This document provides an overview of neurophysiology and local anesthetics. It discusses the structure of neurons, nerve conduction, definitions of local anesthesia, and theories of local anesthesia mechanisms. It describes the properties, composition, classification, pharmacokinetics and complications of local anesthetics. Specific local anesthetic drugs like lidocaine, prilocaine and bupivacaine are also discussed. Factors affecting local anesthetic action and contraindications are summarized. Topical local anesthetics like benzocaine and lidocaine are also reviewed.

1. NEUROPHYSIOLOGY AND DRUGS OF LOCAL ANAESTHESIA

2. CONTENTS
 Structure of neuron
 Nerve conduction
 Definition of LA
 mechanism of LA
 theories of LA
 Properties of LA
 Dissociastion of LA
 LA in infected tissues
 Factors affecting LA
 Contraindications of LA
 Composition of LA
 classification of LA
 pharmacokinetics of LA
 individual drugs
 Vasoconstrictors
 Maximum recommended dose
 Complication
 conclusion

3. PAIN
Pain is the most commonly encountered symptom in dentistry
It is an unpleasant feeling that is conveyed to the brain by the sensory neurons
due to the signals produced by the actual or potential injury to the body

4. STRUCTURE OF A NEURON
SENSORY NEURON
MOTOR NEURON
MYELINATED AND UNMYELINATED NERVE FIBRES

5. NERVE CONDUCTION
The ions mainly involved in the nerve conduction are the sodium, chlorine and potassium ions
The sequence of nerve conduction depends on 2 factors:
 The concentration of ions within the neurons and extracellular fluids
 Permeability of nerve membrane to sodium and potassium ions
Resting state
Membrane excitation

6. RESTING STATE
 The nerve has a negative electrical potential of -70mV across the nerve membrane produced by different concentration
of ions on either side of the nerve membrane.
 In resting state the nerve membrane is:
 slightly permeable to sodium ions
 Freely permeable to potassium ions
 Freely permeable to chloride ions
 The K remain within the axoplasm because the positively charged ions are being restrained by the negatively charged
ions of the membrane by electrostatic attraction
 The chloride remains outside the nerve membrane as the electrostatic influence of the nerve membrane pushes the ions
outwards
 The Na ions migrate inwardly as the concentration ( greater outside) and the electrostatic gradient ( positive ions being
attracted by negative intracellular potential)
Na+(140mEq/L)
Cl- (110mEq/L)
K+ (110 mEq/l)

7. MEMBRANE EXCITATION
 DEPOLARISATION (0.3 sec)
Excitation of the nerve segment Permeability of the cell membrane to
sodium ions depolarisation of the nerve membrane decrease in
transmembrane potential of 15mV(-55mV) firing threshold furthur increase in
entry of sodium ions into the axoplasm electrical potential of +40mV in nerve
REPOLARISATION (0.7 sec)
Voltage gated sodium channels will close and voltage gated potassium channels
will open efflux of K+ return to its resting potential
A slight excess of sodium exists within the nerve along with slight excess of
potassium extracellularly oxidative metabolism of ATP gives off energy which
is used to move these excess Na ions out of the nerve membrane against the
concentration gradient and the same process happens to potassium ions
ABSOLUTE REFRACTORY PERIOD-after a stimulus has initiated a action
potential, a nerve is unable for some time to respond to another stimulus
RELATIVE REFRACTORY PERIOD- new impulse can be initiated but only by a
stronger stimulus

8. DEFINITION
Local anesthesia is defined as the loss of sensation in a
circumbscribed area of the body caused by depression of excitation
in the nerve ending or inhibition of conduction process in peripheral
nerves

9. PROPERTIES OF LOCAL ANAESTHETIC
 It should not be irritating to the tissues to which it is applied
 It should not cause any permanent alteration of nerve structure
 Its systemic toxicity should be low
 It must be effective regardless of whether it is injected into the tissues or is
applied locally to mucous membrane
 The time of onset of anaesthesisa should be as short as possible

10.  The duration of action must be long enough to permit completion of
procedure yet not so long as to require an extended recovery
 It should have potency sufficient to give complete anaesthesia without the use
of harmful concentrated solution
 It should be relatively free from producing allergic reaction
 It should be stable in solution and should readily undergo biotransformation
in body
 It should be sterile or capable of being sterilised by heat without detoriation

