DEPT.OF ORAL &MAXILLOFACIAL
Presented By Dr Haneef
Different Agents , Vasoconstrictors
Mechanism of Action
Ancient time – dental treatment associated with pain
Earliest pain relief – Coca shrub mood elevator
Cocoa shrub – foot hills of Andes
Introduced by Europeans to South America
1855 – Gaedicke extracted alkaloid Erythroxylin
1860 – Dr. Scherzer cocaine from this alkaloid
1844 – Francis Rynd (Dublin)
Acetate of morphine + Creosote
Skin incision TGN treatment
First time liquid used - intradermally
1884 – marks birth of LA
Sigmund Freud Carl Koller
Cocaine for eye operation
William Steward Halsted
Cocaine for inferior dental nerve
1886 – BDJ William Alfred Hunt et al
Cocaine - dental anesthetic documented
1901 – E Mayers
Vasoconstrictor + cocaine
1946 – Lignocaine introduced Dental practice
1948 – Lignocaine ; published in BDJ – Lofgren
Sweden – Birth place of newer LA agents
It is defined as an unpleasant emotional
experience usually initiated by a noxious
stimulus and transmitted over a specific
neural pathway to the central nervous system
where it is interpreted as such.
Accupuncture Analgesia --
Originated-CHINA,between600BC to 200AD
Still employed—susceptible patients,
Time consuming, lasts for less time
Audio Analgesia –
1959 Gardner and licklider
Loud noise used to produce analgesia
Electric analgesia --
Peripheral nerve- Direct electric current
Elos-1,powered by 18v battery- Siemens
Never more than 30 ma
Breech loading, metallic cartridge-aspirating
Aspiration- 1 hand
Rust resistance, Long lasting
Possibility of infection
Breech loading plastic cartridge-aspirating
Rust resistance, Long lasting
Size – Too big / small
Possibility of infection
Repeated autoclaving – Plastic looses
Breech loading metallic cartridge-Self aspirating
Easier to aspirate
Piston is scored – Qty Known
Possibility of infection
Finger has to be moved from thumb
ring to disc-Aspiration
Takes time to accustom
Does not require – needle
Very small volume – Delivered
Inadequate – Pulpal / Regional block
Patient disturbed by jolt of jet.
PDL damage – common
It is defined as a transient loss of sensation to a
painful or potentially painful stimulus, resulting from a
reversible interruption of peripheral conduction along a
specific neural pathway to its central integration and
perception in the brain.
Its action must be reversible
It must be nonirritating to the tissues and produce no secondary local reaction
It should have a low degree of systemic toxicity
It should have a potency sufficient duration to be advantageous.
It should have a potency sufficient to give complete anesthesia without the
use of harmful concentrated solutions
It should have sufficient penetrating properties to be effective as a topical
It should be relatively free from producing allergic reactions.
It should be stable in solution and undergo biotransformation readily within
It should be either sterile or capable of being sterlized by heat without
ROOT CANAL TREATMENT FOR PULPAL
EXTRACTION OF CARIOUS ,PRE PROSTHETIC
EXTRACTIONS,MALPOSED AND IMPACTED TEETH.
SURGICAL EXCISION AND INSICION OF
MAXILLARY ND MANDIBULAR # REDUCTIONS
DRUG ALLERGY OR HYPERSENSTIVITY REACTION
IN HEPATIC FAILURE PATIENTS Amides are metabolized in
the liver. Patients with significant liver disease who have poor
hepatic blood flow will have trouble metabolizing amides and
Patients administered prilocaine may develop
HEART FAILURE (ASA IV OR VI)
LIDOCAINE is used as an ACLS drug for patients with
ventricular dysrythmias. However high levels of lidocaine will
decrease contractility and cardiac output and can lead to
circulatory collapse. Systemic actions on the central nervous
system include CNS depression, seizures and analgesia.
In addition, one of the metabolites of lidocaine may actually
cause some sedation. These metabolites are excreted in the
kidney.IN RENAL FAILURE PATIENTS HAS TO BE USED
BLEEDING DISORDERS PERTICULARLY REGIONAL BLOCKS
Topical Surface contact.
