Local anesthesia

LOCAL ANESTHESIA
- Dr. Ibrahim Shaikh
1st Year MDS Periodontology
Seminar No. 1
1
Guide – Dr. Varsha Rathod.

Local anesthetics are effective means of pain
control, provided necessary precautions are
taken along with thorough knowledge of the
drugs.
2

CONTENTS :
 Introduction
 History
 Neurophysiology
 Pharmacology of local anesthetics.
 Pharmacology of vasoconstrictors.
 Clinical aspects of local anesthetics.
 Future trends.
3

PAIN :
 Unpleasant emotional experience usually
initiated by a noxious stimulus and transmitted
over a specialized neural network to the
central nervous system where it is interpreted
as such.
Monheim’s Handbook of Local Anesthesia
5

Methods Of Pain Control :
1. Removing the cause
2. Blocking the pathway of painful impulses
3. Raising the pain threshold
4. Preventing pain reaction by cortical depression
5. Using psychosomatic methods
6
Monheim’s Handbook of Local Anesthesia

What Is Anesthesia ?
 Anesthesia – It is a temporary state consisting
of unconsciousness, amnesia, analgesia,
muscle relaxation and loss of autonomic
reflexes.
 Proposed by Oliver Wendell Holmes in 1846.
7

OF LOCAL ANESTHESIA
8 HISTORY

History :
 Dentists, not doctors, were responsible for the
discovery of anesthesia.
 Dr. Horace Wells (1815-1848) with nitrous oxide
in 1844
 Dr. William Thomas Green Morton (1819- 1868)
with ether in 1846.
9
History of periodontology

Controversy :
10
 Crawford Long (1815 - 1878) : physician from
Jefferson, Georgia.
 Horace Wells (1815-1848) : Dentist from
Hartford , Connecticut.
 William Morton (1819-1868) : Dentist from
Boston, Massachusetts.

Dr. Horace Wells :
11

History of Periodontology
13
 December 11, 1844 John Riggs extracted a molar from
Dr. Wells – The First painless extraction of the
modern era of medicine.

14
 John Collins Warren, Professor of surgery,
Massachusetts General Hospital, Boston.
 January 20, 1845 – Wells nervously attempted
to extract a student’s tooth in front of an
audience of incredulous staff and students.

Dr. William Morton :
History of periodontology.
15
Helped wells in his failed demonstration and in 1846 consulted
with Charles Jackson, professor of chemistry about other
drugs that could have a similar effect. Jackson suggested
ether.

16
 On September 30, 1846 –
extracted a patients tooth in
a painless procedure.
 On October 16, performed
a successful demonstration
at Massachusetts General
Hospital in which he
removed a tumor from the
neck of a patient.

$1,00,000
17
Horace Wells
William Morton
Charles Jackson
Crawford Long

The COCA Leaf :
 Coca leaves – genus Erythroxylum.
(Erythroxylaceae family)
 Erythroxylum coca – highest concentration of
alkaloid known as cocaine in its leaves (up to
0.7 – 1.8% by weight)
 Arhuaco, a tribe from the Negro river region,
were the first to discover the properties of this
drug.
 In 1653, Bernabé Cobo, a Spanish Jesuit
mentioned in one of his manuscripts that
toothaches can be alleviated by chewing coca
leaves
18
History of the development & evolution of local anesthesia since the coca leaf. Calatayud, Jesus
Journal of Anesthesiology, June 2003:98 – 6:1503-1508

Cocaine :
 In 1860 German chemist Albert Niemann
managed to isolate the active principle, which
he named cocaine.
 Steps were then taken to apply it as the first
local anesthetic by several people.
Lossen(1865),Thomas
Moreno(1868),Basil Von Anrep (1880)
19

Sigmund Freud :
20
 Sigmund Freud (1856-
1939) – German military
experiment, providing
cocaine to soldiers
during maneuvers to
help them overcome the
hardships of military
campaigns.
 Drug induced a euphoric
stage that lifted him out
of his periods of
depression.

Carl Koller :
21
Sep 11, 1884 - Carl Koller an ophthalmologist
performed the first operation using local
anesthetic on a patient with glaucoma.

