local anesthesia

LOCAL ANESTHESIA

- Dr. Ibrahim Shaikh

1st Year MDS Periodontology

Seminar No. 1

Guide – Dr. Varsha Rathod.

1

Local anesthetics are effective means of pain

control, provided necessary precautions are

taken along with thorough knowledge of the

drugs.

2

CONTENTS :

Introduction

History

Neurophysiology

Pharmacology of local anesthetics.

Pharmacology of vasoconstrictors.

Clinical aspects of local anesthetics.

Future trends.

3

INTRODUCTION4

PAIN :

Monheim’s Handbook of Local Anesthesia

Unpleasant emotional experience usually

initiated by a noxious stimulus and transmitted

over a specialized neural network to the

central nervous system where it is interpreted

as such.

5

Methods Of Pain Control :

1. Removing the cause

2. Blocking the pathway of painful impulses

3. Raising the pain threshold

4. Preventing pain reaction by cortical depression

5. Using psychosomatic methods

6

Monheim’s Handbook of Local Anesthesia

What Is Anesthesia ?

Anesthesia – It is a temporary state consisting

of unconsciousness, amnesia, analgesia,

muscle relaxation and loss of autonomic

reflexes.

Proposed by Oliver Wendell Holmes in 1846.

7

OF LOCAL ANESTHESIA

HISTORY8

History :

Dentists, not doctors, were responsible for the

discovery of anesthesia.

Dr. Horace Wells (1815-1848) with nitrous oxide

in 1844

Dr. William Thomas Green Morton (1819- 1868)

with ether in 1846.

9

History of periodontology

Controversy :10

Crawford Long (1815 - 1878) : physician from

Jefferson, Georgia.

Horace Wells (1815-1848) : Dentist from

Hartford , Connecticut.

William Morton (1819-1868) : Dentist from

Boston, Massachusetts.


Dr. Horace Wells :11


Gardner Q. Colton

12

History of Periodontology

13

December 11, 1844 John Riggs extracted a molar from

Dr. Wells – The First painless extraction of the

modern era of medicine.

14

John Collins Warren, Professor of surgery,

Massachusetts General Hospital, Boston.

January 20, 1845 – Wells nervously attempted

to extract a student’s tooth in front of an

audience of incredulous staff and students.


Dr. William Morton :

History of periodontology.

15

Helped wells in his failed demonstration and in 1846 consulted

with Charles Jackson, professor of chemistry about other

drugs that could have a similar effect. Jackson suggested

ether.


16

On September 30, 1846 –

extracted a patients tooth in

a painless procedure.

On October 16, performed

a successful demonstration

at Massachusetts General

Hospital in which he

removed a tumor from the

neck of a patient.

$1,00,00017

Horace Wells

William Morton

Charles Jackson

Crawford Long


The COCA Leaf :

Coca leaves – genus Erythroxylum. (Erythroxylaceae family)

Erythroxylum coca – highest concentration of alkaloid known as cocaine in its leaves (up to 0.7 – 1.8% by weight)

Arhuaco, a tribe from the Negro river region, were the first to discover the properties of this drug.

In 1653, Bernabé Cobo, a Spanish Jesuit mentioned in one of his manuscripts that toothaches can be alleviated by chewing coca leaves

18

History of the development & evolution of local anesthesia since the coca leaf. Calatayud, Jesus

Journal of Anesthesiology, June 2003:98 – 6:1503-1508

Cocaine :

In 1860 German chemist Albert Niemann

managed to isolate the active principle, which

he named cocaine.

Steps were then taken to apply it as the first

local anesthetic by several people.

Lossen(1865),Thomas

Moreno(1868),Basil Von Anrep (1880)

19



Sigmund Freud :20

Sigmund Freud (1856-1939) – German military experiment, providing cocaine to soldiers during maneuvers to help them overcome the hardships of military campaigns.

Drug induced a euphoric stage that lifted him out of his periods of depression.


Carl Koller :21

Sep 11, 1884 - Carl Koller an ophthalmologist

performed the first operation using local

anesthetic on a patient with glaucoma.





Dec 6, 1884 Dr. William Stewart Halsted

published a report on the first successful nerve

block, in context of dentistry.

