Local Anaesthesia

1. DEPT.OF ORAL &MAXILLOFACIAL
SURGERY
Presented By Dr Haneef

2.  History
 Armamentarium
 Definition &Classification
 Composition
 Different Agents , Vasoconstrictors
 Mechanism of Action
 Bio Transformation
 Systemic Action

3.  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.  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.  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
 Electric analgesia --
Peripheral nerve- Direct electric current
 Elos-1,powered by 18v battery- Siemens
 Never more than 30 ma

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

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

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

14. PLASTIC REUSABLE SYRINGE

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

16. SELF ASPIRATING SYRINGE

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

18. PRESSURE
SYRINGE

19. WILCOX- JEWETT OBTUNDER

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

21. JET INJECTOR

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

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

24. Rubber diaphragm
Aluminum cap
NECK
GLASS TUBE
RUBBER PLUNGER

25.  Additional Armamentarium –
 Topical antiseptic
 Topical anesthetic
 Cotton Gauge
 Hemostat
 Applicator Stick.

26. 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.

27. 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
anesthetic.
It should be relatively free from producing allergic reactions.
It should be stable in solution and undergo biotransformation readily within
the body
It should be either sterile or capable of being sterlized by heat without
deterioration.

28.  ROOT CANAL TREATMENT FOR PULPAL
ANESTHESIA
 PERIODONTAL SURGERY
 ORTHODONTIC EXTRACTIONS
 EXTRACTION OF CARIOUS ,PRE PROSTHETIC
EXTRACTIONS,MALPOSED AND IMPACTED TEETH.
 PREPROSTHETIC SURGERY
 SURGICAL EXCISION AND INSICION OF
PATHOLOGICAL LESIONS.
 ORTHOGNATHIC SURGERY
 MAXILLARY ND MANDIBULAR # REDUCTIONS
OPEN/CLOSED

29. ABSOLUTE:
 DRUG ALLERGY OR HYPERSENSTIVITY REACTION

30.  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
other agents.
 Patients administered prilocaine may develop
methemoglobinemia.
 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
WITH CAUTION.
 ATYPICAL PSEUDOCHOLINESTERASE.
 BLEEDING DISORDERS PERTICULARLY REGIONAL BLOCKS

31. Topical Surface contact.
Paste, ethyl chloride. May be adequate for simple incision and drainage,
preinjection,
Infiltration Deposition of solution at or close to site of surgery.
a) Sub mucous - for simple soft tissue surgery - includes long buccal
infiltration.
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
local anaesthetic.

32. 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
C.FIELD BLOCKS
D.NERVE BLOCKS
E.Regional Block: Remote from site of
surgery.
Contraindicated in patients with bleeding
diatheses even if controlled!Success
depends on knowledge of local anatomy
and good technique.

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

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

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

36.  Injectables -- Surface --
 Ultra short acting *Soluble - eg
<80 min eg Lignocaine Cocaine
Lignocaine
 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

37.  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.
 Vasoconstrictor
 Merits
 Reduces toxic effects by retarding the absorption of the
constituents
 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
procedures.

38.  Demerits
 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
damage.
 The vasoconstrictors in general uses are
 Adrenaline.
 Noradrenaline
 Felypressin

39.  Anti oxidant
 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.
 Preservative
 Modern LA solutions are very stable and have a shelf – life of 2 years or more.
 Most frequently used bacteriostatic agents are methylparaben, propylparaben
and chlorobutanol.
 Fungicide Thymol is added.
 Vehicle
 The anaesthetic agent and the additives are dissolved in modified Ringer’s
solution. This automatic vehicle minimizes the discomfort during injection.

40. Anesthetic pKa Onset Duration
(with
Epinephrine)
in minutes
Max Dose
(with
Epinephrine)
Procaine 9.1 Slow 45 - 90 8mg/kg –
10mg/kg
Lidocaine 7.9 Rapid 120 - 240 4.5mg/kg –
7mg/kg
Bupivacaine 8.1 Slow 4 hours – 8
hours
2.5mg/kg –
3mg/kg
Prilocaine 7.9 Medium 90 - 360 5mg/kg –
7.5mg/kg
Articaine 7.8 Rapid 140 - 270 4.0mg/kg –
7mg/kg

41. 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

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

43.  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.

44.  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

45. N
NH.CO
C4H9
CH3
CH3
BUPIVACAINE

46.  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 .

47.  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.

48.  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.

49. 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 LAAgent with thiophene ring,little potential to diffuse
through soft tissue.
 Adverse reaction-methymoglobinemia-Rx by using
methylene blue 1mg/kg.

50. 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.

51.  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

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

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

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

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

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

57.  Altering the basic RMP of nerve
 Altering the threshold potential
 Decreasing the rate of depolarization
 Prolonging rate of repolarization

58.  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

59.  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.

60. 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.

61. 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.

