About local anesthesia used in dentistry .

1. LOCAL ANATHESIA
PRESENTED BY: GUIDED BY:
DR MAITRI PATEL DR SANTOSH KUMAR
PG PART -1 ( HOD AND PG GUIDE )
DR SURABHI
( PROF. AND PG GUIDE)

2.  INTRODUCTION
 DEFINATION
 WHY LOCAL ANAESTHTICS
 PROPERTIES OF AN IDEAL LA
 MECHANISM OF ACTION OF LA
 THEORIES OF LA’S MECHANISM OF ACTION
 COMPOSITION OF LOCAL ANESTHETIC CARTIDAGE
 VASOCONSTRICTORS
 CLASSIFICATION OF LA
 ANAESTHETICS FOR TOPICAL APPLICATION
o COMPLICATIONS OF LOCAL ANESTHESIA
 CONCLUSION
 REFERENCES
CONTENTS

3. INTRODUCTION
• A study of contemporary records reveals that dentistry in the past
was often a painful.

• Pain that may accompany dental treatment is often due to
instrumentation. It is thus practical to employ a local anesthetic
agent either to reduce or abolish the excitability of nerve endings or
to block the pathways along which painful impulses are conveyed to
the brain
INTRODUCTION.

4. DEFINATION
• Analgesia is loss of pain sensation accompanied by loss of other forms
of sensibility.
• Anaesthesia is loss of all forms of sensation including pain, touch,
temperature and pressure perception and may be accompanied by loss
of motor function.
• 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.
- Covino
BG, et al , 1976.
• Local anaesthetics are drugs, which upon topical application or
local injection cause reversible loss of sensory perception, especially
pain, in a restricted area of the body.
• General anaesthetics are drugs that produce reversible loss of all
sensation and consciousness.
DEFINATIONS

5. General Local
Site of action CNS
Peripheral nerves
Peripheral nerves
Area Whole body Restricted areas
Consciousness Lost Unaltered
Preferential use Major surgery Minor surgery
Use in non-coperative
Patients
Possible Not possible
Poor health patient Risky Safer
Care for vital functions Essential Not needed
Reflexes not seen normal
LA VS GENERAL ANESTHESIA

6. • Safety : Local anaesthesia, although it is uncommon for a fit
patient to die because of administration of GA, it is extremely
rare for a fatality to occur for LA
• Ease of Administration : Most anaesthetists recommend that
their patients has nothing to eat or drink for atleast 4 hours
prior to GA. While LA has an advantage, if patient has eaten
be forehand to reduce likelihood of fainting during treatment.
• Comparing with the administration of GA, LA administration
seems a comparatively simple procedure.
• Cooperation of the patient : not got when the patient is under
GA
WHY LOCAL ANAESTHETICS?

7. • Unlimited operating time : Most general anaesthesics administered to
outpatients last only for a few minutes and hence the dental surgeon is
unable to carry out prolonged operative procedures. With the progress in
modern anaesthesia this situation is altering.
• If the effect of LA is wearing off before treatment is completed, then it is a
simple matter for the dental surgeon to inject a further quantity.
• Reduced bleeding during surgical treatment : most LA’s contain a
vasoconstrictor which, besides prolonging the action of the analgesic, also
reduces the severity of hemorrhage.
• When the patient is unfit for a general anaesthetic:
• Airway problems example : ludwig’s angina, nasal obstruction.
• Respiratory inflammatory such as coryza, pneumonia, asthama
• CV disease causing ankle edema, dyspnoea at rest
• Mechanical problems such as difficult in opening of mouth.
• Sickle cell anemia.

8. PROPERTIES OF AN IDEAL LOCAL ANAESTHETIC
• Non irritating
• Not cause any permanent alteration of nerve structure.
• systemic toxicity should be low.
• It must be effective regardless of whether it is injected into the
tissue or applied locally to mucous membranes.
• Time of onset of anesthesia should be short.
• The duration of action should be long enough .
PROPERTIES OF AN IDEAL LOCAL ANAESTHETIC

9. In addition to these qualities BENNETT lists other properties of an
ideal local anesthetic- Bennet CR, 1974.
• sufficient potency to give complete anesthesia.
• free from producing allergic reactions.
• free in solution and relatively undergo biotransformation in the body.
• sterile or be capable of being sterilized by heat without deterioration

10. - LA are weak bases. To make them injectable they should be water soluble
and therefore a hydrochloride salt is added to the la.
- In aqueous solution this salt dissociated into inonised and nonioniesd
forms and equilibriates between two
- for la to be effective it has to first diffuse into the nerve cell membrane. The
nonionized base has lipophilic properties and responsible for the diffusion
into the nerve cell membrane
. Once the base diffuse into the nerve cell ;due to ph of the axoplasm , the la
reequlibrates into ionised and nonionised forms.now the ionised form is
responsible for binding to the sodium channel receptor and thus blocking
the sodium channel to prevent depolarization.
-
MECHANISM OF ACTION OF LA

11. - therefore the lipid solubility of the la solution is essential .since
more than 90% of the nerve membrane is made of lipids,for la
to diffuse into the nerve membrane lipid solubility is important.
-The nonionised part helps in diffusion through the cell
membrane and decrease in the ph of the surrounding tissue
shifts the equlibrium toward the ionised form.