11. THEORIES OF LOCAL ANAESTHESIA
Many theories have been evolved over years to explain the mechanism of action
of LA
 Acetylcholine theory
 Calcium displacement theory
 Surface charge theory
 Membrane expansion theory
 Specific receptor theory

12. THEORIES OF LOCAL ANAESTHESIA
 Acetylcholine theory
It states that the acetyl choline besides being a chemical neurotransmitter
acting at the nerve synapses, it also help in nerve conduction.
Failed:No evidence proves this theory
 Membrane expansion theory
The membrane consist of 2 layer of lipid molecules each layer has an outer
hydrophilic end and a hydrophobic end towards the middle of membrane.
The LA which is highly lipid diffuse to the hydrophobic regions and leads to
expansion of the nerve membrane.this leads to decrease in diameter of the
sodium channels inhibition of sodium conduction and neural excitability
Failed:
No direct evidence suggest that nerve conduction is entirely blocked by
membrane expansion

13. THEORIES OF LOCAL ANAESTHESIA
 Surface charge theory
It states that the cationic(RNH+) molecules present in the LA bind to the nerve membrane and make the
electrical potential of the nerve membrane more positive which leads to increased threshold potential
thus decreasing the excitability
Failed:
 It does not explain the activity of the uncharged ananesthetic molecule which blocks the nerve impulse
 Local anaesthetic act within the nerve membrane rather than the surface of the nerve membrane
 Calcium displacement theory
It states that the membrane site that controlled the permeability to sodium was displaced by calcium
Failed: the potency of the local anaesthetic does not change despite altering the concentration of the
calcium ions around the nerve

14. THEORIES OF LOCAL ANAESTHESIA
 Specific receptor theory
It is the currently accepted theory
It states that local anaesthetics act by binding to specific receptors on the sodium channel
The specific receptor site are located in the external or internal axoplasmic surface of the sodium
channels
Once the LA gained access to the receptors,permeability to sodium ions is decreased and nerve
conduction is interrupted

15. MECHANISM OF ACTION
Conduction blockade
Lack of propagated action potential
Failure to achieve threshold potential
Depression in rate of electrical deploarisation
Decrease in sodium conductance
Blockade of sodium channel
Binding of LA molecules to the receptor site
Displacement of calcium ions from the sodium channel receptor site

16. COMPOSITION OF LOCAL ANAESTHETIC SOLUTION
COMPONENTS Agent used In 1 ml
Local anaesthetic
drug
Lidocaine HCL 2% (20mg/ml)
vasoconstrictor Adrenaline 1:80000 (0.0125mg)
Reducing agent Sodium metabisulphite (0.5mg)
Preservative Methylparaben (1mg)
Isotonic solution Sodium chloride (6mg)
fungicide Thymol
Diluting agent Sterile water
Nitrogen bubble 1-2mm in diameter

17. COMPOSITION OF LOCAL ANAESTHETIC SOLUTION
COMPONENTS FUNCTION
Local anaesthetic drug Blockade of nerve conduction
Sodium chloride Isotonicity of the solution
Sterile water Volume
Vasopressor depth and duration of anaesthesia and
vasopressor
Sodium bisulfite antioxidant
Methyl paraben Bacteriostatic agent
Nitrogen bubble To prevent oxygen from being trapped in

18. DISSOCIATION OF LOCAL ANAESTHETIC
Local anesthetic are tertiary amine( weak base)- poorly soluble and unstable in air
Thus they are dispensed into acid salts(hydrochloride salts) to make it stable
R=N +HCl R=NHCl
Local anaesthetic salts(R=NHCl ) is dissolved in saline or sterile water=it exists as base (RN) and as
cation(RNH+)
RNH+ RN + H+
In lower ph (more of hydrogen ions) most of the anaesthetic solution exists in cation form
RNH+ > RN + H+
In higher ph (less of hydrogen ions) most of the anaesthetic solution exists in free base form
RNH+ < RN + H+

