Local anesthetics work by reversibly blocking sodium channels in nerve cell membranes, preventing the propagation of action potentials and interrupting pain signal transmission. When injected, they take effect within a few minutes and last 1-2 hours on average. The first widely used local anesthetic was cocaine, but modern agents like lidocaine and bupivacaine are safer and longer-lasting. Vasoconstrictors like epinephrine are often added to prolong the effects. Local anesthetics provide pain relief for dental procedures and surgeries.

1. LOCAL ANAESTHESIA
INDIAN DENTAL ACADEMY
Leader in continuing dental education
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2. Contents
History
Armamentarium
Definition &Classification
Composition
Different Agents , Vasoconstrictors
Mechanism of Action
Bio Transformation
Systemic Action

3. INTRODUCTION
‘No pain no gain’
Ancient time – dental treatment associated with pain
Earliest pain relief – Coca shrub  mood elevator

Incas
Cocoa shrub – foot hills of Andes
Introduced by  Europeans to South America
Cocaine

4. 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

5. 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

6. 1905
13 lives claimed – addiction
 A Einhorn & E Uhlfelder(Sweden)

Synthesized  Procaine hydrochloride
 Procaine  sterilizable, non-additive, non-toxic

1943

N Lofgren(Sweden)
Synthesized  Anilide called Lignocaine
 Lignocaine – amide linked synthetic derivative


7. 1946 – Lignocaine introduced  Dental practice
1948 – Lignocaine ; published in BDJ – Lofgren
Sweden – Birth place of newer LA agents

Bupivacaine

Ropivacaine

8. Pain and pain control
DEFINITION - 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.

9. Methods of pain control.
Accupuncture Analgesia -
Originated-CHINA,between600BC to 200AD
Hypnotism –
Still employed—susceptible patients,
 Time consuming, lasts for less time

Audio Analgesia –
1959 Gardner and licklider
 Loud noise used to produce analgesia


10. Electric analgesia -Peripheral nerve- Direct electric current

Elos-1,powered by 18v battery- Siemens

Never more than 30 ma
Analgesia by Cold air–

Inability to conduct AP at low tempr

Nondolar-French-60 lts/min-Cold air

Dis adv-Mucosa dry, Cotton stick to mucosa,ulcers-if not
moistened.

11. Armamentarium
Syringe
Breech loading, metallic cartridge-aspirating
Advantage
Disadvantage
Visible cartridge
Weight
Aspiration- 1 hand
Size-Too big
Autoclavable
Possibility of infection
Rust resistance, Long lasting

12. PISTON WITH
HARPOON
NEEDLE ADAPTOR
FINGER
GRIP
SYRINGE BARREL
THUMB
RING

14. Breech loading plastic cartridge-aspirating
Advantage
Disadvantage
Light weight
Size – Too big / small
Cartridge visible
Possibility of infection
Rust resistance, Long lasting
Repeated autoclaving – Plastic looses
its properties
Low cost

15. PLASTIC REUSABLE SYRINGE

16. Breech loading metallic cartridge-Self aspirating
Advantage
Disadvantage
Cartridge visible
Weight
Autoclavable
Possibility of infection
Easier to aspirate
Finger has to be moved from thumb
ring to disc-Aspiration
Piston is scored – Qty Known
Takes time to accustom

17. SELF ASPIRATING SYRINGE

18. Pressure syringe -Advantage
Disadvantage
Measured dose
Cost
Overcomes tissue resistance
Inject too rapidly -Possibility
Non threatening – Cartridge
protected

19. PRESSURE
SYRINGE

20. WILCOX- JEWETT OBTUNDER

21. Jet injectors
Advantage
Disadvantage
Does not require – needle
Inadequate – Pulpal / Regional block
Very small volume – Delivered
Patient disturbed by jolt of jet.
Topical anesthesia-effective
Cost
PDL damage – common

22. JET INJECTOR

23. Disposable syringe
Advantage
Disadvantage
Single use
Does not accept – Dental cartridge
Sterile-Till opened
Aspiration – Difficult – 2 hands
Light weight

24. Needle

Type – Stainless steel – Disposable
Platinum
Iridium platinum
Ruthenium platinum

Parts – Bevel
Shank
Hub-Leur lock, Friction grip.