13. RNH+ displaces calcium ions for the sodium channel receptor site.
↓ which causes
Binding of the local anesthetic molecules to this receptor site
↓ which produce
Blockade of sodium channel
↓ and
Decrease in sodium conduction
↓ leads to
Depression of the rate of electrical depolarization
↓ and
Failure to achieve the threshold potential level

Lack of development of propagated action potentials
↓ called
Conduction blockade

14. ACETYCHOLINE THEORY
CALCIUM DISPLACEMENT
THEORY
SURFACE
CHARGE(REPULSION)
THEORY
Stated that acetylcholine was involved in
nerve conduction in addition to its role as
a neurotransmitter at nerve synapses.
Dettbarn Wd et al,1967
Proposed that local anesthetic acted by
binding to nerve membrane and changing
the electrical potential at the membrane
surface.
Wei LY , 1969
States that local anesthetic nerve block was
produced by displacement of calcium from
some membrane site that controlled
permeability of sodium.
Goldmann DE et al, 1966
THEORIES OF LA’S MECHANISM OF ACTION

15. MEMBRANE EXPANSION
THEORY
It states that local anesthetic
molecule diffuse to hydrophobic
regions of excitable membranes,
producing a general disturbance of
bulk membrane structure, thus
preventing an increase in
permeability to sodium ions.
-Lee AG, 1976
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.

16. SPECIFIC RECEOTOR
THEORY
The most favored today, proposed that
local anesthetics act by binding to specific
receptors on sodium channel
Ritchie JM, 1987
The action of the drug is direct, not
mediated by some change in general
properties of cell membrane.
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.

17. LA agent
Vasoconstrictor
Sodium metabisulfite
(0.5 mg/ml)
Methylparaben (1 mg/ml)
Thymol
Sodium chloride (5.6 mg)
Sterile Water
Conduction blockade
↓se absorption of LA into
blood,thus
↑sing duration of anesthesia
Antioxidant for
vasoconstrictor
Preservative to ↑se shelf life,
bacteriostatic
Fungicide
Isotonicity of solution
For Dilution
COMPOSITION OF LOCAL ANESTHETIC CARTIDAGE

18.  Vasoconstrictors are the drugs that constricts the
blood vessels and thereby control tissue perfusion.
They are added to local anesthesia to oppose the
vasodilatory action of local anesthetic agent. E.g.-
adrenaline, noradrenaline, felypressin.
WHY DO WE NEED VASOCONSTRICTORS?
1) Constrict blood vessels  decrease blood flow to the surgical site
2) Cardiovascular absorption is slowed  lower anesthetic blood levels
3) Local anesthetic blood levels are lowered  lower risk of toxicity
4) Local anesthetic remains around the nerve for longer periods 
increased duration of anesthesia
5) Decrcreases bleeding
VASOCONSTRICTORS

19. Plain local anesthetics are vasodilators by nature
1) Blood vessels in the area dilate
2) Increase absorption of the local anesthetic into the
cardiovascular system (redistribution)
3) Higher plasma levels  increased risk of toxicity
4) Decreased depth and duration of anesthesia  diffusion
from site
5) Increased bleeding due to increased blood perfusion to
the area.
WHAT HAPPENS IF YOU DON’T USE A
VASOCONSTRICTORS?

20. • B.P. > 200/115 mm/Hg.
• Severe cardiovascular disease.
• Acute myocardial infection in last 6 months.
• Anginal episodes at rest.
• Cardiac disrhythmias that are refractory to drug treatment.
• Pt. is in hyperthyroid state of observable distress.
• Asthma Patients: avoid usage of ADRENALINE/
LEVONORDEFRIN as it contains sulphites.( may cause
wheezing)
CONTRAINDICATION OF USING A
VASOCONSTRICTOR

