GOOD MORNING

LOCAL ANAESTHESIA

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

• Conclusion

INTRODUCTION Widely used method of pain control

Painless treatment

Comfort to the patient.

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.

• 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.

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

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)

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.

PHARMOCOLOGYCLASSIFICATION

•Butacaine•Cocaine•Benzocaine•Hexylcaine•Tetracaine

•Chlorprocaine•Procaine•propoxycaine

•Artricaine•Bupivacaine•Dibucaine•Etidocaine•Lidocaine•Mepivacaine•Prilocaine

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

Based on mode of

application

Topical Injectable

Soluble Insoluble

•Cocaine•Lidocaine•Tetracaine•Benoxinate

•Benzocaine•Butylamino- benzoate

•Lidocaine•Mepivacaine•Tetracaine•Bupivacaine•Dibucaine

Based on duration of

action

Ultra short Short Medium Long

Pulpal = < 10 minSoft tissue = 30 – 45 min

•Chlorprocaine•Procaine

Pulpal = 5-10 minSoft tissue = 60 – 120 min

•Lidocaine •Prilocaine

Pulpal = 45 – 90 minSoft tissue = 120 – 240 min

•Mepivacaine•Artricaine

Pulpal = 90 – 180 minSoft tissue = 240 – 540 min

•Bupivacaine •Etidocaine

Based on potency

LOW Intermediate HIGH

•Procaine•Chlorprocaine

•Lidocaine•Mepivacaine

•Tetracaine•Bupivacaine•Dibucaine

IMPULSE PROPAGATION

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.

• 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

MAXIMUM RECOMMENDED DOSE

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

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.

CALCIUM DISPLACEMENT THEORY

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

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.

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.

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.

MECHANISM OF ACTION OF LOCAL ANESTHETICS

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

• 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.

PHARMACOKINETICS • Uptake

– Oral route

– Topical route

– Injection

• Metabolism – Esters

– Amides

• Excretion

VASOCONSTRICTORS• Decrease blood flow

• Lower anesthetic blood levels

• Decrease the risk of toxicity

• Increases duration of action

• Decrease bleeding

VASOCONSTRICTORS CLASSIFICATION

CATECHOLAMINES

– Epinephrine

– Norepinephrine

– Dopamine

– Levonordefrin

– Isoproterenol

NON CATECHOLAMINES

– Amphetamine

– Methamphetamine

– Hydroxy-amphetamine

– Ephedrine

– Mephetermine

EPINEPHRINEMaximum 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

FACTORS IN SELECTION OF A LA FOR A PATIENT

1. Length of time pain control is necessary.

2. Potential need for post treatment pain control3. Possibility of self-mutation in the postoperative

period

4. Requirement for haemostasis

5 . Presence of any contraindication to the LA solution selected for administration

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?

• Careful preoperative assessment

• History

• A clear explanation of what to expect

PREPARATION OF THE PATIENT

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:

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.

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.

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.

LOCAL ANESTHETIC USE IN MEDICALLY COMPROMISED PATIENTS

2000 JOURNAL OF THE CALIFORNIA DENTAL ASSOCIATION

TECHNIQUES OF LOCAL

ANAESTHESIA

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

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

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

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.

SUPRAPERIOSTEAL

0

TECHNIQUE 1-DIRECT METHOD

Technique-5 METHOD OF SUNDER J. VAZIRANI 1960

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

PAIN CONTROL REGIMEN FOR SURGICAL PROCEDURE

COMPLICATIONS OF LA LOCAL1. Needle breakage2. Prolonged anesthesia3. Facial nerve paralysis4. Trismus5. Soft tissue injury6. Hematoma7. Pain or burning sensation8. Failure to achieve

anesthesia9. Local necrosis10. Post anesthetic intraoral

lesions

SYSTEMIC

1. Overdose

2. Allergic reaction to Local

Anesthesia

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

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

• 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

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

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

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.

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

PRECAUTIONS: Secure intravenous access before injection

of any dose .

Always have adequate equipment and drugs available before starting to inject

ESSENTIAL PRECAUTIONS AND TREATMENT

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

TREATMENT OF CV TOXICITY

Substitute: amiodarone for lidocaine

vasopressin for epinephrine

Consider cardiopulmonary bypass or lipid infusion if standard drugs fail

• 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:

• 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.

RECENT ADVANCES AND FUTURE TRENDS IN PAIN CONTROL

• 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

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.

• 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.

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

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