PERIODONTAL- SURGERY.

1. GOOD MORNING

2. LOCAL
ANAESTHESIA

3. CONTENTS
• Introduction
• Historical background
• Definition
• Desirable properties of L.A
• Pharmacology of L.A(CLASSIFICATION)
• Lidocaine
• Theories of mechanism of action of local anesthesia
• Mechanism of action of local anaesthetics
• Composition
• Pharmocokinetics
• Vasoconstrictors
• Factors in selection of a L.A for a patient
• Common questions to ask patient
• Stress reduction protocol
• Local anaesthetic used in medically compromised patients
• Techniques of local anaesthesia.
• Local and systemic complications
• Recent Advances and future trends in pain control
• Conclusion.
• References

4. INTRODUCTION
 Widely used method of pain control
 Painless treatment
 Comfort to the patient.

5. 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 & diethyl amino ethanol.

6. • Its 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.
• Thereafter, series of potent anesthetic soon
followed with a wide spectrum of clinical
properties.

7. 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. STANLEY
F.MALAMED (1980)
 Important feature of L.A-
It produces loss of sensation without inducing a loss of
consciousness.(STANLEY F.MALAMED)
 Local anesthetics are drugs which upon topical
application or local injection cause reversible loss of
sensory perception, especially of pain in a localized
area of the body.
 No structural damage to the neurons

8. DESIRABLE PROPERTIES OF LOCAL ANESTHESIA
 It should not be irritating to tissue to which it is applied
 It should not cause any permanent alteration of nerve
structure .
 Its systemic toxicity should be low .
 Time of onset of anesthesia should be short .
 It should be effective regardless of whether it is injected
into the tissue or applied locally to mucous membrane.
 The duration of action should be long enough to permit
the completion of procedure.(yet not so long as to require
an extended recovery)

9.  In addition to these qualities,BENNET lists other desirable
properties of ideal L.A
 It should have the potency sufficient to give complete
anesthesia without the use of harmful concentration
solutions.
 It should be free from producing allergic reactions.
 It should be stable 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. PHARMOCOLOGY
CLASSIFICATION
•Butacaine
•Cocaine
•Benzocaine
•Hexylcaine
•Tetracaine
•Chlorprocaine
•Procaine
•propoxycaine
•Artricaine
•Bupivacaine
•Dibucaine
•Etidocaine
•Lidocaine
•Mepivacaine
•Prilocaine

11. Based on biological site
& mode of action
Class A Class B Class C Class D
• Tetrodotoxin
• Saxitoxin • Quaternary
ammonium
analogues of
lidocaine
•Scorpion venom
•Benzocaine
• Lidocaine
• Mepivacane
• Prilocaine

12. Based on
mode of
application
Topical Injectable
Soluble Insoluble
•Cocaine
•Lidocaine
•Tetracaine
•Benoxinate
•Benzocaine
•Butylamino-
benzoate
•Lidocaine
•Mepivacaine
•Tetracaine
•Bupivacaine
•Dibucaine

13. Based on
duration of
action
Ultra short Short Medium Long
Pulpal = < 10 min
Soft tissue = 30 –
45 min
•Chlorprocaine
•Procaine
Pulpal = 5-10 min
Soft tissue = 60 –
120 min
•Lidocaine
•Prilocaine
Pulpal = 45 – 90 min
Soft tissue = 120 –
240 min
•Mepivacaine
•Artricaine
Pulpal = 90 – 180
min
Soft tissue = 240
– 540 min
•Bupivacaine
•Etidocaine

14. Based on
potency
LOW Intermediate HIGH
•Procaine
•Chlorprocaine
•Lidocaine
•Mepivacaine
•Tetracaine
•Bupivacaine
•Dibucaine

15. IMPULSE PROPAGATION

16. LIDOCAINE
• Lidocaine, Xylocaine or lignocaine is a common local
anesthetic and antiarrhythmic drug.
• Most widely used LA effective by all routes.
• Faster onset .
• Available as Injections, topical solution, jelly and ointment
etc.
• Lidocaine is used topically to relieve itching, burning and
pain from skin inflammations, injected as a dental
anesthetic or as a local anesthetic for minor surgery.
• More intense, longer lasting, than procaine.

