handbook of local anesthesia – Stanley F
Malamed – 6th edition
 Netter, F. Atlas of Human Anatomy. CIBA. 1989.
82

83. THANK YOU
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