21. CLASSIFICATION OF LOCAL ANAESTHETICS
CLASSIFICATION OF LOCAL ANAESTHETICS
AMIDES QUINOLINE
Esters of
Para-amino
benzoic acid
Chloroprocaine
Procaine
Propoxycaine
Articaine
Bupivacaine
Dibucaine
Etidocaine
Lidocaine
Mepivacaine
prilocaine
Centbucridine
ESTERS
Esters of
benzoic acid
Butacaine
Cocaine
Benzocaine
Hexylcaine
Piperocaine
Tetracaine

22. Based on duration of
action
Short Intermediate
Long
Short duration –
eg: Lidocaine HCl 2%, Mepivacaine HCl 2%
Intermediate duration –
eg: Lidocaine HCl 2% + epinephrine 1:1,00,000
Long duration–
eg: Bupivacaine HCl 0.5% + epinephrine 1:2,00,000, 2% Etidocaine
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.
Short duration –
eg: Lidocaine HCl 2%, Mepivacaine HCl 2%
Intermediate duration –
eg: Lidocaine HCl 2% + epinephrine 1:1,00,000
Long duration–
eg: Bupivacaine HCl 0.5% + epinephrine 1:2,00,000, 2% Etidocaine
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.

23. 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
ACCORDING TO BIOLOGICAL SITE AND MODE OF ACTION

24. 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)

25. INDIVIDUAL LOCAL ANESTHETIC AGENTS
Drug pka ph Conc
used
Onset ½ life
Procaine 9.1 5-6.5
3.5-5.5
2-4% 6-10 min ½ hr
Lidocaine 7.9 6.5
5-5.5
2% 2-3 min 1.6 hr
Mepivacaine 7.6 4.5
3-3.5
3%
2%
1.5-2
min
1.9 hr
Prilocaine 7.9 4.5
3-4
4% 2-4 min 1.6 hr
Articaine 7.8 4.4-5.2 4% 2-3 min 1.25 hrs
Bupivacaine 8.1 4.5-6
3-4.5
0.5% 6-10 min 2.7 hr
Etidocaine 7.7 4.5
3-3.5
1.5% 1.5- 3 min 2.6 hr

26. ANAESTHETICS FOR TOPICAL APPLICATION
BENZOCAINE:
• Poor soluble in water
• Poor absorption into
CVS
• Not suitable for
injection
• Localized allergic
reaction may occur
following prolonged
and repeated use
• Inhibit the
antibacterial action of
sulfonamides
LIDOCAINE
• Available in two forms
for topical application
lidocaine base and
lidocaine hydrochloride.
LIDOCAINE BASE:
• is poorly soluble in
water
• Used in 5%
concentration
• Indicated in ulcerated,
abraded or lacerated
tissue.
LIDOCAINE
HYDROCHLORIDE:
• available as a
water soluble
preparation
• Used in 2%
concentration
• Penetrates tissue
more efficiently
then base form
• Greater risk of
toxicity then base
form.

27. Lidocaine is available in 3
Fprmulations:
 2% without vasoconstrictor,
 2% with epinephrine 1:50,000
 and 2% with epinephrine 1: 100,000
 Also, eutectic mixture of local anaesthesia (EMLA) has
been developed to provide surface anaesthesia for intact
skin. Other uses- venepuncture, lumbar puncture, arterial
cannulation.
 General definition: eutectic--said of a mixture which has
the lowest melting point which is possible to obtain by the
combination of the given components.
 Melting point of combined drug is lower then either
lidocaine (Xylocaine) or prilocaine (Citanest) alone.
LIDOCAINE

28. MAXILLARY NERVE BLOCK
POSTERIOR SUPERIOR ALVEOLAR NERVE
BLOCK
Other common names - tuberosity block
, zygomatic block
Nerves anesthetized – posterior superior
and branches
Areas anesthetized – pulps of maxillary
third , second, first molars (entire tooth
72%, mesiobuccal root of maxillary first
molar not anesthesized 28%)
MAXILLARY NERVE BLOCK

29. Anterior Superior Alveolar Nerve Block (Infraorbital Nerve Block)
Nerves Anesthetized
Anterior superior alveolar
Middle superior alveolar
Infraorbital nerve
Inferior palpebral
Lateral nasal
Superior labial
Areas Anesthetized
Pulps of the maxillary central incisor
through the canine on the injected side
In about 72% of patients, pulps of the
maxillary premolars and mesiobuccal root of
the first molar
Buccal (labial) periodontium and bone of
these same teeth
Lower eyelid, lateral aspect of the nose,
upper lip

30. GREATER PALATINE NERVE BLOCK
Anterior Palatine Nerve
Areas anesthetized:
Posterior portion of hard palate and
overlying soft tissues
Anteriorly to 1st premolar
Medially to midline
Landmarks:
Greater palatine foramen
Junction of alveolus and palatine bone
Area of Insertion:
Soft tissue anterior to foramen, from opposite side

