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Oral surgery
Local anesthesia
Oral surgery
Local anesthesia
Terminology
• Anesthesia =• Analgesia =
• Local anesthesia• General anesthesia• Sedation == general analgesia
• Paraesthesia
• Pain threshold
Local anesthesia
• 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
Mandatory• Potent and
reliable• Reversible• Minimal
toxicity(MOS)• Rapid onset• Acceptable
duration• Non irritating• Stable in solution• Easily
metabolized
Preferable• 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
RelativeAdvanced liver diseaseThyrotoxic goiter Uncontrolled cardiovascular
disease
Advantages of local anesthesia
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
Mantle fiber
core fiber
Structure of nerve fiber
Nerve bundle of different fibers separated from other bundles by dens fibrous tissue
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
--70+35
Na++
K+
Generation of action potential
Intracellular axoplasm
Extra cellular
Potassium efflux
Repolarization
0.7 second
Sodium influx
Depolarization
0.3 second
Threshold level (firing level)
Impulse propagationtransmittion 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 inhibitedFiring level not reached Action potential inhibited
Theories of action of local anesthesia
Acetylcholine theoryCalcium displacement theorySurface charge theoryMembrane expansion theorySpecific receptor theory
Nerve Blockade Theories
Membrane expansion theoryAgent molecules must be lipid
soluble Membrane is “disordered”Channel changes occurBenzocaine 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
Intracellular axoplasm
Extra cellular
Specific receptor theory
H W
• Type of nerve fiber and their characteristic feature
• Acupuncture as anesthesia in dentistry
Structure of local anesthesia
Ester:
Amide:
Example:
Exception: Benzocaine, which lacks a substituted amino group
R —COO—R —N
R —NHCO—R —N
1 2R
R3
4
21R
R3
4
H N— —COO—(CH ) —N2 2 2
C H2 5
C H2 5
R — Lipophilic aromatic residue.
R — Aliphatic intermediate connector.
R , R — Alkyl groups, occasionally H. Constitute with N the hydrophilic terminus.
1
2
3 4
PH and local anesthesiaDissociation 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 achievedFactors affect onset (induction time)
1. Concentration2. pH3. PKa4. Anatomical barrier5. 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
• Time from induction to complete recovery from local anesthesia
• It depend on:
1. Protein binding
2. Vasoactivity
3. concentration
4. Vascularity of the site
Recovery slower than induction ?
Protein binding capacity
Principle of reinjection
Profound anesthesia:
• Increase concentration gradient to mantle fiber then to the core fiber
Failure ??1. Edema
2. Localized hemorrhage
3. Clot formation
4. Reduced pH (poor buffer capacity)
5. hypernatremia
After reinjection in prolonged procedure 2 situation may occur
Progression of local anestheticfunction
• 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