19. LA ON INFECTED TISSUES
 Let us take 1000molecules of local anesthesia is deposited in a
tissue which is infected and inflamed and has a Ph of 6
 At this low ph level there 990 molecules of RNH+(99%) and 10 RN
molecules(1%)
[ RNH+ > RN + H+ ]
These RN molecules diffuse across the nerve sheath
Extracellularlly the equilibrium which is disrupted is reestablished by
newly formed RN.
Now these newly formed RN diffuse into the nerve sheath and the
entire process starts again
Intracellularly, 75% of RN gets converted to RNH+ and the remaining
25% remains unchanged
The RNH+ molecules bind to the receptor sites within the sodium
channel resulting in blockade
Ph 6
Ph 7.4
RNH
+(990
)
RN
(10)
RN
(10)
RNH
+

20. FACTORS AFFECTING LOCAL ANESTHETIC ACTION
factor Action affected description
pKa onset Lower pKa- rapid onset of action
Lipid solubility Anaesthetic potency Increased lipid solubility- increased potency
Protein binding duration Increased protein binding allows local anaesthetic
cations to be firmly attached to the proteins in
receptor site,prolonging duration
Vasodialator activity Anaesthetic potency and
duration
Greater vasodialator activity-increased blood flow
to the region- rapid removal of anaesthetic
molecules from injection site- anaesthetic potency
and durationis decreased
Non nervous tissue
diffusibility
onset Increased diffusibility- decreased time of onset

21. ABSOLUTE CONTRAINDICATION FOR LOCAL ANAESTHETIC
Medical problem Drugs to avoid Alternative drug
LA allergy All local anaesthetic in
the same class
Local anesthetic in
different chemical class
Bisulfite allergy Vasoconstrictor
containing local
anesthetic
Any local anesthetic
without vasoconstrictor

22. RELATIVE CONTRAINDICATION OF LOCAL ANESTHETIC
Medical problem Drugs to avoid Alternative drug
Atypical plasma cholinesterase esters amide
methemoglobinemia prilocaine Other amides or esters
Liver dysfunction amides Amides or esters, but judiciously
Renal dysfuction Amides or esters Amides or esters, but judiciously
Significant cardiovascular disease
Clinical hyperthyroidism
Higher concentration of
vasoconstrictors
Local anaethetic with epinephrine
concentration of 1:200000 or
mepivacaine 3% or prilocaine 5%

23. CLASSIFICATION OF LOCAL ANESTHETIC ACCORDING TO
BIOLOGICAL SITE
classification definition Chemical substance
Class A Agents acting at the
receptor site on the external
surface of nerve membrane
Biotoxin( tetrodotoxin,
saxitoxin)
Class B Agents acting at receptor
site on internal surface of
the nerve membrane
Quaternary ammonium
analogue of lidocaine
Scorpion venom
Class C Agents acting by a receptor
independent physio
chemical mechanism
Benzocaine
Class D Agents acting by
combination of receptor and
receptor independent
mechanism
Most of the LA agents

24. CLASSIFICATION OF LOCAL ANESTHETIC
ESTERS
Esters of benzoic acid
Butacaine
Cocaine
Ethyl aminobenzoate(
benzocaine)
Hexylcaine
Piperocaine
Tetracaine
Esters of para amino benzoic
acid
Chloroprocaine
Procaine
propoxycaine
AMIDES
Articaine
Bupivacaine
Dibucaine
Etidocaine
Lidocaine
Mepivacaine
Prilocaine
Ropivacaine
Quinolone
Centbucridine

25. ESTER TYPE LOCAL ANESTHETIC
INFORMATION PROCAINE PROPOXYCAINE
Potency 1(procaine=1) 7 to 8 (procaine =1)
Toxicity 1 (procaine=1) 7 to 8 (procaine =1)
Metabolism Hydrolyzed in plasma Hydrolyzed in plasma and liver
Excretion More than 2% is unchanged in urine Via kidney: mostly hydrolysed
Vasodialating properties Produces greatest vasodialating effect Not much as procaine
Onset of action 6-10 min 2-3 min
Effective dental
concentration
2-4% 0.4%
Anaesthetic half life 6 min Not available
comments • Its vasodialating property is used in
breaking arteriospasm
• It is used in immediate
management of intra arterial
injection of a drug
Because of its higher toxicity it is
available in a combination with
procaine

