Local anesthetics work by blocking sodium channels in nerve cell membranes, preventing the propagation of action potentials and conduction of sensations. This document discusses the classification, composition, mechanisms of action, and examples of commonly used local anesthetic drugs and vasoconstrictors. It also covers the techniques for maxillary nerve blocks and factors that influence the onset and duration of local anesthesia.

1. LOCAL ANAESTHESIALOCAL ANAESTHESIA

2. Classification--Classification--
Based on composition –
 A) Natural – eg – cocaine.- PABA derivative
 B) synthetic nitrogenous compound –
para amino benzoic acid-procaine ( freely soluble), amethocaine ,
orthocaine( poorly soluble)
benzoic esters- benzocaine , pipercaine
acetanilide - lignocaine
quinolene - cinchocoline( nupercaine) ,buricaine( acridine derivative
 C) non Nitrogenous compounds – benzyl alcohol, propanediol
 D) miscellaneous with local action – clove oil , phenol , chlorpromazine,
diphenhydramine

3. Based on intermediate group --
Esters –
Benzoic acid
Cocaine
Benzocaine
piperocaine
Hexylcaine
Tetracaine
Amethocaine
Meprylcaine
isobucaine
Amides –
Articaine
Bupivacaine(marcaine)
Dibucaine
Lignocaine
Mepivacaine
Prilocaine(citanert)
Mepivacaine(carbocaine)
Etidocaine(duranest)
PABA
Chlorprocaine
Procaine(novocaine)
Propoxycaine(ravocaine)
butethamine
Quinolene derivative
Cenbucridine/buricaine

4. 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 mediated and
independent physico
chemical mechanism.
Biotoxin -eg
tetrodotoxin, sacrotoxin
Quaternary amonium-
scorpion venom
Benzocaine, N butyl
benzyl alcohol
Clinically useful agents
–Lignocaine etc

5. 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
5% Bupivacaine with 1:2 epin

6. Short Duration (approx. 30 minutes)
Lidocaine HCl 2%
Mepivacaine HCl 3%
Prilocaine HCl 4% (by infiltration)
Intermediate Duration (approx. 60 minutes)
Articaine HCl 4% + epinephrine 1:1,00,000
Articaine HCl 4% + epinephrine 1:2,00,000
Lidocaine HCl 2% + epinephrine 1:50,000
Lidocaine HCl 2% + epinephrine 1:1,00,000
Mepivacaine HCl 2% + levonordefrin 1:20,000
Mepivacaine HCl 2% + epinephrine 1:1,00,000
Prilocaine HCl 4% (via nerve block only)
Prilocaine HCl 4% + epinephrine 1:2,00,000
Long Duration (approx. 90 + minutes)
Bupivacaine HCl 0.5% + epinephrine 1:2,00,000

7. Composition--Composition--
Local anesthetic drug –eg lignocaine (20mg/ml) causes vasodilation.
Vasoconstrictor - eg adrenaline (1:80000 – 0.012mg) – decrease
blood flow to the site and absorption of LA.
Reducing agent - eg Sodium metabisulfite.
preservative – eg methylparaben/propylparaben/caprylhydrocuprino
toxin
For isotonicity – Normal Saline .
Vehicle – RL
Fungicide – thymol
Diluting agent – distilled water
Sodium hydroxide to adjust ph .

8. Individual Agents --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
 Pka (dissociation constant) –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

9.  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,

10.  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,

11.  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.

12. 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.

13. 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.

