MAXILLARY AND MANDINULAR INJECTION TECHNIQUES LA- COMPOSITION

2. LOCAL ANESTHESIA

3. CONTENTS
 History
 Definition
 Ideal Requirements of Local anesthetic
 Neurophysiology
 Classification
 Composition
 Pharmacology of LA
 Individual Local anesthetics
 Topical anesthetics
 Vasoconstrictors
 Armamentarium
 Local complications
 Systemic complications
 Recent advances in local anesthetic delivery
 Conclusion
 Reference

4. History
 1842 Ether used as anesthetic by Dr. Crawford W. Long
 1850’s Cocaine isolated
 1853 Chloroform used as anesthetic by Dr. John Snow
 1884 Carl Koller introduces cocaine into medical practice
1884 Halsted injects cocaine directly into
mandibular nerve and brachial plexus
Carl Koller
1857 -1944
William S. Halsted

5.  1905 Procaine synthesized by Einhorn
 1921 Cartridge syringe marketed by Cook
 1947 Aspirating syringe developed
 1943 First anilide L.A (Lidocaine) synthesized by Lofgren
 1948 Lidocaine marketed
 1959 Disposable needle introduced

6. Methods of pain control
 Acupuncture Analgesia --
 Originated- CHINA, between 600BC to 200AD
 Hypnotism –
 Still employed
 Time consuming
 Audio Analgesia –
 1959 Gardner and licklider
 Loud noise used to produce analgesia

7.  Electric analgesia --
Peripheral nerve- Direct electric current
 Analgesia by Cold air–
 Inability to conduct action potential at low temperature
 Disadvantages - Mucosa dry, Cotton stick to mucosa, ulcers - if not
moistened.

8. Definition
Local anesthetics are drugs that reversibly inhibit nerve
conduction in peripheral nerve or depress excitation in
nerve endings, causing loss of sensation in a circumscribed
area.
- MALAMED

9.  Action must be reversible
 Non irritating to the tissues and produce no secondary reaction.
 Low degree of systemic toxicity
 Rapid onset
 Sufficient duration to be advantageous
PROPERTIES OF LA

10.  Potency to give complete anesthesia without the use of harmful
concentrated solution
 Sufficient penetrating power to be used as topical anesthetic
 Should be relatively free from producing allergic reactions.
 Stable in solution and undergo bio transformation readily within the body
 Either sterile or capable of being sterilized by heat without deterioration

11. NEUROPHYSIOLOGY

12.  Neuron or nerve cell-structural unit
of nerve system
 Transmits message from CNS and
all parts of body
 2 basic types of neuron: motor (efferent) and Sensory(afferent)
The Neuron

13. sensory neuron
 Peripheral process called (dendritic zone) -composed of arborization of
free nerve endings
 Free nerve endings respond to stimulus produced in the tissues
provoking an impulse that is transmitted centrally along the axon

14. motor neurons
 Nerve cell that conducts impulses from the CNS to the Periphery
 Structurally different
 Cell body is integral component of impulse transmission system but
also provides metabolic support

15. THE AXON
 The single nerve fiber axon is a long cylinder of neuron
 Cytoplasm(axoplasm) encased in a thin sheet-the nerve membrane
(axolemma)
 The axoplasm is separated from extracellular fluid by a continuous
nerve membrane.
 In some nerve this membrane is itself covered by a lipid rich layer of
myelin
 Sensory nerve excitability and conduction are both attributed to
changes developing within the nerve membrane

16.  The membrane is defined as flexible
 Non stretchable
 Bilipid layer of phospholipids
 And associated proteins , lipids and carbohydrates
 The lipids are oriented with their hydrophilic (polar)ends facing the outer
surface and the hydrophobic(nonpolar) end projecting to the middle of
the membrane

17.  CHANNEL PROTEINS are thought to be continuous pores through
membrane allowing some ions to flow passively where as other channels
are GATED permitting ion when the gate is open.
 The nerve membrane separates the highly diverse ionic concentrations
within the axon from outside
 The resting nerve membrane has an electric resistance 50 times > than
intracellular and extra cellular fluids-preventing the passage of Na, K, Cl
ions down their concentration gradient
When a nerve impulses passes , electric conductivity of the nerve membrane
increases 100 fold. This permits the passage of Na and K ions along their
concentration gradient thro’ nerve membrane

18. In myelinated nerve fiber
 75% lipid, 20% protein ,5% carbohydrate
 Myelinated nerve fibers enclosed in its own myelin sheath
 Nodes of Ranvier-constrictions along the myelinated nerve fiber
forms gap and is exposed directly to the extracellular fluid

19. Physiology of Nerve conduction
Once an impulse is initiated by a stimulus –
 The amplitude and shape of the impulse remains constant
 Regardless of the change in quality of stimulus and strength because:
 The energy used for its propagation is derived from the energy that is
released from the nerve fiber along its length and not solely from the
initial stimulus

20. • Nerve posses a resting negative electric
potential of -70mV that exists across the membrane.
• The interior of the nerve is negative relative to the
exterior
• Stimulus excites the nerve leading to
following sequences:
 Initial phase of slow depolarization the
electric potential within the nerve becomes
slightly negative
 When falling electric potential reaches critical
level, an extremely rapid phase of depolarization
results –threshold potential or firing potential

21.  This phase of rapid depolarization results in a reversal of the electrical
potential across the nerve membrane.
 The interior of the nerve is now electrically positive in relation to the
exterior.
 An electric potential of +40 mV exists on the interior of the nerve cell.

22.  After the steps of depolarization, repolarization occurs.
 The electric potential gradually becomes more negative inside the nerve cell
relative to outside until the original resting potential of -70 mV is again
achieved
 The entire process takes 1 millisecond , depolarization takes .3 msec,
repolarization .7msec

23. ELECTROCHEMISTRY OF NERVE
CONDUCTION
RESTING STATE : nerve membrane is –
 Slightly permeable to Na ions
 Freely permeable to K ions
 Freely permeable to Cl ion

24.  Potassium remains within the axoplasm , despite ability to diffuse
because the negative charge of the nerve membrane restrains the
positively charge ions by electrostatic attraction

25. Sodium migrates inwardly because both the concentration gradient and
electrostatic gradient favors this. Resting nerve membrane is relatively impermeable
to sodium prevents massive influx of sodium ions.
Chloride remains outside the nerve membrane
because the opposing, nearly equal ,electrostatic influence(electrostatic gradient
from inside to outside) forces outward migration.net result –no diffusion of chloride
through membrane

26. MEMBRANE EXCITATION - DEPOLARIZATION
0.3msec
 The rapid influx of the sodium ions into the interior of the nerve cell
because of the widening of the transmembrane ion channels causes
depolarization of the nerve membrane from its resting level to its
firing threshold
 Decrease in negative transmembrane potential of 15mv is necessary
for firing threshold
 Exposure of the nerve to LA raises its firing threshold.
 Elevating firing threshold means more sodium must pass through the
membrane to decrease the negative transmembrane potential to a
level where depolarization occurs.