31. Nasopalatine Nerve Block
Target area- incisive
foramen
Technique:
Position - open wide, extend head
Landmarks - incisive papilla, central
incisors
Approach - lateral to incisive papilla,
starting with cotton swab, topical
Deposit approx. 0.4 ml / 30 sec

32. Inferior alveolar nerve block
Nerves Anesthetized:
Inferior alveolar, a branch of the posterior
division Of the mandibular
Incisive
Mental
Lingual (commonly)
• Landmarks:
• Coronoid notch (greatest concavity on the anterior border
of the ramus)
• Pterygomandibular raphe
• Occlusal plane of the mandibular posterior teeth

34. BUCCAL NERVE BLOCK/ LONG BUCCAL/ BUCCINATOR NERVE
BLOCK
•Nerve Anesthetized: Buccal (a branch of the anterior
division of the mandibular)
•Area Anesthetized: Soft tissues and periosteum buccal to
the mandibular molar teeth
Area of insertion: mucous membrane distal and buccal to
the most distal molar tooth in the arch
Target area: buccal nerve as it passes over the anterior
border of the ramus
Landmarks: mandibular molars, mucobuccal fold

35. COMPLICATIONS OF LOCAL ANAESTHESIA
LOCAL COMPLICATION
 Needle breakage
 Persistent anesthesia and paresthesia
 Facial nerve paralysis
 Trismus
 Soft tissue injury
 Pain on injection
 Burning on injection
 Infection
 Edema
 Sloughing of tissue
 Post anesthetic intraoral lesions

36. CAUSES:
 Sudden unexpected movement by patient
 Needle of smaller gauge
 Previously bend needle
PREVENTION:
 Use larger gauge needle
 Use long needles
 Don’t insert the needle into tissues to the hub unless it is
absolutely essential for the success of technique
 Don’t redirect the needle once it is inserted into tissues
NEEDLE BREAKAGE

37. WHEN THE NEEDLE BREAKS:
1. Remain calm and don’t panic
2. Instruct the patient not to move
3. If the fragment is visible try to remove it with cotton pliers or with small
hemostat
IF THE NEEDLE IS LOST AND CANNOT BE READILY RETRIEVED
1. Do not proceed with incision
2. Calmly inform the patient and attempt to allay fear and apprehension
3. Note the incident in patients record
4. If the needle is superficial and is easily located through radiological and
clinical examination then removal by competent oral surgeon is possible
5. If the needle is located in the deeper tissue or is hard to locate permit it to
remain with out an attempt at removal
.
MANAGEMENT

38. CAUSES
 Trauma to any nerve
 Injection of contaminated LA
 Trauma to nerve sheath
 MANAGEMENT
 Most cases of parasthesia resolve approximately with in 8
weeks with out treatment only if damage to nerve is severe
then the parasthesia will be permanent
PERSISTANT ANESTHESIA-PARASTHESIA

39. CAUSES
 Introduction of LA solution into the capsule of parotid
gland
MANAGEMENT
 Reassurance the patient
 Advice the patient for periodically close the eyelid
 Contact lens should be removed
 Record the incident on patients chart
FACIAL NERVE PARALYSIS

40. Defined as motor disturbance of trigeminal nerve especially
spasm of masticatory muscles with difficulty in opening the
mouth
CAUSES
 Trauma to muscles or blood vessels in the infra temporal
space
 Local anesthetic cartilages into which alcohol or other cold
sterilizing solutions have diffused produce irritation of the
tissues
 Hemorrhage
 Low grade infection
 Excessive volume of local anesthetic solution
TRISMUS

41. PREVENTION
1)Use sharp and sterile disposable needles
2)Clean the site of injection with an antiseptic solution
3)Use aseptic technique
4)Practice a traumatic insertion
5)Avoid repeat injections
6)Use minimal effective volume
7)Hinton and associates reported onset of trismus 1-6 days post
treatment
MANAGEMENT
1)Heat therapy
2)Warm saline rinse
3)Analgesic ( Aspirin 325 mg)
4)Muscle relaxants
5)Physiotherapy
6)Chewing gums

42. CAUSES
 Inadvertent nicking of blood vesicles
PREVENTION
 Know the normal anatomy
 Modify the injection technique
 Use a short needle for PSA nerve block
 Minimize the number of needle penetration
 Never use a needle as probe in tissue
HEMATOMA

43. MANAGEMENT
IMMEDIATE: when swelling becomes evident direct pressure
should be applied to the site of bleeding
INFERIOR ALVIOLAR NERVE BLOCK: pressure is applied
to the medial aspect of ramus
INFRA ORBITAL NERVE BLOCK : pressure applied to the
skin directly over the infra orbital foramen
MENTAL OR INCISIVE : pressure over mental foramen
BUCCAL NERVE BLOCK: pressure at the site of bleeding
PSA NERVE BLOCK: infra temporal space can
accommodate a large volume of blood digital pressure can
be applied to the soft tissue in the mucobuccal fold as far as
distally as can be tolerated.

