Local anesthesia in dentistry

LOCAL ANESTHESIA IN
DENTISTRY
Guided by Presented by
Dr. P.SURESH,MDS. CH.SUMA PRIYANKA
Professor & HOD 1st year PG
Dept. of Periodontics Dept. of Periodontics

CONENTS:
Definition
Historical Background
Local Vs General anesthesia
Methods of inducing LA
Electro Physiology of Nerve Conduction
Electro Chemistry of Nerve Conduction
Where do LA work?
Classification of local anesthetic agents
How LA works??
Composition of LA

Pharmacology of Local Anesthetic agents
Armamentarium
Techniques for Maxillary & Mandibular anesthetic techniques
Supplemental Anesthetic techniques
LA in patients with Systemic disorders
Complications of LA
Recent advances in LA.
Conclusion
Bibliography

DEFINITION:
Local anesthesia has been defined as “a loss of sensation in a circumscribed area of the body
caused by depression of excitation in nerve endings or inhibition of the conduction process in
peripheral nerves”.
(Stanley F. Malamed)
“Local anesthesia is the temporary loss of sensation or pain in one part of the body produced
by a topically applied or injected agent without depressing the level of consciousness.
(Steven Schwartz)

HISTORICAL BACKGROUND:
• In Peru, the ancient Incas were believed to had
used the leaves of Coca plant as a local
anesthetic in 1532.
• Cocaine was isolated in 1860 by “Niemann”
and 1st used as a local anesthetic in 1884 by
“Karl Koller”.

• The search for a less toxic and less addictive
substitute led to the development of the
amino-ester LA ‘Stovaine’ in 1903 and
‘Procaine’ in 1904.
• Procaine was 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 in 1943 by “Lofgren”.
• Anesthetic properties in 1949 & clinical use by
“T. Gordh”.

• Intravenous regional anesthesia was 1st
described by “August Bier” in 1908.
• Epidural anesthesia by a caudal approach had
been known in the early 20th century.
• Lumbar injection was developed in 1921
when “Fidel pages” published his article
“Anestesia metamerica”.

LOCAL Vs GENERAL ANESTHESIA:
GENERAL ANESTHESIA LOCAL ANESTHESIA
Site of action CNS Peripheral nerves
Area Whole body Restricted areas
Consciousness Lost Un altered
Preferential use Major surgery Minor surgery
Use in un-cooperative patients Possible Not possible
In Poor health patients Risky Safer
Care for vital functions Essential Not needed

ADVANTAGES OF LA OVER GA:
Safety (intra-operatively & post-operatively)
Ease of administration
Less cost
Co-operation of the patient
Reduced bleeding time

METHODS OF INDUCING LA:
Mechanical trauma (Compression of tissues)
Low temperature
Anoxia
Chemical irritants
Neurolytic agents
Chemical agents like Local Anesthetics.

PROPERTIES OF LA:
Not be irritating to the tissues
Not cause any permanent alteration of nerve structure
Systemic toxicity should be low
Must be effective regardless whether it is injected or topically applied
Time of onset should be as short as possible
Duration of action must be long.

Should have potency sufficient to give complete anesthesia without the use of harmful
concentration solutions.
Should be free from producing allergic reactions.
Should be free in solution & relatively undergo biotransformation in the body.
Should be either sterile or be capable of being sterilized by heat without deterioration.

ELECTROPHYSIOLOGY OF NERVE CONDUCTION:
• A nerve possess a “Resting potential” of -70mV that exists across the nerve membrane, produced
by differing concentrations of ions on either side of the membrane.
• The interior of the nerve is negative relative to the exterior.

STEP1: A stimulus excites the nerve, leading to the following events:
a. An initial phase of “Slow depolarization” the electrical potential within the nerve becomes
slightly negative. (-50mV to -60mV).
b. When the falling electrical potential reaches a critical level, an extremely “Rapid phase of
depolarization” results. This is called “Threshold potential” or “Firing threshold”.

C. This phase of rapid depolarization results in a reversal of the electrical potential across the nerve
membrane. The interior of the nerve is now electrically positive relative to the exterior (+40mV).

STEP2: After these steps of depolarization, “Re-polarization” occurs.
The electrical potential becomes more negative (-60mV to -90mV) inside the
nerve cell relative to outside until the original resting potential of -70mV is again achieved.

ELECTROCHEMISTRY OF NERVE CONDUCTION:
• In resting state, nerve is slightly permeable to Na+ ions & freely permeable to K+ & Cl- ions.
ION INTRACELLULAR (m
eq/L)
EXTRACELLULAR
(m eq/L)
RATIO
Potassium 110-170 3-5 27:1
Sodium 5-10 140 1:14
Chloride 5-10 110 1:11

ABSOLUTE REFRACTORY PERIOD:
Immediately after a stimulus has initiated an action potential, a nerve is unable, for
a time, to respond to another stimulus regardless of its strength.
RELATIVE REFRACTORY PERIOD:
Here, a new impulse can be initiated, but only by a stimulus stronger than normal.

