LOCAL ANAESTHESIA IN

ENDODONTICS

BY MODERATOR
DR.SAURAV KUMAR DUTTA DR.SAUMMYA MAM
 INTRODUCTION
“ 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.”
Stanley F. Malamed 7th edition
• Cocaine was isolated in 1860 and is obtained from Coca leaves. It was first used by Carl Koller as
a local anesthetic in 1884.
• At the same time LA was used in dentistry by Halsted and Hall.
• The search for a less toxic and less addictive substitute led to the development of the amino ester
local
anesthetic procaine in 1904 by Einhorn and its anesthetic properties were reported by Biberfield
• . Since then, several synthetic local anesthetic drugs have been developed and put into clinical use,
notably lidocaine in 1943 was marketed by Lofgren, bupivacaine in 1957 and prilocaine in 1959
was introduced.
 DESIRABLE PROPERTIES OF LOCAL ANESTHETICS

• Non-irritant to tissue
• Should not cause any permanent alteration of nerve structure
• Low systemic toxicity
• Should be effective whether injected or applied locally to mucous membranes
• Short time of onset of anaesthesia
• Adequate duration of action
• Should be stable in solution and readily undergo biotransformation
• Should be sterile or be capable of being sterilized by heat without deterioration
 THEORIES O N ME C HANISM O F AC TIO N O F LA
Acetylcholine theory: Calcium displacement the theory:
Membrane expansion theory: Surface charge theory:
 1) The ACETYLCHOLINE THEORY states that acetylcholine is
involved in nerve conduction, in addition to its role as a
neurotransmitter at nerve synapses. No evidence exists indicating that
acetylcholine is involved in neural transmission along the body of the
neuron.

2) The CALCIUM DISPLACEMENT THEORY, once popular,

maintains that local anesthetic nerve block is produced by
displacement of calcium from some membrane site that controls
permeability to sodium. Evidence that varying the concentration of
calcium ions bathing a nerve does not affect local anesthetic potency
has diminished the credibility of this theory
 3) The SURFACE CHARGE (REPULSION) THEORY proposes that
local anesthetics act by binding to the nerve membrane and changing the
electrical potential at the membrane surface.

Cationic (RNH+) drug molecules are aligned at the membrane-water

interface, and because some of the local anesthetic molecules carry a net
positive charge, they make the electrical potential at the membrane
surface more positive, thus decreasing the excitability of the nerve by
increasing the threshold potential.

Current evidence indicates that the resting potential of the nerve

membrane is unaltered by local anesthetics (they do not become
hyperpolarized), and that conventional local anesthetics act within
membrane channels rather than at the membrane surface.
 4) The MEMBRANE EXPANSION THEORY states that local
anesthetic molecules diffuse to hydrophobic regions of excitable
membranes, producing a general disturbance of the bulk membrane
structure, expanding some critical region(s) in the membrane, and
preventing an increase in permeability to sodium ions.
 5) The SPECIFIC RECEPTOR THEORY, the most favored today,
proposes that local anesthetics act by binding to specific receptors on the
sodium channel. The action of the drug is direct, not mediated by some
change in the general properties of the cell membrane.

Both biochemical and electrophysiologic studies have indicated that a

specific receptor site for local anesthetics exists 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, and nerve
conduction is interrupted.
CLINICAL IMPLICATIONS OF PH AND LOCAL ANESTHETIC
ACTIVITY
• Most commercially prepared solutions of local anesthetics without a vasoconstrictor have a pH
between 5.5 and 7.
• When these solutions are deposited into tissue, the vast buffering capacity of the tissue fluids
rapidly returns the pH at the injection site to a normal 7. 4 .
• Local anesthetic solutions that contain a vasopressor (e.g., epinephrine) are acidified by the
manufacturer to retard oxidation of the vasoconstrictor, thereby prolonging the period of the
drug’s effectiveness.
• Sodium bisulphite in a concentration between 0.05% & 0.1% is a commonly used antioxidant
for the epinephrine.
• A 2% solution of lidocaine with a pH of 6.8 is acidified to 4.2 by the addition of sodium
bisulphite. This reduced pH takes a longer time for the onset of action.
• The buffering capacity of mucous membrane is less and thus a greater concentration of the local
anaesthetic agent (atpH between 5.5 & 6.5) is needed to provide topical anaesthesia.
FACTORS AFFECTING LOCAL ANESTHETIC ACTION
 C LASSIFIC ATIO N:

Chemical nature: Based on bioavailability: According to biological

A) ESTERS: site and mode of action:
a) Benzoic Acid esters a) Natural – eg. Cocaine
• Benzocaine a) Class A: external surface
• cocaine b) Synthetic nitrogenous Biotoxins such as tetrodotoxin
b) Parabenzoic acid esters compound – eg. procaine, & saxitoxin
• Procaine benzocaine, lignocaine & Class B: on internal surface
• Chloroprocaine bupivacane Quaternary Ammonium
• Tetracaine
analogues of lid.ocaine,
B) AMIDES: c) Non Nitrogenous compounds –
a) Articaine Scorpion venom
benzyl alcohol
b) Bupivacaine Class C-: receptor independent
c) Etidocaine Benzocaine
d) Miscellaneous – clove oil , phenol
d) Lidocaine Class D: receptor & receptor
e) Mepivacaine independent
f) Prilocaine -
C) quinolones: MOST CLINICALLY USEFUL LOCAL ANAESTHETIC AGENTS:
a) centbucridine
ARTICAINE,LIDOCAINE,BUPIVACAINE,MEPIVACAINE,
PRILOCAINE, ETC.
 CLASSIFICATION
Classification based on potency &
clinical use:
a)Injectable:
a) Low potency
Procaine, Chloroprocaine
b)Intermediate potency
Lidocaine (Lignocaine),
Prilocaine, Articaine
c)High potency Tetracaine
(Amethocaine), Bupivacaine,
Ropivacaine, Dibucaine
(Cinchocaine
Surface anaesthetics
Soluble:Cocaine, Lidocaine,
Tetracaine
Insoluble: Benzocaine,
Butylaminobenzoate (Butamben),
Oxethazine
According to duration of action
Ultra Short acting anesthetic – less than 30 min
• Procaine without a vasoconstrictor
• 2% chloroprocaine without vasoconstrictor
• 2% lidocaine without a vasoconstrictor
2) Short acting local anesthetic – 45 to 75 min
• 2% lidocaine with 1:100000 epinephreine
• 2% mepivacaine with 1: 20000 lavonordefrin
• 4% prilocaine when used to nerve block
3) Medium acting anesthetics- 90 – 150min
• 4% prilocaine with 1:200000 epinephrine
• 2% lidocaine and 2% mepivacaine with a vasoconstrictor
• May produce pulpal anesthesia of this duration
4) Longer acting anesthestic – 180 min or longer
• 0.5% bupivacaine with 1: 200000 epinephrine
• 0.5% or 1.5% etidocaine with 1:200000 epinephrine
 PHARMACOKINETICS OF LOCAL ANESTHETIC