Dr. Nash of New York was able to block the

infraorbital plexus with approx. 0.5ml of 4%

cocaine hydrochloride to obturate an upper

incisor.

Dr. Halsted on the other hand blocked the inferior

dental nerve in a medical student using the same

solution.

22



1905 – Novocaine appeared for the first time and was found

to be safe and quickly became the standard local anesthesia.

(rechristened procaine in United states)

1943-1946 – Nils Löfgren & Bengt Lundquist developed a

xylidine derivative they called lidocaine.

1957 – Bo af Ekenstam et al. synthesized mepivacaine and

bupivacaine.

1969 – prilocaine : Nils Löfgren & cläes Tegner

23

After Cocaine :

Local Anesthesia :

Local Anesthesia has been defined as a loss of

sensation in a circumscribed area of the body

caused by a depression of excitation in nerve

endings or an inhibition of the conduction

process in peripheral nerves.

It produces this loss of sensation without

inducing a loss of consciousness.

Handbook of Local Anesthesia, Stanley F. Malamed

24

Properties :

Should not be irritating to tissues.

Should not cause any permanent alteration of nerve

structure.

Should have very low systemic toxicity.

Effective regardless of mode of administration.

Short time of onset of anesthesia.

Long duration of action of anesthetic effect.


25

Bennett’s additional requirements

:

Potency sufficient to give complete anesthesia without the

use of harmful concentrated solutions.

Relatively free from producing allergic reactions.

Should be stable in solution and should readily undergo

biotransformation in the body.

Should either be sterile or should be capable of being

sterilized by heat without deterioration.


26

NEUROPHYSIOLOGY27

The Neuron :

Structural unit of the nervous system.

Transmits messages between the CNS & all parts of

body.

Types –

a) Sensory

b) Motor

28


The Sensory Neuron :29


The Motor Neuron :


30

The Axon :


Long cylinder of neural cytoplasm encased in a thin

sheath, the nerve membrane, or axolemma.

Axoplasm is separated from extracellular fluids by a

continuous nerve membrane.

Sensory nerve excitability and conduction are both

attributed to changes developed within the nerve

membrane.

31

The Nerve Membrane :


The nerve membrane is 70 – 80 A° thick.

Flexible non stretchable layer consists of two layers of

lipid molecules

32


Proteins are primary organizational elements of the

membranes.

Proteins are classified as transport proteins and receptor

sites.

Channel proteins are continous pores through the

membrane allowing some ions (Na+, K+, Ca++) to pass

passively.

Other channels are gated, permitting ion flow only when

the gates are open.

33

Nerve Conduction :


35

Action Of Local Anesthetics :


Local Anesthetics interfere with the excitation process in

nerve membrane by one of the following mechanism:

1. Altering the basic resting potential of the nerve

membrane.

2. Altering the threshold potential

3. Decreasing the rate of depolarization

4. Prolonging the rate of repolarization

It has been established that the primary effects of local

anesthetics occur during the depolarization phase of the

action potential.¹

36

Theories Of Local Anesthetics :


Acetylcholine theory

Ach involved in nerve conduction

Calcium displacement theory

Ca2+ displaced from membrane site, alters Na2+

permeability

Surface charge (repulsion) theory

Cationic drug molecules bind to nerve membrane making it more positive, thus increasing the threshold potential causing decreased excitability

37



Membrane Expansion Theory :Drug molecule penetrates the lipid portion of membrane & brings about a change in the configuration of lipoprotein matrix, preventing Na ions permeability thereby inhibiting neural excitation.

38



Specific Receptor Theory :

Local Anesthetics act by binding to specific receptors on the sodium channel.

Action of the drug is direct & not mediated by some change in the general properties of the cell membrane.

Specific receptor site for local anesthetic agents exist in the sodium channel either on its external surface or on the internal axoplasmic surface.

Once the local anesthetic has gained access to the receptors, permeability to sodium ions is decreased or eliminated & nerve conduction is eliminated.