14. VASOCONSTRICTORSVASOCONSTRICTORS
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

15. CLASSIFICATION OF V.CCLASSIFICATION OF V.C
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

16. Proprietary
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

17. 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

18. 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

19. UNMYELINATED NERVE :
The spread of impulse is relatively slow forward creeping process
Conduction rate in C fibers is 1.2 msec compared with 14.8 to 120
msec in myelinated A-alpha and A-delta
MYELINATED NERVE:
Impulse conduction occurs by means of current leaps from node to
node , a process termed Saltatory conduction, it proves to be faster
and more energy effeciant
Conduction is usually progressive from one node to next in stepwise
manner
A minimum of perhaps 8 to 10 mm of nerve must be covered by
anesthatic solution to insure through blockade

20. MODE & SITE OF ACTIONS OF LA:
Local anesthetic interferes with the excitation process
in a nerve membrane in one or more of the
following ways:
1.Altering the basic resting potential of the nerve
membrane
2.Altering the threshold potential(firing level)
3.Decreasing the rate of depolarization.
4.Prolonging the rate of repolarization.

21. THEORIES OF ACTION OF L.ATHEORIES 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
SURFACE CHARGE THEORY:
 Action by binding to nerve membrane and changing its electric potential.
 Demerits- RMP not altered by LA.
LA act on nerve channel rather than surface

22. MEMBRANE EXPANSION THEORY-
LA molecules diffuse to hydrophobic regions of excitable membranes, producing a
general disturbance of the bulk membrane structure and expanding some critical
regions and preventing an increase in sodium permeability.
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.

23. MODE OF ACTIONMODE OF ACTION
Displacement of Ca+ Ions
↓
Binding of L A to receptor site
↓
Blockade of sodium channel
↓
Decrease in Sodium conductance
↓
Depression of rate of depolarization
↓
Failure to achieve threshold potential
↓
Lack of development of Propagated action potential
↓
Conduction blockade

24. Local anesthetic molecules
LA are Amphipathic, possess both Lipophillic & hydrophilic
molecules, generally at opposite end of molecules
Intermediate hydrocarbon chain, either Ester or Amide linkage
As prepared in laboratory LA are basic compounds, poorly soluble in
water, unstable on exposure to air --- little or no clinical value
So they are combined with acid (HCl) to form salts, soluble in water
& stable hence they are acidic salts of weak bases (AIPG-96)

25. Mechanism of actionMechanism 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.
 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.
•LA is ineffective in an areas of localized
infection since a low tissue pH is found in
these areas which prevents liberation of
free base (RN) thus interfering with
development of anesthesia [AIPG-92, 98;
MAHE-95, 99, 02; AP-98)

26. Factors affecting LA actionFactors affecting LA action
pKa – lower pka more rapid onset of action, more
number of free base forms
Increased lipid solubility – increased potency
Increased protein binding – more number of cationic
forms are attached to proteins at receptor sites hence
duration of action increased
Non nervous tissue – increased diffusibilty-
decreased time of onset
Vascularity – higher- duration & potency decreased

27. Ideal requirements-
 its 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

28. Technique for Maxillary BlockTechnique 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
 Contra-indication :Infection ,Dense bone covering
 Target area : Behind apices of tooth
 Landmarks : Mucobuccal fold/Crown & root length

29. Posterior Superior Alveolar Nerve Block
 Common names- Zygomatic block , Tuberosity block
 Area anaesthetized: Maxillary 3rd
, 2nd
& 1st
molar
(except mesiobuccal root of 1st
molar ),Bone & periodontium
 Landmarks:
 Mucobuccal fold
 Zygomatic process of maxilla
 Infratemporal surface of maxilla
 Anterior border of ramus and coronoid process
 Tuberosity of maxilla
 Direction : height of the mucobuccal fold of second molar
Upward-superiorly at 45 angle to occlusal plane
inward- medially toward the midline at 45 angle to occlusal plane
Backward- posteriorly at 45 angle to long axis second molar
Depth – 14-16mm,, 1.8ml of solution
No subjective symptoms, only objective
Complications – hematoma- pterygoid plexus of veins , mandibular anesthesia

