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Local Anaesthesia
By,
Rushda
Malek
3rd BDS
Contents
 Definition
 Classification
 Common uses
 Composition
 Indications & Contraindications
 Nerve physiology
 Mechanism of Action
 Dosage
 Complications
 Basic Technique
Definition of LA
Local Anaesthesia has been defined as a
“ Reversible loss of sensation in a
circumscribed area of the body caused by a
depression of excitation in nerve endings or
an inhibition of conduction process in
peripheral nerves”
classification
•Cocaine,prilocaine,
lignocaineTopical
• Lignocaine,mepivacaine
Injectable
Based on site
Based on chemical structure
Esters
• Cocaine
• Procaine
• Benzocaine
• Tetracaine
Amides
• Articaine
• Bupivacaine
• Lidocaine
• Mepivacaine
• Prilocaine
• Ropivacaine
Based on duration of action
• 2% Lignocaine without vasoconstrictorUltra short duration
• Procaine
• 2% Lignocaine with 1:1,00,000
Epinephrine
Short duration
• Articaine
• Mepivacaine
• Prilocaine
• 2% Lignocaine with 1:2,00,000
Epinephrine
Intermediate
Duration
• Bupivacaine
• Etidocaine
• 5% Lignocaine with 1:2,00,000
Epinephrine
Long Duration
Common uses
Excision Dermatology Dentistry
Spinal Anaesthesia
Composition
• Local anaesthetic solution contains:
1. Local anaesthetic agent-
Ester linkage- procaine,cocaine,tetracaine
Amide linkage-Lignocaine, prilocaine,
bupivacaine , mepivacaine
2. Vasoconstrictor-
Adrenaline- a synthetic substance similar to that
secreted in human body. Concentration from
1:50,000-1:250,000 (optimal 1:200,000)
Advantage
• Reduces toxic effect by retarding the absorption of
the constituents.
• It increases the depth & duration of the anaesthesia
and produces bloodless field for the surgical
procedure.
3. Reducing agent – Sodium bimetasulphite.
• Small quantity in the solution prevents oxidation of
the vasoconstrictor as they are unstable in solution
especially on exposure to sunlight.
4. Preservative- caprylhydrocupeinotoxin
• It helps to maintain sterility of the solution & also
increases its shelf life.
5. Fungicide- Thymol
• To prevent proliferation of the minute fungi which
cause cloudiness of the solution.
6. Vehicle – Ringer’s solution.
• In which all constituents are dissolved to minimize
discomfort during injection of the L.A.
7. Sodium chloride - Isotonicity of the solution
Indications
• The patient remains awake and cooperative.
• Poor risk patients.
• Low incidence of morbidity
• Patients leaves office unescorted.
• No additional trained personnel is necessary.
• Techniques are not difficult to master.
• % of failure is small
• No additional expense to patient
• Patient need not omit the previous meal
Contraindications
• Patient refuses regional anaesthesia because
of fear or apprehension
• Infection
• Allergy
• Patient is below the age of reason
• Major surgery- regional anaesthesia
unfeasible
• Anomalies
Nerve physiology and
Mechanism of action
Electrophysiology of nerve
conduction
• Electrical events occur within a nerve during
the conduction of an impulse.
• A nerve possesses a resting potential which is
-70mV that exists across the nerve membrane,
produced by differing concentration of ions on
either side is the membrane.
• A stimulus excites the nerve, in the following
sequence of events:-
• Step 1a- An initial phase of slow
depolarization.
• Step 1b- Falling electrical
potential reaches a critical level,
it gives result of rapid phase of
depolarization. This is termed as
Threshold or firing potential.
• Step 1c- This phase of rapid
depolarization results in a
reversal of electrical potential
across the nerve membrane.
Electric potential of +40mV
exists on the interior of the
nerve cell.
Depolarization
• Excitation of the nerve
segment leads to an
increase in permeability of
the cell membrane to
sodium ions. The rapid influx
of the sodium ions to the
interior of the nerve cell
causes depolarization of the
nerve membrane from its
resting level to its firing
threshold of approx. -50 to -
60mV. Exposure of the nerve
to Local anaesthetic raises
its firing threshold.
• The action potential is terminated when the
membrane repolarises. This is caused by the
inactivation of the increased permeability to
sodium. In many cells potassium also
increases, resulting in the reflux of K+ , and
leading to more rapid membrane
repolarisation and return to its resting
potential.