25. Gauge –23 (IM) – Length 23 mm
25 (D) – Length 36/26 mm - +ve asprn
Blood – 100%
27 (D) – Length 27 mm - +ve asprn
Blood – 87%
30 (D) – Length 22 mm - +ve asprn
Blood – 2-5%

26. Cartridge—
Consists of -
Cylindrical glass tube

Stopper

Aluminum cap

Diaphram

27. Aluminum cap
NECK
Rubber diaphragm
GLASS TUBE
RUBBER PLUNGER

28. Additional Armamentarium –

Topical antiseptic

Topical anesthetic

Cotton Gauge

Hemostat

Applicator Stick.

29. Definition of L.A -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.

30. Classification-Based on composition –

A) Natural – eg – cocaine.

B) synthetic nitrogenous compd –
para amino benzoic acid-procaine,
benzocaine.
acetanilide quinoline -

lignocaine
cinchocoline
C) non Nitrogenous compounds benzyl
alcohol

D) miscellaneous – clove oil , phenol .

31. Based on intermediate group -Esters –
Benzoic acid
Amides –
Para Amino benzoic Acid Articaine
Butane
Chloroprocaine
Bupivacaine
Cocaine
Procaine
Dibucaine
Benzocaine
Propoxycaine
Lignocaine
Hexylcaine
Mepivacaine
Tetracaine
Prilocaine

32. According to biological site and mode of action—

Class A
Agents acting at receptor Biotoxin -eg
site –external surface.
tetrodotoxin

Class B
Agents acting at receptor Quaternary amoniumsite- internal surface..
scorpion venom

Class C

Class D
Agents acting at receptor Benzocaine
independent physico
chemical mechanism.
Agents acting in combn Clinically useful
agents –Lignocaine etc
of receptor and
independent mechanism.

33. Injectables - Ultra short acting
<80 min eg Lignocaine

Short acting 45-50
Min 2% ligno with
1:1 lakh VC

Surface -*Soluble - eg
Cocaine
Lignocaine
*Insoluble- eg
Benzocaine
Medium acting 90-150
2% ligno with Vc or
4% prilocaine with 1:2 epin

Long acting > 180
5% Bupivacaine with 1:2 epin

34. Composition-Local anesthetic drug –eg lignocaine .
Vasopressor drug - eg adrenaline.
Preservative - eg Sodium meta bi sulfide.
Germicide – eg methyl paraben.
For isotonicity – Normal Saline .
Distilled water to equal the desired amount .

35. Individual Agents -Lignocaine--
Classified under – Amide
2-diethylamino 2,6 acetoxylidide hcl
 1943 – Nils Lofgrens- intro 1948(dentistry)
 Metabolised- Liver by microsomal fixed function
oxidases to monoethyl glycerine and xylidide
 Excretion -<10% unchanged, >80%-metab
 Vasodilaton ->Procaine,
<Mepivacaine
 Pka –7.9 , ph(plain)-6.5,ph(with Vc)5 –5.5,Onset of
action 2-3 min,Anesthetic half life 1.6hrs,topical
anesthetic -yes


36. CH3
C2H5
NH.CO.CH2.N
CH3
LIGNOCAINE
C2H5

37. Recommended dose – 7mg/kg not>500mg with VC
4.4mg/kg not>300mg
 For children with VC 3.2 mg/kg
 Council for dental therapeutics- ADA
4.4mg/kg
 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 respiratory
arrest.


38.  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-

39. CH3
NH.CO
CH3
N
C4H9
BUPIVACAINE

40. 
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 .

41.  Procaine- Classified under –Esters

2Diethylamino ethyl 4aminobenzoate hcl

Metabolised-in Plasma by plasma pseudocholine esterases

Excretion >2%unchanged, 90% -PABA,8% diethyl aminoethanol
in urine.

Pka-9.1,High degree of vasodilation, 2% procaine 15-30min soft
tissue LA
no pulpal anesthesia , > incidence allergy, drug of choice for intra
arterial injection and accidents.

42.  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.

43.  Articaine- classified- Amide
2 Carboxymethoxy 4 methylthiophene hcl
 Metabolised- Liver
 Excretion – Kidney 10% - unchanged.
 Pka 7.8, Anesthetic half life-1.2-2 hrs,
 Maximum dose – 1mg/kg , Absolute maximum dose –
500mg
 first LA Agent with thiophene ring,little potential to
diffuse through soft tissue.
 Adverse reaction-methymoglobinemia-Rx by using
methylene blue 1mg/kg.