IMPULSE PROPAGATION:
• After initiation of an action potential by a stimulus, the impulse must move along the surface of
the axon.—
• The stimulus disrupts the resting membrane equilibrium of the nerve membrane, with interior of
the cell changing from –ve to +ve, and the exterior changing from +ve to –ve.
• This new electrical equilibrium produces local currents that begin to flow between the
depolarized segment and the adjacent resting areas.
• The local currents flow from +ve to –ve, extending for several mm along the nerve membrane.

IMPULSE SPREAD:
Propagated impulse travels along the nerve membrane towards the CNS.
UNMYELINATED NERVE:
• Long cylinder with a high- electrical resistance cell membrane surrounding a low-conducting core of
axoplasm.
• Produce a rapid decrease in density of current within a short distance of depolarized segment.
• Spread of an impulse is characterized as a relatively slow, forward-creeping process.
• Conduction rate is 1.2 m/sec.

MYELINATED FIBRES:
• Impulse spread within a myelinated nerves differs from un-myelinated, because of the layer of
insulating material separating the intracellular and extracellular charges in myelinated fibers.
• Farther apart are the charges, the smaller is the current necessary to charge the membrane.
• Local currents thus can travel much farther in a myelinated nerve than in an un-myelinated nerve.
• Impulse conduction in myelinated nerves occurs by means of current leaps from node to node,
termed as “Saltatory conduction”.
• Conduction rate is 14.8 m/sec-120 m/sec.

Where do LA work??
i. Acetyl choline theory
ii. Calcium displacement theory
iii. Surface charge (repulsion) theory
iv. Membrane expansion theory
v. Specific receptor theory

CLASSIFICATION OF LOCAL ANESTHETICS:
ACC. TO BIOLOGICAL SITE & MODE OF ACTION:

MODE AND ACTION OF LOCAL ANESTHETICS:
Local anesthetics interferes with the excitation process in a nerve membrane in one or more
of the following ways:
i. Altering the basic resting potential of the nerve membrane.
ii. Altering the threshold potential (firing level)
iii. Decreasing the rate of depolarization
iv. Prolonging the rate of repolarization

HOW LA WORKS??
• Calcium ions, which exists in bound forms within the cell membrane, are thought to exert a
regulatory role on the movement of Na ions across the nerve membrane.
• Release of bound Ca from the ion channel receptor site may be the 1ry factor responsible for
increased Na permeability of the nerve membrane. This represents the 1st step in nerve membrane
depolarization.

Displacement of Ca ions from Na channel receptor site
Binding of LA molecules to this receptor site
Blockade of Sodium channel
Decrease in Sodium conductance
Depression at the rate of electrical depolarization
Failure to achieve the threshold potential
Lack of development of action potential
CONDUCTION BLOCKADE

HENDERSON-HASSELBACH EQUATION:
Determines how much of LA will be in a non-ionized vs ionized state, based on
tissue pH and anesthetic Pka.
• Injectable LA’s are weak bases (Pka-7.5-9.5).
• When a local anesthetic is injected into tissue, it is neutralized and a part of the ionized form is
converted into non-ionized form. The non-ionized base is what that diffuses into the nerve.
• Hence, if the tissue is infected, PH is lower (more acidic) and according to the HH equation, there
will be less of the non-ionized form of the drug to cross into the nerve (rendering the LA less
effective).
pH = pKa + log (Conjugate base)/ (Acid)

FACTORS AFFECTING LOCAL ANESTHETIC ACTION:
FACTOR ACTION AFFECTED DESCRIPTION
Pka Onset Pka rapid onset of
action
Lipid solubility Anesthetic property lipid solubility 
anesthetic property
Protein binding Duration Protein binding 
duration of action
Non-nervous diffusibility Onset diffusibility  time of
onset
Vasodilator activity Anesthetic potency &
duration
vasodilator activity 
anesthetic potency &
duration.

COMPOSITION OF LA CARTRIDGE:
• Local anesthetic agent - Xylocaine/Lignocaine 2%
• Vasoconstrictor - Adrenaline 1:80,000
• Reducing agent – Sodium metabisulphite
• Preservative – Methyl paraben, Capryl hydrocuprienotoxin
• Fungicide – Thymol
• Vehicle – Distilled water , Nacl.

