Transcript Oral surgery

Oral surgery
Local anesthesia
Terminology
• Anesthesia =
• Analgesia =
• Local anesthesia
• General anesthesia
• Sedation == general analgesia
• Paraesthesia
• Pain threshold
Local anesthesia
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Methods for inducing local anesthesia:
Mechanical trauma
Low temperature
Anoxia
Chemical irritant…….euginol
Neurolytic agent ……….alcohol
Chemical agent
Ideal properties of a local anesthetic
agent
Preferable
Mandatory
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Potent and reliable
Reversible
Minimal toxicity(MOS)
Rapid onset
Acceptable duration
Non irritating
Stable in solution
Easily metabolized
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Minimal allergisity
Adequate shelf life
Surface anesthesia
Easy to sterile
Indications of local anesthesia
• Diagnosis
• Reduce or eliminate pain during
dental treatment
Contraindications of local anesthesia
Systemic
• Uncooperative patient
like child
• Uncontrolled
hemorrhagic patient
• Allergic patient to
local anesthesia
Local
• Patient received
radiotherapy
• Acute infection at
injection site
• Vascular abnormality at
operation site
Contraindications of local anesthesia
Relative
Advanced liver disease
Thyrotoxic goiter
 Uncontrolled cardiovascular disease
Advantages of local anesthesia
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Simple technique
Minimal equipment
Transportable
Minimal
contraindication
 Hemorrhage could
be controlled by
vasoconstrictor
No airway impairment
Minimal postoperative
care
No need for
anesthetist
Duration could be
controlled
Co-operative patient
simplify the work
Disadvantages of local anesthesia
• Difficult to achieve co-operation
• Mechanical obstruction by large tongue or
limited mouth opening
• Failure due to anatomical variation or
incomplete anesthesia
• Prolonged parasthesia
• Spread of acute infection
Mode of action of local anesthesia
• Prevention of generation and or conduction
of nerve impulse
• Act as chemical roadblock between source of
impulse and brain
Sensory neuron
Afferent neuron
Structure of nerve fiber
Nerve bundle of
different fibers
separated from other
bundles by dens
fibrous tissue
core fiber
Mantle fiber
Generation of nerve impulse
Resting membrane
potential (RMP)
(-70) mv due to
impermeability of
membrane to sodium
ion
Concentration of
sodium ion is more in
the extra cellular area
- 70 mv
Generation of action potential
Extra cellular
Na ++
Intracellular axoplasm K+
+35
Threshold level--70
Potassium efflux Sodium influx (firing level)
Repolarization
0.7 second
Depolarization
0.3 second
Impulse propagation
transmittion of nerve impulse along the
neuron
• Movement of the impulse along the axon:
Saltatory movement (jumping)
Creep conduction
Mode of action of local anesthesia
Local anesthetics interfere with
propagation of the action potential by
blocking the increase in sodium
permeability during depolarization.
Depolarization inhibited
Firing level not reached
Action potential inhibited
Theories of action of local anesthesia
Acetylcholine theory
Calcium displacement theory
Surface charge theory
Membrane expansion theory
Specific receptor theory
Nerve Blockade Theories
Membrane expansion theory
Agent molecules must be lipid
soluble
Membrane is “disordered”
Channel changes occur
Benzocaine as example for this
theory
Extra cellular
Intracellular axoplasm
Membrane expansion theory
Nerve Blockade Theories
Specific Receptor Theory
–Anesthetic agent receptor in
channel
–Accessed from intracellular side
Extra cellular
Intracellular axoplasm
Specific receptor theory
HW
• Type of nerve fiber and their characteristic
feature
• Acupuncture as anesthesia in dentistry
Structure of local anesthesia
R3
Ester:
R 1—COO—R 2 —N
R 1 — Lipophilic aromatic residue.
R4
R3
Amide:
R 1—NHCO—R 2—N
R4
R 2 — Aliphatic intermediate connector.
R 3, R 4 — Alkyl groups, occasionally
H. Constitute with N the hydrophilic
terminus.
Example:
C 2H 5
H2 N—
—COO—(CH 2) 2—N
C 2H 5
Exception:
Benzocaine, which lacks a substituted amino group
PH and local anesthesia
Dissociation constant PKa:
• pH at which 50% of drug present in free
base form and 50% in cationic form (water
soluble)
• Most local anesthetic Pka(7-9)
How can local anesthesia cross nerve membrane?
• Local anesthetic solution prepared as weak
acid form at 4-5 pH to prevent precipitation of
free base in neutral solution, thus it present
as cataionic form that must converted to
base form to be lipid soluble and cross cell
membrane
Buffering
capacity
• Local anesthetic agent after injection
and with function of plasma buffering
will dissociate into free base form
and cataionic form
• Free base form cross the cell
membrane
• After crossing the membrane an
other dissociation occur and
cataionc form resulted will bind the
receptor
Onset (induction time)
Time from injection of local anesthesia to the
sign of adequate surgical anesthesia
achieved
Factors affect onset (induction time)
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Concentration
pH
PKa
Anatomical barrier
Lipid solubility
Mixing pen
Recovery
• Time from early sign appeared to the
complete loss of all effects of drug
occur
• This results from reduced
concentration of drug with no
binding with the receptors
Recovery time
Concentration gradient depleted by:
• Dilution by interstitial fluid
• Action of capillary and lymph
• Absorption by other tissue
• Hydrolysis of ester
Extraanuronal
Diffusion from intranuronal tissue (mantle fiber)
Duration
Recovery slower than induction ?
Protein binding capacity
• Time from induction
to complete recovery
from local anesthesia
• It depend on:
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Protein binding
Vasoactivity
concentration
Vascularity of the
site
Principle of reinjection
After reinjection in prolonged procedure 2
situation may occur
Failure ??
Profound anesthesia:
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• Increase
concentration
gradient to mantle
fiber then to the core
fiber
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Edema
Localized hemorrhage
Clot formation
Reduced pH (poor buffer
capacity)
hypernatremia
Progression of local
anestheticfunction
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Dull pain
Temprature
Sharp pain
Touch
Deep pressure
Proprioception
Motor function
H. W.
• Why infected area presents a poor site for
action of local anesthesia