44. PAIN ON INJECTION
CAUSES
1)Careless injection technique
2)Dull needle
3)Rapid deposition of solution
4)Needle with barbs
PREVENTION
1)Proper technique of injection
2)Use sharp needle
3)Use topical anesthetic
prior to injection
4)Use sterile local anesthetic solution
5)Slow injection technique
CAUSES
1)pH of the solution
2)Wahl and associates compared the
pain on injection of prilocaine plain
to lidocaine with epinephrine
(1:100,000) and found no difference
3)When bupivacaine with
epinephrine (1:200,000) compared
with prilocaine plain more pain was
reported
4)Rapid injection of LA
5)Contamination of LA cartridges
PREVENTION
1)Slow injection
2)LA should be at room temperature
BURNING ON INJECTION

45. CAUSES
 Contamination of needle prior to injection
 Improper technique in handling the LA equipment
PREVENTION
 - use disposable needles
 - properly care for and handle needles
 - properly care for and handle cartridges
 - properly prepare the tissue
MANAGEMENT
 - ANTIBIOTICS
 ANALGESICS
 MUSCLE RELAXANTS
 -PHYSIOTHERAPY
INFECTION

46.  CLASSIFICATION OF ADVERSE DRUG REACTIONS
SYSTEMIC COMPLICATIONS
1. Toxicity caused by direct extension of
pharmacological effects
a)Side effects
b)Over dose
c)Local toxic effects
2. Toxicity caused by alteration in the recipient
a)Presence of disease
b)Emotional disturbances
c)Genetic aberrations
d)Idiosyncrasy
3. Toxicity caused by allergy to the drug

47.  PRE DISPOSING FACTORS
1 PATIENT FACTORS
 Age
 Weight
 Sex
 Presence of disease
2. DRUG FACTORS
 Vasoactivity
 Concentration
 Dose
 Route of administration
 Rate of injection
 Vascularity of injection site
 Presence of vasoconstrictor
LOCAL ANESTHETIC OVERDOSE

48. CLINICAL MANIFESTATION OF LOCAL ANESTHETLC
OVERDOSE
•SIGNS:
•MINIMAL TO MODERATE OVERDOSE LEVELS:
•Apprehension
•Talkativeness
•Excitability
•Slurred speech
•Generalized stutter
•Muscular twitching, tremor of face and distal extremities
•Nystagmus
•Sweating , vomiting
•Elevated BP, heart rate and respiratory rate

49. MODERATE TO HIGH BLOOD LEVELS:
Generalized tonic clonic seizure, followed by
Generalized CNS depression
Depressed BP, heart rate and respiratory rate
SYMPTOMS:
Light headedness
Restlessness
Nervousness
Numbness
Metallic taste
Visual disturbances
Auditory disturbances (tinnitus)
Drowsiness
Loss of consciousness

50. • Local anesthesia is required for almost all the
procedures performed in present day dentistry.
• Hence we as the dentists should be aware of various
techniques, adverse effects, actions and indications
along with the pharmacological aspects so that we
can use it judiciously according to the patient’s
condition and choice of the dentist.
CONCLUSION

51. REFERENCES
TEXTBOOK OF LOCALANESTHESIA - STANLEY F. MALAMED
•MONHEIMS LOCALANESTHESIA AND PAIN CONTROL IN DENTAL
PRACTICE
•ESSENTIALS OF PHYSIOLOGY- K SEMBULINGAM
•TEXTBOOK OF PHARMACOLOGY- KD TRIPATHI
•TEXTBOOK OF ORAL SURGERY – NEELIMA MALIK
•TEXTBOOK OF ORAL SURGERY- M LASKIN

52. REFERENCE
• TEXTBOOK OF LOCALANESTHESIA - STANLEY F.
MALAMED
• MONHEIMS LOCALANESTHESIAAND PAIN
CONTROL IN DENTAL PRACTICE
• ESSENTIALS OF PHYSIOLOGY- K SEMBULINGAM
• TEXTBOOK OF PHARMACOLOGY- KD TRIPATHI
• TEXTBOOK OF ORAL SURGERY – NEELIMA MALIK
• TEXTBOOK OF ORAL SURGERY- M LASKIN