VASOCONSTRICTORS:
Epinephrine
Nor-epinephrine
Levonordefrin
Phenylephrine.
MOA: Attach to and directly stimulate adrenergic receptors.
Acts indirectly by provoking the release of endogenous catecholamines from
intranueronal storage sites.

Constricts blood vessels and decreases blood flow to the site of injection.
Absorption of LA into the blood stream is slowed, producing lower levels in blood.
Decreased risk of overdose.
Increasing the duration of action of LA.
Minimizes bleeding at the site of administration.

CONTRA-INDICATIONS OF VASOCONSTRICTORS:
• Hypertension
• Arteriosclerosis or other cardiac diseases
• Cerebro - vascular insufficiency
• Uncontrolled Diabetes mellitus.
DOSAGE:
Healthy pt – 0.2mg
Cardiac pt – 0.04mg

• Vasoconstrictors are unstable in solution and may oxidize especially on prolonged exposure to
sunlight which results in turning of the solution brown indicating that the solution must be
discarded.
• To overcome this, a small quantity of reducing agent is added – competes for the available
oxygen, increasing the shelf life of the solution.

PHARMACOLOGY OF LA AGENTS:
Ester i. An aromatic, lipophilic group
Local anesthetic agent ii. An intermediate chain containing ester / amide linkage
Amide iii. A hydrophilic group.

ABSORPTION:
• When injected, LA agents exert a pharmacological action on blood vessels in the area.
• All LA’s possess a degree of vasodilation except “Cocaine”, the only local anesthetic that
consistently produces vasoconstriction.
• Initial action of cocaine is vasodilation, which is followed by an intense and prolonged
vasoconstriction.

ORAL ROUTE:
Except Cocaine, all are poorly absorbed. Most LA’s esp. Lidocaine undergo hepatic 1st pass
metabolism after oral administration.
TOPICAL ROUTE:
Absorbed at differing rates after application to oral mucosa. In
Tracheal mucosa – almost as rapid as i.v
Pharyngeal mucosa – slower
Esophageal/ bladder mucosa – still slower.
• A Eutectic mixture of local anesthetics (EMLA) has developed that is able to provide surface
anesthesia of intact skin.

INJECTION ROUTE:
Rate of uptake after parenteral administration is related to both Vascularity of injection site &
Vaso activity of the drug.
DISTRIBUTION:
Once absorbed into blood, LA’s are distributed throughout the body to all the tissues.
B Slow
L
Site of injection O
O Rapid
D
FAT
MUSCLE
BRAIN
HEART
LUNGS
LIVER

• Skeletal muscle, though not as highly perfused as these areas, it contains the greatest % of LA of
any tissue or organ in the body as it constitutes the largest mass of tissue in the body.
• The blood level of LA is influenced by following factors:
i. Rate at which the drug is absorbed into CVS.
ii. Rate of distribution of drug from vascular compartment to the tissues.
iii. Elimination of drug through excretory pathways.
All LA’s readily cross BBB & Placenta.

METABOLISM:
ESTERS: hydrolyzed in plasma by “Plasma Psuedocholinesterase”.
• ‘Chlorprocaine’ is most rapidly hydrolyzed  least toxic.
• ‘Tetracaine’ hydrolyzed 16 times more slowly than chlorprocaine, hence has the greatest potential
toxicity.
• ‘Procaine’ undergoes hydrolysis to PABA, which is excreted unchanged in urine, and to diethyl amine
alcohol , which undergoes further biotransformation before excretion.
• Allergic reactions that occur in esters are due to PABA.
• App. 1 of every 2800 persons has an atypical form of Psuedocholinesterase which causes an inability
to hydrolyze esters. Its presence leads to a prolongation of higher LA in blood and increased potential
for toxicity.

AMIDES:
• More complex than esters.
• 1ry site is liver.
• ‘Prilocaine’ undergoes 1ry metabolism in liver, with some possibly in lungs.
• App. 70% of a dose of injected lidocaine undergoes in normal liver function.
• Patients with lower than usual hepatic blood flow ( htn, CHF) or poor liver function (Cirrhosis) are
unable to bio-transform amides at a normal rate leading to increased blood levels  increased
toxicity.
• Biotransformation products of certain LA’s can possess significant clinical activity if they are
increased in blood.
Eg; Methemoglobinemia by Prilocaine

EXCRETION:
• Kidneys are the 1ry excretory organs.
• ‘Procaine’ appears in urine as PABA (90%) & 2% unchanged.
• 10% of Cocaine is found unchanged in urine.
• Amides are present in urine as a parent compound in a greater % than esters.

ARMAMENTARIUM:
i. Needles
ii. Cartridges containing anesthetic solutions
iii. Syringes.