Paste, ethyl chloride. May be adequate for simple incision and drainage,
Infiltration Deposition of solution at or close to site of surgery.
a) Sub mucous - for simple soft tissue surgery - includes long buccal
Not suitable for pulpal anaesthesia.
b) Supraperiosteal - the commonest technique - solution diffuses
through cortical bone into apical area. Usually adequate especially
in maxilla but adult mandibles to thick in posterior buccal cortex.
c) Subperiosteal - painful! - use if (b) fails.
d) Intraosseous - very painful! again use if (b) fails. Drill small
access hole over appropriate tooth apex and deposit 0.25ml of
e) Intraseptal - variation of (d) - similar indications but inject through
softer crestal bone to reach apex.
f) Intraligamentous - painful but occasionally very useful especially
for acute pulpitis where regional block fails to give adequate depth
of anaesthesia. Must use special syringe to avoid breaking
cartridge. Push needle along root surface to apex - inject small
volume of solution - effect is rapid so proceed with surgery
E.Regional Block: Remote from site of
Contraindicated in patients with bleeding
diatheses even if controlled!Success
depends on knowledge of local anatomy
and good technique.
Based on composition –
A) Natural – eg – cocaine.
B) synthetic nitrogenous compd –
para amino benzoic acid-procaine,
acetanilide - lignocaine
quinoline - cinchocoline
C) non Nitrogenous compounds -
D) miscellaneous – clove oil , phenol .
Based on intermediate group --
Benzoic acid Para Amino benzoic Acid
According to biological site and mode of action—
Agents acting at receptor
site –external surface.
Agents acting at receptor
site- internal surface..
Agents acting at receptor
Agents acting in combn
of receptor and
agents –Lignocaine etc
Injectables -- Surface --
Ultra short acting *Soluble - eg
<80 min eg Lignocaine Cocaine
Short acting 45-50 *Insoluble- eg
Min 2% ligno with Benzocaine
1:1 lakh VC
Medium acting 90-150
2% ligno with Vc or
4% prilocaine with 1:2 epin
Long acting > 180
Bupivacaine with 1:2 epin
Local anesthetic agent
This is the active ingredient in the solution, but despite the
constant development of new drugs, the ideal L.A. agent is yet
to be introduced into clinical practice.
Reduces toxic effects by retarding the absorption of the
By confining the anesthetic agent to a localized area it
increases the depth and duration of anesthesia.
It produces a relatively blood less field of operation for surgical
In higher doses can cause systemic effects that are undesirable,
practically in individuals suffering from cardiovascular disease.
Vasoconstrictor may also cause a delay in wound healing,
edema and tissue necrosis. This is because sympathomimetic
amines may increase O2 consumption of tissues. This, together
with vaso constriction leads to hypoxia and local tissue
The vasoconstrictors in general uses are
Most often is sodium meta-bi sulphite
Amount varies from 0.0065 to 0.002 mg/CC.
Since this substance is more readily oxidized than adrenaline or noradrenaline it
protects their stability.
Modern LA solutions are very stable and have a shelf – life of 2 years or more.
Most frequently used bacteriostatic agents are methylparaben, propylparaben
Fungicide Thymol is added.
The anaesthetic agent and the additives are dissolved in modified Ringer’s
solution. This automatic vehicle minimizes the discomfort during injection.
Recommended dose – 7mg/kg not>500mg with VC
For children with VC 3.2 mg/kg
Council for dental therapeutics- ADA
It is non allergic available in three
formulations Ligno2% with out Vc
Ligno2% with VC 1:80,000
Ligno2% with VC 1:100,000
Adverse reactions- CNS stimulation then
Depression,Overdose causes unconsciousness and
Bupivacaine –Classified under amide
1-butyl 2,6 pipecoloxylidide
Toxicity <4 times – Lignocaine, Mepivacaine
Metabolism –Liver by Amidases
Excretion by kidney (16% unchanged)
Vasodilation- relatively significant
Pka-8.1,ph(plain)- 4.5-6, ph(vc)- 3-4.5
Onset of action –6-10 min,Anesthetic half life-2.7hrs,Dose 1.3mg/kg
,Maximum dose-not >40mg,Absolute maximum dose-not> 90mg
Available as 0.5% soln 1:2,00,000 (vc)
Indicaton- pulpal anesthesia->90- min.
Full mouth recontruction.
Extensive perio surgery.
management of post op pain.
Duration –Pulpal- 90- 180 min
Soft tissue-4-12 hrs
Contra indication- burning sensation at site of injecton, in children-
anticipating self trauma .