26. AMIDE TYPE LOCAL ANESTHETIC
INFORMATION LIDOCAINE PRILOCAINE
Potency 2 (compared with procaine) 2(when procaine =1)
Toxicity 2 (compared with procaine) 1 ( when procaine=1)
Metabolism In the liver by microsomal fixed function
oxidase to monoethylgycine and xylidide
It is hydrolysed by hepatic amides to
orthotoludine and N- propylalanine.
Orthotoludine can induce formation of
methemoglobinemia.
Excretion Via kidneys-less than 10%unchanged Via kidneys
Vasodialating properties Lesser than procaine Lesser than lidocaine
Onset of action 3-5 min 3-5 min
Effective dental
concentration
2% 4%
Anaesthetic half life 1.6 hrs 1.6 hrs
comments • It is available without vasoconstrictor and
with vasoconstrictor with epinephrine
concentrations of 1:50000, 1:1,00,000,
It provides shorter duration of
anaesthesia in infiltration than regional
blocks

27. AMIDE TYPE LOCAL ANESTHETIC
INFORMATION ARTICAINE BUPIVACAINE
Potency 1.5 times that of lidocaine 4 times that of lidocaine
Toxicity Similar to lidocaine (2) Less than 4 times that of lidocaine
Metabolism It is a hybrid molecule . It undergoes
biotransformation in the plasma(
plasma esterase) and liver( hepatic
microsomal enzymes)
Metabolised in liver by amidase
Excretion Via kidneys( 5-10% unchanged) Via kidney;16% unchanged
Vasodialating properties Similar to lidocaine Greater than lidocaine
Onset of action Infiltration- 1-2 min
Mandibular block-2-3 min
6-10 min
Effective dental
concentration
4% 0.5%
Anaesthetic half life 27 min 2.7 hrs
comments • Used in caution in people with
hepatic disease, in females who are
Used for lengthy dental procedures
Management of post operative pain

28. TOPICAL ANAESTHESIA

29. BENZOCAINE
 It is an ester of local anesthetic
 Not suitable for injection
 Poor solubility in water
 Poor absorption in cardiovascular system
 Remains at the site of application longer, providing a prolonged duration of anaesthesia
 Localised allergic reaction may occur after prolonged use
 It in available in the form of gels, patches, oilment, aerosol and solution

30. LIDOCAINE
Maximum recommended dose following topical application is 200mg
Two forms of
topical
application
LIDOCAINE BASE
Used as 5% concentration
Poorly soluble in water
Available as aerosol, spray,
oilment, patch , solution
LIDOCAINE HYDROCHLORIDE
Used as a 2% concentration
Water soluble form
Available as oral topical solutions:
20mg/ml ( viscous)
40 mg/ml( solution)

31. EUTECTIC MIXTURE OF LOCAL ANESTHESIA (EMLA)
 EMLA cream is composed of lidocaine 2.5% and prilocaine 2.5%
 It provides surface anaesthesia for intact skin , venipuncture, leg ulcer
debridement
 It must be applied 1 hour before the procedure, reaches at a maximum at 2-3
hrs and last for 1- 2 hrs after removal
 it is supplied :
 Tube- 5 g and 30 gm
 Disc- white round cellulose disc preloaded with EMLA, packed in protective laminate
foil surrounded by adhesive tape
 The EMLA cream on the oral mucosa can be used for procedures that do not
involve deep tissue and only require short term anesthesia
 EMLA is contraindicated in patients with congenital or idiopathic
methemoglobinemia, infants younger than 12 months who are receiving
treatment with methemoglobin inducing drugs,and patients who are known
sensitivity to amide type local anesthetics

32. VASOCONSTRICTORS
Vasoconsrictors are drugs that constrict the blood vessels and thereby controlling tissue perfusion. The
oppose the vasodialatory effect of LA
 By constricting the blood vessels, vasoconstrictors decrease the blood flow to the site of drug
administration
 Absorption of local anaesthetic into the cardiovascular system is slowed, resulting in lower anaesthetic
blood levels, thereby decreasing the risk of local anaesthetic toxicity
 It increases the duration of action of most local aneasthetic