17. • Sets on quickly and produces a desired
anesthetic effect for several hours
• Good alternative for those allergic to ester type
• More potent than procaine but about equal toxicity
• It relieves pain during the dental surgeries
• Quicker CNS effects than others
• Anti arrhythmic
• Cause little allergenic reaction; it is hypoallergenic

19. MAXIMUM RECOMMENDED DOSE

20. USE :
a) 2% lignocaine with 1: 50000 epi. – hemostasis
b) 2% lignocaine with 1: 100000 or 1: 200000 –
localanesthesia
COMPARISON OF LIDOCAINE WITH PROCAINE
- More rapid onset of action
- More profound anesthesia
- Longer duration of action
- Greater potency

21. THEORIES MECHANISM OF ACTION OF LOCAL
ANESTHETICS
• Many theories have been promulgated over the
years to explain the mechanism of action of local
anesthetics.
ACETYLCHOLINE 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.

22. CALCIUM DISPLACEMENT THEORY
• States that local anesthetic nerve block was
produced by displacement of calcium from some
membrane site that controlled permeability of
sodium.

23. 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.

24. 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.

26. 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.

28. MECHANISM OF ACTION OF LOCAL ANESTHETICS

29. COMPOSITION
• LOCAL ANESTHETIC AGENT(DRUG) (xylocaine, lignocaine 2%)
Blockade of nerve conduction.
• VASOCONSTRICTOR (adrenaline 1: 80,000)
 Increase depth and increase duration of anesthesia;
decreases aborption of local anesthetic .
• SODIUM METABISULPHITE  reducing agent (antioxidant)
• METHYLPARABEN,CAPRYL HYDROCUPRIENOTOXIN
 Bacteriostatic agent
• THYMOL  Fungicide
• VEHICLE (DISTILLED WATER and NACL)  Volume and
Isotonicity of solution

30. • 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.

31. PHARMACOKINETICS
• Uptake
– Oral route
– Topical route
– Injection
• Metabolism
– Esters
– Amides
• Excretion

32. VASOCONSTRICTORS
• Decrease blood flow
• Lower anesthetic blood levels
• Decrease the risk of toxicity
• Increases duration of action
• Decrease bleeding

33. VASOCONSTRICTORS CLASSIFICATION
CATECHOLAMINES
– Epinephrine
– Norepinephrine
– Dopamine
– Levonordefrin
– Isoproterenol
NON CATECHOLAMINES
– Amphetamine
– Methamphetamine
– Hydroxy-amphetamine
– Ephedrine
– Mephetermine

34. EPINEPHRINE
Maximum Dose for Dental Appointment
- Normal healthy patient:
0.2 mg. per appointment
- Significant cardiovascular impairment:
0.04 mg per appointment
NOREPINEPHRINE
Maximum dose :
 Healthy pt – 0.34 mg per appointment or 10 ml of 1:30000
solution
 pt. with CV disease : 0.14 mg per appointment or 4 ml of
1:30000 solution

35. FACTORS IN SELECTION OF A LA FOR A
PATIENT
1. Length of time pain control is necessary.
2. Potential need for post treatment pain control
3. Possibility of self-mutation in the postoperative
period
4. Requirement for haemostasis
5 . Presence of any contraindication to the LA
solution selected for administration

36. COMMON QUESTIONS TO ASK THE
PATIENT
• Allergic to any medications?
• Have you ever had a reaction to local
anesthesia?
• If yes, describe what happened
• Was treatment given? If so, what?

37. • Careful preoperative assessment
• History
• A clear explanation of what to expect
PREPARATION OF THE PATIENT

38. Data should be documented includes:
1.Baseline vital signs: 1.blood pressure
2.laboratory values
3.Results of ECG
monitoring
4.any other tests.
2. Weight, height, and age:
 Dosage of some drugs is calculated on the
basis of body weight in kilograms (mg/kg).
Some drugs are contraindicated for age
extremes (i.e., pediatric or geriatric patients).
PREOPERATIVE ASSESSMENT:

39. 3. Current medical problem(s) past history of
medical events, including a history of substance
abuse.
4. Current medications or drug therapy, such as
insulin for diabetes or hypertensive drugs.
5. Allergy, or hypersensitivity reactions to previous
anesthetics or other drugs.
6. Mental status, including emotional state and
level of consciousness.
7. Communication ability A patient with hearing
impairment or language barrier may be unable
to understand verbal instructions during the
procedure or to respond appropriately.