NEEDLES:
Should range from 20-25 gauge and from ½ - 4 inches in length.
• Needle that is used for administration of LA is divided into 5 segments.
A. Bevel
B. Shank
C. Hub
D. Syringe adaptor
E. Syringe end of the needle.

GAUGE:
Denotes the diameter of the lumen of the shank.
Generally, 25 or 27 gauge needles are used in dentistry. Higher gauge denotes the smaller diameter
of the shaft.
20 gauge – 0.81mm diameter
27gauge – 0.45mm diameter.
30gauge – 0.35mm diameter

LENGTH:
Measured from hub to the point of bevel.
• Usually dental needles are 
Long (32-40mm)
Short (20-25mm)
Extra-short (15mm)

RECOMMENDATIONS FOR NEEDLE UTILIZATION:
Sterile needle should be used.
If multiple injections are to be administered, needles should be changed after 3-4 insertions in a
patient.
Must ever be used on more than one patient.
Should not be inserted into tissue to their hub to allow for easy retrieval, if breaks.
To change a needle direction while it is still in tissues, withdraw the needle almost completely
then change direction..
Never force a needle against resistance (bone) as it can increase the chance of breakage.
Do not bend needles except for intra-pulpal injections.
Should remain capped until used and then re-capped immediately after injection.
Should be discarded and destroyed after use.

CARTRIDGES:
Cartridge is a glass tube sealed at one end by a rubber stopper and the other end is sealed
by an Aluminum cap over rubber diaphragm.
• COMPONENTS i) Cylinder
ii) Plunger
iii) Diaphragm
• Store them in a cartridge dispenser and the wipe the rubber diaphragm with 91% isopropyl alcohol
or 70% ethyl alcohol.

COMPONENTS:
i. Needle adaptor
ii. Piston with harpoon
iii. Syringe barrel
iv. Finger grip
v. Thumb ring.

ADA criteria for acceptance of LA syringes:
Durable and re-sterilizable or packed in a sterile container (if disposable)
Accept a wide variety of cartridges and needles of different manufacturers (Universal use).
Inexpensive, light weight, and simple to use with one hand.
Provide effective aspiration and the blood be easily observed in the cartridge. The incidence of
positive aspiration may be as high as 10% - 15% in some injection techniques.

INJECTION PROCEDURE:
• Sterile the cartridge by 70% alcohol and then thaw to body temperature by water.
• Bevel of the needle towards bone.
• Syringe should contain no air.
• In critical areas with neighboring blood vessels, use aspiration syringe.
• Slow injection.
• The site of injection should be dis-infected.
• Stretch the tissues on injection.
• Follow shortest way inside tissue.
• Never bend to change direction.

TECHNIQUES FOR MAXILLARY ANESTHESIA:
Supra-periosteal injection
Posterior Superior Alveolar nerve block
Middle Superior Alveolar nerve block
Anterior Superior Alveolar nerve block
Maxillary nerve block
Greater palatine nerve block
Nasopalatine nerve block
Anterior Middle Superior Alveolar nerve block.

TECHNIQUES FOR MANDIBULAR ANESTHESIA:
Inferior Alveolar Nerve Block
Buccal nerve block
Mandibular nerve block
Mental nerve block
Incisive nerve block.

SUPRA-PERIOSTEAL INJECTION: 0.6ml/20 secs

POSTERIOR SUPERIOR ALVEOLAR NERVE BLOCK: 0.9-1.8ml for 30-60secs

ANTERIOR MIDDLE SUPERIOR ALVEOLAR NERVE BLOCK:
0.5ml/min

GREATER PALATINE NERVE BLOCK: 0.45-0.5ml/30secs

NASOPALATINE NERVE BLOCK: 0.45ml/15-30secs

INFERIOR ALVEOLAR NERVE BLOCK: 1.5ml/min

MENTAL NERVE BLOCK: 0.6ml/20secs

SUPPLEMENTAL ANESTHETIC TECHNIQUES:
Intra - Osseous technique
Intra - Ligamentary technique
Intra – Pulpal technique
Topical anesthesia

INTRA – LIGAMENTARY TECHNIQUE:
• Also known as “Periodontal ligament injection”.
• “The most Universal of all the supplemental injection techniques”.
• Usually administered when IANB is inadequate or ineffective.
• Indicated for:
i. Single tooth anesthesia
ii. Low anesthetic dose
iii. Contra-indication for nerve blocks
iv. Presence of systemic health problems.

INJECTION METHODOLOGY:
PDL provides an accessible route to the Cancellous bone, and the anesthetic reaches
the pulpal nerve via natural perforation of intraoral bone tissue.
27 or 30 gauge Ultra-short needle
Inserted along the long axis , at 30-degree angle
Orient bevel towards the root.
Deposit 0.2ml per root, over 20 secs.

