Local anesthesia

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 traumaLow temperatureAnoxiaChemical irritant…….euginolNeurolytic agent ……….alcoholChemical 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

Relative Advanced liver disease Thyrotoxic 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 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 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
2
R
R
3
4
2
1
R
R
3
4
H N— —COO—(CH ) —N 2
2
2
C H
2
5
C H
2
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 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) Concentration pH PKa Anatomical barrier Lipid solubility

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:
Protein binding Vasoactivity concentration 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 ?? Edema Localized hemorrhage Clot formation Reduced pH (poor buffer capacity) 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