UPTAKE:
• When injected into soft tissues, local anesthetics exert pharmacologic action on
blood vessels in the area. All local anesthetics possess a degree of vasoactivity,
most producing dilation of the vascular bed into which they are deposited,
although the degree of vasodilation may differ, and some (e.g., cocaine) may
produce vasoconstriction
• Procaine, the most potent vasodilator
• Tetracaine, chloroprocaine, and propoxycaine also possess vasodilating
properties to differing degrees but not to the degree of procaine
• Cocaine is the only local anesthetic that consistently produces vasoconstriction
• The rates at which local anesthetics are absorbed into the bloodstream and reach their peak blood level vary
according to the route of administration:
A) ORAL ROUTE
• With the exception of cocaine, local anesthetics are absorbed poorly
• most local anesthetics (especially lidocaine) undergo a significant hepatic first-pass effect after oral administration.
• 72% of the drug undergoes first pass metabolism
B) TOPICAL ROUTE
• Local anesthetics are absorbed at differing rates after application to mucous membrane: in the tracheal mucosa,
absorption is almost as rapid as with intravenous (IV) administration.
• Wherever no layer of intact skin is present, topically applied local anesthetics can produce an anesthetic effect
eg::Sunburn remedies
• A eutectic mixture of local anesthetics lidocaine and prilocaine (EMLA) has been developed that is capable of providing
surface anesthesia of intact skin. EMLA is frequently used as an aid before venipuncture in needle-phobic patients
C) INJECTION:
• IV administration of local anesthetics provides the most rapid elevation of blood levels and is used clinically in the
primary management of ventricular dysrhythmias.
• Rapid IV administration can lead to significantly high local anesthetic blood levels, which can induce serious
adverse reaction
 DISTRIBUTION:
• Highly perfused organs (and areas), such as the brain, head, liver, kidneys, lungs, and
spleen, initially will have higher anesthetic blood levels than less highly perfused organs
• Skeletal muscle, although not as highly perfused as these areas, contains the
greatest percentage of local anesthetic of any tissue or organ in the body because it
constitutes the largest mass of tissue in the body
• The blood level of the local anesthetic is influenced by:
1. the rate at which the drug is absorbed into the CVS
2.the rate of distribution of the drug from the vascular compartment to the tissues (more rapid
in healthy patients than in those who are medically compromised [e.g., congestive heart
failure], thus leading to lower blood levels in healthier patients)
3. Elimination of the drug through metabolic or excretory pathways
• All local anesthetics readily cross the blood-brain barrier
• They also readily cross the placenta and enter the circulatory system of the developing
 METABOLISM (BIOTRANSFORMATION,
DETOXIFICATION )
• ESTER LOCAL ANESTHETICS are hydrolyzed in AMIDE LOCAL ANESTHETICS
the plasma by the enzyme pseudocholinesterase.. The • The primary site of biotransformation of amide local
rate at which hydrolysis of different esters occurs anesthetics is the liver
varies considerably
• the entire metabolic process occurs in the liver for
• Chloroprocaine, the most rapidly hydrolyzed, is the lidocaine, mepivacaine, etidocaine, and bupivacaine
least toxic
• Prilocaine undergoes primary metabolism in the liver,
• Tetracaine, hydrolyzed 16 times more slowly than with some also possibly occurring in the lung.
chloroprocaine, has the greatest potential toxicity
• •Articaine, a hybrid molecule containing both ester and
Procaine undergoes hydrolysis to p-aminobenzoic
amide components, undergoes metabolism in both the
acid (PABA) Allergic reactions that occur (rarely) in blood (primarily) and the liver. It has a shorter half life as
response to ester local anesthetic administration are some of its biotransformation occurs in blood.
usually related not to the parent compound (e.g.,
procaine) but rather to PABA, which is a major • relative contraindication -.Significant liver dysfunction,
metabolic product of many ester local anesthetics. heart failure (ASA class 4 or 5)
 EXCRETION:

• The kidneys are the primary excretory organ for both the local anesthetic and its metabolites
• Esters appear only in very small concentrations as the parent compound in the urine
because
they are hydrolyzed almost completely in the plasma.
a) Procaine appears in the urine as PABA (90%) with 2% unchanged.
b) Ten percent of a cocaine dose is found in the urine unchanged.
• Amides are usually present in the urine
a) less than 3% lidocaine
b) 1% mepivacaine, and
c) 1% etidocaine is found unchanged in the urine
 SYSTEMIC ACTIONS OF LA
• Central Nervous System
• Local anesthetics readily cross the blood-brain barrier
• Their pharmacologic action on the CNS is one of depression.
• low (therapeutic, nontoxic) blood levels, no CNS effects of any clinical significance have been noted. At
higher (toxic, overdose) levels the primary clinical manifestation is a generalized tonic-clonic convulsion
Cardiovascular System

• Local anesthetics have a direct action on the myocardium and peripheral vasculature.
• Local anesthetics produce a myocardial depression related to the local anesthetic blood level.
They decrease the electrical excitability of the myocardium, decrease conduction rate, and
decrease the force of contraction
• On peripheral vasculature: Increased local blood flow increases the rate of drug absorption, in
turn leading to decreased depth and duration of local anesthetic action, increased bleeding in
the treatment area, and increased local anesthetic blood levels.
• The primary effect of local anesthetics on blood pressure is hypotension. Procaine produces
hypotension more frequently and significantly than does lidocaine

Respiratory System
• They have a direct relaxant action on bronchial smooth muscle
• whereas at overdose levels, they may produce respiratory arrest as a result of generalized
CNS
depression. In general respiratory function is unaffected by local anesthetics until near-
 CLINICAL ACTION OF SPECIFIC AGENTS:
• Lidocaine (Xylocaine, Octocaine, Lignocaine):
• Lidocaine (diethyl-2,6-dimethylacetanilid) is the first non ester type of local anesthetic
compoundto be used in dentistry, having synthesized in 1943 by Lofgren.
• pH of plain solution = 6.5; with vasoconstrictor = 5 to 5.5
• Rapid onset of action – 2- 3min & half life = 1.6hrs
• Lidocaine diffuses readily through interstitial tissues and into the lipid-rich nerve, giving a
rapid onset of anesthesia.
• This agent is approximately two times as potent as toxic as procaine. Produces profound
anesthesia.
• Duration of action depends on the type of injection (for example, nerve blocks will have longer
duration than infiltration) and the amount of vasoconstrictor included in the solution.
• Allergy to this local anesthetic is extremely rare
 BUPIVACAINE (MARCAINE, SENSORCAINE)
• Chemistry: Bupivacaine (l-butyl-2', 6 '-pipecoloxylidine) is a white crystalline powder freely soluble in
95% ethanol and water and slightly soluble in chloroform or acetone.
• The pH is 4.5 to 6.5, and the p Ka is 8.1.
• The time of onset is comparable to the other amides, but the duration of action of pulpal anesthesia is
increased to 3 hours.
• Duration of soft tissue anesthesia following a major nerve block may extend to 12 hours.
 ARTICAINE