30. Infra orbital nerve block
 Areas anaesthetized:
 Pulp of maxillary Central incisors – mesio buccal root of first molar
 Buccal periodontium, lower eyelid, lateral aspect of nose
 Upper lip
Methods:
a) intra oral – central incisor approach/premolar approach
b) Extra oral
Nerves anesthetized: anterior and middle superior alveolar nerves
Landmarks:
Supra orbital ridge , Infra orbital ridge ,Infra orbital notch
. Infra orbital depression ,Pupils of the eye
. Upper 2nd
premolar or anterior teeth
Depth- above the apex of tooth, 1-1.5ml
Complications- hematoma

31. Greater palatine nerve block
 Common – anterior palatine nerve block
 Areas anesthetized: posterior portion of
hard palate & overlying soft tissues,
anteriorly upto first premolar , medially to
midline
 Landmarks
 Greater palatine foramen – junction of
the maxillary alveolar process &
palatine bone
 Between the 2nd
& 3rd
molars – 1-1.5cms
away from gingival margin
Depth: 5mm, from opposite side , 0.45-0.6ml ,
45 angle to the mucosa

32. Nasopalatine nerve block
 Areas anesthetized :Anterior portion of Hard palate and over lying structures
back to the bicuspid area.
 Landmarks : Central incisor & incisive papilla
 Technique
 Single needle penetration – lateral to incisive papilla
 Multiple needle penetration
First- labial frenum, second- right angle to interdental papilla, third – 45
angle to incisive papilla
Depth: >5mm, 0.3-0.45ml

33. ANTERIOR MIDDLE SUPERIOR ALVEOLAR NERVE BLOCK
Developed by Friedman and hochman (AMSA)
Described as field block of terminal branches- subdural neural plexus
Area of insertion: on the hard palate about halfway along a imaginary line
connecting midpalatal suture to free gingival margin; the location is at the contact
point between first and second premolar
Areas anesthetized: pulpal anesthesia of incisors, canines, premolars along buccal
gingiva and palatal gingiva ( 0.5ml/min : 1.4-1.8ml)
Note: muscles of facial expression and upper lip not anesthetized
PALATAL APPROACH – ANTERIOR SUPERIOR ALVEOLAR( P-ASA)
Similar to Nasopalatine block but differs in final position where needle is positioned within
incisive canal
Areas – pulps of incisors & to lesser extent canines with labial and palatal gingiva

34. Maxillary nerve block
INTRA ORAL – high Tuberosity approach / greater palatine
foramen approach
Target area: 1) superior and medial of PSA block as maxillary nerve
passes through the pterygopalatine fossa 2) Through the greater
palatine foramen reaching pterygopalatine fossa ( depth: 30mm,
1.8ml)
Complications: hematoma- maxillary artery ,
penetration of the orbit-Volume displaces orbital structures,
periorbital swelling, proptosis, 6th
nr block – Diplopia, transient
loss of vision, optic nerve blocked, retrobulbar block /
hemorrhage, opthalmoplegias (common) .
penetration of the nasal cavity- Patient complains – LA running
down the throat – to prevent keep mouth wide open

35. EXTRAORAL-
- Midpoint of zygomatic arch
- Sigmoid notch
- Zygomatic notch
- Coronoid process
- Lateral pterygoid plate
Depth of insertion: max 45 mm
Direction: upward, forwards, inwards
Needle passes anterior to lateral pterygoid plate into
the pterygopalatine fossa
Depth of insertion 5 cm
Direction: upwards ,laterally ,backwards ,
inwards
Needle passes posterior to lateral pterygoid plate
below the foramen ovale

36.  Common- mandibular block, Halstead technique
 Areas anesthetized
 Mandibular teeth upto midline
 Body of mandible
 Inferior portion of ramus
 Buccal periosteum & mucous membrane
 Area of insertion???
 Landmarks
 Coronoid notch
 Vertical portion of Pterygomandibular raphe
 Occlusal plane of posterior mandibular teeth
 Depth: 20-25mm, 1-1.8ml
 Complication
 Hematoma
 Trismus
 Transient facial paralysis (parotid gland)
 Failure of anesthesia greatest: 15-20%
Inferior alveolar nerve block