44.  Etidocaine- classified –Amide

Metabolism –Liver

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.

45. VASOCONSTRICTORS
Added – to counteract vasodilation effect of
injectable L.A

Decreases rate of absorption

Reduces the risk of overdose reaction

Increases duration of action

Reduces bleeding at the site

46. CLASSIFICATION OF V.C
Based on chemical stc  (Catechol nucleus)
Catecholamines
Non catecholamines
Epinephrine
Nor epinephrine
Dopamine
Amphetamine
Meta amphetamine
Based on mode of action
Direct acting
Epinephrine
Nor epinephrine
Indirect acting
Mixed acting
Amphetamine
Tyramine
Ephedrine

47. EPINEPHRINE
Proprietary Adrenaline
name
Mode of
α1& β receptors
action
Systemic
Systolic &
1) CVS
Diastolic pressure
FELYPRESSIN
Octopressin
Direct stimulation of
vasculature
No direct effect on
Myocardium
Heart rate
Non-arrythmagenic
Oxygen consumption High doses – impaired
coronary flow
Stroke volume

48. 2) CNS
CNS stimulation Adrenergic nerve – no
effect
3) RS
Bronchodilator
4) Vasculature α1 –
vasoconstriction
β 2 – vasodilation
oxygen
5)Metabolism
consumption
blood sugar level
Vasoconstriction –
coronary blood vessels
Anti-diuretic action
Oxytocin like action –
uterus

49. 6) Clinical Allergy, hemostasis
As vaso-constrictor in
application
L.A
7) Max
0.2 mg – healthy
dose
0.04mg – CVS impaired
8) Side
CVS & CNS symptoms
effect
Cerebral hemorrhage
0.04mg

50. MECHANISM OF ACTION
Resting membrane potential

Excitation of nerve

Stimulus – slow depolarization – electric potential less negative
 increase in permeability to Na

Electric potential – critical level – firing / threshold potential

Rapid depolarization – reversal of electric potential

Reaches peak +35 mv - +40 mv  rapid depolarization
(0.3msec)

Repolarize to RMP  -60 to –70mv (0.7msec)

51. Conduction / propagation

Depolarization – 1segment – local current  affects
RMP next segment

Current flow +ve  –ve; never backwards – prevented by
previous unexcitable refractory segm.
Spread
Sequential depolarization - non myelinated
 Saltatory conduction – myelinated – faster & energy
efficient


53. Rate
Non-myelinated 1.2m/s
 Myelinated 14.8 – 120m/s

Site of action

Outer bimolecular lipoprotein layer in nerve membrane

54. MODE OF ACTION
Altering the basic RMP of nerve
Altering the threshold potential
Decreasing the rate of depolarization
Prolonging rate of repolarization

55. THEORIES OF ACTION OF L.A
ACTEYLCHOLINE THEORY:

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

56. SURFACE CHARGE THEORY:

Action by binding to nerve membrane and changing its
electric potential.


Cationic molecules aligned at membrane water interface –
surface elec potn more positively charged - electric potn ,
threshold potn.
Demerits- RMP not altered by LA.
LA act on nerve channel rather than surface –cannot
explain how uncharged LA molecule causes nerve
blockage.

57. 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
LA .

No evidence to tell that the whole blockade is due to this
phenomenon.

58. Specific receptor theory—

LA act by binding to specific receptors- sodium channelon 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.

59. Mechanism of action.

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 base.

BNH which is hydrophilic further dissociates to BN and
H. BN is now lipophilic.

60. 
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.

61. LA Solution .

62. Biotransformation.
Esters- eg- Procainehydrolyzed to pseudo cholinesterase's
Para amino benzoic acid
Diethyl amino alcohol
Excreted unchanged urine further transformed-urine
Atypical cholinesterase's --- increase toxicity

63. Amide eg lidocaine -Mono ethyl xylidide
Glycine xylidide
xylidide
Xylidide
Hydroxy xylidide.
Excreted kidney .
Significant renal diseases – contra

64. Systemic action.
CNS –
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/
symptom
>7.5mg/ml-tonic clonic seizures.
Anti convulsive property –
As it causes depression of CNS.
Seizure threshold- excitability nerve

65. CVS
Action on Heart

Electrical excitability of myocardium .

conduction rate

Tone of contraction.
clinically effective level-1.8-5mg/ml –anti arrhythmic
used in premature ventricular contractures , arrhythmias.

