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
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
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.
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
39.
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
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
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
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
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
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
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
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 )
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
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
148.
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
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
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
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.
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
167.
168.
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
Non decremental conduction – unhindered conduction of impulse… all or none law – a nerve fibre responds to a stimulus irrespective of the strength of the stimulus. If stimulus is beyond the threshold level, it’ll show response otherwise 0 response.
Hyperpolarised state – much more negative
Hydrated Na ion – 3.4 A0, hydrated K – 2.2 A0. Na channel diameter - .3-.5 nm
Conduction velocity unmyelinated – 1.2m/sec, myelinated a alpha -120 m/sec, a delta – 14.8 m/sec
Potency – ability or stength
Ph of normal tissue – 7.4, inflamed tissue – 5.5-5.6
EMLA – 2.5% lidocaine + 2.5% prilocaine
for ventricular dysrhthemia doseof la -.5-.75,max 1-1.5
Pre of atypical cholinesterase cannot able to hydrolyse ester compounds – increased ester LA drug causes toxicity
Monoethyl glycine xylidide & glycine xylidide can cause sedation
Pulpal anesthesia – 20-40 min
needle types – platinum, iridium platinum
Contact lenses should be removed
Kenalog –corticosteroid , it’s antiinflammatory component increases the viral and bacterial component
Otherdrugs – desipramine (tricyclic antidepressant), quinidine (antidysrhthymic), cimetidine (H2 histamine blocker) increases the drug overdose by slowing the biotransformation