Potency 1.5 times that of lidocaine and 1.9 times that of procaine.
• Toxicity Similar to lidocaine and procaine.
• Excretion via the kidneys; approximately 5% to 10% unchanged, approximately 90% metabolites
• Articaine is the first and only anesthetic of the amide type to possess a thiophene ring as its lipophilic moiety.
• Articaine has been available in two formulations:
• 4 % with 1:100,000 - provides approximately 75 minutes of pulpal anesthesia
• 4 % with 1:200,000 - formulation, approximately 45 minutes.
• Side effects: Methemoglobinemia is a potential side effect of the administration of large doses of articaine
especially in intravenous routes and less in dental injections.
• Contraindications: Articaine is contraindicated in patients with idiopathic or congenital methemoglobinemia,
anemia, or cardiac or respiratory failure evidenced by hypoxia and the presence of a documented allergy to sulfur-
containing drugs.
 ANESTHETICS FOR TOPICAL APPLICATION
• The concentration of a local anesthetic applied topically is typically greater than
that of the injectable form of the local anesthetic. This higher concentration
facilitates diffusion of the drug through the mucous membrane.
• Many injectable local anesthetics are ineffective when applied topically
because the concentrations necessary to produce anesthesia via topical
application are high, with significantly increased overdose and local tissue
toxicity potential
• Cocaine Hydrochloride
• Used exclusively via topical application
• Onset of topical anesthetic action is quite rapid, usually occurring within 1 minute
• Cocaine is occasionally applied topically prior to surgical procedures by otolaryngologists and ophthalmologists. 

EMLA (Eutectic Mixture of Local Anesthetics)

• Composed of 2.5% lidocaine and 2.5% prilocaine. Emulsion in which the oil phase is a eutectic
mixture of lidocaine and prilocaine in a ratio of 1:1 by weight
• EMLA must be applied 1 hour before the procedure.
• EMLA is supplied in a 5- or 30-g tube
• USES: 1) provide surface anesthesia for intact skin. Like before painful procedures such as
venipuncture and other needle insertions.
2) routinely during circumcision, during leg ulcer débridement, and during gynecologic
procedures.
 CONTRAINDICATED :
• Congenital or idiopathic methemoglobinemia
• Children younger than 12 months who are receiving treatment with methemoglobin inducing agents
• patients with known sensitivity to amidetype local anesthetics or any other component of the product

• ORAQIX-The dental formulation of EMLA

• Application of the periodontal gel (Oraqix) to periodontal pockets produces an anesthetic effect
in 30 seconds
• Indications:
1. localized anesthesia in periodontal pockets during scaling and/or root planning
2. prosthodontics for pain management during intraperiodontal gingival retraction
3. provide palatal anesthesia before palatal needle penetration
LIDOCAINE
Available in two forms :
1. lidocaine base, which is poorly soluble in water, used as a 5% concentration
• indicated for use on mucous membrane, ulcerated, abraded, or lacerated tissue
• Lidocaine base is available as an ointment, patch, and solution in various dosage form
2. lidocaine hydrochloride- its water-soluble preparation, which is used as a 2% concentration. More
commonly used

TETRACAINE HYDROCHLORIDE

Tetracaine (3%) with the vasoconstrictor oxymetazoline has been shown to provide pulpal
anesthesia of maxillary non molar teeth when administered by aerosol mist.
 USE O F L O C A L ANAESTHETICS IN DENTISTRY

• To reduce pain
• In diagnosis: to find the location from which pain is originating
• To decrease hemorrhage: with agents containing vasoconstrictors
• In conjunction with sedation techniques: as an adjunct to nitrous
oxide analgesic
• As a vehicle for Calcium Hydroxide during intracanal medication
• Component of pulp devitalizer – Depulpin.
 CO M P O S I T I O N