66.  Action
on vasculature-
normal value no change.
over dose- hypo tension.( myocardial
contractility)
Lethal dose- cardio vascular collapse
( myocardial contractility, massive peripheral vaso
dilatation )

67. Action on Respiratory system–

Normal levels- no over dose- bronchial muscles
relaxation .

Over dose – Respiratory arrest due to CNS depression.

68. Query
Least toxic LA- 2 chlorprocaine.
Most toxic LA- tetracaine- for topical-dicyclomine
If allergic to LA –diphenhydramine- anti histamine
+ mild anesthetic
For children - 2 chlorprocaine
LA is added with bi carbonate in infections
Allergy – delt in detail part II

69. Ideal requirementsits action must be reversible
 Must be non irritant and not produce any secondary
irritation
 Low degree of systemic toxicity
 Must be potent enough
 Have sufficient penetrating properties


70. LOCAL ANAESTHESIA
part II
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71. Techniques of Injection
Basic points
Use a Sterile Sharp Needle

Check The flow of Solution

Determine Whether to Warm soln before use or not.

Position the patient

Dry the tissue/ wipe once.

Apply topical anesthetic

72. 
Topical antiseptic /optional

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

73. Technique for Maxillary Block
Supra periosteal injection:

Anaesthetize buccal soft tissue & hard tissue

Nerves anaesthetized – large terminal branches

Indication :

1 or 2 teeth need to be anaesthetized / small area

74. 
Contra-indication :



Infection
Dense bone covering
Target area :


Behind apices of tooth
Landmarks :

Muco-buccal fold

Crown & root length

76. Posterior Superior Alveolar Nerve Block

Area anaesthetized:
Maxillary 3rd, 2nd & 1st molar (except mesio-buccal root of 1st
molar
 Bone & periodontium over these


Indication:
Treatment of 2 or more molars required
 Supra-periosteal injection – ineffective
 Acute inflammation


77. 
Contra-indication:


Pt with bleeding disorders
Disadvantage:
More of soft tissue landmarks used
 2nd injection for 1st molar


Landmarks:
Mucobuccal fold
 Zygomatic process of maxilla
 Infratemporal surface of maxilla
 Anterior border and coronoid process of mandible
 Tuberosity of maxilla


78. 
Complications:

Hematoma –

Non visible - pterygoid plexus posteriorly

Visible – buccal aspect

Accidental mandibular Anaesthesia

Orbital contents – anaesthetized accidentally

Accidental - parotid gland  facial nerve affected

80. Anterior superior alveolar nerve block

Areas anaesthetized
Pulp of maxillary C.Is – Canine
 Buccal periodontium, lower eyelid, lateral aspect of nose
 Upper lip


Indications


More than 2 anterior teeth
Contraindications
Discreet treatment areas
 Hemostasis of localized area – not adequately achieved


81. 
Landmarks

Mucobuccal fold, infra-orbital notch, infra-orbital foramen
2 methods:

Intra-oral



Premolar approach
Incisal approach
Extra-oral

83. Palatal Anaesthesia
Pressure Anaesthesia
Slow deposition
 Small quantity
 Effect only a very small area

Greater palatine nerve block

Areas anaesthetized
Palatal soft tissue – posterior aspect
 Palatal hard tissue


84. 
Indication
Surgical procedures posterior portion of hard palate
 Palatal Anaesthesia in conjunction with posterior superior
alveolar nerve block.


Landmarks
Greater palatine foramen – junction of the maxillary alveolar
process & palatine bone
 Between the 2nd & 3rd molars – 1-1.5cms away from gingival
margin


86. Nasopalatine nerve block

Areas anaesthetized


Anterior portion of Hard palate and over lying structures back
to the bicuspid area.
Indications
Anterior palatal procedures supplementing infraorbital nerve
blocks
 Anaesthesia of nasal septum


Landmarks

Central incisor & incisive papilla

87. 
Complications



Hematoma
Necrosis
Technique

Single needle penetration

Multiple needle penetration
Usually most discomforting block for patient – very painful

88. Maxillary nerve block

Areas anaesthetized
Pulpal Anaesthesia
 Maxillary teeth – 1 side
 Periodontium / soft tissue – 1 side


Indications
Extensive oral / periodontal / endodontal procedures
 Other regional nerve blocks not possible
 Therapeutic procedure to diagnose neuralgias


89. 
Contra-indications
Pediatric patients
 Infection / inflammation
 Hemorrhage – anticipated
 Greater palatine canal approach not possible – bony obstr.