37. CLOSED MOUTH TECHNIQUECLOSED MOUTH TECHNIQUE
 Common- Akinosi technique, tuberosity technique,
 Indication: patients unable to open mouth
 Nerves anesthetized – IAN, lingual, mylohyoid, incisive, mental
 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, Mucogingival junction maxillary teeth,
Anterior border of ramus, Orientation of bevel must be oriented away from the bone of
mandibular ramus (bevel faces toward mid line).
 Area of insertion: soft tissue overlying the medial border of the mandibular ramus
directly adjacent to the maxillary tuberosity at the height of the mucogingival junction
adjacent to maxillary third molar
 Depth : 25mm, 1.5-1.8ml
 Complications: hematoma and trismus (rare) , transient facial nerve paralysis
Akinosi (1977)/Vazirani (1960)

38. Gow gates technique- 1973Gow gates technique- 1973
Nerves anesthetized – inferior alveolar, mental, incisive, lingual, mylohyoid,
auriculotemporal and buccal.
Area anesthetized –all mandibular hard and soft tissue Upto mid line.
Landmarks:
Extraoral- corner of mouth, lower border of the tragus, intertragic notch.
Intraoral- height of injection established by placement of the needle tip just below
the mesiolingual cusp of maxillary second molar & penetration of soft tissues just
distal to the maxillary second molar
Area of insertion: mucous membrane on the mesial of mandibular ramus, on a line
from the intertragic notch to the corner of the mouth, just distal to second molar.
Target area: lateral side of the condylar neck, just below the insertion of lateral
pterygoid muscle insertion – 25mm depth , 1.8-3ml, wait for 3 to 5 min

39. Lingual nerve block – around 0.5ml, lingual nerve is Anteromedial to that of IAN
to mandibular foramen
 Area anesthetized :Anterior2/3rd
tongue, floor of mouth, lingual mucoperiosteum
Only used singly to operate on tongue, floor of mouth
Buccinator / long buccal nerve block
 Area anesthetized –Buccal mucosa & mandibular molar – mucoperiosteum
 Land marks -External oblique ridge, retromolar triangle
Distobuccal aspect of lower third molar at occlusal level
Retromolar pad sub mucosal at occlusal level
Advancing needle till resistance 2 to 4 mm depth
Right opposite to the tooth at the buccal gingivae or vestibule
SLOMAN’S technique: 1 cm above occlusal plane& few mm medial to anterior border
When infection: 1 cm below Stensons duct & approaching backwards

40. Mental nerve block
 Areas anesthetized: Lower lip, mucous membrane – anterior to mental foramen
 Landmarks :Mandibular bicuspids
 Indications :Surgery of lower lip or mucous membrane
 Area of insertion: mucobuccal at or just anterior to mental foramen
 Depth: until the periosteum of mandible, around 0.5ml
 Incisive nerve block- entry has to be made into mental foramen
 Extraorally the needle has to be oriented anteriorly and downwards

41. ComplicationsComplications
LOCAL COMPLICATIONS
 Needle breakage
 Pain on injection
 Burning on injection
 Persistent anesthesia or paresthesia
 Trismus
 Hematoma
 Sloughing of the tissue / soft tissue injury
 Facial nerve paralysis
SYSTEMIC COMPLICATIONS
Toxicity
Idiosyncrasy
Tachyphylaxis
Allergy
Anaphylactic reaction
Syncope

42. Needle breakageNeedle breakage
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
Prevention
 Correct gauge – 25 gauge
 Long needles – prevent penetration till hub
 Not to redirect when in tissue
Management
 Patient – not to move –
 Fragment visible – remove it
 Fragment not visible – inform patient – not necessary for
intervention immediately – Radiograph suggested

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

44. Burning on injectionBurning on injection
Causes
 Due to pH of solution
 Rapid injection
 Contamination
 Warm solution
Problems
 pH  disappears upon LA action – no residual effect
 Contaminated solution  other complications – trismus, edema, paraesthesia
Prevention
 Slow injection – 1ml / minute(ideal) , optimal – 1ml/10sec(6ml/min)
 Cartridge stored at room temperature – away from containers with alcohol /
other agents