• The entire process requires 1 millisecond;
depolarisation(step1)takes 0.3msec;
repolarisation (step2) takes 0.7 msec.
Theories for Mechanism of LA
The Acetylcholine theory.
The Calcium displacement theory.
The surface charge theory.
Membrane Expansion theory
Specific Receptor theory
The Acetylcholine theory
• Stated that acetylcholine was involved in
nerve conduction in addition to its role as
a neurotransmitter at nerve synapse.
The Calcium Displacement theory
• Local Anaesthetic nerve block was produced
by displacement of the calcium from some
membrane site that controlled permeability of
sodium. That varying the concentration of
calcium ion bathing a nerve does not affect
local anaesthetic potency has diminished the
credibility of this theory.
The Surface charge theory
• Proposed that La acts by binding to the nerve
membrane and changing the electrical
potential at the membrane surface.
Membrane expansion theory
• Stated that Local anaesthetic molecules diffuse to
hydrophobic regions of excitable membranes,
producing a general disturbance in the bulk
membrane structure, expanding some critical
regions in the membrane & preventing an increase
in the permeability to sodium ions.
Specific receptor theory by strichartz
1987
• Drug molecules bind to specific receptors present
on the external or internal axoplasmic surface of
the sodium channel & by acting directly on them,
decrease or eliminate permeability to Na2⁺ leading
to interruption of nerve conduction.
Local anaesthesia acts as follows:
Displacement of calcium ions from
the sodium channel receptor site,
which permits
Binding of L.A molecules to the
receptor site, which thus produces
Blockade of the sodium channel
Decrease in sodium conductance, which
leads to
Depression of the electrical
depolarization
Failure to achieve the threshold
potential level along with
Lack of development of the propagated
action potential, which is called
Conduction blockade
Doses and Duration of Block
Drug Conc. Total dose (mg) Dose(mg/kg) Duration of
block
Procaine 1-2% 400 6 30-60 min.
Lidocaine 0.5-2% 300 4.5 60-120 min.
Bupivacaine 0.25-0.5% 90 1.4 180-360 min.
Tetracaine 0.25-0.5% 80 1.3 180-480 min.
Cardiac patients
• Vasoconstrictor content should be kept
minimum or eliminated.
• Epinephrine- max- 0.04 mg
Complications
• CNS stimulation (more sensitive than cardiac)
• Dose related spectrum of effects and all effects are due
to depression of neurons.
• First an apparent CNS stimulation ( convulsion most
serious)
• Premonitory signs include: ringing in ears, metallic
taste, numbness around lips
• Followed by CNS depression (death due to respiratory
depression)
• Cocaine- Euphoria
• Lidocaine – Sedation even at non toxic dose
ARRHYTHMIAS
• Decrease cardiac
excitability and
contractibility
• Decreased conduction rate
• Increased refractory rate
(bupivacaine)
• ALL can cause arrhythmias
if conc. Is high enough
• ****Cocaine is exception
(it stimulates heart)
HYPOTENSION: Arteriolar
dilation as a result of:
• Direct effect(procaine and
lidocaine have most effect)
• Block of postganglionic
sympathetic fibre function
• CNS depression
• Avoid by adding
vasoconstrictor to the
preparation
• Cocaine is exception
(produces
vasoconstriction)
• Hypersensitivity:
• Common with ester linked LA
• Rashes, angio oedema, dermatitis an rare
anaphylaxis
• Sometimes typical asthmatic attack
• Neurotoxicity:
• La can cause concentration dependent nerve
damage to central and peripheral NS
• Mechanism not clear
• Permanent neurologic injury is rare
• May account for transient neurological
symptoms.
• Others:
• Ischemia and necrosis of soft tissues when
highly conc. Vasoconstriction solution used for
homeostasis over a prolonged period
• Hematoma is possible but rarely occurs
• Inflammation or infection at the injection site
• Palatal ulcers
• Facial paralysis
• Trismus
• Needle breakage
• Pain/burning on injection site
• Sloughing of tissue
Post anaesthetic complications
• Lip biting- seen in children
Cheek biting
Blanching due to
vasoconstriction
Hematoma due to Local anaesthesia
The Armamentarium
4 PARTS:
1) The Syringe
2) The Needle
3) The Cartridge
4) Preparation
The syringe
The Needle
The 25 gauge needle is the most
preferred needle for local
anaesthesia.