39

Classification of Local Anesthetic substances

according to biological site & mode of action


CLASS

A

CLASS

B

CLASS

C

CLASS

D

40

Mode Of Action Of LAs :


Displacement of Ca ions from the Na channel receptor

site,

Binding of the local anesthetic molecule to this receptor

site

Blockade of the sodium channel

Decrease in sodium conductance

Decrease of the rate of electrical depolarization

Failure to achieve the threshold potential level

Lack of development of propagated action potentials

Conduction blockade.

41


All Local Anesthetics are amphipathic.

The hydrophilic part is an amino derivative of

ethyl alcohol or acetic acid.

The lipophilic part is the largest. Aromatic in

structure, it is derived from benzoic acid, aniline,

or thiophene.

The structure is completed by an intermediate

hydrocarbon chain containing either an ester or

an amide linkage.

OOOO N

42

Dissociation of Local

Anesthetics :


Local anesthetics are basic compounds, poorly soluble in water and unstable on exposure to air.

They combine with acids to form local anesthetic salts, which are water-soluble and stable.

Local anesthetic are dissolved in either sterile water or saline

In this solution, it exists as uncharged molecules (RN) called base and positively charged molecules (RNH+) called the cation.

43


Both base and cation exist simultaneously

RNH+ RN + H+

As the pH decreases, equilibrium shifts to the

left

RNH+ > RN + H+

As the pH increases, equilibrium shifts to the

right

RNH+ < RN + H+

44

pKa and Anesthesia :


pKa (dissociation constant) is the measure of a molecule’s

affinity for hydrogen ions.

When pH = pKa, the drug exists in exactly 50% RNH+ and

50% RN form

The two factors involved in the action of a local anesthetic

are diffusion of the drug through the nerve sheath and

binding at the receptor site in the ion channel

The uncharged free base form RN is responsible for the

diffusion through the nerve sheath.

45


1000 molecules of LA (pKa-7.9) – injected in tissue (pH 7.4)

By Henderson-Hasselbalch equation- 75% RNH+ form & 25% RN form

Diffusibility & binding are responsible for LA effectiveness, but the diffusibility is much more important in actual practice.

46

Barriers :


Peripheral nerve

composed of hundreds

to thousands of tightly

packed axons.

Endoneurium

Perineurium – Fascicle

Perilemma – innermost

layer of perineurium

Epineurium

Epineural sheath or

nerve sheath

47

FACTORACTION

AFFECTEDDESCRIPTION

pKa Onset

Lower pKa = more rapid onset of action,

more RN molecules present to diffuse

through nerve sheath, thus onset time is

decreased

Lipid solubility Anesthetic

potency

Increased lipid solubility = increased

potency

Protein binding Duration

Increased protein binding allows anesthetic

cations (RNH+) to be more firmly attached

to protein located at receptor sites, thus

duration of action is increased

Tissue

diffusibility Onset

Increased diffusibility = decreased time of

onset

Vasodilator

activity

Anesthetic

potency and

duration

Greater vasodilator activity = increased

blood flow to region = rapid removal of

anesthetic molecules from injection site,

thus decreased anesthetic potency and

decreased duration Handbook of Local Anesthesia, Stanley F. Malamed

48

OF LOCAL ANESTHETICS

PHARMACOLOGY49


Based on Chemical structure

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

Classification :50

Procaine :


51

Vasodilation- clean surgical field difficult to maintain

because of increased bleeding.

Procaine is used in cases of inadvertent intra-arterial(IA)

injection of a drug; vasodilating properties are used to

aid in breaking arteriospasm.

Lidocaine :


52

Compared with procaine, lidocaine possesses

a significantly more rapid onset of action,

produces more profound anesthesia, has a

longer duration of action, and has a greater

potency.

Mepivacaine :


53

Provide longer duration of anesthesia than most other

local anesthetics when the drug is administered without

a vasoconstrictor.

Mepivacaine plain is the most used local anesthetic in

pediatric patients & is often quite appropriate in the

management of geriatric patients.

Prilocaine :


54

Integral part of EMLA(eutectic mixture of local

anesthetics) cream, which permits the anesthetics to

penetrate the imposing anatomic barrier of intact skin.

Prilocaine plain frequently is able to provide anesthesia

that is equal in duration to that obtained from lidocaine

or mepivacaine with a vasoconstrictor.