2% Lidocaine Hydrochloride - Local Anaesthetic

Agent

• 1:80,000 to 1:1,00,000 Epinephrine -

Vasoconstrictor

• Sodium metabisulphate – Oxidising agent

• Methyl Paraben – Preservative

• Thymol – Antifungal

• Water – Solvent
 VASOCONSTRICTORS

Vasoconstrictors are added to a local anesthetic solution for the following reasons:

1.By constricting blood vessels, vasoconstrictors decrease blood flow (perfusion) to the site of
injection.
2. Absorption of the local anesthetic into the cardiovascular system is slowed, resulting in
lower anesthetic blood levels.
3. Lower local anesthetic blood levels decrease the risk of local anesthetic toxicity.
4. Higher volumes of the local anesthetic agent remain in and around the nerve
for
longer periods, thereby increasing the duration of action of most local anesthetics.
5. Vasoconstrictors decrease bleeding at the site of their administration and are
useful,
CLASSIFICATION
 SE L E C TIO N O F A
VASO C O NSTRIC TO R:
Length of the Dental Procedure Requirement for Hemostasis:
• Average duration of pulpal and hard tissue
• Epinephrine is effective in preventing or
anesthesia expected from commonly used local
anesthetics are: minimizing blood loss during surgical procedures.

-2% Lidocaine - 5 to 10 minutes; with • Vasoconstrictors used to achieve hemostasis must

adrenaline be deposited locally into the area of bleeding.
– 6 0 min
- 3 % Mepivacaine - 20 to 40 minutes
Medical Status of the Patient:
• Felypressin has minimum cardiovascular
stimulatory actions and is non dysrhythmogenic; it
is the recommended drug for cardiovascular risk
patients.
• Epinephrine should not be used as a
vasoconstrictor during general anesthesia when a
patient (in any high risk category) is receiving a
halogenated anesthetic (halothane, methoxyflurane,
SAFE DOSE
 EPINEPHRINE

Most potent and widely used vasoconstrictor in dentistry.

• Epinephrine as the acid salt is highly soluble in water.
• Slightly acid solutions are relatively stable if they are protected from air.
• Epinephrine acts directly on both alfa and beta-adrenergic receptors; beta effects predominate.
 ADVANTAGES O F LA OVER G A

• Safety especially in medically compromised patients

• Ease of administration

• Cost effective

• Good cooperation from the patient

• Normal patient physiology not altered

• Reduced bleeding during treatment

 REGIONAL ANAESTHESIA

(A) Topical Or Surface Anesthesia,

(B) Local Infiltration,
(C) Peripheral Nerve Block,
(D) Intervenous Regional Anesthesia (Bier Block),
(E) Epidural Anesthesia, And
(F) Spinal (Subarachnoid)Anesthesia.
 TECHNIQUES OF LOCAL ANESTHESIA
Local infiltration: Posterior Superior Alveolar Nerve Block, Tuberosity block,
zygomatic block
TECHNIQUES OF MAXILLARY ANESTHESIA

Middle superior alveolar Infraorbital nerve block (Anterior

nerve block superior alveolar nerve block):
TECHNIQUES OF MAXILLARY ANESTHESIA

Greater palatine nerve block Nasopalatine nerve block (incisive nerve

block, sphenopalatine nerve block):
(anterior palatine nerve block):
 MANDIBULAR NERVE BLOCK

1.Inferior alveolar nerve 2.Buccal nerve block 3. Gow-Gates mandibular nerve

block:
block
 MANDIBULAR NERVE BLOCK

VAZIRANI – AKINOSI CLOSED MENTAL NERVE BLOCK INCISIVE NERVE BLOCK

MOUTH TECHNIQUE
 LOCAL COMPLICATIONS

NEEDLE BREAKAGE
• Burning on
• Prolonged anesthesia or paresthesia injection
• Facial nerve paralysis • Infection
• Trismus
• Edema
• Soft tissue injury
• Hematoma • Sloughing of tissues
• Pain on injection
• Postanesthetic intraoral
lesions
NEEDLE BREAKAGE:
Causes:
• Unexpected movements by patients
• Sudden deflection of needle during injection
•Poor quality needle
•Bending
•Use of thinner needles Management:
•Instruct patient not to move
•Keep patient’s mouth open
•If fragment visible-removed with hemostat or Magill’s intubation forceps
• If invisible –surgeon’s attention is sought with the help of thorough radiological and clinical
examination.
• In deeper tissues- no attempt to remove.
Pain on injection: Causes: traumatic injection with blunt needle,
• rapid injection,
• needle with barbs
Burning sensation: Paresthesia:
Cause: Causes:
• pH of solution (Acidic), •trauma to nerve sheath, use of contaminated
•rapid injection, needle,
•contamination of cartridges with alcohol •hemorrhage around or into nerve sheath.
etc., •Other causes:
•solutions warmed to body temperature Inferior dental nerve lesion after
Prevention: endodontic traumatism can be the result of
•slow injection, physical trauma,
•proper storage at room temperature irritative chemical trauma or a
combination of both.
Management:
•usually resolved within 8 weeks without
treatment.
•Assurance to patient. If still persists,
advice
neurological management.
Trismus: Soft tissue injury:

Causes: Cause:
• trauma to blood vessel and muscles •self-inflicted,
especially in the infratemporal fossa, •common in children
•distention of tissues,
•low-grade infections, Prevention:
• hematoma formations, •cotton rolls placed between lips and teeth,
•contaminated LA solutions, •warn the patient and Guardian,
• multiple needle penetration, •watch – me stickers
• excess volumes deposited into a restricted
area Management:
Management: Analgesics,
antibiotics,
lukewarm saline rinses,
•hot moist towels for 20 min every hour lubricants like petroleum jelly
•warm saline rinse,
•anti-inflammatory drugs,
•if needed muscle relaxants,
Hematoma: Infection:

Causes: Causes:
• nicking of blood vessel, •contaminated needles,
•common with posterior superior alveolar nerve •poor oral hygiene
block.
Prevention:
Management: •proper sterilization protocols

•Immediate pressure packs, ice cold packs. Management:

• No heat to be applied for 4-6 hrs. •Antibiotics
•Then warm moist towels 20min every hour •Analgesic
after 1 day.
•This heat acts as an analgesic and increases rate
of resorption of blood elements. Discoloration
as a result of extravasation of blood and
swelling usually resolves over 7-14 days.
 FACIAL NERVE PARALYSIS:
Cause:
• introduction of LA into parotid during inferior alveolar nerve block especially.

Prevention:
• overinsertion of needle,
•contact with bone during inferior alveolar nerve block,

Management:
•assurance to patient, usually transient,
•resolves without residual effect,
•eye patch to the affected eye.
• Contact lenses should be removed until muscular movements return.
 SYSTEM IC C O M PL IC ATIO NS O F L A

1)Due to overdose
Causes of overdose:
• injection into blood vessel
• injection into a highly vascularized tissue
• inability of liver to detoxify the drug
To prevent overdose:
• Aspirate in 2 planes
• slow rate of injection
• Gels 5% should be applied carefully
2)Allergy:
• Methyl paraben - preservative in LA – common cause of allergy. Sodium bisulphite of
sodium metabisulphite
– common.
• Cross reactivity between local anaesthetics within ester or amide groups present.
• Skin test for allergy: primary mode of assessing allergy. 0.1ml of test solution into patient’s
forearm.
Signs & symptoms:
• Dermatological - Urticaria, angioedema
• Respiratory – bronchospasm, laryngeal edema
• Generalized anaphylaxis
• Management:
• Basic life support(BLS), adrenaline 1:1000, 0.3 ml subcutaneously or im,
hydrocortisone hemisuccinate iv or im (Efkerlin salts), oxygen therapy, anti
histaminics, bronchodilators.
 CONTRAINDICATIONS:
Absolute:
Known hypersensitivity of any of the contents of local anaesthetics.

Relative :
1. Abnormal bleeding tendency
• Anticoagulant therapy
• Thrombocytopenia

2. Compromised immune system

• HIV,cancer
• Chronic illness
• Rheumatoid arthritis etc.

3.Cardiovascular diseases
4.Kidney diseases
 DRUG INTERACTIONS

• Drugs can interfere with the action of one another at various points
• An example of an absorption interaction is the use of one drug to reduce the plasma concentration of
another; for example, the addition of epinephrine to lidocaine solutions delays the entry of the local
anaesthetic into the circulation:‘
• An example of a metabolic interaction is that between lidocaine and beta-adrenergic blocking drugs. The
metabolism of the local anaesthetic is reduced during concurrent therapy with beta-blockers as hepatic
blood flow is reduced by the latter.
Cardiovascular Drugs
• beta-adrenergic blocking drugs increase the toxicity of amide local anaesthetics (such as lidocaine,
prilocaine and bupivacaine) by decreasing hepatic blood flow and inhibiting liver enzymes.
• calcium-channel blockers increase the cardiotoxicity of the long acting local anaesthetic bupivacaine.
Antimicrobials :
• One of the side-effects of prilocaine is methaemoglobinaemia.
• This presents as cyanosis and is caused by the iron in haemoglobin being in the ferric rather than
the ferrous form, thus reducing its oxygen-carrying capacity.
• This hematological problem is also caused by other drugs such as sulfonamide antibacterials.