 Dec 6, 1884 Dr. William Stewart Halsted
published a report on the first successful nerve
block, in context of dentistry.
 Dr. Nash of New York was able to block the
infraorbital plexus with approx. 0.5ml of 4%
cocaine hydrochloride to obturate an upper
incisor.
 Dr. Halsted on the other hand blocked the inferior
dental nerve in a medical student using the same
solution.
22

23
After Cocaine :
 1905 – Novocaine appeared for the first time and was found
to be safe and quickly became the standard local anesthesia.
(rechristened procaine in United states)
 1943-1946 – Nils Löfgren & Bengt Lundquist developed a
xylidine derivative they called lidocaine.
 1957 – Bo af Ekenstam et al. synthesized mepivacaine and
bupivacaine.
 1969 – prilocaine : Nils Löfgren & cläes Tegner

Local Anesthesia :
 Local Anesthesia has been defined as a loss of
sensation in a circumscribed area of the body
caused by a depression of excitation in nerve
endings or an inhibition of the conduction
process in peripheral nerves.
 It produces this loss of sensation without
inducing a loss of consciousness.
Handbook of Local Anesthesia, Stanley F. Malamed
24

Properties :
 Should not be irritating to tissues.
 Should not cause any permanent alteration of nerve
structure.
 Should have very low systemic toxicity.
 Effective regardless of mode of administration.
 Short time of onset of anesthesia.
 Long duration of action of anesthetic effect.
25

Bennett’s additional requirements
:
 Potency sufficient to give complete anesthesia without the
use of harmful concentrated solutions.
 Relatively free from producing allergic reactions.
 Should be stable in solution and should readily undergo
biotransformation in the body.
 Should either be sterile or should be capable of being
sterilized by heat without deterioration.
26

The Neuron :
 Structural unit of the nervous system.
 Transmits messages between the CNS & all parts of
body.
 Types –
a) Sensory
b) Motor
28

The Sensory Neuron :
29

The Motor Neuron :
30

The Axon :
 Long cylinder of neural cytoplasm encased in a thin
sheath, the nerve membrane, or axolemma.
 Axoplasm is separated from extracellular fluids by a
continuous nerve membrane.
 Sensory nerve excitability and conduction are both
attributed to changes developed within the nerve
membrane.
31

The Nerve Membrane :
 The nerve membrane is 70 – 80 A° thick.
 Flexible non stretchable layer consists of two layers of
lipid molecules
32

 Proteins are primary organizational elements of the
membranes.
 Proteins are classified as transport proteins and receptor
sites.
 Channel proteins are continous pores through the
membrane allowing some ions (Na+, K+, Ca++) to pass
passively.
 Other channels are gated, permitting ion flow only when
the gates are open.
33

Nerve Conduction :
35

Action Of Local Anesthetics :
 Local Anesthetics interfere with the excitation process in
nerve membrane by one of the following mechanism:
1. Altering the basic resting potential of the nerve
membrane.
2. Altering the threshold potential
3. Decreasing the rate of depolarization
4. Prolonging the rate of repolarization
 It has been established that the primary effects of local
anesthetics occur during the depolarization phase of the
action potential.¹
36

Theories Of Local Anesthetics :
 Acetylcholine theory
 Ach involved in nerve conduction
 Calcium displacement theory
 Ca2+ displaced from membrane site, alters Na2+
permeability
 Surface charge (repulsion) theory
 Cationic drug molecules bind to nerve membrane
making it more positive, thus increasing the
threshold potential causing decreased excitability
37

Membrane
Expansion
Theory :
Drug molecule
penetrates the lipid
portion of membrane &
brings about a change in
the configuration of
lipoprotein matrix,
preventing Na ions
permeability thereby
inhibiting neural
excitation.
38

 Specific Receptor Theory :
 Local Anesthetics act by binding to specific
receptors on the sodium channel.
 Action of the drug is direct & not mediated by some
change in the general properties of the cell
membrane.
 Specific receptor site for local anesthetic agents
exist in the sodium channel either on its external
surface or on the internal axoplasmic surface.
 Once the local anesthetic has gained access to the
receptors, permeability to sodium ions is decreased
or eliminated & nerve conduction is eliminated.
39

Classification of Local Anesthetic substances
according to biological site & mode of action
40
CLASS
A
CLASS
B
CLASS
C
CLASS
D