40. STRESS REDUCTION PROTOCOL
 Morning appointments are usually best.
 Keep appointments as short as possible.
 Freely discuss any questions, concerns, or fears
that the patient has
 Establish a honest, supportive relationship with
the patient.
 Maintain a calm, quiet, professional environment.
 Provide clear explanations of what the patient
should expect and feel.

41. Premedicate with benzodiazepines if needed.
 Ensure good pain control through judicious
selection of local anesthetic agents appropriate
for treatment.
Maintenance of patient comfort throughout
the procedure.
 Use nitrous oxide as needed (avoid hypoxia).
 Use gradual position changes to avoid postural
hypotension.
 End the appointment if the patient appears
overstressed.

42. LOCAL ANESTHETIC USE IN MEDICALLY
COMPROMISED PATIENTS
2000 JOURNAL OF THE CALIFORNIA DENTAL ASSOCIATION

43. TECHNIQUES
OF LOCAL
ANAESTHESIA

44. 1. LOCAL INFILTRATION (0.6 – 1.0 ml)small
terminal nerve endings are anaesthetized.

45. 2. FIELD BLOCK deposited in proximity to the
larger nerve branches

46. 3. NERVE BLOCK (1.8 – 2.0 ml)depositing the
LA solution within close proximity to a
main nerve trunk

47. 4.INTRALIGAMENTARY (0.2 ml)
• depositing the LA solution within PDL
through gingival sulcus.
• Provides 30-35 min of anesthesia.
• Indicated in patient with bleeding
disorder& young handicapped patients .
5.INTRASEPTAL (0.1 ml)
• Similar in technique and design to the PDL
injection.
• Useful in providing osseous and soft tissue
anesthesia and hemostasis for periodontal
curettage and surgical flap procedures.

51. SUPRAPERIOSTEAL

63. 0

91. TECHNIQUE 1-DIRECT METHOD

95. Technique-5 METHOD OF SUNDER
J. VAZIRANI 1960

113. DURATION OF LOCAL ANESTHETICS
Examples
Lidocaine Bupivacaine
• local infiltration 30-60 min 120-240
• Minor nerve block 60-120 180-360
• Major nerve block 120-240 360-720
• Epidural 30-90 180-300
• Addition of epi improved improved

114. PAIN CONTROL REGIMEN FOR SURGICAL
PROCEDURE

115. COMPLICATIONS OF LA
LOCAL
1. Needle breakage
2. Prolonged anesthesia
3. Facial nerve paralysis
4. Trismus
5. Soft tissue injury
6. Hematoma
7. Pain or burning sensation
8. Failure to achieve
anesthesia
9. Local necrosis
10. Post anesthetic intraoral
lesions
SYSTEMIC
1. Overdose
2. Allergic reaction
to Local
Anesthesia

116. 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

117. 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

118. • Hypersensitive state as a result of exposure
to an allergen
• Re-exposure can heighten the initial reaction
• Incidents of allergy are low
• Often allergic reaction is to one of the
ingredients within the cartridge, not the local
anesthesia itself
ALLERGIC REACTIONS TO LOCAL ANESTHETIC
AGENTS

119. CLINICAL MANIFESTATIONS OF AN ALLERGY
• Fever
• Angioedema
• Urticaria
• Dermatitis
• Depression of blood-forming organs
• Photosensitivity
• Anaphylaxis

120. When excessive blood levels occur.
Usually due to:
1. Accidental rapid intravenous injection.
2. Rapid absorption from mucous membranes.
3. Absolute overdose if the dose used is excessive.
TOXICITY FROM LOCAL ANAESTHETIC DRUGS

121. SIGNS AND SYMPTOMS OF LA TOXICITY
 It involves the CNS and CVS.
 CNS is more sensitive to LA than the CVS.
 CNS manifestations tend to occur earlier.
 Brain excitatory effects occur before the
depressant effects.

