local ansthesia

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

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 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

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

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:
• 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