Landmarks
Mucobuccal fold distal to maxillary 2nd molar
 Maxillary tuberosity
 Zygomatic process
 Greater palatine foramen


90. 
Complications
Hematoma
 Penetration into orbit



Penetration into nasal cavity


Volume – displaces orbital structures, periorbital swelling,
proptosis, 6th nr block – diplopia, transient loss of vision, optic
nerve blocked, retrobulbar block / hemorrhage, opthalmoplegias
(common)
Patient complains – LA running down the throat – to prevent
keep mouth wide open
Technique
High tuberosity approach
 Greater palatine canal approach


92. Maxillary nerve block – Extra Oral

Areas anaesthetised
Anterior temporal & zygomatic region
 Lower eyelid
 Side of nose
 Anterior cheek
 Upper lip
 Maxillary teeth / alveolar bone & overlying structures – 1side
 Hard & soft palate
 Tonsils – parts of pharynx
 Nasal septum – floor of nose


93. 
Indications
Extensive surgery – 1 half of maxilla
 Others blocks not possible
 Therapeutic purposes


Technique
mid point of zygomatic process
 Needle gently contact lateral pterygoid plate
 Maximum length of 4.5cms directed slightly upward & forward


Note:
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


95. Mandibular Nerve Blocks
Inferior alveolar nerve block

Areas anaesthetised
Mandibular teeth upto midline
 Body of mandible
 Inferior portion of ramus
 Buccal periosteum & mucous membrane
 Lingual soft tissue
 Anterior 2/3rd of tongue


Indications
Multiple mandibular teeth – procedures
 Buccal / Lingual soft tissue anaesthesia


96. 
Contraindications
Infection / acute inflammation
 Young children / mentally handicapped


Landmarks
Coronoid notch
 Pterygomandibular raphe
 Occlusal plane of posterior mandibular teeth


Complication
Hematoma
 Trismus
 Transient facial paralysis (parotid gland)


97.  Anatomical
structures - final position
 Superiorly –
Inferior alveolar nerves & vessels
 Insertion of medial pterygoid
 Mylohyoid nerves & vessels

 Anteriorly

–
Deep part of parotid gland
 Laterally
–
Lingual nerve
 Internal pterygoid
 Spehnomandibular ligament

 Medially-
ramus of mandible.

100. Closed mouth/ Akinosis technq—

Area anesthetized


one half of mandible upto mid line including lingual tissue.
Land markoccluding plane of the teeth.
 Muco gingival junction maxillary teeth.
 Antr border of ramus.


More popular now
Land marks easy
 One prick – mandibular, buccal, lingual n anesthetised.
 Patient more comfortable.


102. Gow gates technique– 1973.
deposit soln at neck of condyle
 Area –all mandibular hard and soft tissue Upto mid line.
 Land marks


antr border of ramus, tendon of temporalis, corner of mouth,
inter tragic notch of ear and exter nal ear.
Final position needle is just inferior to condyle.and
insertion of lateral pterygoid.
Gained popularity – single needle penetration, relies on
soft tissue landmarks – differ from patient to patient

104. 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
Land marks

External oblique ridge, retromolar triangle

106. Mental nerve block

Areas anaesthetised


Landmarks


Lower lip, mucous membrane – anterior to mental foramen
Mandibular bicuspids
Indications

Surgery of lower lip or mucous membrane

108. Extra Oral Technique
Mandibular nerve

Area anaesthetised
Temporal region with auricle of ear & external auditory
meatus
 TMJ, salivary glands
 Anterior 2/3rd of tongue
 Mandible – hard & soft tissue – midline


Landmarks
mid point of zygomatic arch
 Zygomatic notch
 Cornoid process of mandible
 Lateral pterygoid plate


109. 
Indications

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 cms

111. Mental & Incisive nerve block

Area anaesthetised


Mandibular hard & soft tissue – labial aspect with lower lip
Landmarks
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 & downwards