Procaine- Classified under –Esters
2Diethylamino ethyl 4aminobenzoate hcl
Metabolised-in Plasma by plasma pseudocholine esterases
Excretion >2%unchanged, 90% -PABA,8% diethyl aminoethanol in
Pka-9.1,High degree of vasodilation, 2% procaine 15-30min soft
no pulpal anesthesia , > incidence allergy, drug of choice for intra
arterial injection and accidents.
Mepivacine- classified -amide type
1 Methyl 2,6 pipecoloxylidide hcl
Metabolism-microsomal fixed funcn oxidasea in liver.
Maximum dose 4.4 mg/kg , absolute max dose-300mg.
Excretion-1-10% unchanged urine.
Pka-7.6,Anesthetic half life-90min,
Mild vasodilator, 3% mepivacaine used in patients with vc
contraindicaton. Low reported cases-allergy.over dose CNS
stimulation followed by depression.
Articaine- classified- Amide
2 Carboxymethoxy 4 methylthiophene hcl
Excretion – Kidney 10% - unchanged.
Pka 7.8, Anesthetic half life-1.2-2 hrs,
Maximum dose – 1mg/kg , Absolute maximum dose –
first LAAgent with thiophene ring,little potential to diffuse
through soft tissue.
Adverse reaction-methymoglobinemia-Rx by using
methylene blue 1mg/kg.
Etidocaine- classified –Amide
Excretion –urine- Kidney
Pka 7.7 ,Anesthetic half life-56 min.
Maximum dose 8mg /kg, Absolute max dose 400 mg
Employed mainly in epidural or caudal regional block.
Added – to counteract vasodilation effect of injectable
Decreases rate of absorption
Reduces the risk of overdose reaction
Increases duration of action
Reduces bleeding at the site
Based on chemical stc (Catechol nucleus)
Based on mode of action
α1& β receptors
Direct stimulation of
No direct effect on
High doses – impaired
0.2 mg – healthy
0.04mg – CVS impaired
CVS & CNS symptoms
As vaso-constrictor in
Myelinated 14.8 – 120m/s
Site of action
Outer bimolecular lipoprotein layer in nerve membrane
Altering the basic RMP of nerve
Altering the threshold potential
Decreasing the rate of depolarization
Prolonging rate of repolarization
Involved in nerve conduction in addition to its role as a
neurotransmitter at nerve synapses
No such evidence
CALCIUM DISPLACEMENT THEORY:
L.A causes nerve block by displacement of Ca from some
membrane site that controls entry of Na
Varying conc. Of Ca in nerve – not seen
SURFACE CHARGE THEORY:
Action by binding to nerve membrane and changing its
Cationic molecules aligned at membrane water interface –surface
elec potn more positively charged - electric potn , threshold
Demerits- RMP not altered by LA.
LA act on nerve channel rather than surface –cannot explain
how uncharged LA molecule causes nerve blockage.
Membrane expansion theory-
LA lipid soluble – enters nerve membr and changes
configuration of membr. There by reduced space for sodium
to enter and thus cause inhibition.
Explains how non ionised drug causes- blockade, nerve
membrane do expand and become more fluid when exposed to
No evidence to tell that the whole blockade is due to this
Specific receptor theory—
LA act by binding to specific receptors- sodium channel-on
external/ axoplasmic surface.
Once it binds there is no permeability of sodium- no conduction.
LA molecule replace calcium molecule at calcium gate – thus
prevent sodium entry.
This is by far the most accepted theory.
All LA are available as acid salt of weak bases.
Weak base(BNHOH) combined with acid (HCL) to give
acid salt(BNHCL)& water.
In mucosa BNHCL dissociates into BNH and CL . Normal
tissue PH 7.4 is necessary for conversion of acid salt to free
BNH which is hydrophilic further dissociates to BN and H.
BN is now lipophilic.
Lipophilic BN diffuses through nerve membrane (lipid).
Inside the nerve it combines with intrinsic H. (H in nerve
formed by buffering action.)
Newly formed ionised BNH displaces calcium from the
sodium channel receptor site to cause conduction blockade.
Low levels – no action
Toxic dose – tonic clonic convulsions
Blood- 0.5-4.0 mg/ml-no complication
4.5-7.0 mg/ml-pre seizure sign/
>7.5mg/ml-tonic clonic seizures.
Anti convulsive property –
As it causes depression of CNS.
Seizure threshold- excitability nerve
Action on Heart
Electrical excitability of myocardium .
Tone of contraction.
clinically effective level-1.8-5mg/ml –anti arrhythmic
used in premature ventricular contractures , arrhythmias.