27. Action Potential
(Impulse)
 The change or “overshoot” in electrical potential of nerve or muscle
fiber
 The basic unit of conduction in the nervous system
 Characteristic of axons
Because of absence of voltage-gated channels in cell body &
dendrites, Action potential does not reach there.

28. Action Potential Sequence
Involves the action of voltage-gated
channels
Exchanges of ions in and out of the
cell

29.  Voltage-gated Na+ Channels open and Na+ rushes into the cell
 Depolarization of nerve membrane from its resting potential to its firing threshold
= -50mV to -60mV

30. At about +40 mV, Sodium channels close, but now, voltage-gated potassium
channels open, causing an outflow of potassium, down its electrochemical
gradient
Repolarization begins and action potential is terminated

31. The return of membrane to its
resting potential
The voltage-gated K+ channels
close, but excess Potassium
accumulates outside the cell and
excess Na inside the cell.
equilibrium potential of the cell is restored

32.  The Sodium – Potassium Pump is left to clean up the mess…

33. The Sodium-Potassium Pump
 The energy necessary for this process is
obtained from the hydrolysis of ATP (an
energy carrying molecule)
Because the pump moves Na and K against their net electrochemical gradients,
energy is required to drive these actively transported fluxes.

34. REPOLARIZATION
 Caused by extinction (inactivation) of increased permeability to
sodium
 Many cells permeability to k ions also increases resulting in efflux
of k+ ions leading to more rapid membrane repolarization and return
to its resting potential

35. ABSOLUTE REFRACTORY PERIOD
 Immediately after a stimulus has initiated an action potential, nerve is
unable for a time to respond to another stimulus regardless of its strength
 When Na+ channels close, at peak of AP, they do not reopen for a time
RELATIVE REFRACTORY PERIOD
 New impulse can be initiated but only by a stronger than normal stimulus
 Membrane hyperpolarized
 Some Na+ channels still refractory

36. MEMBRANE CHANNELS
 Aqueous pores through the excitable nerve membrane called sodium
channels are molecular structures that mediate its sodium
permeability
 Sodium ion is thinner than either K ion or Cl ion but does not diffuse
freely down its concentration gradient because these ion attracts
water molecules and become hydrated.
 Sodium ions are therefore too large to pass through when the nerve
is at rest

37.  During depolarization sodium ions readily pass because of transient
widening of these channels
 This concept is visualized as opening of a gate during depolarization that
is partially occluding the channel in resting membrane

38. MYELINATED FIBRES
Impulse conduction in myelinated nerves
occur by means of current leaps from node to
node: saltatory conduction
If conduction of current is blocked at one
node it leaps (skips) over that node to the
next node to its firing potential producing
depolarization
Minimum of 8-10mm of nerves must be
covered by anesthesia to ensure thorough
blockade

40. MODE AND SITE OF ACTION OF LOCAL ANESTHETICS
By interfering the excitation process:
 Altering the basic resting potential of the nerve membrane
 Altering the threshold potential
 Decreasing the rate of depolarization
 Prolonging the rate of repolarization

41. Classification of Local Anesthetics
Based on Chemical structure
 Ester Group
Benzoic acid esters
– Benzocaine, Cocaine, Butacaine, Tetracaine, Piperocaine
Para amino benzoic acid esters
– Procaine, Chloroprocaine, Propoxycaine
 Amide Group
Lignocaine, Bupivacaine, Mepivacaine, Prilocaine, Articaine, Dibucaine,
Etidocaine, Ropivacaine
 Quinolone
Centbucridine

42. Based on duration of action
 Ultra short acting < 30 min
 2 % Lignocaine without a vasoconstrictor
 Short acting 45-75 min
 Procaine HCL 4%, 2 % Lignocaine with 1:1,00,000
Epinephrine
 Medium acting 90-150 min
 Mepivacaine, Prilocaine, 2 % Lignocaine with 1:2,00,000
Epinephrine
 Long acting ≥ 180 min
 Bupivacaine (400-450 min), Etidocaine, 5 % Lignocaine with
1:2,00,000 Epinephrine

43. Classification according to mode of delivery
Injectable
 Low potency
i. Procaine
ii. Cholroprocaine
■ Intermediate potency
i. Lidocaine
ii. Prilocaine
 High potency
i. Tetracaine
ii. Bupivacaine
iii. Ropivacaine
iv. Dibucaine

44.  Surface anesthesia
 Soluble
i. Cocaine
ii. Lidocaine
iii. Tetracaine
 Insoluble
i. Benzocaine
ii. Oxethazine
iii. Butylaminobenozoate

45. Based on its biological site & mode of action
 Class A :- Acting on receptor site located on external surface of nerve membrane –
biotoxins
( eg : Tetradotoxin , saxitoxin )
 Class B :- Acting on receptor site located on internal surface of nerve membrane –
Quaternary ammonium analogues of lidocaine , scorpion venom
 Class C :- Acting by a receptor-independent physico-chemical mechanism -
Benzocaine
 Class D :- Acting by combination of receptor & receptor-independent mechanisms
- most cinically useful local anesthetics ( eg ; Lidocaine, Mepivacaine , prilocaine )

46. ESTER GROUPS COMPOSED OF:
 An aromatic , lipophilic group
 An intermediate chain containing an ester linkage
 Hydrophilic secondary or tertiary amino group which forms water
soluble salts when combined with acids
 Another group of ester type compounds that lack the hydrophilic
substituted amino portion are useful as topical anesthetic. They are
almost insoluble in water

47. AMIDE GROUPS
Composed of:
 An aromatic ,lipophilic group
 An intermediate chain containing a amide linkage
 An hydrophilic secondary or tertiary amino group, which forms water
soluble salts when combined with acids

48. The synthetic compounds used as injectable LA are weakly basic in nature
and poor soluble in water they are however combined with HCl acid to
form salts that are soluble in water and acid in reaction
 Their chemical characteristic are so balanced that they have both
lipophilic and hydrophilic properties
 If hydrophilic group pre dominates the ability to diffuse into lipid rich
nerves is diminished. If the molecule is too lipophilic it is of little
clinical value as an injectable anesthetic since its insoluble in water and
unable to diffuse through interstitial tissues

49. Theories of Action of LA
 Acetylcholine theory
Ach involved in nerve conduction – Disapproved
 Calcium displacement theory
Ca2+ displaced from membrane site alters Na2+
permeability – Disapproved
 Surface charge (repulsion) theory
Cationic drug molecules bind to nerve membrane making it
more +ve, thus increasing the threshold potential causing
decreased excitability
–Disapproved

50. MEMBRANE EXPANSION THEORY -
Drug molecule penetrates the lipid portion of
membrane & brings about a change in the configuration of
lipoprotein matrix, leading to inhibition of Na2+ conductance
hence inhibiting neural excitation.
SPECIFIC RECEPTOR THEORY - Drug molecules bind to specific
receptors present on the external or internal axoplasmic surface of
sodium channels & by acting directly on them, decrease or eliminate
permeability to Na2+ leading to interruption of nerve conduction.