Articaine :


55

Clinically, it is claimed that maxillary buccal

infiltration of Articaine, provides palatal soft-

tissue anesthesia, obliterating the need for the

more traumatic palatal anesthesia.

Also claimed that it can provide pulpal and

lingual anesthesia when administered by

infiltration in adult mandible.

Bupivacaine & Etidocaine :


56

Lengthy dental procedures for which pulpal

anesthesia in excess of 90 minutes is

necessary.

Difference between the two is that Etidocaine

has an onset of action of about 3 minutes,

whereas Bupivacaine has an onset of 6 to 10

minutes.

Topical Anesthetics :57

Topical anesthetics diffuse through the mucous membranes and injured skin to reach the free nerve endings.

But the diffusion is limited and they are rapidly absorbed in the circulation, thus effective block is not obtained.

Thus, to increase their efficacy, their concentration is increased.

5% or 10% lidocaine,1% or 2% tetracaine-most common


Pharmacokinetics of Local Anesthetics :


Uptake

Distribution

Metabolism (Biotransformation)

Excretion

58

Uptake


All local anesthetics possess some degree of

vasoactivity; most producing some level of

vasodilation

Ester local anesthetics are potent vasodilating

drugs

Cocaine is the only local anesthetic that

consistently produces vasoconstriction

initial vasodilation intense vasoconstriction

59


Vasodilation leads to an increased rate of absorption of the

local anesthetic into the blood, thus decreasing the duration

and depth of pain control while increasing the anesthetic

blood concentration and potential for overdose (toxic reaction)

60

Distribution of Local Anesthetics :


Once in the blood, local anesthetics are distributed to all

tissues

Brain, head, liver, lungs, kidneys and spleen have high

levels of local anesthetics due to their high level of

perfusion

Skeletal muscle has the highest level because it has the

largest mass of tissue in the body

61

Factors influencing the blood levels

:


1) Rate at which the drug is absorbed into the

cardiovascular system.

2) Rate of distribution from the vascular compartment to

the tissues.

3) Elimination of the drug through metabolic or excretory

pathways.

62


All local anesthetics cross the

blood brain barrier

All local anesthetics cross the

placenta and enter the

blood stream of the developing

fetus

63

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Metabolism :64

Ester Local Anesthetics:

Hydrolyzed in the plasma by the enzyme

pseudocholinesterase

The rate of hydrolysis is related to the degree of toxicity

Tetracaine is hydrolyzed the slowest which makes it 16

times more toxic than Chloroprocaine which is

hydrolyzed the fastest

Slower Hydrolyzation = Toxicity

65

Esters - Procaine-

Para amino benzoic acid Diethyl amino alcohol

Excreted unchanged urine further transformed-urine


66

Amide Local Anesthetics:

Primary site of metabolism of amide local anesthetics is

the liver.

Virtually the entire metabolic process occurs in the liver

for Lidocaine, Mepivicaine, Articaine, Bupivacaine and

Etidocaine.

Prilocaine is metabolized in the liver and lung.


67

Biotransformation :

Mono ethyl xylidide

Glycine xylidide

Xylidide

Hydroxy xylidide.

Excreted by kidney .


68

Liver function and hepatic perfusion greatly affect the

rate of metabolism (biotransformation) of amide local

anesthetics

Significant liver dysfunction or heart failure represents a

relative contraindication to the use of amide local

anesthetics

Articaine has a shorter half-life than other amides

because a portion of its metabolism occurs in the blood

by plasma cholinesterase


69

Metabolism byproducts of amide local anesthetics can

possess clinical activity if allowed to accumulate in the

blood

All local anesthetics have the ability to cause sedation.


70

U.S. Air Force and U.S. Navy pilots are

grounded for 24 hours following

administration of Lidocaine due to its mild

effects of sedation and/or drowsiness


71

If the local anesthetic has two “i”s in its name; it’s

an amide

Lidocaine

Prilocaine

Bupivacaine

Articaine

Mepivacaine


Composition :72

Local anesthetic drug –e.g. lignocaine .

Vasopressor drug - e.g. adrenaline.

Anti-oxidant - egg Sodium meta bi sulfite.