Mode Of Action Of LAs :
 Displacement of Ca ions from the Na channel receptor
site,
 Binding of the local anesthetic molecule to this receptor
site
 Blockade of the sodium channel
 Decrease in sodium conductance
 Decrease of the rate of electrical depolarization
 Failure to achieve the threshold potential level
 Lack of development of propagated action potentials
 Conduction blockade.
41

OOOO N
 All Local Anesthetics are amphipathic.
 The hydrophilic part is an amino derivative of
ethyl alcohol or acetic acid.
 The lipophilic part is the largest. Aromatic in
structure, it is derived from benzoic acid, aniline,
or thiophene.
 The structure is completed by an intermediate
hydrocarbon chain containing either an ester or
an amide linkage.
42

Dissociation of Local
Anesthetics :
 Local anesthetics are basic compounds,
poorly soluble in water and unstable on
exposure to air.
 They combine with acids to form local
anesthetic salts, which are water-soluble and
stable.
 Local anesthetic are dissolved in either sterile
water or saline
 In this solution, it exists as uncharged
molecules (RN) called base and positively
charged molecules (RNH+) called the cation.
43

 Both base and cation exist simultaneously
RNH+ RN + H+
 As the pH decreases, equilibrium shifts to the
left
RNH+ > RN + H+
 As the pH increases, equilibrium shifts to the
right
RNH+ < RN + H+
44

pKa and Anesthesia :
 pKa (dissociation constant) is the measure of a molecule’s
affinity for hydrogen ions.
 When pH = pKa, the drug exists in exactly 50% RNH+ and
50% RN form
 The two factors involved in the action of a local anesthetic
are diffusion of the drug through the nerve sheath and
binding at the receptor site in the ion channel
 The uncharged free base form RN is responsible for the
diffusion through the nerve sheath.
45

 1000 molecules of LA (pKa-7.9) – injected in tissue (pH 7.4)
 By Henderson-Hasselbalch equation- 75% RNH+ form &
25% RN form
 Diffusibility & binding are responsible for LA effectiveness, but
the diffusibility is much more important in actual practice.
46

Barriers :
 Peripheral nerve
composed of hundreds
to thousands of tightly
packed axons.
 Endoneurium
 Perineurium – Fascicle
 Perilemma – innermost
layer of perineurium
 Epineurium
 Epineural sheath or
nerve sheath
47

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
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
Tissue
diffusibility
Onset
Increased diffusibility = decreased time of
onset
Vasodilator
activity
Anesthetic
potency and
duration
Greater vasodilator activity = increased
blood flow to region = rapid removal of
anesthetic molecules from injection site,
thus decreased anesthetic potency and
Handbdooekc oref Laosceadl A dneusrtahetisoian, Stanley F. Malamed
48

49 PHARMACOLOGY
OF LOCAL ANESTHETICS

Classification :
Based on Chemical structure
 ESTER GROUP
 Benzoic acid esters
 Benzocaine, Cocaine, Butacaine, Tetracaine,
Hexylcaine, Piperocaine
 Para amino benzoic acid esters
 Procaine, Chloroprocaine, Propoxycaine
 AMIDE GROUP
 Lignocaine, Bupivacaine, Mepivacaine, Prilocaine,
Articaine, Dibucaine, Etidocaine, Ropivacaine
 QUINOLONE
 Centbucridine
50

Procaine :
51
 Vasodilation- clean surgical field difficult to maintain
because of increased bleeding.
 Procaine is used in cases of inadvertent intra-arterial(IA)
injection of a drug; vasodilating properties are used to
aid in breaking arteriospasm.

Lidocaine :
52
 Compared with procaine, lidocaine possesses
a significantly more rapid onset of action,
produces more profound anesthesia, has a
longer duration of action, and has a greater
potency.

Mepivacaine :
53
 Provide longer duration of anesthesia than most other
local anesthetics when the drug is administered without
a vasoconstrictor.
 Mepivacaine plain is the most used local anesthetic in
pediatric patients & is often quite appropriate in the
management of geriatric patients.

Prilocaine :
54
 Integral part of EMLA(eutectic mixture of local
anesthetics) cream, which permits the anesthetics to
penetrate the imposing anatomic barrier of intact skin.
 Prilocaine plain frequently is able to provide anesthesia
that is equal in duration to that obtained from lidocaine
or mepivacaine with a vasoconstrictor.