Benzodiazepines
• One such combination that is helpful is that between midazolam and lidocaine.
• The benzodiazepine reduces the central nervous system toxicity of the local anaesthetic, which is
useful if doses approaching the maximum recommended are approached.
• this benefit does not apply to all benzodiazepine/local anaesthetic combinations - for instance,
diazepam increases the serum levels of bupivacaine, increasing its toxicity.
 IMPLICATIONS OF LA IN ENDODONTICS:

HOT TOOTH
• The term “HOT TOOTH” refers to a tooth that is difficult to anaesthetize.
• Mandibular molars are frequently affected though other teeth are also
involved.
• Apprehensive patients have a reduced threshold to painful stimuli.
• Local release of nerve growth factor (NGF) in response to pulpitis adds a
further complication to the condition.
• With inflammation, the tetradotoxin sensitive sodium channels become
resistant and hence the LA becomes ineffective
 SEVEN-STEP CASCADE OF APPROACH HAS BEEN SUGGESTED TO DEAL
WITH HOT TOOTH
THE 7 STEPS ARE:

1)Gow-Gates mandibular block - Advantage of overcoming problems associated with accessory

sensory innervation of pulps from branches of the mandibular nerve such as the mylohyoid
nerve.

2) Inferior alveolar nerve block

3) Buccal & lingual infiltration

4) Intraseptal injection

5) Periodontal ligament injection-reaches the pulpal nerve supply by entering the cancellous bone
through natural perforations in the socket wall
• Advantage- smaller doses required,used in patiets with bleeding disathesis
• Disadvantage- chances of bacteremis,damage pdl tissues,may enter the circulation

6) Intraosseous injection- Stabident, X-Tip

 LOCAL ANAESTHESIA FOR ENDODONTIC SURGERIES

• Based on the location and duration of the procedure, the choice and
technique of Local anaesthetic is made.

• A second LA injection following wearing out of the effect of the first LA

injection is often less effective due to a phenomenon called
Tachyphylaxis.

• Hence a longer acting drug such as Bupivacaine is injected for a longer

period of anaesthesia.
 LOCAL ANESTHESIA DELIVERY SYSTEM

Although Cook invented the modern dental syringe nearly 150 years ago, it is only
recently that anesthetic delivery systems have seen major innovations. Although the
traditional aspirating syringe still is the most common method by which local
anesthetics are administered, newer technologies have been developed that can assist
the dentist in providing enhanced pain relief with reduced injection pain and minimum
adverse effects.

Some of the delivery system are - VIBROTACTILE DEVICES, COMPUTER-

CONTROLLED LOCAL ANESTHETIC DELIVERY (CCLAD) SYSTEMS, JET
INJECTORS, SAFETY DENTAL SYRINGES AND DEVICES FOR INTRA-
OSSEOUS (IO) ANESTHESIA.
VIBROTACTILE DEVICES

1) VIBRAJECT

It is a small battery-operated attachment that snaps on to the standard dental syringe. It

delivers a high-frequency vibration to the needle that is strong enough for the patient to feel.
2) DENTALVIBE

Another system that uses vibration diversion based on the pain gate theory is recently
introduced DENTALVIBE (BING Innovations LLC, Crystal Lake, IL, USA). It is a cordless,
rechargeable, hand held device that delivers soothing, pulsed, percussive micro-oscillations to
the site where an injection is being administered.
Its U-shaped vibrating tip attached to a microprocessor-controlled Vibra-Pulse motor
gently stimulates the sensory receptors at the injection site, effectively closing the neural pain
gate, blocking the painful sensation of injections. It also lights the injection area and has an
attachment to retract the lip or cheek.
3)ACCUPAL

The Accupal (Hot Springs, AR, USA) is a cordless device that uses both vibration and
pressure to precondition the oral mucosa. Accupal provides pressure and vibrates the injection site
360° proximal to the needle penetration, which shuts the "pain gate," according to the
manufacturer.