51. ACETYLCHOLINE THEORY
 States acetylcholine was involved in nerve conduction in addition to
its role as a neurotransmitter at nerve synapses
 There is no evidence that acetylcholine is involved in neural
transmission along the body of the neuron

52. CALCIUM DISPLACEMENT THEORY
 Nerve block was produced by displacement of calcium from some membrane
site that controlled permeability to sodium
 Evidence states that varying the concentration of calcium ions binding a nerve ,
does not effect LA potency –decrease credibility of the theory

53. SURFACE CHARGE( REPULSION ) THEORY
 LA acted by binding to the nerve membrane and changing the
electric potential at the membrane surface
 Cationic drug (RNh+) were aligned at the membrane water interface
and because some of the LA molecules carried a net positive charge,
--they made the electric potential at the membrane surface more
positive --thus decreasing the excitability of the nerve by increasing
the threshold potential

54.  Conventional LA act with in the membrane channels rather than at the
membrane surface
 Also the theory cannot explain the activity of the uncharged anesthetic
molecules in blocking nerve impulses (eg. Benzocaine)

55. MEMBRANE EXPANSION THEORY
 LA molecules diffuse to hydrophobic regions of excitable
membrane
 Producing general disturbance of the bulk membrane structure ,
expanding some critical regions in the membrane
 And preventing increase in the permeability to Na+ ions

56.  LA that are lipid soluble penetrate the lipid portion of the cell membrane
, producing a change in configuration of the lipoprotein matrix of nerve
membrane—decrease diameter of Na channels , which leads to inhibition
of both Na conductance and neural excitation
 This explains the LA activity of benzocaine which does not exist in
cationic form yet still exhibits potent topical anesthetic activity

57. SPECIFIC RECEPTOR THEORY
 Proposes LA act by binding to specific receptors on Na channel
 the action of the drug is direct and not mediated by some change in
general properties of the cell membrane
 both biochemical and electrophysiological studies have been
indicated that specific receptor site for LA agents exist in Na channel
either on its external surface or internal axoplasmic surface
 once the LA has gained access to the receptors permeability to the Na
ions is decreased or eliminated and nerve conduction is interrupted

58. There are 4 sites within the sodium
channels at which the drugs can alter
nerve conduction
1. Within the Na channel (tertiary amine
LA)
1. At the outer surface of Na channel
(tetradotoxin, saxitoxin)
1. At either the activation or inactivation
gates (scorpion venom)

59. Mechanism of action of LA
 Although the exact site at which the action of LA occurs is still
debated, there is a general agreement that LA agent progressively
lowers the amplitude of action potential, retards its rise, increases the
firing threshold, slows the velocity of impulse conduction and
lengthens the refractory period, leading to a CONDUCTION
BLOCKADE

60. Mechanism of action of LA at normal pH
BNHOH + HCl > BNHCl + HOH
Weak base strong acid acid salt water
BNHCl > BNH+ + Cl-
free base
BN + H+ > BNH+
+ + + + + + + + + + + + + + +
BNH+ > BN + H+
Ca ++
Nerve cell membrane
- - - - - - - - - - - - - - - - - - - - - - - -

61. Mechanism of action of L. A. at low pH - infection
BNHOH + HCl > BNHCl + HOH
Sub-mucosa
BNHCl > BNH+ + Cl-
Interstitial fluid
space
BN + H+ > BNH+
Nerve cell membrane
- - - - - - - - - - - - - - - - - - - - - - - - Ca ++
“Little”

62. HOW LA WORKS?
 Action of LA is to produce a conduction block to decrease the
permeability of the ion channels to Na ions
 LA selectively inhibits the peak permeability of Na whose value is
normally 5-6 times greater than the minimum necessary for impulse
conduction

63.  LA decreases both the rate of rise of action potential and its conduction
velocity
 LA produces very slight , virtually insignificant decrease in K+
conductance thro’ the nerve membrane

64. SEQUENCE OF ACTION OF LA
Displacement of Ca ions from the Na channel receptor site
↓
Permits
↓
Binding of LA molecule to this receptor site
↓
Produces
↓
Blockade of Na channels
↓
and decreases Na conductance

65.  LEADS TO
Depression of the rate of electric depolarization and failure to achieve the
threshold potential level along with a lack of development of propagated action
potential which is called conduction blockade
Nerve block produced by LA is called non depolarizing nerve block

66.  The mechanism where by sodium ions gains entry to the axoplasm –
initiating an action potential is altered by local anesthetics
 The nerve membrane remains in polarized state because ionic movement
fail to develop
 Because electric potential remains unchanged, local currents do not
develop and the self perpetuating mechanism of impulse propagation is
stalled.

67. ACTIONS ON NERVE MEMBRANES
 Two factors involved :
 Diffusion of the agent through the nerve
sheath.= lipid soluble, free base form (RN) is
responsible for diffusion
 Binding at the receptor site in the cell
membrane
 Clinical implication
LA with low pKa has high no:
of Lipophilic free be to diffuse , but
anesthetic action inadequate as at
intracellular pH 0f 7.4, only very small base
molecule dissociate to cationic form .
L.A with a high pKa, has very few molecules
available in RN form at tissue pH of 7.4. The
onset of action thus slow

68.  pKa or dissociation constant – It is the measure of a molecule’s affinity for hydrogen
ions (H+).
 When pH of the solution has the same value as the pKa of the local anaesthetic ,
exactly 50% of the drug exists in the RNH+ form and 50% in the RN form.
 The percentage of the drug existing in either form can be determined from the
Henderson – Hasselbalch equation
 Log Base/Acid = pH - pKa

69. Clinical Implications
LA solutions containing vasoconstrictors , contain sodium bisulfite
as an antioxidant , to prevent oxidation of LA solution
Due to this pH of solution is reduced .
When this solution injected , it takes time for LA to act as compared
to its plain counterpart , because it takes time for the tissue buffering
capacity to maintain normal pH

70. THE EFFECTIVENESS OF LA DEPENDS ON
CHEMICAL NATURE OF INDIVIDUAL DRUG
 Concentration of drug used
 Volume of solutions injected
 Rate of diffusion of both the anesthetic salt and free base
 Addition of vasoconstrictor which influences the time during which
the free base remains in contact with the nerves

71. FACTORS AFFECTING LOCAL ANESTHETIC ACTION
factor Action affected description
pKa Onset Lower pKa = more rapid onset of action, more RN molecules present
to diffuse through nerve sheath, thus onset time is decreased
Lipid
solubility
Anesthetic
potency
Increased lipid solubility = increased potency
Etidocaine produces conduction blockade at very low concentrations
whereas procaine poorly suppresses nerve conduction, event at higher
concentrations
Protein
binding
Duration Increased protein binding allows anesthetic cations (RNH+) to be more
firmly attached to protein located at receptor sites, thus duration of
action is increased
Non-nervous
tissue
diffusibility
Onset Increased diffusibility = decreased time of onset
Vasodilator
activity
Anesthetic
potencyand
duration
Greater vasodilator activity = increased blood flow to region = rapid
removal of anesthetic molecules from injection site, thus decreased
anesthetic potency and decreased duration

72. Local Anesthetic Molecule
● Ester-linked L.A= readily hydrolyzed in aqueous solution.
● Amide-linked L.A= relatively resistant to hydrolysis.
● Anesthetic amine or base = poorly soluble in water and unstable on
exposure to air. =has little or no clinical value = local anesthetics that
are used for injection are dispensed as salts, most commonly the
hydrochloride salt dissolved in either sterile water or saline .
A, Typical local anesthetic. B, ester type. C, Amide type.