Articaine :
55
 Clinically, it is claimed that maxillary buccal
infiltration of Articaine, provides palatal soft-tissue
anesthesia, obliterating the need for the
more traumatic palatal anesthesia.
 Also claimed that it can provide pulpal and
lingual anesthesia when administered by
infiltration in adult mandible.

Bupivacaine & Etidocaine :
56
 Lengthy dental procedures for which pulpal
anesthesia in excess of 90 minutes is
necessary.
 Difference between the two is that Etidocaine
has an onset of action of about 3 minutes,
whereas Bupivacaine has an onset of 6 to 10
minutes.

Topical Anesthetics :
57
 Topical anesthetics diffuse through the mucous
membranes and injured skin to reach the free
nerve endings.
 But the diffusion is limited and they are rapidly
absorbed in the circulation, thus effective block
is not obtained.
 Thus, to increase their efficacy, their
concentration is increased.
 5% or 10% lidocaine,1% or 2% tetracaine-most
common

Pharmacokinetics of Local Anesthetics :
 Uptake
 Distribution
 Metabolism (Biotransformation)
 Excretion
58

Uptake
 All local anesthetics possess some degree of
vasoactivity; most producing some level of
vasodilation
 Ester local anesthetics are potent vasodilating
drugs
 Cocaine is the only local anesthetic that
consistently produces vasoconstriction 
initial vasodilation  intense vasoconstriction
59

 Vasodilation leads to an increased rate of absorption of the
local anesthetic into the blood, thus decreasing the duration
and depth of pain control while increasing the anesthetic
blood concentration and potential for overdose (toxic reaction)
60

Distribution of Local Anesthetics :
 Once in the blood, local anesthetics are distributed to all
tissues
 Brain, head, liver, lungs, kidneys and spleen have high
levels of local anesthetics due to their high level of
perfusion
 Skeletal muscle has the highest level because it has the
largest mass of tissue in the body
61

Factors influencing the blood levels
:
1) Rate at which the drug is absorbed into the
cardiovascular system.
2) Rate of distribution from the vascular compartment to
the tissues.
3) Elimination of the drug through metabolic or excretory
pathways.
62

All local anesthetics cross the
blood brain barrier
All local anesthetics cross the
placenta and enter the
blood stream of the developing
fetus
63

Metabolism :
64
Ester Local Anesthetics:
 Hydrolyzed in the plasma by the enzyme
pseudocholinesterase
 The rate of hydrolysis is related to the degree of toxicity
 Tetracaine is hydrolyzed the slowest which makes it 16
times more toxic than Chloroprocaine which is
hydrolyzed the fastest
Slower Hydrolyzation = Toxicity

65
Esters - Procaine-
Para amino benzoic acid Diethyl amino alcohol
Excreted unchanged urine further transformed-urine

66
Amide Local Anesthetics:
 Primary site of metabolism of amide local anesthetics is
the liver.
 Virtually the entire metabolic process occurs in the liver
for Lidocaine, Mepivicaine, Articaine, Bupivacaine and
Etidocaine.
 Prilocaine is metabolized in the liver and lung.

67
Biotransformation :
Mono ethyl xylidide
Glycine xylidide
Xylidide
Hydroxy xylidide.
Excreted by kidney .

68
 Liver function and hepatic perfusion greatly affect the
rate of metabolism (biotransformation) of amide local
anesthetics
 Significant liver dysfunction or heart failure represents a
relative contraindication to the use of amide local
anesthetics
 Articaine has a shorter half-life than other amides
because a portion of its metabolism occurs in the blood
by plasma cholinesterase

69
 Metabolism byproducts of amide local anesthetics can
possess clinical activity if allowed to accumulate in the
blood
 All local anesthetics have the ability to cause sedation.

70
U.S. Air Force and U.S. Navy pilots are
grounded for 24 hours following
administration of Lidocaine due to its mild
effects of sedation and/or drowsiness

71
If the local anesthetic has two “i”s in its name; it’s
an amide
Lidocaine
Prilocaine
Bupivacaine
Articaine
Mepivacaine

Composition :
72
 Local anesthetic drug –e.g. lignocaine .
 Vasopressor drug - e.g. adrenaline.
 Anti-oxidant - egg Sodium meta bi sulfite.
 Germicide, Preservative – e.g. methyl
paraben.
 For isotonicity – Normal Saline .
 Distilled water to equal the desired amount .