112. Complications
Definition

An anaesthetic complication may be defined as any
deviation from the normal expected pattern during or
after securing regional anaesthesia

2 types

Local

Systemic

113. LOCAL COMPLICATIONS
Needle breakage
 Pain on injection
 Burning on injection
 Persistent anaesthesia or paresthesia
 Trismus
 Hematoma
 Sloughing of the tissue / soft tissue injury
 Facial nerve paralysis


114. SYSTEMIC COMPLICATIONS

Toxicity

Idiosyncracy

Allergy

Anaphylactoid reaction

Syncope

115. Classification

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

116. 
Transient / permanent

Transient – is one that is severe at occurrence – no residual
effects

Permanent – residual effect; lasts for a life time even though it
is mild
Complications could be a combination of any of the above
mentioned types
Majority are either Primary Mild & Transient or Secondary Mild
& Transient

117. Complications

Attributed to solutions – toxicity, allergy, idiosyncrasy,
anaphylactoid reaction, local irritation

Attributed to technique / needle – syncope, muscle
trismus, pain, edema, hematoma

118. Needle breakage
Cause –

Unexpected movement – patient (if patient movement is
opposite to path of needle insertion)

Usually at Hub – Magill forceps – hemostat used

If needle has penetrated soft tissue – not usually more
than few mms deep – encased in scar tissue in few weeks
– removed later on if necessary

Multiple used needle

119. Prevention
Correct gauge – 25 gauge
 Long needles – prevent penetration till hub
 Not to redirect when in tissue

Management
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


120. Precautions

Avoid bony contact

Avoid heavy pressure

Avoid movement of needle and patient

121. Pain on injection
Causes –
Careless injection technique
 Multiple used needle
 Rapid deposition

Problems –

Pain – patient anxiety – unexpected movements
Prevention –




Proper technique – sharp needles
Enter topical anaesthetics
Inject slowly – solution sterilized
Check temperature of solution

122. Burning on injection
Causes
Due to pH of solution  5 (LA) – 3 (LA+VC)
 Rapid injection
 Contamination
 Warm solution

Problems
pH  disappears upon LA action – no residual
sensitivity
 Contaminated solution  other complications – trismus,
edema, paraesthesia


123. Prevention

Slow injection – 1ml / minute

Cartridge stored at room temperature – away from
containers with alcohol / other agents

124. Persistent anaesthesia / paresthesia
Causes
Direct trauma to nerve – bevel of needle
 LA solution containing neurotoxic substance – alcohol
 Injection of wrong solution
 Hemorrhage / infection – near to nerve

Problem
Persistent anaesthesia – usually rare
 Biting / thermal / chemical insult – without patient
awareness
 When lingual nerve is involved – taste impaired


125. Prevention
Proper care & handling of dental cartridge
 Adherence to injection protocol

Management
Usually resolve in 8 weeks
 Periodic recall & check up of patients
 Persistence – consult neurosurgeon
 LA – not to be injected in the same region


126. Trismus
Definition

“difficulty in opening the jaws due to muscle spasm”
Causes
Trauma – muscle / blood vessel
 Irritating solution – hemorrhage
 LA have been known to have slight myotoxicity
 Excessive volume – distension of tissues

Problems

Pain / hypomobility

127. Prevention

Use of sharp, sterile, disposable needle

Aseptic technique

Practice atraumatic methods

Avoid repeated injections

Use minimum volume

128. Management

Heat therapy


Analgesics


Aspirin, Codeine (30-60mg)
Initial physiotherapy


Warm saline rinses, moist hot packs
Thrice a day
Antibiotic regime

Possibility of infection

129. Hematoma
Causes

Arterial & venous puncture – common in PSA & Inf Alv
nerve blocks
Problem
Bruise – may / may not be visible extraorally
 Complications – pain & trismus
 Swelling & discolouration

Prevention
Knowledge of normal anatomy – proper technique
 Shorter needle – PSA, minimise the number of
penetration


130. Management

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, heat application next day

131. Infection
Comparitively rare complication
Instrument needle solution to be as aseptic as
possible
Area & operative hands – cleaned
Avoid passing needle through infected area

132. Edema
Causes
Trauma during injection
 Infection, hemorrhage
 Allergy (Angioedema)
 Injection of irritating solution

Problems
Pain & dysfunction
 Airway obstruction


133. Prevention



Proper care & handling of armamentarium
Atraumatic injection technique
Complete medical evaluation prior to injection
Management