Action on vasculature-
normal value no change.
over dose- hypo tension.( myocardial
Lethal dose- cardio vascular collapse
( myocardial contractility, massive peripheral vaso dilatation )
Action on Respiratory system–
Normal levels- no over dose- bronchial muscles relaxation .
Over dose – Respiratory arrest due to CNS depression.
DEPT.OF ORAL &MAXILLOFACIAL
Presented By Dr Haneef
Local anaesthesia technique- Maxilla
Local anaesthesia technique- Mandible
The right and left trigeminal nerves provide among other
functions, the overwhelming majority of sensory innervation
from the teeth, bone, soft tissues of the oral cavity.
i. Motor:- a. Masseter
c. lateral/medial pterygoid
e. Anterior belly of digastric
f. Tensor tympani
g. Tensor veli palatini
ii. Sensory: V1 Opthalmic nerve
V2 Maxillary division
V3 mandibular division
Use a Sterile Sharp Needle
Check The flow of Solution
Determine Whether to Warm solution before use or not.
Position the patient
Dry the tissue/ wipe once.
Apply topical anesthetic
Communicate with patient apply firm hand rest
Inject few drops of soln, communicate with patient,
Advance to the target slowly ,aspirate , inject
Withdraw the needle slowly
Observe the patient & check for anesthetic symptoms
Supra periosteal injection:
Anaesthetize buccal soft tissue & hard tissue
Nerves anaesthetized – large terminal branches
1 or 2 teeth need to be anaesthetized / small area
Dense bone covering
Target area :
Behind apices of tooth
Crown & root length
Maxillary 3rd, 2nd & 1st molar (except mesio-buccal root of 1st
Bone & periodontium over these
Treatment of 2 or more molars required
Supra-periosteal injection – ineffective
Pt with bleeding disorders
More of soft tissue landmarks used
2nd injection for 1st molar
Zygomatic process of maxilla
Infratemporal surface of maxilla
Anterior border and coronoid process of mandible
Tuberosity of maxilla
Only in present in about 20% of the poplation thereby
limiting its clinical usefulness of this block.
Mesiobuccal root of the 1st molar, pulps of maxillary first 1st and
Buccal periodontal tissues
When ifra orbital block fails to provide anaesthesia to maxillary
Dental procedures involving both maxillary premolars
When infection or inflammation
Pulp of maxillary C.Is – Canine
Buccal periodontium, lower eyelid, lateral aspect of nose
More than 2 anterior teeth
Discreet treatment areas
Hemostasis of localized area – not adequately achieved
1.Nasopalatine nerve block/spenopalatine nerve block/
incisive nerve block
Anterior portion of Hard palate and over lying structures back to
the bicuspid area.
Anterior palatal procedures supplementing infraorbital nerve
Anaesthesia of nasal septum
Central incisor & incisive papilla
Single needle penetration
Multiple needle penetration
Usually most discomforting block for patient – very painful
2.Greater palatine nerve block/ anterior palatine nerve block
Palatal soft tissue – posterior aspect
Palatal hard tissue
Surgical procedures posterior portion of hard palate
Palatal Anaesthesia in conjunction with posterior superior
alveolar nerve block.
Greater palatine foramen – junction of the maxillary alveolar
process & palatine bone
Between the 2nd & 3rd molars – 1-1.5cms away from gingival
First reported by freidman and hochman in 1997 during development of
Muscles of facial expression and upper lip anesthesized.