Significant resistance is experienced when the needle reaches between the root and crestal bone.
 Slower than other injections as there is pressure build-up from the anesthetic administration.
Not recommended for patients with active periodontal inflammation.
Not be administered at tooth sites with 5mm or more of periodontal attachment loss.

TOPICAL ANESTHESIA:
Acts on the peripheral nerves and reduce the pain sensation at the site of
application.
• In dentistry, they are used to control local pain caused by-
i. Needling
ii. Placement of orthodontic bands
iii. Scaling & root planing
iv. Vomiting reflex
v. Oral mucositis
vi. Rubber dam placement
Contain Lidocaine or Benzocaine as active ingredients and are used in the form of
solutions, creams, gels, and sprays.

• Generally, applied by after drying the mucous
membrane or skin where the anesthesia will
be administered by spraying or using a cotton
swab to apply the minimal amount.
• Duration of action is about 10 minutes.

HURRIPAK PERIODONTAL ANESTHETIC KIT:
• A 20% Benzocaine solution that is sold as a needle-free periodontal anesthetic kit.
• The product comprises of a plastic syringe (3 ml) and disposable plastic tips , which are inserted deep
within the gingival sulcus.
• The onset of action is 30 seconds and duration of action is approximately 15 minutes.
• Fifteen minutes is generally not enough time for performing procedures in adults, so re-
administration of the solution, infiltration anesthesia, or periodontal ligament anesthesia using
needle injections may be needed.

CETACAINE TOPICAL ANESTHETIC:
• Contains 14% Benzocaine, 2% Butamben, and 2% Tetracaine-hydrochloric acid and is used for
controlling local pain in all mucous membranes.
• The anesthetic kit is comprised of the solution, a syringe, and applicator tip that enables access to the
periodontal pocket.
• The solution may be applied using a cotton swab or microbrush.

ORAQIX SUBGINGIVAL ANESTHETIC:
• In 2004, the FDA approved Oraqix for dental use.
• Oraqix contains 2.5% Lidocaine and 2.5% Prilocaine and is packaged with 20 cartridges and tips.
• It is a non-injectable gel anesthetic that is administered by insertion into the gingival sulcus, where it
produces its anesthetic effects to enable deep scaling and root planing.
• It has been reported that Oraqix is also effective for application of orthodontic bands.

EMLA:
Widely used for topical anesthesia to treat lacerations and lumbar punctures.
2.5% Lidocaine + 2.5% Prilocaine
Onset of action depends on blood supply of the area.
Max. depth of anesthesia is 5mm and can be achieved
in 120 mins.
Should be given 1-2mg at-least 1hour before the
procedure for an area of 10sq.cm

Studies have shown that analgesic effect of EMLA for periodontal probing and scaling is more than 5%
Prilocaine ointment.
Study of Hassio showed no significant difference between 10% Lidocaine spray and
EMLA for topical anesthesia of gums.

LMX: *Consists of liposomal capsules containing Lidocaine.
*Given 1-2mg 30 mins before surgical intervention for an area of 10sq.cm
In a study in 2002, liposomal capsules of Ropivacaine were compared to EMLA for
topical anesthesia of palatal mucosa during needle entrance into the tissues in which EMLA was
significantly more successful than encapsulated Ropivacaine.

LET:
4% Lidocaine + 0.1% epinephrine + 5% Tetracaine.
• Often used to repair lacerations in children and because of the presence of epinephrine, this drug
should not be used in extremities such as fingers, ears and nose.
• Should be given on the area 20 mins before procedure and lasts for 40 mins.
MICRO-PARTICULATE FORMULATIONS:
Various drugs and combinations are added to local anesthetic drugs to increase the duration
of anesthesia and to reduce the side effects.
Eg; Addition of Dexamethasone to lipid-protein-sugar particles containing Ropivacaine can be
used for chronic facial pain or to facilitate physiotherapy in muscle dysfunction.

TAC:
Combination of 4-11% Cocaine , 0.025-0.05% Epinephrine & 0.25-0.5% Tetracaine.
• Begins to work in 10-15 mins and has a duration of 15-25mins.
• Used to treat lacerations but has complications like HTN, Seizures & Systemic toxicity.

LOCAL COMPLICATIONS:
i. Needle breakage
ii. Prolonged anesthesia or paresthesia
iii. Facial nerve paralysis
iv. Trismus
v. Soft tissue injury
vi. Hematoma
vii. Pain on injection
viii. Burning on injection
ix. Infection
x. Edema
xi. Sloughing of tissues

NEEDLE BREAKAGE:
CAUSES:
• Unexpected movement of the patient
• Small needle size
• Bent needles
• Defective needles.
PREVENTION:
Use large needles
Use long needles for deep injections
Never insert to hub
Redirect only when adequately withdrawn.