Germicide, Preservative – e.g. methyl

paraben.

For isotonicity – Normal Saline .

Distilled water to equal the desired amount .


How much LA can be injected :73

Without adrenaline is : 300mg or 4.4mg/kg

With adrenaline : 500mg or 7mg/kg

Safe dose adrenaline : 0.2mg/visit

2% Lignocaine - 2g in 100 ml

2000mg - 100 ml

20 mg - 1ml

1 mg - 1/20ml

500mg = 1/20 500 = 25ml can be given safely for a normal

pt


Effects of LA on CNS :74

The pharmacological action of local anesthetics on the

CNS is depression.

At high levels, local anesthetics will produce tonic-clonic

convulsions.

Procaine, Lidocaine, Mepivacaine, Prilocaine and

Cocaine generally produce anti-convulsant properties;

this occurs at a blood level considerably below that at

which the same drugs cause seizures.


Preconvulsive Signs and Symptoms :75

Numbness of tongue & circumoral regions.

Shivering, Slurred speech, Muscular twitching.

Visual/auditory disturbances.

Dizziness, Drowsiness, Disorientation & Tremors.

If excitation or sedation occurs in the first 5 to 10 minutes after

local anesthetic delivery, it should serve as a warning that

convulsive activity could be possible


Cardiovascular Effects of LA’s :76

Local anesthetics have a direct action on the

myocardium and peripheral vasculature

CVS is more resistant to the effects local anesthetics

than the CNS

Increased local anesthetic blood levels result in

decreased myocardial depolarization, however, no

change in resting membrane potential and no

prolongation of the stages of repolarization


77

Local anesthetics decrease myocardial excitation,

decrease conduction rate and decrease the force of

contraction

Lidocaine is used therapeutically for pre-ventricular

contractions (PVCs) and ventricular tachycardia

Local anesthetics cause hypotension from the direct

relaxant action on vascular smooth muscle


Lung Toxicity :78

Local anesthetics have a direct relaxant action on bronchial

smooth muscle.

Generally, respiratory function is unaffected by local

anesthetics until near overdose levels are achieved.

Skeletal muscle will heal within two weeks of being injected

with local anesthetic.

Longer acting local anesthetics (Bupivacaine) produce more

damage to skeletal muscle than do shorter acting agents.


Of Vasoconstrictors.

Pharmacology79

Vasoconstrictor’s :80

All clinically effective injectable L.A have some degree of

vasodialating activity ↑ absorption of L.A into CVS → removal from injection site

Rapid diffusion of L.A from injection site → ↓ duration of action &

depth of anesthesia.

Higher plasma level of L.A → ↑ risk of toxicity

↑ bleeding at injection site.

Addition of vasoconstrictor to L.A.. Constriction of blood vessels → ↓ tissue perfusion

Slow absorption into CVS → low anesthetic blood level → ↓ risk

of toxicity.

Higher volume of L.A around nerve → ↑ duration of action

↓ bleeding at injection site


Classification :81

Catecholamines : Epinephrine

Norepinephrine

Levonordefrin

Isoproterenol

Dopamine

Noncatecholamines : Amphetamine

Methamphetamine

Ephedrine

Mephentermine

Hydroxyamphetamine

Metaraminol

Methoxamine


Selection Of Vasoconstrictors :82

The length of surgical procedure

Duration of pulpal and soft tissue anesthesia with 2% lidocaine lasts for only 10 min; the addition of 1:50,000, 1:80,000,1:100,000,increases this to app 60 min

Requirement for haemostasis during surgical procedure.

Epinephrine is effective in preventing blood loss during surgical procedures, however it also produces rebound vasodilatory effect.


83

Requirement for post operative pain control.

plain LA produce pulpal anesthesia for short duration

Medical Status of the Patient.

Benefits and risk of using LA with vasoconstrictor should be weighed against benefits and risks of using plain LA in medically compromised patients


Contraindications :84

Patients with more significant cardiovascular disease (ASA Ш and IV)

Patients with certain non-cardiovascular diseases (e.g., thyroid dysfunction , and sulfite sensitivity)

Patients receiving Monoamine oxidases inhibitors, Tricyclic antidepressant , and phenothiazines


Of Local Anesthesia

Applied Aspects85

Which type of LA should be given

in inflammation?86

• Mepivacaine is suitable for infected areas

which have

acidic medium , because it has less pKa

(7.6)

Allergic to both groups :87

If a pt is sensitive to both groups .