73. Composition of LA Solution
 Lignocaine Hcl --- (Anesthetic) 24.64 mg (2 %)
 Adrenaline --- (Vasoconstrictor) 0.0125 mg (1:80,000)
 Sodium metabisulphite (Reducing Agent) 0.5 mg
 Methyl paraben --- (Preservative) 1 mg
OR
Cupryl hydrocuprinotoxin 1 mg
 Thymol --- (Fungicide)
 Distilled Water --- (Vehicle) 100 ml
OR
Ringer’s Lactate

74. PHARMACOLOGY OF LOCALANESTHETICS
UPTAKE
 Most local anesthetics , vasodilating properties
 Procaine= most vasodilating
 Cocaine = only L.A =vasoconstriction
 Vasodilatation =  the rate of absorption of L.A. into the blood=  duration and depth
of anesthesia.
ORAL ROUTE
 Except cocaine , L.A are absorbed poorly , if at all from the G.I. tract
 Also they undergoes significant hepatic first pass effect
TOPICAL ROUTE
 Applied to intact skin = No anesthetic action
 EMLA= can be used on intact skin
INJECTION
 Rate of uptake after s.c., i.m., or i.v., is related to the vascularity of the site of injection.
 I.V administration of L.A., is used for the management of ventricular
Dsyrhythmias

75. Biotransformation
Esters - Hydrolyzed in plasma by enzyme Pseudo cholinesterase
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

76. Amide =Primary site of biotransformation is liver
e.g. lidocaine --
Mono ethyl xylidide
Glycine xylidide xylidide
Xylidide
Hydroxy xylidide. Excreted kidney .
Significant renal diseases – contra indication.

77. Individual Agents
 Lignocaine
 Classified under – Amide
 Chemical formula -2-diethylamino 2,6 acetoxylidide Hcl
 Prepared by : 1943 – Nils Lofgrens- intro 1948(dentistry)
NH.CO.CH2.N
CH3
CH3
C2H5
C2H5

78.  Metabolised- Liver by microsomal fixed function oxidases to monoethyl glycerine and xylidide
 Excretion -<10% unchanged, >80%-metab
 Vasodilation Properties -less than Procaine, more than Mepivacaine
 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
 Effective dental conc. = 2%
 Topical anesthetic action–yes , in 2% in the form of gel
=5% in the form of ointment
=10%- 15% in the form of spray

79.  Recommended dose
With V.C = 7mg/kg not>500mg
Without V.C= 4.4mg/kg not>300mg
 For children with VC 3.2 mg/kg
 Council for dental therapeutics- ADA suggest
4.4mg/kg ( with /without VC)
 It is 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.

80. Individual Agents
Bupivacaine
 Classified under- amide
 Potency - 4 times that of lidocaine , prilocaine
 Toxicity- <4 times – Lignocaine, Mepivacaine
 Metabolism –Liver by Amidases
 Excretion by kidney (16% unchanged)
 Vasodilation- relatively significant, greater than those of lidocaine, prilocaine and mepivacaine
 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 BW
 Absolute maximum dose-not> 90mg

81.  Available as 0.5% solution 1:2,00,000 (vc)
 Indication- Lengthy dental procedure/deep anesthesia-e.g. Pulpal
anesthesia->90- min.
Full mouth reconstruction.
Extensive perio surgery.
Management of post op pain.
 Duration –Pulpal- 90- 180 min
Soft tissue- 4-12 hrs.
 Contra indication- in children-anticipating self trauma .

82. Procaine
 Classified under –Esters
 Chemical formula- 2Diethylamino ethyl 4aminobenzoate hcl
 Metabolism- hydrolyzed in Plasma by plasma pseudocholine esterases
 Excretion >2%unchanged, 90% -PABA, 8% diethyl aminoethanol in urine.
 Pka - 9.1,
 Vasodilating property –High
 Effective Dental concentration -2%-4%
 Anesthetic half life -6min
 Topical Anesthetic action – not clinically acceptable
 Max recommended dose for peripheral blocks -1000mg
 Onset of action - slow
 no pulpal anesthesia ,
 > incidence allergy,
 Used in breaking arteriospasm

83. Mepivacaine
 classified -amide type
 Metabolism - microsomal fixed function oxidases in liver.
 Maximum dose 4.4 mg/kg , absolute max dose-300mg.
 Excretion-1-10% unchanged urine.
 Pka-7.6, pH plain – 4.5, pH with vasoconstrictor- 3.0-3.5
 Onset of action – 1 ½ to 2 min
 Anesthetic half life - 90min
 Mild vasodilator, 3% mepivacaine is used in patients in whom a vasoconstrictor is not
indicated.
 Low reported cases-allergy.
 over dose -CNS stimulation followed by depression.

84. Properties of local anesthetics
85
notes main unwanted effects plasma
half-life
tissue
penetration
duration onset drug
Rarely used, only as spray for upper
respiratory tract
cardiovascular and CNS effects
due to block of amine uptake
~1h good medium medium cocaine
no longer used CNS: restlessness, shivering,
anxiety, occasionally convulsions
followed by respiratory
depression
CVS: bradycardia and decreased
cardiac output, vasodilatation,
which can cause cardiovascular
collapse
<1h poor short medium procaine
widely used for local anaesthesia .also
used i.v. For treating ventricular
arrhythmias mepivacaine is similar
less tendency to cause CNS
effects
~2h good medium rapid lignocaine
(lidocaine)
used mainly for spinal and corneal
anaesthesia
as lignocaine ~1h moderate long very slow amethocaine
widely used because of long duration
of action. Ropivacaine is similar, with
less cardiotoxicity
as lingocaine, but greater
cardiotoxicity
~2h moderate long slow bupivacaine
widely used, not for obstetric
analgesia because of risk of neonatal
methaemoglobinaemia
no vasodilator activity, can cause
methaemoglobinaemia
~2h moderate medium medium prilocaine

85. Anesthetics for topical applications
 Component of Atraumatic intra oral administration.
 Conventional Topically applied anesthetics – unable to penetrate intact skin.
 To be effective Topically applied LA- Greater conc.-Greater degree of
toxicity- few agents can be used safely
 Topically Applied LA lack vasoconstrictor- greater absorption – greater
blood levels
 Effective only on the surface (2-3mm)
 Available as ointments, sprays, emulsions and strips, aerosol , gels.