ASA and MSA
Pulpal anesthesia of maxillary incisors,canines and premolars
Buccal and palatal attached gingiva
Performed with CCLAD
When anterior cosmetic procedures are performed
When anesthesia is desired from a single injection
Patients with thin palatal tissues
Patients who cannot tolerate the 3-4 minute adminstration time
Long procedures >90 mins
Less amount of LA is deposited 0.5ml/min
Allows for accurate smile line assesment in case of aesthetic
Very slow adminstration
Can cause operator fatigue
Maybe uncomfortable for the patient
Maxillary division of trigeminal nerve
Maxillary teeth – 1 side
Periodontium / soft tissue – 1 side
Extensive oral / periodontal / endodontal procedures
Other regional nerve blocks not possible
Therapeutic procedure to diagnose neuralgias
Penetration into orbit
Volume – displaces orbital structures, periorbital swelling,
proptosis, 6th nr block – diplopia, transient loss of vision,
optic nerve blocked, retrobulbar block producing mydriasis,
corneal anesthesia / hemorrhage, opthalmoplegias
Penetration into nasal cavity
Patient complains – LA running down the throat – to
prevent keep mouth wide open
High tuberosity approach
Greater palatine canal approach
I. Anterior and middle superior alveolar nerve block –
Inferior palpebral, lateral nasal and superior labial nerves
Incisors and bicuspids on the effected side
Labial alveolar plate and associated tissues
Pupil of the eye
When Intra oral route is not feasable
When attempts of intra oral anaesthesia have been ineffective
II. Maxillary nerve block –
Anterior temporal & zygomatic region
Side of nose
Maxillary teeth / alveolar bone & overlying structures – 1side
Hard & soft palate
Tonsils – parts of pharynx
Nasal septum – floor of nose
Extensive surgery – 1 half of maxilla
Others blocks not possible
mid point of zygomatic process
Needle gently contact lateral pterygoid plate
Maximum length of 4.5cms directed slightly upward & forward
In final position – internal maxillary artery – inferior to needle
Temporal vessels on either sides
Posteriorly foramen ovale with mandibular nerve & foramen spinosum
with middle meningeal artery
Anteriorly pterygomaxillary fissure
INFERIOR ALVEOLAR NERVE BLOCK
Other common name- Mandibular block
Different techniques are:
METHOD OF CLARKE & HOLMES
METHOD OF ANGELO SARGENTI
VAZIRANI- AKINOSI TECHNIQUE
KURT THOMA EXTERNAL APPROACH
Classical inferior alveolar nerve block
Nerves anaesthetised- inferior alveolar nerve block and its
Mandibular teeth upto midline
Body of mandible
Inferior portion of ramus
Buccal periosteum & mucous membrane
Lingual soft tissue
Anterior 2/3rd of tongue
Multiple mandibular teeth – procedures
Buccal / Lingual soft tissue anaesthesia
Anatomical structures - final position
• Rate of indequate anesthesia is high 10-20%
• Intra oral landmarks are not consistently reliable
• Highest positive aspiration of about 10-20%
• Partial anesthesia where bifid inferior alveolar nerve and bifid
mandibular canal are present
Stages in the indirect technique :- Initial insertion of the
needle more laterally,thus immediately strikes the bone, needle
is partially withdrawn after touching the bone, syringe is
moved parallel to the lower molars on the other side, insertion
of the needle beyond theinternal oblique ridge, the syringe is
returned to it’s original direction, ie over the lower premolars
and deposit 1.5ml of solution in the pterygomandibular space.
It involves deposition of solutions @ a higher level than usual. It is a
modification of indirect technique. In the standard direct/indirect technique,
the analgesic is placed immediately behind the mandibular foramen, which
is 1cm above the occlusal plane of molar teeth. At this level the nerve is
concealed by lingula & sphenomandibular ligament. Depositing the solution
at a higher level causing complete anesthesia.
This technique is a modification of direct method. The difference is that the
nerve is approached from a higher level than usual.
TECHNIQUE: Syringe with 1 5/8 inch 26gauge needle is used.The index
finger is placed in the retro molar fossa with nail facing lingually. The
needle is inserted opposite to the mid point of the finger nail. The barrel of
the syringe is now placed between and in contact with the upper premolars
of the opposite side. Needle is slowly inserted in a downwards & backwards
direction until it touches the bone, depth is 1cm. 1.5ml of solution is
Nerves anesthetized – inferior alveolar nerve, lingual nerve
one half of mandible upto mid line including lingual tissue and inferior
portion of the ramus of the mandible.
occluding plane of the teeth.
Muco gingival junction maxillary teeth.
Antr border of ramus.
Orientation of bevel must be oriented away from the bone of mandibulaar
ramus (bevel faces toward mid line).
More popular now
Land marks easy
One prick – mandibular, buccal, lingual n anesthetised.
Patient more comfortable.
• pats. with restricted mouth opening.
• fewer post op complications.
• Difficult to visualize the path of needle and depth of
• hematoma, transient facial n. paralysis.
Nerves anaesthetised – inferior alveolar, mental,
incisive, lingual, mylohyoid, auriculotemporal and
Area –all mandibular hard and soft tissue Upto mid line.
Indications- multiple procedures on mandibular teeth,
buccal soft tissue anaesthesia from third molar to midline,
conventional inf. alv. n. block is unsuccessful.