Antihistamines like diphenhydramine can be

given for Local anesthetic action

What happens in case of alcoholics &

smokers?88

• In case of acute alcoholics there is vasodilatation present at the site so rapid absorption of LA into circulation resulting in decreased depth and decreased duration of anesthesia

• In cases of chronic alcoholics the pain threshold is raised also resulting in decreased depth of anesthesia & need for larger doses which may lead to increased chances of overdose reactions

• In smokers , there is peripheral vasoconstriction present = increased duration of action and increased intensity of LA

Complications :89

LOCAL

Needle breakage Persistent

anesthesia Facial nerve

paralysis Trismus Soft-tissue injury Hematoma Pain on injection Burning on injection Infection, edema Sloughing of tissues

SYSTEMIC

Overdose

Allergy

Syncope


Overdose :90

• A drug over dose reaction has been defined as those

clinical signs & symptoms that result from an overly high

blood level of drug in various target organs and tissues.

• Under normal condition there is a constant absorption

of local anesthetic from the site of deposition into the

CVS & a constant removal of drug from the blood by the

liver.


91

Elevated blood levels of LA may result from one or

more of the following:

1. Biotransformation of the drug is usually slow

2. The unbiotransformed drug is too slowly eliminated

from the body through the kidneys.

3. Too large a total dose is administered

4. Absorption from the injection site is unusually rapid

5. Inadvertent intravascular administration occurs


92

Symptoms:

Restlessness, Visual disturbances

Nervous & Auditory disturbances

Numbness & Metallic taste

Light-headedness and dizziness

Drowsiness and disorientation

Losing consciousness

Sensation of twitching (before actual

twitching is observed)


Allergy :93

• Allergy is a hypersensitive state, acquired throughexposure to a particular allergen, re-exposure towhich produces a heightened capacity to react .

Allergens in LOCAL ANESTHETICS :

1. Esters - usually to the Para-amino-benzoic-acid product

2. Na bisulfite or metabisulfite - found in anesthetics as preservatives for vasoconstrictors, antioxidants

3. Methylparaben - no longer used as preservative.


In Local Anesthetics

Future Trends94

Centbucridine :95

Quinoline derivative

Five to eight times the potency of lidocaine

Rapid onset and an equivalent duration of action

Does not affect the central nervous system or

cardiovascular system


Ropivacaine :96

Long acting amide anesthetic

Structurally similar to mepivacaine and bupivacaine.

Unique in that it is prepared as an isomer rather than asa racemic mixture.

Has demonstrated decreased cardiotoxicity.

Potential for use in dentistry appears great, but awaitsclinical evaluation.


Carbonated Local Anesthetics :97

Carbon dioxide enhances diffusion of local anesthetic through nerve membranes, providing a more rapid onset of nerve block .

As CO2 diffuses through the nerve membrane, intracellular pH is decreased, raising the intracellular concentration of charged cations (RNH+) Since the cationic form of the drug does not readily diffuse out of the nerve, the anesthetic becomes concentrated within the nerve trunk (termed “ion trapping”), providing a longer duration of anesthesia.


98

The problem = if the carbonated LA agent is not

injected almost immediately after opening of the

vial the CO2 will diffuse out of solution,

significantly diminishing the solution’s

effectiveness.


Electronic Dental Anesthesia :99

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


Reference : 100

Handbook of Local Anesthesia ; Stanley F.

Malamed.

Monheim’s Handbook of Local Anesthesia.

History of Periodontology ; Fermin carranza,

Vincenzo Guerini

History of the development & evolution of local

anesthesia since the coca leaf; Calatayud,

Jesus, Journal of Anesthesiology, June

2003:98-6: 1503-1508

…for the patience.

THANK YOU101

local anesthesia

Health & Medicine

local theater

history of periodontology16on

discovery of anesthesia

helped wells

pain threshold

pain reaction

professor of surgery

methods of pain control