Oral surgery Oral surgery Local anesthesia 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 Preferable Minimal allergisity Adequate shelf life Surface anesthesia Easy to sterile Mandatory Potent and reliable Reversible Minimal toxicity(MOS) Rapid onset Acceptable duration Non irritating Stable in solution Easily metabolized

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

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 Threshold level (firing level) Extra cellular Na ++ K+ +35 Intracellular axoplasm Threshold level (firing level) --70 Potassium efflux Repolarization 0.7 second Sodium influx 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

Membrane expansion theory Extra cellular Intracellular axoplasm Membrane expansion theory

Nerve Blockade Theories Specific Receptor Theory Anesthetic agent receptor in channel Accessed from intracellular side

Specific receptor theory Extra cellular Intracellular axoplasm Specific receptor theory

H W Type of nerve fiber and their characteristic feature Acupuncture as anesthesia in dentistry

Structure of local anesthesia 3 Ester: R —COO—R —N R — Lipophilic aromatic residue. 1 2 1 R 4 R — Aliphatic intermediate connector. 2 R 3 R , R — Alkyl groups, occasionally 3 4 Amide: R —NHCO—R —N 1 2 H. Constitute with N the hydrophilic terminus. R 4 Example: C H 2 5 H N— —COO—(CH ) —N 2 2 2 C H 2 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) 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

Diffusion from intranuronal tissue (mantle fiber) 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)

Protein binding capacity Duration Recovery slower than induction ? Protein binding capacity Protein binding Vasoactivity concentration Vascularity of the site Time from induction to complete recovery from local anesthesia It depend on:

Principle of reinjection After reinjection in prolonged procedure 2 situation may occur Failure ?? Edema Localized hemorrhage Clot formation Reduced pH (poor buffer capacity) hypernatremia Profound anesthesia: Increase concentration gradient to mantle fiber then to the core fiber

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