45. Persistent anaesthesia / paresthesiaPersistent 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
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

46. TrismusTrismus
Definition -“difficulty in opening the
jaws due to muscle spasm”
Causes
 Trauma – muscle / blood vessel
 Irritating solution
 hemorrhage
 Infection
 Multiple needle punctures
 Excessive volume – distension of
tissues
Problems
 Pain / hypomobility
Prevention
Use of sharp, sterile, disposable
needle
Aseptic technique
Practice atraumatic methods
Avoid repeated injections
Use minimum volume
Control infection
Management
Heat therapy- Warm saline rinses, moist
hot packs
Analgesics -Aspirin, Codeine (30-60mg),
muscle relaxants
physiotherapy
Antibiotic regime -Possibility of infection

47. HematomaHematoma
 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

48. InfectionInfection
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

49. EdemaEdema
 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

50. Sloughing of tissueSloughing of tissue
Causes
 Epithelial desquamation – topical anesthesia – long time, heightened sensitivity
to LA
 Sterile abscess – secondary to prolonged ischemia – VC in LA  site – hard
palate
Prevention
 Topical – for not more than 1-2 minutes
 VC – minimal concentration in solution
Management
 Symptomatic – pain – analgesia
 Epithelial desquamation – resolve few days
 Sterile abscess resolve  7-10 days

51. Soft tissue injurySoft 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

52. Facial nerve paralysisFacial nerve paralysis
Cause
 LA solution into parotid gland – usually while giving Inf Alv Nr. Block, Akinosi
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
Management
 Reassure the patient
 Resolves after action of LA is over
 Eye patches to the affected – eye drops
 Contact lenses if any – removed

53. Systemic complicationsSystemic complications
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

54.  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

55.  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
 Medullary depression – mild fall in B.P– severe cases drops to 0 , Pulse ,
Respiration – similar effect

56. 0.00.0
0.50.5
1.01.0
1.51.5
2.02.0
2.52.5
3.03.0
3.53.5
4.04.0
4.54.5
5.05.0
5.55.5
6.06.0
6.56.5
7.07.0
7.57.5
8.08.0
8.58.5
9.09.0
9.59.5
1010
Cardiovascular system Central nervous system
LA Blood levels µg/ml
0.50.50.50.5
2.0
2.0
1.8
5.0
4.0
4.5
7.0
7.5
10.010.0
Normal blood level following I/O
injection. No CNS reaction
0.5 – 4.0 Anticonvulsant action 2
to 3mg/kg
4.5 – 7.0 CNS depression manifest
as excitation
7.5 – 10.0 CNS depression manifest
as tonic –clonic seizures
10.0+ Generalised CNS depression
Normal blood level following
intraoral injection. No CVS
reaction
1.8 – 5.0 Antiarrhythmic actions
5.0 – 10.0 Massive peripheral
vasodilation , Myocardial
depression
10.0 Intensive myocardial
depression, Cardiac arrest

57. MANAGEMENTMANAGEMENT
 Position pt.Position pt.
 Manage seizureManage seizure
 Administer OAdminister O22
 Ensure patent airwayEnsure patent airway
 Monitor vital signsMonitor vital signs
 Anticonvulsant after 4 to 5 mins. Diazepam 2mg/min IVAnticonvulsant after 4 to 5 mins. Diazepam 2mg/min IV
 Artificial ventilation if necessary.Artificial ventilation if necessary.
 Methoxamine 20mg IM for low blood pressureMethoxamine 20mg IM for low blood pressure
 Permit pt to recover before discharge.Permit pt to recover before discharge.

