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Local anesthesia.pptx
1. D E P T O F O R A L A N D M A X I L L O F A C I A L
S U R G E R Y
LOCAL ANESTHESIA
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2. DEFINITION
ACCORDING TO STANLEY F MALAMED (1980),
LOCAL ANESTHESIA IS DEFINED AS THE
REVERSIBLE LOSS OF SENSATION IN A
CIRCUMSCRIBED AREA OF THE BODY CAUSED BY
DEPRESSION OF EXCITATION IN NERVE ENDINGS
AND INHIBITION OF THE CONDUCTION PROCESS
IN PERIPHERAL NERVES WITHOUT THE LOSS OF
CONSCIOUSNESS.
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Based on CHEMISTRY
• AMIDE (ii) (Eg:lignocaine)
• ESTER (i) (Eg:benzocaine)
Based on duration of action
• Short acting (procaine)(less than 60 min)
• Intermediate acting (lidocaine)(60-
120min)
• Long acting (bupivacaine)(more than 120
min)
5. RESTING MEMBRANE POTENTIAL
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A resting (non-signaling) neuron has a voltage across its
membrane called the resting membrane potential.
In a resting neuron, there are concentration gradients
across the membrane for Na+ and K+. Ions move down
their gradients via channels, leading to a separation of
charge that creates the resting potential.
K+ is not allowed to leave and Na+ cannot enter the cell
Maintained by Na/K/ATPase pump
Value is -60 mV
7. DEPOLARISATION
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WHEN THERE IS LESS NEGATIVE
CHARGE INSIDE THE CELL, THE CELL IS
DEPOLARISED.
INNER
OUTER
+ 40 mV
8. REPOLARISATION
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CHANGE IN MEMBRANE POTENTIAL THAT
RETURNS TO NEGATIVE VALUE AFTER
DEPOLARISATION PHASE.
INNER
OUTER
+ 30 mV
9. ACTION POTENTIAL
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STATE OF CELL MEMBRANE WHILE IN AN IMPLUSE
RAPID CHANGE IN THE MEMBRANE POTENTIAL IN
RESPONSE TO A THRESHOLD STIMULUS
FOLLOWED BY A RETURN TO THE RESTING
MEMBRANE POTENTIAL.
13. MECHANISM OF ACTION
ACETYLCHOLINE THEORY
States that acetylcholine is involved in nerve
conduction, in addition to its role as a
neurotransmitter at nerve synapses.
CALCIUM DISPLACEMENT THEORY
The local anesthetic nerve block is produced by the
displacement of calcium from some membrane site
that controls permeability to sodium.
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14. MECHANISM OF ACTION
SURFACE CHARGE/REPULSION THEORY
It proposes that local anesthetics act by binding
to the nerve membrane and changing the electrical
potential at the membrane surface.
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15. MECHANISM OF ACTION
MEMBRANE EXPANSION THEORY
It states that LA molecule diffuse to the
hydrophobic region of excitable membrane,
producing general disturbance of bulk membrane
structure, expanding membrane and thus
prevent the increase in permeability of sodium
ions.
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16. MECHANISM OF ACTION
• SPECIFIC RECEPTOR THEORY
The most favored theory, proposed that the LAs act
by binding to the specific receptors on Na channels.
The action of drugs are directed but not mediated by
some change in general properties of cell membrane.
Biochemical and electrophysiological studies have
indicated that specific sites for LA agents exists in Na
channel either on its external surface or on internal
axoplasmic surface.
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19. COMPONENT FUNCTION
Local anesthetic drug
(lignocaine)
Sodium chloride
Sterile water
Vasopressor (e.g.: Epinephrine,
Adrenaline)
Sodium-bi-sulphite
Methylparaben
Blockade of nerve conduction
Isotonicity of the solution.
Volume
Increases depth and duration
of anesthesia
Antioxidant
Bacteriostatic agent
COMPOSITION
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20. WHAT IF ALLERGIC TO METHYL
PARABEN??
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Amino esters are derivatives of para-aminobenzoic
acid (PABA) which is associated with allergic
reactions.
Preparations of amide anesthetics contain methyl
paraben which is structurally similar to PABA and
may result in allergic reactions.
Allergic manifestations include rashes, utricaria
and rarely anaphylaxis.
Methylparaben free lidocaine or CARDIAC
LIGNOCAINE is obtained for such patients.