Contraindications – infection or acute inflammation in the
area of infection, pats. with restricted mouth opening.
Extraoral- corner of mouth, lower border of the tragus, intertragic
Intraoral – height of injection established by placement of
needle tip just below the mesiolingual cusp of max. 2nd molar,
penetration of soft tissue distal to 2nd molar at the same height.
Final position needle is just inferior to condyle and insertion of lateral
Gained popularity – single needle penetration, relies on soft tissue
landmarks – differ from patient to patient
Buccal nerve block or buccinator nerve block.
Buccal nerve as it passes over the anterior border of the ramus
External oblique ridge
Distal to 3rd molar
1” 25 gauge needle is inserted in to the buccal mucosa just distal to the
lower 3rd molar. 0.25 to 0.5ml of solution is deposited.
Lingual nerve block –
Area anaesthetised –
Anterior 2/3rd tongue, floor of mouth, lingual mucoperiosteum
Only used singly to operate on tongue, floor of mouth
Buccinator / long buccal nerve block
Area anaesthetised –
Buccal mucosa & mandibular molar – mucoperiosteum
External oblique ridge, retromolar triangle
Mental & Incisive nerve block
Mandibular hard & soft tissue – labial aspect with lower lip
Bicuspid teeth, lower ridge of body of mandible
Supra & infra orbital notch
Pupil of the eye
2 inch 22 gauge needle used & introduced slightly anteriorly
Temporal region with auricle of ear & external auditory meatus
TMJ, salivary glands
Anterior 2/3rd of tongue
Mandible – hard & soft tissue – midline
mid point of zygomatic arch
Cornoid process of mandible
Lateral pterygoid plate
When need to anaesthetise entire mandibular nerve
Infection / trauma – makes terminal anaestheisa not possible
Diagnostic / therapeutic
The needle is pointed posteriorly & to a greater depth of 5
This technique is used when there is severe limitation of opening of the
jaws in case of ankylosis of TMJ.
Anatomical land marks/ surface markings:
Lowest point on the anterior border of the masseter
Posterior border of the ascending ramus
Anterior border of masseter is located by clenching the teeth.The point is
marked and a line drawn connecting this with the tragus of the ear.The
mid point of this line shows the position of the mandibular foramen.
21 gauge,7 to 8cm long.
An anaesthetic complication may be defined as any
deviation from the normal expected pattern during or after
securing regional anaesthesia
Pain on injection
Burning on injection
Persistent anaesthesia or paresthesia
Sloughing of the tissue / soft tissue injury
Facial nerve paralysis
Primary / secondary
Primary – caused & manifested at time of anaesthesia
Secondary – manifested later
Mild / severe
Mild – exhibit slight change from normal expected pattern
- reverses itself without treatment
Severe – manifests itself – pronounced deviation
- requires specific treatment
Transient / permanent
Transient – is one that is severe at occurrence – no residual
Permanent – residual effect; lasts for a life time even though it is
Complications could be a combination of any of the above
Majority are either Primary Mild & Transient or Secondary Mild &
Attributed to solutions – toxicity, allergy, idiosyncrasy,
anaphylactoid reaction, local irritation
Attributed to technique / needle – syncope, muscle trismus,
pain, edema, hematoma
Unexpected movement – patient (if patient movement is
opposite to path of needle insertion)
Multiple used needle
Defective manufacture of needles/barbed needles
smaller gauge – more likely to break
Correct gauge – 25 gauge
Long needles – prevent penetration till hub
Not to redirect when in tissue
Patient – not to move – hand in the mouth – mouth open
Fragment visible – remove it
Fragment not visible – inform patient – not necessary for
intervention immediately – Radiograph suggested
Avoid bony contact
Avoid heavy pressure
Avoid movement of needle and patient
Due to pH of solution 5 (LA) – 3 (LA+VC)
pH disappears upon LA action – no residual effect
Contaminated solution other complications – trismus,
Slow injection – 1ml / minute
Cartridge stored at room temperature – away from containers with
alcohol / other agents
Direct trauma to nerve – bevel of needle
LA solution containing neurotoxic substance – alcohol
Injection of wrong solution
Hemorrhage / infection – near to nerve
Persistent anaesthesia – usually rare
Biting / thermal / chemical insult – without patient
When lingual nerve is involved – taste impaired
Proper care & handling of dental cartridge
Adherence to injection protocol
Usually resolve in 8 weeks
Periodic recall & check up of patients
Persistence – consult neurosurgeon
Recall patient every 2 months for check up
“difficulty in opening the jaws due to muscle spasm”
Trauma – muscle / blood vessel
Multiple needle punctures
LA have been known to have slight myotoxicity
Excessive volume – distension of tissues
Pain / hypomobility
Use of sharp, sterile, disposable needle
Practice atraumatic methods
Avoid repeated injections
Use minimum volume
Warm saline rinses, moist hot packs
Aspirin, Codeine (30-60mg), muscle relaxants
Thrice a day
Possibility of infection
“effusion of blood into extra-vascular spaces”
Arterial & venous puncture – common in PSA & Inf. Alv.