58. IdiosyncrasyIdiosyncrasy
“It is an adverse response that is neither an overdose nor an allergic
reaction”
The drug reaction which cannot be explained by any known
pharmacological or biochemical reaction”
Common cause – some underlying pathology/psychological /genetic
mechanism
Psychotherapy may be helpful
Treatment – symptomatic ..remember CAB’s!

59. AllergyAllergy
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 metabisulfite is also increasing

60. TACHYPHYLAXISTACHYPHYLAXIS
“ Increase tolerance to a given drug which is given
repeatedly”
DUE TO –
Edema , localized hemorrhage, clot formation,
transdution, hypernatremia, decrease tissue pH.

61. Alkalization of local anesthesia – speed the onsets of action, increases the efficiency .
Addition of carbondioxide and sodium bicarbonate prior to injection increases greater
comfort and rapid onset. Useful in inflamed and infected tissues.
Type B fibers (sympathetic tone) are the most sensitive followed by Type C (Pain), Type A
delta (temperature), Type A gamma (proprioception), Type A beta (sensory touch and
pressure) and Type A alpha (motor). Although Type B fibers are thicker than Type C fibers,
they are myelinated, and thus are blocked before the unmyelinated, thin C Fiber.
Loss of sensation following LA administration is in the following order- pain, temperature,
touch, proprioception- deep pressure, motor. The return of sensation is in reverse of
preceding order.
Nerve block- LA deposited near main trunk
Field block- L A deposited near large branch of peripheral nerve
Infiltration-L A deposited near small nerve endings
Intraligamentary injection used in vascular diseases, hemophiliacs. 0.2ml/root for 20sec

62. Kurl thoma / kanrowick/sigmoid notch - extra oral inferior alveolar nerve block technique
Clark & holmes- IAN block given higher to bypass sphenomandibular ligament .superior to
finger nail/coronoid notch palpation
Angelo sargenti- directed from maxillary premolar in a downward and backward direction
Fisher 123- indirect technique
Direct technique- first IAN,lingual,buccal
Direct thrust technique- brownlee
Greater palatine foramen directed anteromedially
Dumb bell shaped swelling seen after PSA block due to damage to pterygoid plexus of veins
Inferior alveolar nerve lies lateral to sphenomandibular ligament within pterygomandibular
space
Lidocaine used in management of arrhythmias
One cartridge contains -1.8ml
Mental foramen opens backward and lateral direction

63. Cocaine has intrinsic vasoconstrictive property, has sympathomimetic property
Procaine is a powerful vasodilator
PABA derivatives- have reversible antagonism with sulfonamides
When patient is allergic to ester and amide – diphenhydramine/quinolines can be used
For reversal of LA – vasodilator – phentolamine mesylate
Monoethylglydexylidide & glycinexylidide – two metabolites of lignocaine responsible for
sedative effect
Atracaine should be avoided in patients with sulfur allergy
Among amides bupivacaine has longer duration of action
Prilocaine and atracaine causes methemoglobinemia. Orthotoludine a metabolite of prilocaine
responsible. Symptoms :cyanosis of lips, mucosa, nail bed associated with respiratory
/circulatory problems. Rx – IV 1-2mg/kg of 1% methylene blue
Enzyme responsible for prevention of methemoglobinaemia is erthrocyte nucleotide
diphorase /methemoglobin reductase.
Only effective oral LA is tocainide hydrochloride

64. Drug of choice for malignant hyperthermia- dantrolene sodium
The drug of choice to counteract the CNS stimulation caused by accidental IV injection –
pentobarbital
EMLA – eutectic mixture of 2.5% lidocaine and 2.5% prilocaine. Used for topical intact skin
benzocaine, lidocaine base- water insoluble topical anesthetics
Tetracaine , benzyl alcohol, lidocaine hydrochloride – water soluble topical anesthetics
2- chlorprocaine- short duration of action , least toxic and preferred in children
Pka of lignocaine-7.9, mepivacaine-7.6,etidocaine-7.7,prilocaine-7.9,bupivacaine-
8.1,tetracaine-8.5, procaine-9.1
Lignocaine with less Pka readily dissociates with onset of action 3-5min
Higher the protein binding capacity longer the duration of action .Protein binding capacity of
prilocaine-55, lidocaine-64,tetracaine-75,bupivacaine-85,etidocaine-94
Duration of action of procaine-50min, mepivacaine-100min, lidocaine-100min, tetracaine-
175min, bupivacaine-175, etidocaine-200