33. MODE OF ACTION OF VASOCONSTRICTORS
 Direct acting drugs- acts directly on the adrenergic receptors
 Indirect acting drugs- act by releasing norepinephrine from adrenergic nerve terminals
 Mixed acting drugs- acts both directly and indirectly
Adrenergic receptors:
a receptors- contraction of smooth muscles
A1 receptors- excitatory postsynaptic;
A2 receptors- inhibitory postsynaptic
b receptors-relaxation of smooth muscles and cardiac stimulation
 The indirectly acting drugs has tachyphylaxis phenomenon

34. CATEGORIES OF VASOCONSTRICTORS
Direct acting Indirect acting Mixed acting
Epinephrine Tyramine Metaraminol
Norepinephrine Amphetamine ephedrine
Levonordefrine Methamphetamine
Dopamine hydroxyamphetamine
phenylephrine

35. EPINEPHRINE
 Chemical structure: it is acid salt and it is highy soluble in water. It gets detoriated in presence of heat
and heavy metals by oxidative mechanism. Sodium bisulphite is added to delay deterioration
 Mode of action: it acts on both a and b adrenergic receptor of which b predominates
 Systemic actions:
Myocardium- it stimulates b1 receptors causing an increased force of contraction and rate of contraction
CVS- systolic and diastolic pressure, cardiac output, stroke volume, heart rate, strength of contraction,
myocardial oxygen consumption
This leads to a overall decrease in cardiac efficiency
Hemostasis- injected into surgical site tissue concentration predominate a receptor hemostasis. As
the tissue concentration decreases b2 receptors predominate vasodialation bleeding after 6 hours of
surgical procedure

36. Metabolism:
It increases the oxygen consumption in all the tissues. It undergoes glycogenolysis in liver , elevating the
blood sugar levels in the plasma
Excretion: action is terminated by its reuptake by adrenergic nerves.1% is excreted unchanged in urine
Clinical application;
 In LA to increase depth and duration of ananesthsia
 To produce mydriasis
 For management of acute allergic reaction
 Management of cardiac arrest
 For hemostasis

37. NOREPINEPHRINE ( LEVARTERENOL)
Chemical structure:
It is relatively stable in acid solutions, detoriating on exposure to light and air. Acetone-sodium bisulphite is
added to retard detoriation
Mode of action:it is mostly on a receptors. It also stimulates b receptors in the heart
Systemic action:
CVS: increased systolic pressure, increased diastolic pressure, decreased heart rate, unchanged or slightly
decrease cardiac output, increased stroke volume
Respiratory system: it produce a-induced constriction of lung arterioles which reduces airway resisitance to
some degree

38. Side effects:
Extravascular injection of norepinephrine into the tissues may produce necrosis and sloughing of the
tissues, in oral mucosa it is mostly the hard palate
Clinical application:
 Used as a vasoconstrictor in LA
 Used for the management of hypotension

39. MAXIMUM RECOMMENDED DOSE
Local Anaesthetic MRD (mg/kg)
Lidocaine
With vasoconstrictor
Without vasoconstrictor
7.0
4.7
Mepivacaine
With vasoconstrictor
Without vasoconstrictor
6.6
6.6
Prilocaine
With vasoconstrictor
Without vasoconstrictor
8.0
8.0
Bupivacaine
With vasoconstrictor
With
vasoconstrictor(Canada)
Not listed
2.0
Articaine
With vasoconstrictor 7.0
MRD FOR EPINEPHRINE
normal healthy patient- 0.2mg/
appt
Patients with significant
cardiovascular disease- 0.04
mg/appt

40. CALCULATING THE TOTAL VOLUME OF LA TO BE ADMINISTERED TO
A PATIENT
2% of lidocaine is present in LA solution
2gm of lidocaine=100ml of solution
2000mg= 100ml
20mg of lidocaine= 1 ml
To calculate the volume of LA for 70 kg weight
person,
MRD of lidocaine with epinephrine=7mg/kg
Therefore, for 70 kg 70* 7= 490mg of lidocaine
When converting to ml,
490/20= 24.5 ml
Epinephrine= 0.0125 mg
24.5 ml of LA with epinephrine soln contains 0.3
mg(>0.2mg)
Therefore considering the risk of epinephrine toxicity,
16.3 ml of LA solution is the maximum volume to be
administered to a 70 kg patient