Patients with bleeding disorders
Bruise – may / may not be visible extra-orally
Complications – pain & trismus
Swelling & discoloration
Knowledge of normal anatomy – proper technique
Shorter needle – PSA, minimize the number of penetration
Discard defective needles- barbed needles
Immediate – apply firm pressure 5-10minutes
Inf. Alv. Nr. Block – medial aspect of ramus
Infra orbital, Mental, Incisive block – directly over foramen
PSA – pressure on soft tissue with finger as posteriorly as tolerated by
patient – medial superior direction
Patient to be reviewed after 24 hours, advice analgesics, cold application
upto 4-6 hours, warm- pack application next day
Comparitively rare complication
Instrument needle solution to be as aseptic as possible
Area & operative hands – cleaned
Avoid passing needle through infected area
Use disposable syringes
Proper care & handling of armamentarium
Atraumatic injection technique
Complete medical evaluation prior to injection
Trauma – resolve in few days without therapy
Hemorrhage – resolve slowly 7-14 days
Allergy – life threatening, airway impairment – basic life
support, call medical help, Epinephrine – 0.3mg,
Total airway obstruction – Tracheostomy /
Epithelial desquamation – topical anaesthesia – long time,
heightened sensitivity to LA
Sterile abscess – secondary to prolonged ischemia – VC in
LA site – hard palate
Pain & infection
Topical – for not more than 1-2 minutes
VC – minimal concentration in solution
Symptomatic – pain – analgesia
Epithelial desquamation – resolve few days
Sterile abscess resolve 7-10 days
Trauma occurs – frequently mentally / physically challenged
Primary cause – significantly longer duration of action
Pain & swelling
Infection of soft tissue
Cotton roll between lip & teeth
Patient – guarded against eating / drinking
LA solution into parotid gland – usually while giving Inf
Alv Nr. Block, Akinosis technique
Ipsilateral loss of motor control – Buccinator muscle
Inability to raise the corner of Mouth, close Eye lid
Needle tip to contact bone, redirection of needle to be done
only after complete withdrawal
Reassure the patient
Resolves after action of LA is over
Eye patches to the affected – eye drops
Contact lenses if any – removed
Toxicity / toxic overdose
“Signs and symptoms that result from an overly high blood
level of a drug in various target organs and tissues”
Age – any age
Weight – greater the body weight greater is the amount of dose
tolerated before overdose reaction
Sex – during pregnancy – renal function disturbed – females more
affected at this time
Diseases – hepatic & renal dysfunction reduced breakdown
Congestive heart failure – less liver perfusion
Genetics – pseudocholinesterase deficient – toxicity - Ester LA
Drug factors – Vasoactivity – vasodilation – increase in blood
More concentration – greater risk
Dose- smaller dose should always be preferred
Route of Administration – Intravascular – increased toxicity
Rate of injection – slower rate preferred
Vascularity of injection site – more vascular – greater absorption
Presence of Vasoconstrictor – with VC less absorption
Causes of toxicity –
Biotransformation usually slow
Drug – slowly eliminated by kidney
Too large a total dose
Absorption from injection site - rapid
Accidental intra-vascular injection
CNS – cerebral cortical stimulation – talkative, restless,
Cerebral cortical depression – lethargy, sleepiness,
Medullary stimulation – increased B.P, Pulse rate, Respiration
Medullary depression – mild fall in B.P– severe cases drops to 0 ,
Pulse , Respiration – similar effect
Mild overdose reaction – slow onset reaction – > 5 mins administer
Oxygen (prevent acidosis), monitor vital signs, in case of
convulsions – anti-convulsants (diazepam/midazolam infusion)
Slower onset - >15 mins – same procedure
Severe overdose reaction – rapid onset – 1 minute –
unconsciousness with or without convulsion, patient in supine
position, convulsions – protect hand, leg, tongue, BLS, administer
anti-convulsant,use of vasopressor(phenyl ephrine) i.m if
post seizure – CNS depression usually present
“It is an adverse response that is neither an overdose
nor an allergic reaction”
Common cause – some underlying
pathology/psychological /genetic mechanism
Psychotherapy may be helpful
Treatment – symptomatic ..ABC
“transient loss of consciousness that is caused due to cerebral
ischemia (neurogenic shock)”
Anxiety – increased blood supply to muscles, sitting position
2mm Hg, less pressure – cerebral arteries
Clinically pallor, light headedness, dizziness, tachycardia &
palpitation – may further lead to Unconsciousness
Treatment – discontinue procedure, supine position-
(trendelenburg position), deep breathing, O2 administration if
“hypersensitive state acquired through exposure to a
particular allergen reexposure to which produces a
heightened capacity to react”
1 % of all reaction in LA is allergy
Hyper sensitivity to ester more common-procaine
Most of patients allergic to methyl paraben
Recently allergy to sodium meta bi sulfide is also increasing
Ho of allergy to be recorded
Ho any asthmatic attack to be noted.