65. Needless anesthesia – electronic dental anesthesia, based on gate control theory
WAND is the name of equipment used for computer controlled local anesthesia(CCLAD).
Delivers: slow rate of 0.5ml/min & fast rate of 1.8ml/min.
Jet injection (syrijet) are given under high pressure through small opening into the mucosa
or skin without much trauma. used for topical anesthesia(painless anesthesia)
Dentipatch – controlled realeased devices
Peripress, ligmaject, wilcox-jewett obtunder is an intraligamentary injection method.
Peridental injection is also known as intraligamental injection
STA –intraligamentary injection – using CCLAD instrument
Stabident, intraflow HTP anesthesia delivery system- intraosseous
Last resort of local anesthesia is intra pulpal
Wydase is hyaluronidase which enhances diffusion of local anesthetic
Extra oral mandibular nerve block – the needle directed posterior to the lateral pterygoid
plate below the foramen ovale
Extraoral maxillary nerve block- the needle directed anterior to the pterygoid plate into the
pertygopalatine fossa

66. Maximum dose of adrenaline in normal patient – 0.2mg, cardiac patient- 0.04mg
The bubble 1-2mm seen in cartridge is – nitrogen gas –prevent oxygen from being trapped
inside the cartridge potentially destroying the vasopressor
Nor adrenaline not recommended – predominant action on A receptors causes intense
vascular constriction – lack of blood supply and tissue necrosis
Felpypressin synthetic analogue of ADH used in hyperthyroidism patients, contraindicated in
pregnancy
1:200000 means 1000mg /200000ml= 0.005mg/ml
Lidocaine with vasoconstrictor maximum dose is 7mg/kg upto-500
Lidocaine without vasoconstrictor maximum dose is 4.4mg.kg upto 300
Topical anesthesia effective only upto 2-3mm
Sodium metabisulfite acts as reducing/antioxidant for vasopressor
Adrenline not used in ring block used in circumcision / minor surgical procedures of fingers
Cocaine increases the vasoconstrictive action of adrenaline. If LA with adrenaline is given,
risk of death is more in cocaine abusers. Hence known as walking bombs

67. Lidocaine 2% in dental , 5% in spinal most common
2% means 2gm in 100ml , 1ml =20mg
Maximum effective concentration of LA for topical use is 5%
Ropivacaine causes – cutaneous vasoconstriction
LA which does not vasocontrictor / least vasodilator- mepivacaine
Most toxic LA is dibucaine, topical- dyclomine
Excretion of LA is by kidney
Amides undergo total biotransformation in liver by microsomal enzymes
Esters hydrolysed by plasma cholinesterases
Inferior alveolar nerve block given into mandibular sulcus
Huber point – within needle- prevents deflection
The bevel of the needle is at 45
Recapping of needle- scoop technique

68. Permanent vision loss in oneeye following administration of localPermanent vision loss in oneeye following administration of local
anesthesia for a dental extractionanesthesia for a dental extraction
The exact mechanism of unilateral visual loss is not well understood. A proposed
mechanism is that an intraarterial injection of certain quality and pressure allows for
retrograde flow with the arteries, and may lead to occlusion of retinal and choroidal
vasculature. A variety of anatomic variants may explain this phenomenon. One
mechanism may be via the maxillary artery to the middle meningeal artery which
can anastomose with the ophthalmic artery. It is also possible that anesthetic
solution entered the inferior alveolar artery, passed through the middle meningeal
artery and anastomosed in the face, to occlude the ophthalmic artery.
Any occlusion of the ophthalmic artery may obstruct circulation to the choroid and
retina. Another possible mechanism may involve an injection through vascular
abnormalities that may exist due to chronic inflammation or previous trauma or
surgery, and that may cross the midline and a vegetative embolic phenomenon from
valve colonization