41. PHARMACOKINETICS OF LOCAL ANESTHESIA

42. UPTAKE
 The rate at which the local anaesthetic are absorbed into the circulation and reach their peak level vary
according to route of administration:
Oral route- LA is absorbed poorly. After passing the GIT into the enterohepatic circulation, most of the
molecules are metabolised into inactive forms
Topical route-absorption rates in tracheal mucosa> pharyngeal mucosa>esophageal mucosa
Parental route- the rate of absorption is rapid. It leads to rapid elevation of blood level and there is possible
risk of toxic reactions

43. DISTRIBUTION
 Once absorbed into the blood the local anaesthetics are distributed throughout the body to all the
tissues
 Highly perfused organs like brain, lungs, spleen will initially have higher anaesthetic blood levels. Skeletal
muscles also constitute the greatest percentage of LA
 The blood level of LA is determined by:
 Rate at which drug is absorbed into the circulation
 Rate at which drug is distributed from the vascular compartment to the tissues
 Elimination of drug through metabolic pathways
 The rate at which the LA is removed from the blood is called elimination half life.it is the time required
for 50% reduction in blood level
 All LA readily cross the blood brain barrier and the placenta

44. METABOLISM
 Ester groups are hydrolysed in the plasma by enzyme pseudocholinesterase and that of amide group
occur in the liver
 When there is pseudocholinesterase deficiency, it leads to prolongation of higher LA blood levels and
increased potential of toxicity therefore ester groups are relative contraindicated
 Procaine gets metabolised to para amino benzoic acid(PABA) and diethyl amine alcohol . PABA may
cause allergic reaction
 Prilocaine gets metabolised to orthotoludine – methemoglobin formation - methemoglobinemia
 Articaine being a hybrid molecule gets metabolised by pseudocholinesterase and liver

45. EXCRETION
 The kidneys are the primary excretory organ for both the local anesthetic and its metabolites
 Amides are usually present in the urine as a parent compound in a greater percentage than esters,
because of their more complex process of biotransformation
 Patients with significant renal impairment may be unable to eliminate the parent local anaesthetic
compound from the blood, resulting in elevated blood levels and therefore increased potential for
toxicity
 Thus it is relatively contraindicated in patients undergoing renal dialysis, and those with chronic
glomerulonephritis

46. SYSTEMIC EFFECTS OF LOCAL ANESTHESIA

47. CENTRAL NERVOUS SYSTEM
 Local anaesthesia readily crosses the blood brain barrier
 Their pharmacologic action on the CNS is seen as depression
 Clinical situations:
Anticonvulsive effect
Preconvulsive effects
Tonic- clonic seizure
Anticonvulsive effect (0.5-4 µg/ml)
It is effective in temporarily arresting the seizure activity
Epileptic patients have hyperexcitable neurons in the epileptic focus
LA having the depressant action , decreases the excitability of these neurons
Preventing or terminating seizures

48. CENTRAL NERVOUS SYSTEM
Preconvulsive effect( 4.5-7 µg/ml)
The cerebral cortex has pathways of neurons that are
inhibitory and excitatory
The LA depresses the action of inhibitory neurons
In order to compensate the excitatory levels are
elevated
Tonic clonic seizure( >7.5µg/ml)
The seizure activity is usually self limiting and
terminates within 1 min
Increased partial pressure of CO2
The blood level of LA necessary for seizure decreases
Increase in duration of seizure
Increased blood flow to the brain
Increase in volume of LA delivered to the brain
Prolong seizure
Signs
Slurred speech
Shivering
Muscular twitching
Tremor of the muscle
Dizziness
Drowsiness
disorientation
Symptoms
Numbness of the
tongue
Warm flushed feeling
of the skin
Pleasant dream like
state

49. CARDIOVASCULAR SYSTEM
Direct action on myocardium
LA decreases the electrical excitability of the
myocardium
Decreases the excitability rate
Decreases the force of contraction
It is used in ventricular tachycardia
It is used in the management of cardiac arrest
caused by ventricular fibrillation
Direct action on the peripheral vasculature
LA produces relaxation of the smooth muscles of
the walls in blood vessels
Peripheral vasodialation
Increased absorption of the drug
Decrease the depth and duration of LA