21. WHAT IF ALLERGIC TO SODIUM
META-BI-SULPHITE?
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PATIENTS MAY PRESENT WITH THE PROBLEMS
OF SULFITE ALLERGY.
SODIUM META BI SULPHITE ALLERGY CAN
CAUSE BRONCHOSPASM, UTRICARIA,
ANGIOEDEMA, SEIZURES, HYPOTENSION,
NAUSEA AND ANAPHYLACTIC REACTIONS.
22. WHY IS NITROGEN BUBBLE PRESENT
IN LA CARTRIDGE?
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1-2 mm diameter nitrogen bubble is present to
prevent oxygen from being trapped in the cartridge
which potentially destroy the vasopressor or
vasoconstrictor.
23. IDEAL PROPERTIES
Reversible
Non-irritant
Produce no allergic reaction
No systemic toxicity
Rapid onset of action
Longer duration of action
Potent
Sufficient penetrating properties
Stable in solution and undergo biotransformation in body
Can be sterilized
Not interfere with healing of local tissues
Have vasoconstrictor action
Not expensive/economically feasible
Ease of metabolism and excretion
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24. IDEAL PROPERTIES BY
C RICHARD BENNET
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IT SHOULD HAVE THE SUFFICIENT POTENCY TO GIVE
COMPLETE ANESTHESIA WITHOUT THE USE OF HARMFUL
CONCENTRATION SOLUTIONS.
IT SHOULD BE FREE FROM PRODUCING ALLERGICREACTIONS
IT SHOULD BE STABLE IN SOLUTION AND RELATIVELY
UNDERGO BIOTRANSFORMATION IN THE BODY
IT SHOULD BE EITHER STERILE OR CAPABLE OF BEING
STERILISED BY HEAT WITHOUT DETERIORATION
25. WHAT IS pH ?
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pH (POTENTIAL HYDROGEN)
Expresses the acidity and alkalinity of a
solution on a logarithmic scale on
which 7 is the neutral value.
Lower values are more acidic and
higher values are more alkaline.
26. EFFECT OF pH ON LOCAL ANESTHETICS
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LA action is strongly pH dependent.
They are weak bases.
Inflammation increases the acidity of the medium.
Therefore, administration of local anesthetics at sites
of inflammation increases their ionization.
This leads to lesser penetration into the nerves and,
therefore, lesser activity of the anesthetic.
27. SUBSTITUTE FOR ADRENALINE
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IT IS RECOMMENDED THAT WHEN THE USE OF
ADRENALINE IS CONTRAINDICATED ,
ALTERNATIVE LOCAL ANESTHETIC AGENTS
LIKE MEPIVACAINE CAN BE USED.
29. BIOTRANSFORMATION
ESTER GROUP
Metabolized in
Plasma by plasma pseudo-cholinesterase enzyme
Liver by the esterase enzyme
AMIDE GROUP
Metabolized in
Liver by the liver microsomal enzymes
Toxicity (high toxic blood level) occurs in patients
with impaired liver function (liver dysfunction)
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30. EXCRETION
Both group of local anesthetics and their
metabolites are excreted by kidneys.
Esters appear in very small concentrations in urine
as they are almost completely hydrolyzed in the
plasma
Patients with renal dysfunction may be unable to
eliminate the waste materials from the blood with
increased risk of toxicity
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31. HOW MUCH LA CAN BE INJECTED?
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WITHOUT ADRENALINE : 4.4 mg/kg
WITH ADRENALINE: 7mg/kg
SAFE DOSE ADRENALINE: 0.2mg/visit
2% lignocaine = 2g in 100 ml
2000mg = 100ml
20mg = 1ml
1mg = 1/20 ml
32. SYSTEMIC COMPLICATIONS
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Over dosage
Allergy
Anaphylactic reactions
Cardiovascular system complications
Nervous system complications
Liver complications
Syncope/Unconsciousness
33. LOCAL COMPLICATIONS
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Needle breakage
Paraesthesia
Facial nerve paralysis
Trismus
Soft tissue injury
Pain
Edema
Infection
Post anesthetic intra oral lesions
34. COMMON QUESTIONS TO ASK THE
PATIENTS
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1. ALLERGIC TO ANY MEDICATIONS?
2. HAVE YOU EVER HAD A REACTION TO LOCAL
ANESTHESIA? IF YES, DESCRIBE WHAT
HAPPENED??
3. WAS TEATMENT GIVEN?IF SO WHAT?