69. Trigeminal Nerve or GasserianTrigeminal Nerve or Gasserian
Ganglion BlockGanglion Block
Indications:
 Trigeminal Neuralgia
 Cancer related pain
 Cluster headaches
 Atypical facial pain
 Neurolytic block

70. Technique:Technique:
Maneuver must be done with X – ray or
fluoroscopic guidance to confirm needle
position
Patient under sedation
Patient in supine position with neck extended
Sterile preparation of the face is done

71. Technique:Technique:
Needle is directed perpendicular to the skin
above & lateral to the molars and should travel
superior & toward the medial aspect of External
Auditory Meatus
The needle is advanced until it touches the base
of the skull (appx – 50mm from the skin)
The needle is repositioned into the foramen
ovale

74. Concerns:Concerns:
Tough & Challenging
Painful procedure [either sedation or GA is
mandatory]
False negative aspiration can occur (CSF)
Complications: LOC, cardiac arrest, & apnea
Resuscitation team must be ready if needed
Hematoma & echymosis due to injury by the
needle

75. Int J Oral Surg. 1975 Dec;4(6):251-7.Int J Oral Surg. 1975 Dec;4(6):251-7.
Adler P.
The use of bupivacaine for blocking the Gasserian
ganglion in trigeminal neuralgia.
The patients remained free from typical paroxysmal attacks for
several months or even years.

76. Supraorbital & SupratrochlearSupraorbital & Supratrochlear
Nerve BlocksNerve Blocks
Indications:
Neuropathies
Surgical procedures
Localized trigeminal neuralgia
Neurolytic procedure may be done if diagnostic
injections provide excellent but short lived relief

79. Concerns:Concerns:
Hematoma formation & echymosis at the needle site
Damage to the Supraorbital artery
Apply pressure after the injection

80. Surg Radiol Anat. 2001;23(2):97-104.Surg Radiol Anat. 2001;23(2):97-104.
AndersenNB,BovimG,SjaastadO.
The frontotemporal peripheral nerves. Topographic
variations of the supraorbital, supratrochlear and
auriculotemporal nerves and their possible clinical
significance.
The optimum injection site for a selective SON block is 20-
30 mm from the midline (range 15-33 mm)
Distance between the main SON and STN branches (mean
15.3 mm)
The ATN is best blocked at a point located at the level with
and 10-15 mm (range 8-20 mm) anterior to the upper
origin of the helix.

81. Auriculotemporal Nerve Block:Auriculotemporal Nerve Block:
Indications:
TMJ analgesia
Neuralgia & atypical facial pain

83. Concerns:Concerns:
Hematoma
Entry into auditory meatus

84. Oral Surg Oral Med Oral Pathol Oral RadiolOral Surg Oral Med Oral Pathol Oral Radiol
Endod. 1998 Aug;86(2):165Endod. 1998 Aug;86(2):165
Schmidt BL, Pogrel MA, Necoechea M, Kearns G
The distribution of the auriculotemporal nerve around
the temporomandibular joint.
The average vertical distance between the superior condyle and
the nerve was 7.06 mm (+/- 3.21 mm); the range was 0 to 13
mm.
The auriculotemporal nerve trunk has a close anatomic
relationship with the condyle and the temporomandibular joint
capsular region

85. Cranio. 2003 Jul;21(3):165-71Cranio. 2003 Jul;21(3):165-71
Fernandes PR, de Vasconsellos HA, Okeson JP, Bastos RL,
Maia ML.
The anatomical relationship between the position of the
auriculotemporal nerve and mandibular condyle.
Nerve was found to be between 10-13 mm inferior to the
superior surface of the condyle and 1-2 mm posterior to the
neck of the condyle.