86. Water insoluble topical anesthetics
Insoluble in water- soluble in vehicle such as alcohol, polyethylene glycol,
propylene glycol, or carboxymethyl cellulose -make them amenable to
surface application
Advantage=1. By incorporating the anesthetic into a viscous liquid, a gel,
or an ointment, they remain in contact with the area for a longer period,
thereby increasing the duration of action.
2. poorly absorbed into the circulation

87. Benzocaine : Poor solubility in water
Poor absorption into CVS
Remains longer at the site of application
Prolonged use – localized allergic reaction
Systemic Toxic reaction unknown
Availability as: Aerosol, Gel, Gel patch, Ointment , Solution
Lidocaine Base : Available as flavored gels, ointments,, aerosol spray
Produce anesthesia within 15 sec, duration of action = 30 min

88. Cocaine hydrochloride :
 Used exclusively as Topical Anesthetic
 Rapid onset of topical anesthesia
 Absorbed rapidly, eliminated slowly
 Duration of action =2hrs
 Cause Habituation, so use as topical anesthetic in dentistry not recommended
Lidocaine Hydrochloride :
 Used in a 2% or 4% concentration.
 Water soluble , so tends to penetrate tissue better than lidocaine base.
 Maximum recommended dose is 200 mg.
 Lidocaine viscous 2% is a flavored syrup that may be used as an oral rinse or gargle or
swallowed to provide topical anesthesia of the mouth and pharynx. In this form it is
particularly useful in those patients who tend to gag during dental procedures.

89. EMLA (Eutectic Mixture Of Local Anesthetics)
 Cream (Lidocaine 2.5% +Prilocaine 2.5%)
 Emulsion in which oil phase is eutectic mix of lidocaine and
prilocaine in a ratio of 1:1 by wt.
 Supplied as 5g or 30 gm tube or as an EMLA disc.
 Can be used to provide surface anesthesia on intact skin.
 Contraindicated=pts with congenital idiopathic
methemogloulinemia, infants under age of 12 months who are
receiving methemoglobin inducing agents
pts. with known sensitivity to amide type local anesthetics

90. Vasoconstrictors

91. Need….
 All clinically effective injectable LA have some degree of vasodilating activity
 ↑ absorption of LA into CVS → removal from injection site
 Rapid diffusion of LA from inj site → ↓ duration of action & depth of
anesthesia.
 Higher plasma level of LA → ↑ risk of toxicity
 ↑ bleeding at inj site.
 Addition of vasoconstrictor to LA..
 Constriction of blood vessels → ↓ tissue perfusion
 Slow absorption into CVS → low anesthetic blood level → ↓ risk of toxicity.
 Higher volume of LA around nerve → ↑ duration of action
 ↓ bleeding at inj site

92. Classification
 Pyrocatechin derivatives
- Epinephrine & Norepinephrine
 Benzol derivatives
- Levonordefrin
 Phenol derivatives
- Phenylephrine
 Catecholamines
 Epinephrine, Norepinephrine
Dopamine, Isoproterenol, Levonordefrin
►Noncatecholamines
 Amphetamine, Ephedrine, Methoxamine

93. Epinephrine
( Adrenaline )
 A sympathomimetic amine produced by adrenal medulla.
 Acts directly on both ά and β adrenergic receptors ( β effect predominate )
Biotransformation :
- Re uptake by adrenergic nerves
- inactivated in blood by catechol-O-methyltranferase (COMT) & monoamine oxidase
(MAO)( in liver)
- 1 % excreted unchanged in urine
Clinical application :
- Acute allergic reactions
- Bronchospasm
- Cardiac arrest
- For hemostasis
- With L.A

94. SELECTION OF VASOCONSTRICTOR
 The length of surgical procedure
(Duration of pulpal and soft tissue anesthesia with 2% lidocaine lasts for only 10 min;
the addition of 1:50,000, 1:80,000,1:100,000,increases this to app 60 min)
 Requirement for hemostasis during surgical procedure.
(Epinephrine is effective in providing blood loss during surgical procedures, however
it also produces rebound vasodilatory effect. Felypressin constricts venous
circulation more than arteriolar so minimum value in hemostasis)
 Requirement for post operative pain control.
(plain LA produce pulpal anesthesia for short duration )
 Medical Status of the Patient.
( Benefits and risk of using LA with vasoconstrictor should be weighed against
benefits and risks of using plain LA in medically compromised patients )

95. Contraindications for the use of vasoconstrictor in
LA
Patients with more significant cardiovascular disease
Patients with certain noncardiovascular diseases (e.g., thyroid
dysfunction , and sulfite sensitivity)
Patients receiving Monoamine oxidases inhibitors, Tricyclic
antidepressant , and phenothiazines)

96. Armamentarium
Essential components :
 Syringe
 Needle
 LA solution in the form of cartridge, or multidose vial
Syringe -
Types:
1. Non Disposable (reusable syringe)
a. Breech- loading metallic cartridge type aspirating
b. Breech- loading plastic cartridge type aspirating
c. Breech- loading metallic cartridge type self aspirating
d. Pressure syringe
e. Jet injector
2. Disposable (Plastic syringe)
3. Safety Syringes.
PISTON WITH HARPOON FINGER GRIP
NEEDLE ADAPTOR
SYRINGE BARREL
THUMB RING
Breech loading, metallic cartridge-aspirating
Breech loading plastic cartridge-aspirating

97. Breech loading metallic cartridge-Self aspirating
Pressure syringe –used for intraligamentary
injection , pulpal anesthesia
Jet injectors

98. PRESSURE SYRINGE (1905) DESIGNED FOR A PERIODONTAL
INJECTION
WILCOX- JEWETT OBTUNDER

99. ADVANTAGES DISADVANTAGES
Breech loading, metallic cartridge-
aspirating
Visible cartridge
Aspiration- 1 hand
Autoclavable
Rust resistance, Long lasting
Weight
Size-Too big
Possibility of infection
Breech loading plastic cartridge-
aspirating
Light weight
Cartridge visible
Rust resistance, Long lasting
Low cost
Size – Too big / small
Possibility of infection
Repeated autoclaving – Plastic looses its
properties
Breech loading metallic cartridge-Self
aspirating
Cartridge visible
Autoclavable
Easier to aspirate
Piston is scored (indicates the volume of
anesthetic administered)
Weight
Possibility of infection
Finger has to be moved from thumb ring
to disc-Aspiration
Takes time to accustom

100. Pressure syringe –used for
intraligamentary injection , pulpal
anesthesia
Measured dose
Overcomes tissue resistance
Non threatening – Cartridge protected
Cost
Inject too rapidly -Possibility
Jet injectors
Does not require – needle
Very small volume – Delivered
Topical anesthesia-effective
Inadequate – Pulpal / Regional block
Patient disturbed by jolt of jet.
Cost
PDL damage – common
Disposable syringe Single use
Sterile-Till opened
Light weight
Does not accept – Dental cartridge
Aspiration – Difficult – requires the use
of both hands

101. Needle
■ Type
● Stainless steel – Disposable with plastic
hub
●steel – reusable for cartridge syringes
●disposable syringes with mounted
needle with safety covering
● disposable cartridge mounted needle
● disposable loaded syringe with mounted
needle and the syringe preloaded with
anesthetic agent
■ Parts – Bevel
Shank
Hub
needles long short
length 30 mm 20 mm
32 mm
35 mm
Gauge 23 25
25 27
27 30
30

102.  Cartridge —
Consists of --
 Cylindrical glass tube
 Stopper
 Aluminum cap
 Diaphragm

103.  Additional Armamentarium –
 Topical antiseptic
 Topical anesthetic
 Cotton Gauge
 Applicator Stick.
 Haemostat

104. COMPLICATIONS

105. Definition
Anesthetic complication :
Any deviation from the normally
expected during or after securing of regional analgesia.