62.  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.

63.  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.

64. LA Solution .

65.  Esters- eg- Procaine-
hydrolyzed to pseudo cholinesterase's
Para amino benzoic acid Diethyl amino alcohol
Excreted unchanged urine further transformed-urine
Atypical cholinesterase's --- increase toxicity

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

67. 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

68. 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.

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

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

71. DEPT.OF ORAL &MAXILLOFACIAL
SURGERY
Presented By Dr Haneef

72.  Anatomical considerations
 Local anaesthesia technique- Maxilla
 Local anaesthesia technique- Mandible
 Complications
 Future trends

73.  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.
 Two parts:-
i. Motor:- a. Masseter
b. temporalis
c. lateral/medial pterygoid
d. Mylohyoid
e. Anterior belly of digastric
f. Tensor tympani
g. Tensor veli palatini
ii. Sensory: V1 Opthalmic nerve
V2 Maxillary division
V3 mandibular division

77.  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

78.  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

79. Intra Oral injection techniques
 Supraperiosteal injection
 Intralegimentry injection
 Intraspetal injection
 Intraosseus 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
Exta oral injection techniques
 Ifraorbital nerve block – anterior, middle superior alveolar nerve
block
 Maxillary nerve block

80.  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

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

83.  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

84.  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

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

87. Only in present in about 20% of the poplation thereby
limiting its clinical usefulness of this block.
 Area anaesthetized:
 Mesiobuccal root of the 1st molar, pulps of maxillary first 1st and
2nd premolar
 Buccal periodontal tissues
 Indication:
 When ifra orbital block fails to provide anaesthesia to maxillary
canine
 Dental procedures involving both maxillary premolars
 contraindication:
 When infection or inflammation

88.  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

89.  Landmarks
 Mucobuccal fold,lforamen supra –orbital notch infra-orbital
notch, infra-orbital foramen, mental foramen
 2 methods:
 Intra-oral
 Premolar approach
 Incisal approach

91. 1.Nasopalatine nerve block/spenopalatine nerve block/
incisive 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

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

93. 2.Greater palatine nerve block/ anterior palatine nerve block
 Areas anaesthetized
 Palatal soft tissue – posterior aspect
 Palatal hard tissue
 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

95.  First reported by freidman and hochman in 1997 during development of
CCLAD system
 Muscles of facial expression and upper lip anesthesized.
 Nerves anesthetized
 ASA and MSA
 Areas anesthetized
 Pulpal anesthesia of maxillary incisors,canines and premolars
 Buccal and palatal attached gingiva
 Indications
 Performed with CCLAD
 When anterior cosmetic procedures are performed
 When anesthesia is desired from a single injection
 contraindications
 Patients with thin palatal tissues
 Patients who cannot tolerate the 3-4 minute adminstration time
 Long procedures >90 mins

96.  Advantage
 Less amount of LA is deposited 0.5ml/min
 Allows for accurate smile line assesment in case of aesthetic
restorations
 Disadvantage
 Very slow adminstration
 Can cause operator fatigue
 Maybe uncomfortable for the patient
 Technique sensitive

97.  Nerve anaesthetized
 Maxillary division of trigeminal nerve
 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

98.  Contra-indications
 Pediatric patients
 Inexperience operators
 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

99.  Complications
 Hematoma
 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
(common)
 Penetration into nasal cavity
 Patient complains – LA running down the throat – to
prevent keep mouth wide open
 Technique
 High tuberosity approach
 Greater palatine canal approach

101. I. Anterior and middle superior alveolar nerve block –
 Nerves anaesthetized
 Infraorbital nerve
 Inferior palpebral, lateral nasal and superior labial nerves
 Area anaesthetized
 Incisors and bicuspids on the effected side
 Labial alveolar plate and associated tissues
 Anatomical landmarks
 Pupil of the eye
 Infraorbital ridge
 Infrorbital notch
 Infraorbital depression
 Indications
 When Intra oral route is not feasable
 When attempts of intra oral anaesthesia have been ineffective

103. II. Maxillary nerve block –
 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

104.  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

106. INFERIOR ALVEOLAR NERVE BLOCK
Other common name- Mandibular block
Different techniques are:
 DIRECT METHOD.
 INDIRECT METHOD.
 METHOD OF CLARKE & HOLMES
 METHOD OF ANGELO SARGENTI
 VAZIRANI- AKINOSI TECHNIQUE
 GOW-GATE’S TECHNIQUE
 KURT THOMA EXTERNAL APPROACH

107.  Classical inferior alveolar nerve block
 Nerves anaesthetised- inferior alveolar nerve block and its
subdivisions
 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

108.  Contraindications
 Infection / acute inflammation
 Young children / mentally handicapped
 Landmarks
 Coronoid notch
 Mucobuccal fold
 External oblique ridge
 Retromolar triangle
 Internal oblique ridge
 Pterygomandibular raphe
 Occlusal plane of posterior mandibular teeth
 Complication
 Hematoma
 Trismus
 Transient facial paralysis (parotid gland)

109.  Anatomical structures - final position
 Disadvantages:
• 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

112. 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.