After placing the device at the injection site and applying moderate pressure, the unit light up
the area and begins to vibrate. The needle is placed through a hole in the head of the disposable tip,
which is attached to the motor. It uses one AAA standard battery.
COMPUTER-CONTROLLED LOCAL ANESTHETIC DELIVERY SYSTEMS

WAND/COMPUDENT SYSTEM

This system enabled operator to accurately manipulate needle placement with fingertip accuracy
and deliver the LA with a foot-activated control.
The lightweight handpiece is held in a pen-like
grasp that provides the user with greater tactile
sensation and control compared to a traditional syringe.

The available flow rates of LA delivery

are controlled by a computer and thus remain
consistent from one injection to the next.
JET INJECTORS

1)SYRIJET

The Syrijet (Keystone Industries [aka Mizzy], Cherry Hill, NJ, USA) has been on the market
for nearly 40 years and has had some minor improvements over the years. Some good features of
the device is that it accepts the standard 1.8 mL cartridges of LA solution (thereby ensuring sterility
of the solution), permits the administration of a variable volume of solution from 0 to 0.2 mL, and
is completely autoclavable.
2)MED-JET H III
MED-JET (Medical International Technologies, Montreal, QC, Canada) has been launched in 2011
with the manufacturer's claim that medication being injected with the device is directed through
a small orifice 7 times smaller than the smallest available needle in the world. This extremely
small stream of liquid under pressure pierces and then the remainder of the dose will be
dispersed into the desired layer of tissue.
SAFETY DENTAL SYRINGES

1)ULTRA SAFETY PLUS XL SYRINGE

The Ultra Safety Plus XL syringe (Septodont, Lancaster, PA, USA) has a sterile disposable protective shield that
is fitted with a dental needle into which anesthetic carpules are placed. The plunger assembly is reusable and
autoclavable. The Ultra Safety Plus XL syringe provides protection from the needle because the needle is covered both
before and after injection, and the needle does not have to be disassembled prior to disposal, which further protects the
worker who is cleaning the dental tray.
2)ULTRASAFE SYRINGE
The UltraSafe syringe (Safety Syringes Inc, Carlsbad, CA, USA) is a disposable syringe and needle with a
transparent, plastic syringe barrel, which has a retractable needle sheath. Providers can view the carpule contents
through the clear plastic syringe barrel; this is further helpful in aspiration and in viewing anesthetic content, and also
protects the provider from injury because the needle is covered before and after injection

The difference between this type of syringe and the Ultra Safety Plus XL syringe is that in the UltraSafe
syringe the entire assembly is disposable and is not autoclavable.
3)REVVAC™ SAFETY SYRINGE

RevVac safety syringe operates the same as a standard conventional syringe. No

additional training, skills, or procedures are necessary. It works on a simple concept;
where retracting and pressing the plunger creates a robust vacuum at the time of use.
When the plunger reaches the bottom, after all medicine is administered, a further push
on the plunger breaks the seal, and the needle retracts into the plunger. The syringe
cannot be reused.
DEVICES FOR INTRA-OSSEOUS ANESTHESIA

1)STABIDENT

The advantages of the product are that it is relatively inexpensive and can be used with equipment already
existing in a dental office: A slow-speed hand piece with a latch contra-angle for the perforator and a standard
dental anesthetic syringe for the needle. The main disadvantage of the device is that the perforation needs to be
made in a reasonably accessible and visible location in the attached gingiva distal to the tooth to be anesthetized.
If the penetration zone is located in alveolar mucosa that moves once the perforator is withdrawn, it can be
extremely difficult to locate the perforation site with the anesthetic needle.
2)INTRAFLOW

The IntraFlow (Pro-Dex Medical Devices, Irvine, CA, USA) device is essentially a dental handpiece
equipped with an injection system built into the body. The biggest advantage of the IntraFlow anesthesia
system is that it allows entry into the penetration zone, injection, and withdrawal in one continuous step,
without the need to relocate the perforation site. This single-step method can be helpful in penetration zones
that are difficult to visualize or access, such as the second and sometimes the first molar areas, or where there
is horizontal bone loss or a limited band of attached gingiva in the desired penetration zone.
 C O N C LUSIO N

• Adequate knowledge on the anatomy and physiology of nerve conduction,

various techniques of anaesthesia is mandatory to achieve good anaesthesia of
the pulp and soft tissues.

• Recent advancements in drug delivery systems has made dental

injections less painful.
 REFEREN C ES

• Handbook of local anaeshesia. Seventh edition.: Stanley F Malamed

• Bennett CR : Monheim’s local anesthesia and pain control in dental
practice, ed 5 , St Louis , Mosby
THANK
YOU!