106. Classification
 Primary or secondary
 Mild or severe
 Transient or permanent
 1. Those attributed to the solutions used.
2. Those attributed to the insertion of needle.
 Local complications
Systemic complications

107. LOCAL COMPLICATIONS
 Classification of Local complications
Complications arising from
 Drugs or chemicals :
Soft tissue injuries
Sloughing of tissues
 Injection techniques :
Needle stick injuries
Needle breakage
Hematoma
Failure to obtain anesthesia

108.  Both drugs and injection techniques
Pain on injection
Burning on injection
Infection
Trismus
Edema
Mucosal blanching
Persistent anesthesia or paresthesia
Persistent or prolonged pain
Post injection herpetic lesions
Bizarre neurological symptoms

109. Needle breakage

110. Causes :
Primary – sudden unexpected movement
Secondary – size/diameter
previously bent
redirection
poor manufacture
forcing against resistance
Problem : Encased in scar tissue
Infection is rare

111. Prevention :
Do not surprise with sudden insertion
An informed patient is always a better patient and is much more cooperative
Do not attempt to force against resistance
Do not attempt to change the direction
Do not use too fine gauge
Do not insert completely
Management :
Shira’s management
If the fragment is
visible
If the fragment is not visible
and cannot be readily retrieved

112. Persistent anesthesia
Persistent anesthesia / paresthesia – Anesthesia or altered sensation well
beyond the expected duration.
 More common with prilocaine
 Leads to self-inflicted injury
 Duration depends on severity and extent of nerve injury

113. Causes :
 Contaminated or wrong solution
 Trauma to nerve or nerve sheath – “electric shock”
 Hemorrhage around nerve sheath
Problem : resolve within 8 weeks
can lead to self inflicted injuries
After the nerve injury,
 Hyperesthesia - increased sensitivity to noxious stimuli
 Dysesthesia - painful sensation to nonnoxious stimuli

114. Prevention :
Strict adherence to injection protocol
Management : Mc carthy’s management
 Reassure
 Examine – degree and extent
 Reschedule the pt. every 2 months
 If persists after 1 year-neurologist consult

115. Bizarre neurological symptoms
 Facial nerve paralysis
 Visual disturbances
1. Squint
2. Diplopia
3. Amaurosis
4. Permanent blindness

116. Facial nerve paralysis
Causes :
when solution is deposited
 Directly : vicinity of terminal branches
- infra orbital nerve block
- Para periosteal inj for maxillary
canine
 Indirectly : deep lobe of parotid gland
- IANB, vazironi-akinosi

117. Problem :
 “Transitory” – few hours
duration = soft tissue anesthesia of drug
 Primary – cosmetic
Face appears lopsided
 Secondary – Unable to close one eye
Protective lid reflex is abolished
Winking and blinking is impossible

118. Prevention :
Adherence to protocol with the inferior alveolar and vazirani akinosi nerve blocks.
Management :
Reassure
Eye patch should be applied
Record the incident the on patient’s chart

119. Visual disturbances
Causes:
 Vascular spasm
 Intra –arterial injection
 Inadvertent anesthesia
Prevention:
 Injection protocol
 Knowledge of anatomy
Management: Pass off within 2-3 hrs.

120.  Diplopia : infraorbital block
- Infiltration into the orbit
- Intra-arterial injection
 Transient squints : PSA and maxillary block
- paralysis of extrinsic muscles
Explanation - diffusion into the orbit from the pterygopalatine ganglion
and infratemporal fossa via infraorbital fissure

121. Trismus
Definition :
A prolonged tetanic spasm of the jaw muscles by which the
normal opening of the mouth is restricted (locked jaw)
 Commonly seen in inferior alveolar nerve block

122. Causes:
 Primary – trauma to muscles and blood vessels in the infratemporal
fossa
 Secondary – contaminated solutions
“myotoxic” properties
hemorrhage
low grade infection
multiple needle penetrations
barbs
excess volume of solution

123. Myotoxicity
Necrotic with edema, fibrin deposits
And numerous macrophages
Damage surrounding the needle track

124.  Barbs
Unused needle Needle after contact
With the bone

125. Trismus
Problem :
Acute phase –pain from hemorrhage leads to muscle spasm,
limitation of movement
Chronic phase – this phase begins if treatment is not begun
● chronic hypo mobility secondary to organisation of clot , fibrosis and
scar contracture
● infection also produces through
increased pain,
increased tissue reaction,
scarring

126. Prevention:
 Use sharp, sterile needle
 Proper care and handle of LA catridges
 Use aseptic techniques
 Atraumatic injection technique
 Avoid multiple insertions
 Use minimum volume
TRISMUS IS NOT ALWAYS PREVENTABLE

127. Management: improvement within 48-72 hrs.
 Heat therapy – 20 min / hr.
 Warm saline rinses
 Analgesic – Aspirin 325 mg
 Muscle relaxation – Diazepam 10 mg BD
 Physiotherapy – 5 min every 3-4 hrs.
 Antibiotics – if pain and dysfunction persists beyond 48 hr.
Complete recovery in 6 weeks (4-20 days )

128. Soft tissue injuries

129. Self inflicted injuries

130. Causes:
 Primary – soft tissue anesthesia last longer than pulpal anesthesia
Problem: usually occurs in young child or handicapped individual
 Pain and Behavioral problems
Prevention:
 Cotton roll
 Warn the patient or guardian
Management: - symptomatic
 Analgesics
 Antibiotics
 Saline rinses
 Petroleum jelly

131. Hematoma
 The effusion of blood into the extra vascular space
 Large – IANB , PSA
Rare – palatal injections
 Causes:
Arterial or venous puncture
Artery – rapidly increases in size
Vein – may not result
Posterior superior alveolar nerve block
Bilateral mental nerve block

132. Problem:
 “bruise”
 Trismus and pain
 Swelling and discoloration- 7-14 days
 Inconvenience to patient
embarrassment to dentist
Prevention:
 Knowledge of anatomy
 Modify injection technique
 Use of short needle for PSA nerve block
 Minimize number of needle penetrations
 Never use needle as probe in tissues
HEMATOMA IS NOT ALWAYS PREVENTABLE

133. Management:
Immediate – direct pressure for 2 min onto the site of bleeding
PSA nerve block & maxillary nerve block
 Largest and most esthetically unappealing
 Accommodate larger volume of blood
 Difficult to apply direct pressure
 Ceases when external pressure exceeds
 Digital pressure and application of ice
Subsequent:
 Trismus – treat
 Discoloration – resorb over 7-14 days
 If Soreness develops – Adv aspirin
 Do not apply heat – for at least 4-6 hrs
 “tincture of time”
With or without treatment hematoma will be present for 7-14 days

134. Pain on injection
Causes :
careless technique
dull needle
rapid deposition
barbs
Problem :
increases patient anxiety
sudden unexpected movement
Prevention :
proper technique :
use topical before injection
use sharp, sterile needles
inject slowly
correct temperature of solution
Management :
No management is necessary

135. Burning on injection
Bupivacaine causes more pain
Causes :
Primary – pH of the solution
without vasoconstrictor – 5
with vasoconstrictor - 3
Secondary – rapid injection especially in the denser tissues
contamination of solution
temperature of solution – solution warmed to normal body temperature
usually considered “too hot” by the patient.