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, Antihistamine,
Corticosteroids
Total airway obstruction – Tracheostomy / Cricothyroidectomy

134. Sloughing of tissue
Causes
Epithelial desquamation – topical anaesthesia – long
time, heightened sensitivity to LA
 Sterile abscess – secondary to prolonged ischemia – VC
in LA  site – hard palate

Problems

Pain & infection
Prevention
Topical – for not more than 1-2 minutes
 VC – minimal concentration in solution


135. Management

Symptomatic – pain – analgesia

Epithelial desquamation – resolve few days

Sterile abscess resolve  7-10 days

136. Soft tissue injury
Causes
Trauma occurs – frequently mentally / physically
challenged children
 Primary cause – significantly longer duration of action

Problem
Pain & swelling
 Infection of soft tissue

Prevention
Cotton roll between lip & teeth
 Patient – guarded against eating / drinking


137. Facial nerve paralysis
Cause

LA solution into parotid gland – usually while giving Inf
Alv Nr. Block, Akinosis technique
Problem
Ipsilateral loss of motor control – Buccinator muscle
 Inability to raise the corner of Mouth, close Eye lid

Prevention

Needle tip to contact bone, redirection of needle to be
done only after complete withdrawl

138. Management
Reassure the patient
 Eye patches to the affected – eye drops
 Contact lenses if any – removed

Some post anaesthetic extra oral lesions – recurrent apthous
stomatitis, herpes simplex seen in susceptible patient
Mixture of Diphenhydramine, milk of magnesia – relief
against ulcers

139. Systemic complications
Toxicity / toxic overdose
Caused by overdose reaction – increased conc. In blood
 Predisposing factors

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


140. 
Mental attitude and environment – pyschological attitude
affects response to various stimuli – larger dose LA needed

Fearful patients – lower seizure threshold for LA

Drug factors – Vasoactivity – vasodilation – increase in blood

Concentration – greater 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

141. 
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


Symptoms –
CNS – cerebral cortical stimulation – talkative, restless,
apprehensiveness, convulsions
 Cerebral cortical depression – lethargy, sleepiness,
unconsciousness
 Medullary stimulation – increased B.P, Pulse rate, Respiration


142. 
Medullary depression – mild fall in B.P– severe cases
drops to 0 , Pulse , Respiration – similar effect
Treatment
Mild overdose reaction – slow onset reaction – > 5 mins
administer Oxygen (prevent acidosis), monitor vital
signs, in case of convulsions – anti-convulsants
 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 ----------- post seizure –
CNS depression usually present


143. Idiosyncrasy
Any reaction neither toxic nor allergic
Common cause – some underlying pathology /
psychological
Pyschotherapy may be helpful
Treatment – symptomatic

144. Syncope
Anxiety – increased blood supply to muscles, sitting
position 2mm Hg, less pressure – cerebral arteries
Clinically light headedness, dizziness, tachycardia
& palpitation – may further lead to Unconsciousness
Treatment – discontinue procedure, supine position,
deep breathing, BLS

145. Allergy
1 % of all reaction in, LA is allergy
Predisposing factors
Hyper sensitivity to ester more common-procaine
 Most of patients allergic to methyl paraben
 Recently allergy to sodium meta bi sulfide is also
increasing
Precautions--Ho of allergy to be recorded
Ho any asthmatic attack to be noted.
Always better to test the patient for allergy before
treatment.


146. 
Consultation and allergy testing



Refer doubtful cases for allergic skin test – sub cutaneous test
most sensitive.
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.

147. 
Laryngeal edema – type of angio neurotic oedema- life
threating.
Edema upper air way – laryngeal edema
 Lower air way affect broncioles- small.


Management

`skin reactions




Delayed – non life threatening - oral histramine blockers- 50 mg
diphenhidramine
Immediate reaction—with conjunctivites rhinitis- vigerous
managemennt.
0.3 mg epinephrine. IM
50 mg diphenhydramine Im
medical help summoned.

148. 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.


Laryngeal edemaPatient position ,oxygen, broncho dilator, oral anti histamines.
 If condition not improving cricothyrotomy - achieve patent air
way if necessary give artificial ventilation.


149. 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.

General anesthesia

alternative method of pain control –

electric anesthesia / hypnosis.