How much LA can be injected :
73
 Without adrenaline is : 300mg or 4.4mg/kg
 With adrenaline : 500mg or 7mg/kg
 Safe dose adrenaline : 0.2mg/visit
2% Lignocaine - 2g in 100 ml
2000mg - 100 ml
20 mg - 1ml
1 mg - 1/20ml
500mg = 1/20  500 = 25ml can be given safely for a normal
pt

Effects of LA on CNS :
74
 The pharmacological action of local anesthetics on the
CNS is depression.
 At high levels, local anesthetics will produce tonic-clonic
convulsions.
 Procaine, Lidocaine, Mepivacaine, Prilocaine and
Cocaine generally produce anti-convulsant properties;
this occurs at a blood level considerably below that at
which the same drugs cause seizures.

Preconvulsive Signs and Symptoms :
75
 Numbness of tongue & circumoral regions.
 Shivering, Slurred speech, Muscular twitching.
 Visual/auditory disturbances.
 Dizziness, Drowsiness, Disorientation & Tremors.
 If excitation or sedation occurs in the first 5 to 10 minutes after
local anesthetic delivery, it should serve as a warning that
convulsive activity could be possible

Cardiovascular Effects of LA’s :
76
 Local anesthetics have a direct action on the
myocardium and peripheral vasculature
 CVS is more resistant to the effects local anesthetics
than the CNS
 Increased local anesthetic blood levels result in
decreased myocardial depolarization, however, no
change in resting membrane potential and no
prolongation of the stages of repolarization

77
 Local anesthetics decrease myocardial excitation,
decrease conduction rate and decrease the force of
contraction
 Lidocaine is used therapeutically for pre-ventricular
contractions (PVCs) and ventricular tachycardia
 Local anesthetics cause hypotension from the direct
relaxant action on vascular smooth muscle

Lung Toxicity :
78
 Local anesthetics have a direct relaxant action on bronchial
smooth muscle.
 Generally, respiratory function is unaffected by local
anesthetics until near overdose levels are achieved.
 Skeletal muscle will heal within two weeks of being injected
with local anesthetic.
 Longer acting local anesthetics (Bupivacaine) produce more
damage to skeletal muscle than do shorter acting agents.

Of Vasoconstrictors.
79 Pharmacology

Vasoconstrictor’s :
80
 All clinically effective injectable L.A have some degree of
vasodialating activity
 ↑ absorption of L.A into CVS → removal from injection site
 Rapid diffusion of L.A from injection site → ↓ duration of action &
depth of anesthesia.
 Higher plasma level of L.A → ↑ risk of toxicity
 ↑ bleeding at injection site.
 Addition of vasoconstrictor to L.A..
 Constriction of blood vessels → ↓ tissue perfusion
 Slow absorption into CVS → low anesthetic blood level → ↓ risk
of toxicity.
 Higher volume of L.A around nerve → ↑ duration of action
 ↓ bleeding at injection site

Classification :
81
 Catecholamines :
 Epinephrine
 Norepinephrine
 Levonordefrin
 Isoproterenol
 Dopamine
 Noncatecholamines :
 Amphetamine
 Methamphetamine
 Ephedrine
 Mephentermine
 Hydroxyamphetamine
 Metaraminol
 Methoxamine

Selection Of Vasoconstrictors :
82
 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 haemostasis during surgical procedure.
Epinephrine is effective in preventing blood loss during
surgical procedures, however it also produces rebound
vasodilatory effect.

83
 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

Contraindications :
84
Patients with more significant cardiovascular disease
(ASA Ш and IV)
Patients with certain non-cardiovascular diseases (e.g.,
thyroid dysfunction , and sulfite sensitivity)
Patients receiving Monoamine oxidases inhibitors,
Tricyclic antidepressant , and phenothiazines

85 Applied Aspects
Of Local Anesthesia

Which type of LA should be given
in inflammation?
86
• Mepivacaine is suitable for infected areas
which have
acidic medium , because it has less pKa
(7.6)

Allergic to both groups :
87
If a pt is sensitive to both groups .
Antihistamines like diphenhydramine can be
given for Local anesthetic action