Gauge= 1
_________________
diameter
Basic Technique for administration of
Local Anaesthesia
References
• Handbook of Local Anaesthesia – Stanley F
Malamed
• Monheim’s Local Anaesthesia And Pain in
Dental practice
Local anesthesia

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Local anesthesia

  • 2. Contents  Definition  Classification  Common uses  Composition  Indications & Contraindications  Nerve physiology  Mechanism of Action  Dosage  Complications  Basic Technique
  • 3. Definition of LA Local Anaesthesia has been defined as a “ Reversible loss of sensation in a circumscribed area of the body caused by a depression of excitation in nerve endings or an inhibition of conduction process in peripheral nerves”
  • 5. Based on chemical structure Esters • Cocaine • Procaine • Benzocaine • Tetracaine Amides • Articaine • Bupivacaine • Lidocaine • Mepivacaine • Prilocaine • Ropivacaine
  • 6. Based on duration of action • 2% Lignocaine without vasoconstrictorUltra short duration • Procaine • 2% Lignocaine with 1:1,00,000 Epinephrine Short duration • Articaine • Mepivacaine • Prilocaine • 2% Lignocaine with 1:2,00,000 Epinephrine Intermediate Duration • Bupivacaine • Etidocaine • 5% Lignocaine with 1:2,00,000 Epinephrine Long Duration
  • 7. Common uses Excision Dermatology Dentistry Spinal Anaesthesia
  • 8. Composition • Local anaesthetic solution contains: 1. Local anaesthetic agent- Ester linkage- procaine,cocaine,tetracaine Amide linkage-Lignocaine, prilocaine, bupivacaine , mepivacaine 2. Vasoconstrictor- Adrenaline- a synthetic substance similar to that secreted in human body. Concentration from 1:50,000-1:250,000 (optimal 1:200,000)
  • 9. Advantage • Reduces toxic effect by retarding the absorption of the constituents. • It increases the depth & duration of the anaesthesia and produces bloodless field for the surgical procedure. 3. Reducing agent – Sodium bimetasulphite. • Small quantity in the solution prevents oxidation of the vasoconstrictor as they are unstable in solution especially on exposure to sunlight.
  • 10. 4. Preservative- caprylhydrocupeinotoxin • It helps to maintain sterility of the solution & also increases its shelf life. 5. Fungicide- Thymol • To prevent proliferation of the minute fungi which cause cloudiness of the solution. 6. Vehicle – Ringer’s solution. • In which all constituents are dissolved to minimize discomfort during injection of the L.A. 7. Sodium chloride - Isotonicity of the solution
  • 11. Indications • The patient remains awake and cooperative. • Poor risk patients. • Low incidence of morbidity • Patients leaves office unescorted. • No additional trained personnel is necessary. • Techniques are not difficult to master. • % of failure is small • No additional expense to patient • Patient need not omit the previous meal
  • 12. Contraindications • Patient refuses regional anaesthesia because of fear or apprehension • Infection • Allergy • Patient is below the age of reason • Major surgery- regional anaesthesia unfeasible • Anomalies
  • 14. Electrophysiology of nerve conduction • Electrical events occur within a nerve during the conduction of an impulse. • A nerve possesses a resting potential which is -70mV that exists across the nerve membrane, produced by differing concentration of ions on either side is the membrane. • A stimulus excites the nerve, in the following sequence of events:-
  • 15. • Step 1a- An initial phase of slow depolarization. • Step 1b- Falling electrical potential reaches a critical level, it gives result of rapid phase of depolarization. This is termed as Threshold or firing potential. • Step 1c- This phase of rapid depolarization results in a reversal of electrical potential across the nerve membrane. Electric potential of +40mV exists on the interior of the nerve cell.
  • 16. Depolarization • Excitation of the nerve segment leads to an increase in permeability of the cell membrane to sodium ions. The rapid influx of the sodium ions to the interior of the nerve cell causes depolarization of the nerve membrane from its resting level to its firing threshold of approx. -50 to - 60mV. Exposure of the nerve to Local anaesthetic raises its firing threshold.
  • 17. • The action potential is terminated when the membrane repolarises. This is caused by the inactivation of the increased permeability to sodium. In many cells potassium also increases, resulting in the reflux of K+ , and leading to more rapid membrane repolarisation and return to its resting potential. • The entire process requires 1 millisecond; depolarisation(step1)takes 0.3msec; repolarisation (step2) takes 0.7 msec.