136. Problem :
duration is few seconds and low intensity
development of edema, paresthesia, post anesthetic trismus etc.
Prevention : slow injection
Ideal rate - 1 ml/min
Recommended – 1.8 ml/min
● proper storage and temperature – cartridge should be stored at room temperature either in the
container in which it was shipped or in a suitable container without alcohol or other sterilizing agents.
● alkalinisation of local anesthetics – by addition of 1ml of 1% sodium bicarbonate
(Alkalinization of amide local anaesthetics by addition of 1% sodium bicarbonate solution. Milner QJ1, Guard BC, Allen JG.
Eur J Anaesthesiol. 2000 Jan;17(1):38-42)
Management : Formal treatment is not indicated , in situations like post injection discomfort, edema ,
paresthesia management of that specific problem is indicated.

137. Infection - become extremely rare after the introduction of sterile needles and
cartridges
Causes : Major – contamination of needle
Other – improper tissue preparation,
injecting into an area of infection
Problem : leads to Trismus if not recognized
Prevention : use sterile needles
proper handling of needles and
cartridges
proper tissue preparation

138. Management : symptomatic
 Analgesics
 Antibiotics – 7-10 day course
 Physiotherapy
 Heat therapy
 Anti inflammatory drugs
 Muscle relaxants
 Incision & drainage if necessary

139. Edema
Causes :
 Trauma during injection
 Infection
 Allergy – Angioedema ( usually occurs as a common response to ester type topical
anesthetics)
 Hemorrhage
 Contaminated solution
 Hereditary Angioedema

140. Problem : pain & dysfunction of the region
angioneurotic edema caused by topical anesthetics can cause air way
obstruction (life threatening)
Prevention : proper handling
atraumatic injection technique
complete medical history
Management : analgesics
antibiotics
hematoma management

141. Hereditary Angioedema
 Sudden onset of non pitting edema
 Affects face, extremities and mucosal surfaces of intestine & respiratory
tract
 Precipitating factors-manipulation in mouth
 Lips, eyelids & tongue are involved
 May lead to laryngeal obstruction

142. Sloughing of tissues
 Prolonged irritation and ischemia of gingival soft tissues may lead to unpleasant
complications including epithelial desquamation and sterile abscess
Causes :
 Epithelial desquamation :
prolonged topical anesthesia
increased sensitivity of tissues
 Sterile abscess :
prolonged ischemia resulting from the use of LA with vc ( usually norepinephrine)
Problem : pain & infection

143. Prevention :
use topical anesthetics as recommended
do not use high concentrated solutions
(vasoconstrictor)
Management : symptomatic
analgesics, topical ointment (orabase)
-Epithelial desquamation resolve in few days
-Sterile abscess resolve in 7-10 days

144. Post anesthetic intra oral lesions
Causes :
Recurrent aphthous stomatitis (common)
Herpes simplex
Problem :
mild burning or itching sensation
acute sensitivity in the ulcerated area
Prevention : no means of prevention
Acyclovir qid – minimizes the acute phase

145. Management : Primarily symptomatic
If complains of severe pain -
 Topical anesthetics
 A mixture of equal amounts of Diphenhydramine (benadryl) & milk of
magnesia oral rinses
 Orabase without kenalog
 Tannic acid preparation
The ulcerations usually last 7-10 days with or without treatment

146. SYSTEMIC COMPLICATIONS

147. Adverse drug reactions
 Overdose reactions : are those clinical signs & symptoms that
manifest as a result of an absolute or relative over administration of a
drug
 Allergy : is a hypersensitive state acquired through exposure to a
particular substance capable of inducing altered bodily reactivity
(allergen)
 Idiosyncrasy :
A qualitatively abnormal , unexpected response to a
drug, differing from its pharmacological actions and thus resembling
hypersensitivity
All instances of idiosyncratic reaction have an underlying
genetic mechanism

149. Comparison of Allergy and Overdose
Clinical response Allergy Over dose
Dose Non dose related Dose related
Signs and symptoms Similar, regardless of
allergen
Relate to the
pharmacology of drug
administered
Management Similar (epinephrine ,
histamine blockers
Different , specific for
drug administered

150. OVERDOSE

151. Causes of Overdose
 Slow biotransformation of drug
 Slow elimination of unbiotransformed drug
 Administration of too large a total dose
MRD of local anesthetics should be determined after consideration of the
patients age, physical status, and body weight.
 Rapid absorption from the injection site
 In advertent intravascular administration

152. Retrograde flow

153. Prevention of intravascular administration
 Use an aspirating syringe
 Use a needle no smaller than 25 Gauge
 Aspirate in at least two planes
 Slowly inject the anesthetic
Intimal obstruction of blood aspiration

154. Anterior superior nerve block 0.7
Long buccal nerve block 0.5

156. Signs & symptoms of overdose (contd)

157. Pathophysiology

160. Management of overdose
mild overdose reaction
 Slow onset ( > 5 min)
P→A→B→C→D
D
1. Reassure
2. Administer oxygen
3. Monitor vital signs
4. Establish IV infusion (optional)
5. Recovery
6. Dental treatment may be continued
Slow onset (> 15 min)
P→A→B→C→D
D
1. Reassure
2. Administer oxygen
3. Monitor vital signs
4. Administer an anticonvulsant (Diazepam
5mg/min or Midazolam 1mg/min)
5. Summon medical assistance
6. Hepatic and renal function test
7. Do not permit to leave patient alone
8. Determine cause of reaction

161. Management of overdose
Severe overdose reaction
 Rapid onset (within 1 min)
P→A→B→C→D
D( in presence of tonic clonic seizures)
1. Protect patient from self injuries
2. Summon medical assistance
3. Continue basic life support
4. Administer anticonvulsants
(Diazepam 5mg/min IV or
Midazolam 1mg/min IV or 5 mg
IM or 0.25 mg/ kg IN)
5. Post seizure management
Slow onset (5 to 15 min)
P→A→B→C→D
D
1.Administer anticonvulsant
2.Summon medical assistance
3.Post seizure management-Use of
vasopressor (Phenylephrine or
Methoxamine IM) if hypotension
persists
4.Recovery of patient
5.The patient should be examined
by physician before discharge.