114. 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.

116. 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
deposited.

118.  Nerves anesthetized – inferior alveolar nerve, lingual nerve
buccinator nerves
 Area anesthetized
 one half of mandible upto mid line including lingual tissue and inferior
portion of the ramus of the mandible.
 Land mark-
 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.

122.  Advantages
• Atraumatic,
• pats. with restricted mouth opening.
• fewer post op complications.
• Disadvantages
• Difficult to visualize the path of needle and depth of
insertion.
• Complications
• hematoma, transient facial n. paralysis.

123. Nerves anaesthetised – inferior alveolar, mental,
incisive, lingual, mylohyoid, auriculotemporal and
buccal.
 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.

124.  Land marks-
 Extraoral- corner of mouth, lower border of the tragus, intertragic
notch
 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
pterygoid.
Gained popularity – single needle penetration, relies on soft tissue
landmarks – differ from patient to patient

126. OTHER NAME
Buccal nerve block or buccinator nerve block.
TARGET AREA
Buccal nerve as it passes over the anterior border of the ramus
LAND MARKS
 External oblique ridge
 Retromolar triangle
 Distal to 3rd molar
TECHNIQUE
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.

128.  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

130.  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

132.  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

133.  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

135. 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
 Tragus
 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.
Needle Used
21 gauge,7 to 8cm long.

138.  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

139.  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

140.  SYSTEMIC COMPLICATIONS
 Toxicity
 Idiosyncracy
 Allergy
 Anaphylactoid reaction
 Syncope

141.  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

142.  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

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

144.  Cause –
 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

145.  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

146.  Precautions
 Avoid bony contact
 Avoid heavy pressure
 Avoid movement of needle and patient

147.  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

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

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

150.  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

151.  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
 TENS
 Recall patient every 2 months for check up

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

153.  Prevention
 Use of sharp, sterile, disposable needle
 Aseptic technique
 Practice atraumatic methods
 Avoid repeated injections
 Use minimum volume
 Control infection

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

155.  “effusion of blood into extra-vascular spaces”
 Causes
 Arterial & venous puncture – common in PSA & Inf. Alv.
nerve blocks
 Patients with bleeding disorders
 Problem
 Bruise – may / may not be visible extra-orally
 Complications – pain & trismus
 Swelling & discoloration
 Prevention
 Knowledge of normal anatomy – proper technique
 Shorter needle – PSA, minimize the number of penetration
 Discard defective needles- barbed needles

156.  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, warm- pack application next day

157.  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

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

159.  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

160.  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

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

162.  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
 Warning sticker

163.  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 withdrawal

164.  Management
 Reassure the patient
 Resolves after action of LA is over
 Eye patches to the affected – eye drops
 Contact lenses if any – removed

165.  Toxicity / toxic overdose
 “Signs and symptoms that result from an overly high blood
level of a drug in various target organs and tissues”
 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

166.  Drug factors – Vasoactivity – vasodilation – increase in blood
concentration
 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

167.  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

168.  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 (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
hypotensiom presists.
 post seizure – CNS depression usually present

169.  “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

170.  “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
required, BLS

171.  “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
 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.

172.  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.

173.  Laryngeal edema – type of angio neurotic oedema-
life threating.
 Edema upper air way – laryngeal edema
 Lower air way affect broncioles- small.

174. Management
skin reactions-
 Delayed – non life threatening - oral histamine
blockers- 50 mg diphenhidramine,10 mg
chlorpheniramine 3-4 days.
 Immediate reaction—with conjunctivitis rhinitis-
vigorous management.
 0.3 mg epinephrine. IM
 50 mg diphenhydramine Im
 medical help summoned.

175.  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
 Laryngeal edema-
 Patient position ,oxygen, broncho-dilator, iv anti histamines.
 If condition not improving cricothyrotomy - achieve patent air way
if necessary give artificial ventilation.

176.  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.

177.  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 patients
 The addition of hyalurodinase for deeper penetration than
plain solutions
 Local anaesthesia without the use of needles
 Exploring the possibility of reversing local anaesthesia at
the conclusion of dental procedure

178. Centbucridine-
 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
Ropivacaine
 Amide anaesthetic similar to mepivicaine and bupvicaine
 Has greater margin of safety
 Decrease cardiotoxicity as compared to others

179.  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
venipuncture
 Consists of 5% cream containing 25mg/g lidocaine and
prilocaine respectively

180.  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

181.  First used described in 1949
 Provides more rapid onset of anaesthesia
 Decrease duration of action
 Possibility for allergic reactions

182.  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
anaesthesia
 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

183. THANK YOU