  • 18. Theories for Mechanism of LA The Acetylcholine theory. The Calcium displacement theory. The surface charge theory. Membrane Expansion theory Specific Receptor theory
  • 19. The Acetylcholine theory • Stated that acetylcholine was involved in nerve conduction in addition to its role as a neurotransmitter at nerve synapse.
  • 20. The Calcium Displacement theory • Local Anaesthetic nerve block was produced by displacement of the calcium from some membrane site that controlled permeability of sodium. That varying the concentration of calcium ion bathing a nerve does not affect local anaesthetic potency has diminished the credibility of this theory.
  • 21. The Surface charge theory • Proposed that La acts by binding to the nerve membrane and changing the electrical potential at the membrane surface.
  • 22. Membrane expansion theory • Stated that Local anaesthetic molecules diffuse to hydrophobic regions of excitable membranes, producing a general disturbance in the bulk membrane structure, expanding some critical regions in the membrane & preventing an increase in the permeability to sodium ions.
  • 23. Specific receptor theory by strichartz 1987 • Drug molecules bind to specific receptors present on the external or internal axoplasmic surface of the sodium channel & by acting directly on them, decrease or eliminate permeability to Na2⁺ leading to interruption of nerve conduction.
  • 24. Local anaesthesia acts as follows: Displacement of calcium ions from the sodium channel receptor site, which permits Binding of L.A molecules to the receptor site, which thus produces Blockade of the sodium channel
  • 25. Decrease in sodium conductance, which leads to Depression of the electrical depolarization Failure to achieve the threshold potential level along with Lack of development of the propagated action potential, which is called Conduction blockade
  • 26. Doses and Duration of Block Drug Conc. Total dose (mg) Dose(mg/kg) Duration of block Procaine 1-2% 400 6 30-60 min. Lidocaine 0.5-2% 300 4.5 60-120 min. Bupivacaine 0.25-0.5% 90 1.4 180-360 min. Tetracaine 0.25-0.5% 80 1.3 180-480 min.
  • 27. Cardiac patients • Vasoconstrictor content should be kept minimum or eliminated. • Epinephrine- max- 0.04 mg
  • 28. Complications • CNS stimulation (more sensitive than cardiac) • Dose related spectrum of effects and all effects are due to depression of neurons. • First an apparent CNS stimulation ( convulsion most serious) • Premonitory signs include: ringing in ears, metallic taste, numbness around lips • Followed by CNS depression (death due to respiratory depression) • Cocaine- Euphoria • Lidocaine – Sedation even at non toxic dose
  • 29. ARRHYTHMIAS • Decrease cardiac excitability and contractibility • Decreased conduction rate • Increased refractory rate (bupivacaine) • ALL can cause arrhythmias if conc. Is high enough • ****Cocaine is exception (it stimulates heart) HYPOTENSION: Arteriolar dilation as a result of: • Direct effect(procaine and lidocaine have most effect) • Block of postganglionic sympathetic fibre function • CNS depression • Avoid by adding vasoconstrictor to the preparation • Cocaine is exception (produces vasoconstriction)
  • 30. • Hypersensitivity: • Common with ester linked LA • Rashes, angio oedema, dermatitis an rare anaphylaxis • Sometimes typical asthmatic attack • Neurotoxicity: • La can cause concentration dependent nerve damage to central and peripheral NS • Mechanism not clear • Permanent neurologic injury is rare • May account for transient neurological symptoms.
  • 31. • Others: • Ischemia and necrosis of soft tissues when highly conc. Vasoconstriction solution used for homeostasis over a prolonged period • Hematoma is possible but rarely occurs • Inflammation or infection at the injection site • Palatal ulcers • Facial paralysis • Trismus • Needle breakage • Pain/burning on injection site • Sloughing of tissue
  • 32. Post anaesthetic complications • Lip biting- seen in children
  • 33. Cheek biting Blanching due to vasoconstriction
  • 34. Hematoma due to Local anaesthesia
  • 35. The Armamentarium 4 PARTS: 1) The Syringe 2) The Needle 3) The Cartridge 4) Preparation
  • 37. The Needle The 25 gauge needle is the most preferred needle for local anaesthesia. Gauge= 1 _________________ diameter
  • 38. Basic Technique for administration of Local Anaesthesia
  • 39. References • Handbook of Local Anaesthesia – Stanley F Malamed • Monheim’s Local Anaesthesia And Pain in Dental practice