162. Epinephrine overdose

163. Management of epinephrine overdose
P→A→B→C→D
 D
1. Reassure the patient
2. Monitor vital signs ( Heart rate and blood pressure to be checked
every 5 min)
3. Administer oxygen if complains of difficulty in breathing
4. Recovery

164. Allergy
Incidence of allergy to amide anesthetics is less than 1%
(Complications of Local Anaesthesia Used in Oral and Maxillofacial Surgery David R. Cummings, DDSa,b ,
Dennis-Duke R. Yamashita, DDS, FACD, FICDc, *, James P. McAndrews, DDS, FACD, FICD 2011)
Predisposing factors:
1. Allergy to Methyl paraben
2. Allergy to sodium bisulphate
3. Allergy to topical anesthetic
4. Latex allergy

165. Prevention of Allergy
 Complete detailed history
 Test dose :
● Intracutaneous injection of the local anesthetic solution (0.1ml) is given into
patient’s forearm
● Intraoral challenge test - after the successful intracutaneous test ( involves the
administration of .1 ml of each of 0.9% sodium chloride, 1% or 2% lidocaine, 3%
mepivacaine , 4% prilocaine ( without methylparaben, bisulphates , vasopressors )
0.9% of the LA solutions that produced no reactions injected intraorally via
supraperiosteal infiltration above maxillary right or left premolar or anterior tooth.
( University of Southern California school of dentistry )

166.  Allergic responses to local anesthetics include
1. Dermatitis (most frequently)
2. Bronchospasm
3. Systemic anaphylaxis
 Amides are essentially free of risk

169. Dental Management in the presence of alleged
local anesthetic allergy
 Elective dental care – Dental treatment requiring local anesthesia should be
postponed until a thorough evaluation of the patient’s allergy is completed.
 Emergency dental care:
1. Emergency protocol no:1- no treatment of an invasive nature
2. Emergency protocol no:2- use GA in place of LA
3. Emergency protocol no:3- Histamine blockers as local anesthetics
(Diphenhydramine Hcl in 1% solution with 1: 100,000 epinephrine provides
pulpal anesthesia for 30 min.
4. Emergency protocol no:4- EDA ( electronic dental anesthesia )

170. Management of skin reactions
 Delayed
P→A→B→C→D
D
1. Oral histamine blocker (
Diphenhydramine 50mg or
Chlorpheniramine 10 mg
QID for 3 to 4 days)
2. Observe for 1 hour before
discharge
3. Obtain medical consultation
4. Do not permit to leave
unescorted
Immediate
P→A→B→C→D
D
1. Administer epinephrine (0.3mg IM
or SC)
2. Administer IM histamine blocker
3. Obtain medical consultation
4. Observe for 1 hour
5. Oral histamine blocker for 3 days
6. Evaluate patient before further
dental care

171. Management of respiratory reactions
 Bronchospasm
P→A→B→C→D
D
1. Terminate treatment
2. Administer oxygen( at a flow of 5
to 6 lit/min)
3. Administer epinephrine or other
bronchodilator via aerosol inhaler
4. Observe for 1 hour
5. Administer histamine blocker ( 50
mg IM diphenhydramine or 10 mg
chlorpheniramine )
6. Medical consultation
7. Oral histamine blocker and
complete evaluation before dental
therapy
Laryngeal edema
P→A→B→C→D
D
1.Epinephrine ( 0.3mg IM or SC)
2.Administer oxygen and summon medical
assistance
3.Maintain airway
4.Additional drug management (histamine
blocker IM/IV, cortico steroid-
hydrocortisone sodium succinate 100mg
IM/IV to inhibit and decrease edema and
capillary dilation)
5.Perform cricothyrotomy

172. Management of Generalized Anaphylaxis
 Signs of allergy present
P→A→B→C→D
D
1. Summon medical assistance
2. Administer epinephrine (0.3 ml
of 1:1000 for adults by IM or IV
)
3. Administer oxygen
4. Monitor vital signs
5. Additional drug therapy (
histamine blocker ,
corticosteroid)
No signs of allergy present
P→A→B→C→D
D
1.Terminate treatment
2.Summon medical assistance
3.Administer oxygen
4.Monitor vital signs
5.Additional management

173. Methemoglobinemia
 It occurs when the iron atom within the
haemoglobin molecule is oxidised. The
iron atom goes from ferrous to ferric .
This state is referred to as
methemoglobin
 prilocaine doses >600 mg are needed
to produce clinically significant
methemoglobinemia
 Can be treated by administration of
methylene blue (1-2 mg/kg of a 1 %
solution over 5 min) or les successfully
with ascorbic acid (2mg/kg)

174. Malignant hyperthermia
 It is one of the most intense and life threatening complications associated with the
administration of general anaesthesia .
 Incidence – 1:15,000 among children receiving general anaesthesia
1:50,000 among adults
Syndrome is transmitted genetically by an autosomal dominant gene
Clinical manifestations
► Tachycardia, tachypnea, unstable BP, cyanosis, respiratory and metabolic
acidosis, fever (42 c or 108 o F) , muscle rigidity and death, mortality ranges from 63-
73%
Treatment - Dantrolene sodium 2.5mg/kg initially and 1mg/kg every 4 hours after the
episode

175. Recent advances in local anaesthetic delivery
 1. Electronic Dental Anesthesia – EDA
 2. Intra-oral Lignocaine Patch - Dentipatch
 3. Jet Injection
 4. Iontophoresis
 5. EMLA
 6. Computer Controlled Local Anaesthetic Delivery Devices – CCLAD
 7. Intra-osseous Systems – IO Systems

176.  Electronic dental anaesthesia –
this technique involves the use of the principle of Transcutaneous
Electrical Nerve Stimulation (TENS) which has been used for the relief of pain. It can be
used a supplement to conventional local anaesthesia.
■ Dentipatch - a patch that contains 10-20% lidocaine is placed on the dried mucosa
for 15 minutes
■ Jet Injection - in this technique a small amount of local
anesthetic is propelled as a jet into the sub mucosa
without the use of a hypodermic syringe/needle from a reservoir.
This technique is particularly effective for palatal injections

177.  Iontophoresis - It is a painless modality of administrating anesthesia.
 EMLA - It contains a mixture of lignocaine and prilocaine bases, which forms an oil
phase in the cream and passes through the intact skin. Use of EMLA cream for
anesthetizing the skin prior to needle insertion as this reduces the incidence of injection
pain.
 CCLAD Systems (Computer Controlled Local Anesthesia
Delivery System) - termed the “WAND” introduced in 1997
►Intra-Osseous Anaesthesia - the use of motor driven perforator
to penetrate the buccal gingiva and bone can be considered as the
first modern technique of IO anesthesia

178. REFERENCES
 Ocular complications after posterior superior alveolar nerve block: a case of
trochlear nerve palsy G. Chisci, C. Chisci, V. Chisci, E. Chisci:
 Monheim’s Local Anesthesia and Pain Control in Dental Practice, eighth edition.
 Malamed SF. Handbook of local anesthesia. 5th ed.
 Essentials of local anesthesia – K G Ghorpade
 Newer Local Anaesthetic Drugs and Delivery Systems in Dentistry – An Update Dr.
S. S. Sharma1, Dr. S. Aruna Sharma2, Dr. C. Saravanan, Dr. Sathyabama
 Complications of Local Anesthesia Used in Oral and Maxillofacial Surgery David
R. Cummings, DDSa,b , Dennis-Duke R. Yamashita, DDS, FACD, FICDc, *, James
P. McAndrews, DDS, FACD, FICD 2011

179. THANK
YOU