PROLONGED ANESTHESIA OR PARASTHESIA:
CAUSES:
• Trauma to nerve
• Neurolytic agents (Alcohol, Phenol)
• Intra-neural injections
• Hematoma
PREVENTION:
• Careful injection techniques

FACIAL NERVE PARALYSIS:
CAUSES:
• Anesthesia of peripheral facial nerve branches
PREVENTION:
• Bone contact when injecting
• Avoid over penetration
• Avoid arbitrary injection.
MANAGEMENT:
• Re-assure patient
• Cornea care
• Defer dental care

TRISMUS:
CAUSES:
• Trauma to muscle or blood vessels
• Contaminated anesthetic solutions
• Hemorrhage
• Infection
• Excessive anesthetic volume
PREVENTION:
• Sharp needles
• Proper care & handling of cartridges
• Aseptic technique & clean injection site
• Atraumatic insertion
• Minimal injection &volume.

MANAGEMENT:
• Examination
• Passive ROM therapy
• Analgesics
• Heat
• Muscle relaxants.

SOFT TISSUE INJURY:
CAUSE:
• Self-inflicted trauma to the lips & tongue is more common.
• Seen in young children , in mentally or physically disabled adults or older patients.
PREVENTION:
• LA of appropriate duration should be selected.
• A cotton roll can be placed between lips and teeth.
• Warn the patient against eating, drinking hot fluids and biting on lips to test for anesthesia.
MANAGEMENT:
• Analgesics
• Antibiotics
• Lukewarm saline rinses to decrease any swelling
• Petroleum jelly or other lubricants to cover lip lesion & minimize irritation.

HEMATOMA:
Effusion of blood into extravascular spaces.
• Vessels commonly associated are-
a) Pterygoid plexus of veins
b) Posterior superior alveolar vessels
c) Inferior alveolar vessels
d) Mental vessels.
PREVENTION:
• Follow basic principles of atraumatic injection technique
• Use a short needle for PSA block.
MANAGEMENT:
 Apply direct pressure immediately
 Once bleeding has stopped, discharge patients with instructions.
 Apply ice intermittently to the site for 6 hours
 Do not apply heat for atleast 6hrs
 Use analgesics

PAIN ON INJECTION:
CAUSES:
• Dull needles
• Rapid deposition of solution
• Needle with barbs
• Careless technique
PREVENTION:
• Careful technique
• Sharp needles
• Topical anesthetic
• Slow injections
• Room temperature solutions.

BURNING ON INJECTION:
CAUSES:
• pH of solution
• Rapid solution
• Contamination
• Warmed solutions.
i. LA with vasoconstrictor are acidic because of the preservative. This acidity can cause the
anesthetic to burn when it is injected into tissues.
ii. If cartridges are immersed in sterilizing solutions and solution seeps into the cartridge , the
sterilizing solutions can cause a burning sensation upon injection.
iii. No treatment is needed.

INFECTION:
CAUSES:
• Needle contamination
• Improper handling of armamentarium
• Infection on injection site
• Improper handling of tissue
PREVENTION:
• Disposable needles
• Proper care of equipment
• Aseptic technique
MANAGEMENT:
• Usual sign is trismus
• Antibiotics

EDEMA:
CAUSES:
• Trauma during injection
• Infection
• Allergy
• Hemorrhage
• Injection of irritating solutions
PREVENTION:
• Properly care for and handle the local anesthetic armamentarium
• Use atraumatic injection technique
• Complete adequate medical evaluation of the patient

SLOUGING OF TISSUES:
Prolonged irritation or ischemia of gingival soft tissues may lead to epithelial desquamation & sterile
abscess.
EPITHELIAL DESQUAMATION:
• Application of a topical anesthetic to the gingival tissues for a prolonged period
• Heightened sensitivity of the tissues to either topical or injectable LA
• Reaction in an area where a topical anesthetic has been applied.
STERILE ABSCESS:
• Secondary to prolonged ischemia resulting from the use of LA with vasoconstrictor.
• Usually develops on the hard palate
PREVENTION:
• Use topical anesthetics as recommended
• When using vasoconstrictors, do not use overly concentrated solutions.