122. Early or mild toxicity:
If LA with Adrenaline :Tachycardia with
Hypertension
If no Adrenaline : Bradycardia with
Hypotension
Severe toxicity:
 CV Collapse is due to the depressant effect of the LA
acting directly on the myocardium (e.g. Bupivacaine)
 Severe and intractable arrhythmias can occur with
accidental iv injection.
CVS SIGNS & SYMPTOMS

123. PRECAUTIONS:
 Secure intravenous access before injection
of any dose .
 Always have adequate equipment and
drugs available before starting to inject
ESSENTIAL PRECAUTIONS AND TREATMENT

125. TREATMENT OF LOCAL ANESTHETIC TOXICITY
Apparent allergy
• Steroids
• Histamine (H1)
blockers
• With severe reactions
– Intravenous
fluid
– Epinephrine
CNS toxicity
• Don’t treat minor reactions
• Seizures: maintain airway,
provide O2
– Terminate seizure with
thiopental, midazolam,
or propofol
– Intubate patients with
full stomach

126. TREATMENT OF CV TOXICITY
 Substitute: amiodarone for lidocaine
vasopressin for epinephrine
 Consider cardiopulmonary bypass or lipid infusion if
standard drugs fail

127. • Aspirate carefully before injecting
 To reduce the risk of unintentional intravascular
injection
• Inject slowly:A maximum rate of 1 min/ capsule
• Monitor the patient both during and after the
injection for unusual reactions
• Select the anesthetic agent with or without a
vasoconstrictor based upon the duration of
anesthesia appropriate for the planned procedure
UNIVERSAL SAFETY GUIDELINES FOR
ADMINISTRATION OF LA TO ALL PATIENTS:

128. • Use the minimum amount of anesthetic solution
 To achieve an adequate level of anesthesia
 To keep the patient comfortable throughout the
dental procedure.
• Adherence to these simple guidelines will reduce
the risk of adverse reactions to the local anesthetic
agents themselves or to the vasoconstrictors
contained in local anesthetics.

129. RECENT ADVANCES AND FUTURE
TRENDS IN PAIN CONTROL

130. • Centbucridine
• Ropivacaine
• EMLA
• TENS ( Transcuteneous Electrical Nerve
Stimulation)
• Hyaluronidase
• Ultra –long acting local anesthetics
• Sprays
• Topical gels
• Intraoral lignocaine patch(dentipatch)
• Iantophoresis
• Jet injection
• Computer controlled system
• Comfort control syringe
• Electronic dental anaesthesia
• Ph alteration

131. CONCLUSION
• Adapting local anaesthetic technique can
overcome difficulties in access and limit soft tissue
anaesthesia
• Local anaesthetic doses must be controlled.
• Vasoconstrictors produce systemic effects.
• Dental epinephrine has drug interactions.
• Local anesthesia remains the backbone of pain
control in dentistry.
• Research has been continued in both medicine and
dentistry to seek new and better means of
managing pain associated with many surgical
treatments.

132. • Painful experiences and poor or prominent
surgical scars are the two most memorable
aspects of a surgical procedure for a patient.
• If one can provide a nearly painless surgical
procedure without the use of general anesthesia
then you have won half the battle.

133. REFERENCES
 Handbook of local anesthesia – Stanley F Malamed – 6th
edition
 Local analgesia in dentistry – by d .h.roberts& j. h.sowray
 Monehim”s local anesthesia and pain control, Benett
 Practical pearls for nearly painless local anesthesia- JOHN K.
GEISSE.
 Principles of anesthesiology, 3rd edition, vol- 2, Vincent J. Collins
 Local anesthesia- mechanism of action and clinical use-
Benjamin G Cohino
 Paincontrol in dental practice by Richard bennet7th edition.
 Essentials of Local Anesthetic Pharmacology : Daniel E Becker
 Advanced techniques and armamentarium for dental local
anesthesia; Clark TM; Dent Clin North Am.
 Vasoconstrictors in local anesthesia for dentistry: A. L. Sisk;
Anesth Prog.
 Practical Local Anaesthesia for Special Needs Patients-John
meechan
 Current trends in pain research and therapy, Vol 4, chronic pain
reactions, mechanism and modes of therapy

134. THANK YOU