What happens in case of alcoholics &
smokers?
88
• In case of acute alcoholics there is vasodilatation
present at the site so rapid absorption of LA into
circulation resulting in decreased depth and decreased
duration of anesthesia
• In cases of chronic alcoholics the pain threshold is
raised also resulting in decreased depth of anesthesia &
need for larger doses which may lead to increased
chances of overdose reactions
• In smokers , there is peripheral vasoconstriction present
= increased duration of action and increased intensity of
LA

Complications :
89
 LOCAL
 Needle breakage
 Persistent
anesthesia
 Facial nerve
paralysis
 Trismus
 Soft-tissue injury
 Hematoma
 Pain on injection
 Burning on injection
 Infection, edema
 Sloughing of tissues
 SYSTEMIC
 Overdose
 Allergy
 Syncope

Overdose :
90
• A drug over dose reaction has been defined as those
clinical signs & symptoms that result from an overly high
blood level of drug in various target organs and tissues.
• Under normal condition there is a constant absorption
of local anesthetic from the site of deposition into the
CVS & a constant removal of drug from the blood by the
liver.

91
 Elevated blood levels of LA may result from one or
more of the following:
1. Biotransformation of the drug is usually slow
2. The unbiotransformed drug is too slowly eliminated
from the body through the kidneys.
3. Too large a total dose is administered
4. Absorption from the injection site is unusually rapid
5. Inadvertent intravascular administration occurs

92
Symptoms:
Restlessness, Visual disturbances
Nervous & Auditory disturbances
Numbness & Metallic taste
Light-headedness and dizziness
Drowsiness and disorientation
Losing consciousness
Sensation of twitching (before actual
twitching is observed)

Allergy :
93
• Allergy is a hypersensitive state, acquired through
exposure to a particular allergen, re-exposure to
which produces a heightened capacity to react .
 Allergens in LOCAL ANESTHETICS :
1. Esters - usually to the Para-amino-benzoic-acid
product
2. Na bisulfite or metabisulfite - found in anesthetics
as preservatives for vasoconstrictors, antioxidants
3. Methylparaben - no longer used as preservative.

In Local Anesthetics
94 Future Trends

Centbucridine :
95
Quinoline derivative
 Five to eight times the potency of lidocaine
Rapid onset and an equivalent duration of action
Does not affect the central nervous system or
cardiovascular system

Ropivacaine :
96
 Long acting amide anesthetic
 Structurally similar to mepivacaine and bupivacaine.
 Unique in that it is prepared as an isomer rather than as
a racemic mixture.
 Has demonstrated decreased cardiotoxicity.
 Potential for use in dentistry appears great, but awaits
clinical evaluation.

Carbonated Local Anesthetics :
97
 Carbon dioxide enhances diffusion of local anesthetic
through nerve membranes, providing a more rapid onset
of nerve block .
 As CO2 diffuses through the nerve membrane,
intracellular pH is decreased, raising the intracellular
concentration of charged cations (RNH+) Since the
cationic form of the drug does not readily diffuse out of
the nerve, the anesthetic becomes concentrated within
the nerve trunk (termed “ion trapping”), providing a
longer duration of anesthesia.

98
 The problem = if the carbonated LA agent is not
injected almost immediately after opening of the
vial the CO2 will diffuse out of solution,
significantly diminishing the solution’s
effectiveness.

Electronic Dental Anesthesia :
99
 A hand held electrode is placed at
the needle penetration site,
providing a very localized area of
intense anesthesia, permitting both
the painless penetration of intraoral
soft tissues with dental needles and
administration of local anesthetics

Reference :
100
 Handbook of Local Anesthesia ; Stanley F.
Malamed.
 Monheim’s Handbook of Local Anesthesia.
 History of Periodontology ; Fermin carranza,
Vincenzo Guerini
 History of the development & evolution of local
anesthesia since the coca leaf; Calatayud,
Jesus, Journal of Anesthesiology, June
2003:98-6: 1503-1508

…for the patience.
101 THANK YOU

Local anesthesia

Empfohlen

Empfohlen

Weitere ähnliche Inhalte

Was ist angesagt?

Was ist angesagt? (20)

Andere mochten auch

Andere mochten auch (7)

Ähnlich wie Local anesthesia

Ähnlich wie Local anesthesia (20)

Mehr von DrIbrahim Shaikh

Mehr von DrIbrahim Shaikh (8)

Kürzlich hochgeladen

Kürzlich hochgeladen (20)

Local anesthesia

Hinweis der Redaktion