SYSTEMIC COMPLICATIONS:
OVERDOSE:
• High drug concentration(>2%) , the absence of vasoconstrictors,
high – speed injection and the vascularity of the injection area can
increase the risk of overdose.
• Aspiration in at-least 2 planes before the injection, slow injection ,
dosage adjustment and review of the patients age , weight ,
diseases and medications can reduce or prevent the risk of overdose.
• If the symptoms of overdose occur, following protocol must be followed-
P - Position
A - Airway
B - Breathing
C - Circulation
D – Definitive cure

ALLERGY:
• Occurs commonly due to PABA , in ester drugs.
• Allergy to an amide drug doesn’t prevent the use of other amides as there is no cross – sensitivity
• If there is sensitive reaction to both types, Diphenhydramine ( 0.5 – 1%) should be used.
• 0.1-0.5ml of 1:1000 Epinephrine injection should be given at the base of the tongue.

METHAMOGLOBINEMIA:
Occurs due to the oxidation of Fe atoms in Hb by drugs like Prilocaine that causes a defect in the
transportation of oxygen and leads to cyanotic conditions in patients 1-3 hrs after the injection of
anesthesia.
Dyspnea , Tachycardia may be seen
 Patients with Methamoglobin reductase and G6PD enzyme deficiency are at higher risk.
Rx – iv infusion of 1-2mg/kg Methylene blue.

MALIGNANT HYPERTHERMIA:
• Determined by increase in body temperature , muscle stiffness & increases oxygen consumption.
• Common in children than adults.
• Role of anesthetic drugs in MH is still controversial.

LA IN PATIENTS WITH SYSTEMIC DISORDERS:
DIABETIS MELLITUS:
The action of vasoconstrictors directly opposes that of insulin. Epinephrine increases
gluconeogenesis and glycogen breakdown in liver, leading to hyperglycemia.
So , well controlled diabetics better tolerate vasoconstrictors , and have fewer episodes of
hyperglycemia than poorly controlled diabetics.
Studies have shown that the amount of epinephrine contained in 1-3 cartridges ( 0.018-0.054mg)
may significantly increase the risk of complications in patients with unstable diabetes, and so should
be avoided until the are brought to normal.

HYPERTENSION:
• Studies have shown that the use of 1-2 cartridges of 2% Lidocaine with 1:1,00,000 epinephrine
( 0.018-0.036) is of little significance in most patients with HTN.
• Elective dental care should be avoided in –
i. Patients with BP ≥ 180/110
ii. Patients who have hypertensive symptoms.
Use of retraction cord with epinephrine and intra – ligamentary , intra – bony
injections should be avoided in these patients.

ISCHEMIC HEART DISEASE:
• Elective dental care is contra-indicated in –
i. Patients with unstable angina
ii. Recent MI
iii. Recent coronary artery bypass graft ( CABG)
Epinephrine dosage should be limited to 1-2 cartridges of 1:1,00,000 solution.

LA IN PREGNANCY:
• The fetal-to-maternal ratio of a local anesthetic is determined by the extent of protein binding of the
local anesthetic.
• Among the amide types, Bupivacaine is known to have the lowest fetal-to-maternal ratio.
• Theoretically, Bupivacaine should have the smallest effects on the fetus among all amide types.
• For this reason, Bupivacaine is widely used as a local anesthetic in the field of obstetrics.
• However, at toxic levels, Bupivacaine inhibits cardiac conduction, which leads to cardiac arrest with
low chances of survival.
• For this reason, high-concentration Bupivacaine is currently not used to induce local anesthesia in
dental treatment.

• Lidocaine is the most commonly used local anesthetic in a dental cartridge.
• The extent of protein binding of lidocaine is smaller than that of bupivacaine.
• The proportion of free lidocaine is relatively high, so the amount of lidocaine transferred from the
mother to the fetus is also relatively high.
• As a result, lidocaine has a relatively high fetal-to-maternal ratio.

• Epinephrine is commonly added to Lidocaine contained in a dental cartridge as a vasoconstrictor.
• Vasoconstriction induced by epinephrine delays the absorption of local anesthetics by the
mother, allowing the absorption of lidocaine to gradually occur in the maternal systemic
circulation, while also allowing blood levels of lidocaine to gradually increase.
• The local anesthetic is transferred to the fetus slowly, and its margin of safety is also increased.
• Considering how local anesthetics have small direct effects on the fetus even at submaximal
doses , lidocaine may be considered relatively safe for use in pregnant women.

RECENT ADVANCES:
TRANS-CUTANEOUS ELECTRICAL NERVE STIMULATION ( TENS):
• Stimulates the nervous system and it starts before injecting and the pulse rate increases to make a
good shake to the patient.
• Needle is inserted at an area between the electrodes of TENS while impulses are generated at the
same level.
• After withdrawing the injection and removing the needle , pulses are slowly reduced and stopped.
• This provides less pain during injection esp. for IANB technique.