Always better to test the patient for allergy before treatment.
Consultation and allergy testing
Refer doubtful cases for allergic skin test – sub cutaneous test most
Informed consent that includes cardiac arest end death to be included.
Signs and symptoms of allergy.
Dermatological------ urticaria –wheal and smooth elevated patch seen, ---
---angio oedema—localised swelling – face hands, common
Respiratory– broncho spasm, respiratory distress,
dysnea, wheezing, flushing, tachycardia etc.
Laryngeal edema – type of angio neurotic oedema-
Edema upper air way – laryngeal edema
Lower air way affect broncioles- small.
Delayed – non life threatening - oral histamine
blockers- 50 mg diphenhidramine,10 mg
chlorpheniramine 3-4 days.
Immediate reaction—with conjunctivitis rhinitis-
0.3 mg epinephrine. IM
50 mg diphenhydramine Im
medical help summoned.
Observe patient for minimum of 60 min
Oral histamine blockers for 5 days.
Respiratory reaction –
patient in comfortable position.
administer - oxygen
Admn epinephrine- bronchodilator
Observe for 60 min , advise anti histamines to prevent relapse.
Histamine blockers Im
Patient position ,oxygen, broncho-dilator, iv anti histamines.
If condition not improving cricothyrotomy - achieve patent air way
if necessary give artificial ventilation.
Patient with confirmed allergy status-
if patient allergic to any one type of anesthetic ester /
amide use the other.
Use histamine blocker like diphenhydramine as anesthetic.
alternative method of pain control –
electric anesthesia / hypnosis.
Efforts have been made to improve to increase the ability
of the anesthetic to cross intact skin
Attempts at making the experience more comfortable for
The addition of hyalurodinase for deeper penetration than
Local anaesthesia without the use of needles
Exploring the possibility of reversing local anaesthesia at
the conclusion of dental procedure
5-8 time potency of lidocaine
Doesn’t effect CNS or CVS except in large doses
When adminstered in overdose the drug acts as a true
stimulant of nervous system
0.5% concentratio effective to 2% lignocaine
Amide anaesthetic similar to mepivicaine and bupvicaine
Has greater margin of safety
Decrease cardiotoxicity as compared to others
Its an oil in water emulsion containing high concentrations
of lidocaine and prilocaine in base form
Provides enouh anaesthesia of intact skin to permit a
Consists of 5% cream containing 25mg/g lidocaine and
The adminsteration of local anaesthetic is usually
uncomfortable for the patient due to difference in PH
Addition of sodium bicarbonate provides more rapid onset
of block, but it has decreased stability
CO2 enhances diffusion, as it increase intracellular PH.
Unstable solution, has short life
First used described in 1949
Provides more rapid onset of anaesthesia
Decrease duration of action
Possibility for allergic reactions
Precursor for TENS
It acts by working at low frequency of 2 Hz
It serotonin, endomorphin levels in blood
It takes about 10 minutes for sufficient rise of blood levels
It causes dilation of vessels
It can be used to reverse partially of totally the effects of local
Can be used in patients who have needle phobia
Its being used with increasing success in chronic TMJ pain
Its contraindicated in patients having cardiac pacemakers,
pregnancy, young and old age patients