50. RESPIRATORY SYSTEM
 At non overdose level they have direct relaxation effect on the bronchial
smooth muscles
 At overdose levels, generalised CNS depression - respiratory arrest - death

51. LOCAL ANESTHETIC OVERDOSE
 A drug overdose reaction may be caused by a level of a drug in the blood that is sufficiently high to
produce adverse effects in various organs and tissues of the body
Predisposing factors:
Patient factor Drug factor
Age vasoactivity
Weight Concentration
Drugs like cimetidine Dose
Sex Route of administration
Presence of disease Rate of injection
Genetics Vascularity at the injection site
Attitude and environment Presence of vasoconstrictor

52. CLINICAL MANIFESTATION
MILD TO MODERATE OVERDOSE MODERATE TO SEVERE OVERDOSE
Signs
Tonic clonic seizure
Generalised CNS depression
Depressed BP, heart rate and respiratory
rate
signs symptoms
Excitability restlessness
Slurred speech Numbness
Euphoria Sensation of twitching
nystagmus Metallic taste
Sweating Auditory and visual
disturbance
Disorientation Drowsiness and
disorientation
Depressed BP, heart rate
and respiratory rate
Loss of consciousness

53. MANAGMENT
Termination of the procedure
Patient is placed in a supine position
Call for emergency medical assistance
Circulation, airway and breathing is maintained
Administer O2
Monitor vital signs every 5 mins
Administer anticonvulsant drugs like diazepam IV 2.5- 5 mg
If patients blood pressure is depressed(> 30 min) vasopressor like ephedrine(25-50 mg IM ) or 5% dextrose
in water soln is given to maintain mild elevation in blood pressure
If the patient is stabilised, patient is recovered

54. EPINEPHRINE OVERDOSE
The inclusion of vasoconstrictors in LA solution has potentially lead to adrenaline- vasoconstrictor overdose
Clinical manifestation:
Signs:
Elevated blood pressure and elevated heart rate
Symptoms:
Fear, anxiety, restlessness, tremor, weakness, dizziness, pallor, headache, sweating, palpitation
Epinephrine overdose may also produce cerebral hemorrhage and cardiac dysrhythmias
Risk of overdose:
 Patients receiving MAO inhibitors to manage depression- cannot eliminate epinephrine
 Epinephrine + propanalol = hypertensive crisis , increasing both systolic and diastolic pressure with
decrease in heart rate

55. EPINEPHRINE OVERDOSE
Termination of the procedure
Patients should be placed in a semi supine position
Circulation, airway and breathing are assessed
Reassurance to the patient
Monitor the vital signs and record them every 5 min
Call for medical emergency if needed
If available, O2 is administered
If blood pressure does not return normal,
• Nitroglycerine- 2 tab sublingually
• Labetalol- IV
When signs and symptoms subsides patient is

56. ALLERGY
 Allergy after administration of LA solution can occur
 In LA agents- esters group mainly causes allergy when compared to amide
 Components such as methyl paraben and sodium metabisulphite may also cause
 A true allergy to local anaesthetics may be either type I or type IV
PROGRESS OF ANAPHYLAXIS
skin
Exocrine glands
stimulation(
runny nose
watery eyes)
Spasm of GI
smooth
muscles
Respiratory
system
Cardiovascular
system

59. MANAGEMENT
Termination of the dental
procedure
Place the patient in a supine
position with legs elevated
Maintain the airway in a head
tilt chin lift manoeuvre
Call for medical emergency
Administer epinephrine
(0.3mlof 1:1000 for >30 kg
patients) IM in vastus lateralis
muscle located in thigh
If it fails to improve another
dose is administered after 5
min
Deliver O2 at a flow of 5-6 L
/min
Monitor and record vital signs
every 5 min
Additional drug therapy of:
histamine blocker or
corticosteroid(IV, IM)

60. CONCLUSION
 Local anesthetic are the most important as well as most commonly used drug in dentistry
 Without their availability, all dental procedures associated with pain would be difficult to manage
 Therefore a thorough knowledge of the mechanism, agents used , technique and the possible risk
factors is essential for a pain free procedure