ELECTRONIC DENTAL ANESTHESIA (EDA):
• Based on TENS and the electronic waves are used to disrupt neural pain transmission to the brain.
CONTRA-INDICATIONS:
Patients with prior history of cerebrovascular accident or other neurological disorders
Pregnant women
Patients with cardiac pacemakers
EDA was less effective than LA in controlling pain during cavity preparation of children aged 6-
12 yrs.

NEEDLE – FREE INJECTIONS:
• Based on a piston – pressure system.
• Several systems like SYRIJET , PED-O-JET , MED-E-JET
• These showed less pain compared to conventional injections with a needle of 25 gauge.

i. COMPUTER CONTROLLED INJECTIONS ( C-CLADS):
Charles Pravaz in 1853.
Here, computer controls the speed & injection pressure.
1st introduced into dentistry in 1997.
Core technology is an automatic delivery system of local anesthetic injection at a fixed pressure ;
volume ratio regardless of variations in tissue resistance.
This results in a controlled, highly effective and comfortable injection even in resilient tissues such as
palate & PDL.
C-CLADS has less pain and discomfort for patients than conventional syringe injections , but greater
facilities , more space and higher costs.

• Currently , available C-CLAD are-
i. WAND / Compudent system
ii. Comfort control syringe
iii. Quick sleeper.

IONTOPHORESIS:
• New technique for the transdermal administration of Lidocaine.
• Here, 2 external electrodes on the skin are used to make the transition of ionized lidocaine from
Stratum Corneum to the Dermis layer to block the nerve ends.
• Drug penetration rate in this technique is higher than passive diffusion.
• 0.6-1ml of 2% Lidocaine with 0-4mA electrical current is used for 10mins which causes 5-7mm of
drug penetration to the tissues to provide anesthesia.

STA SYSTEM DEVICE:
• An auxiliary system for injection especially made for PDL injections where dynamic pressure sensory
system improves the quality and reduces side effects of injection.
• Requires computer system tools.
• Here, low-pressure dynamic injection prevents tissue damage and pain during injection.

INTRA-NASAL LA:
Studies have shown that the use of intra-nasal Tetracaine with a vasoconstrictor like
Oxymetazoline can provide tooth anesthesia for 1st molar on one side to the other.

ELECTROSPUN DRUG – ELUTING SUTURE:
Contains absorbable suture with PLGA chemical structure that are combined with
Bupivacaine. These sutures can slowly release the drug to the surgical site with in 12 days and provides
appropriate analgesia.
• Higher concentrations of the drug may decrease the tensile strength of the suture.

INTRA-ORAL LIDOCAINE PATCH (DENTIPATCH):
Contains 10-20% Lidocaine which is placed on dry mucosa for 15 mins provides suitable
anesthesia.
JET INJECTION:
• A small amount of anesthetic drug is given into the sub-mucosa without a needle.
• Air pressure is used for the infiltration of the drug into the mucosa
through tiny pores.
• Used particularly for topical anesthesia for palatal injection.

VIBRAJECT:
Device that provides high frequency vibrations in the dental injection syringe which causes a
relative decrease in pain during the injection.

ACCUPAL:
A tool to create pressure and vibrations at the injection site. These irritate the larger nerve
fibers and cause the lack of sensitivity during the penetration of the needle.

BIBLIOGRAPHY:
i. Stanley F. Malamed (2012). Handbook of Local Anesthesia 6th Ed.
ii. Monheim’s (1990). Local Anesthesia and Pain Control in Dental Practice 7th Ed.
iii. Carranza’s (2006). Clinical Periodontology 11th Ed.
iv. Mohammed Ali Ghavimi. Overview of Local Anesthetic Techniques,1-32 from
http://dx.doi.org/10.5772/59214.
v. Ananthi Christopher (Oct 2016). Recent Advances in Local Anesthesia- A Review. Int. J Recent Sci
Res. 7(10), pp.13576-13581 , from http://www.recentscientific.com.
vi. Hyo-Soel Lee (2016 Dec 7). Recent Advances in Topical Anesthesia. J Dent Anesth Pain Med
2016;16(4):237-244, https://doi.org/10.17245/jdapm.2016.16.4.237.
vii. https://www.aagbi.org/sites/default/files/la_toxicity_2010_0.
viii. Je Min Lee (2017). Use of Local Anesthetics for Dental treatment during Pregnancy; Safety for
Parturient. J Dent Anesth Pain Med 2017;17(2):81-90,
https://doi.org/10.17245/jdapm.2017.17.2.81
ix. Sharmraaj Subramaniam, Prasanna Neelakantan (2013). Local anesthesia in dentistry - Clinical
Considerations. International Journal of Drug Development and Research 2013.
x. Wikepedia

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