Local Anaesthesia
Topical Anaesthetic
Purpose: Numbs gums/mucous membranes before injections/minor procedures.
Forms: Gels, creams, sprays, liquids, pre-soaked pellets.
Ingredients: Lidocaine, benzocaine, or tetracaine.
Application: Apply to dried area for 1-2 minutes.
Duration: 15-30 minutes.
Indications: Scaling, root debridement, or before LA injections.
Side Effects: Rare; irritation/allergies. Prolonged use: mild ischemia.
Artery Forceps
Purpose: Reduce needle stick injury risk when recapping/removing needle cap.
Cartridge
Contains 1.8ml or 2.2ml of solution.
Parts: Cylindrical tube, rubber stopper, aluminum cap, rubber diaphragm.
Check name, composition, vasoconstrictor, Expiry date.
Needle
Stainless steel/disposable.
Parts: Bevel, shank, hub & syringe end.
Marker indicates bevel direction.
Length:
Long:
Short:
Gauge: Diameter of lumen.
Smaller number = larger diameter.
Typically 27 & 30 gauge.
Bevel oriented towards bone during injection to avoid pain.
Uncap with artery forceps.
Dispose of in sharps container.
The Syringe
Delivers anesthetic solution.
Non-aspirating, aspirating, or self-aspirating types.
Steps For Loading manually aspirating syringe:
Pull back piston/plunger.
Engage piston with rubber stop.
Insert and screw needle onto adapter/thread.
Apply slight pressure to check flow.
Self Aspirating Syringes:
Spring mechanism aids automatic aspiration.
After needle insertion decrease pressure on thumb ring to create negative pressure to assess if the needle is in a blood vessel or not
Positive aspiration: (blood in cartridge) do not deposit solution, discard cartridge and replace
Negative aspiration: SLOWLY deposit solution
What is Local Anaesthesia?
Loss of sensation in a circumscribed area caused by:
Depression of excitation in nerve endings.
Inhibition of conduction in peripheral nerves.
Prevents generation and conduction of nerve impulse.
The Neuron
Sensory (afferent): Transmit pain.
3 parts: Dendritic zone, Axon (synapses with CNS), Cell body.
Motor (efferent)
The Axon
Long cylinder separated from extracellular fluids by nerve membrane.
May be covered by myelin (insulating lipid-rich layer).
Nodes of Ranvier: Constrictions at regular intervals ( to ).
Nerve membrane: Two layers of lipid molecules and phospholipids.
Hydrophilic (polar) end faces outer surface, hydrophobic (non-polar) end faces middle.
Selectively permeable to molecules via channels.
Proteins: Transport proteins (channels, carriers, pumps) or receptor sites.
Depolarization at one Node of Ranvier triggers Na+ channels in adjacent segment.
Waves of depolarization (Salutatory Conduction) continue to axon terminal.
Neurotransmitters: Chemical messengers released from axon and received by effector cells.
Signal Conduction
An action potential (AP) is a rapid, brief reversal in electrical charge across the Axon’s membrane
Voltage-gated Channels
Resting membrane Potential is approx.
Nerve impulse increases membrane conductivity ().
Permits Na+ and K+ ion passage along concentration gradients.
Ion movement provides energy for impulse conduction.
Resting nerve membrane resistance prevents ion passage.
Local anesthetics interfere with excitation, causing temporary anesthesia.
How Local Anaesthetics Work
Displace calcium ions from the sodium channel receptor site
Binding of the LA molecule to the receptor site
Blockade of the sodium channel
Decrease in sodium conductance
Depression of the rate of electrical depolarization
Failure to achieve the threshold potential level
Lack of development of propagated action potentials
Conduction blockade
Properties of LA
Speed on onset: determined by the pKa of the solution and the pH of fluids.
Potency: HIGH lipid solubility are more potent.
Duration of Action
Protein Binding: Higher protein binding =bind to plasma proteins for longer
Vasodilator action: anesthetic agent is carried away from effector site more rapidly for biotransformation
Low tissue pH means more L.A solution in cation form, less free base available to act on Na receptor
Increased Inflammation more blood vessels present in local area.
Local Anaesthetics in Dentistry
Block pain signals in peripheral nerves.
Vasodilators; contain vasoconstrictors to reduce bleeding and retain solution.
Can cause CNS stimulation or depression.
Used topically and subcutaneously.
Weak base, pKa of . Exists as uncharged and +ve charged molecule.
Pharmacokinetics of LA (ADME)
Pharma = medicine, kinetics = movement
The movement of drugs inside the body
ADME
Absorption: Affected by the drug's chemical nature, site of injection, local blood flow, and vasoconstrictors. Greater absorption leads to greater potential for systemic effects.
Distribution: Influenced by protein binding capacity and other drugs. Described by a two-compartment model (rapid and slow disappearance phases).
Metabolism: Occurs in the liver, blood plasma, and lungs. Alters chemical properties of drugs to enable excretion.
Products of metabolism may also have clinical implications.
Excretion: Primarily via the kidneys.
Factors Impacting ADME
Absorption:
Accidental intravenous injection
Volume and concentration of anesthetic
Vasoconstrictors
Local blood flow, Site of injection
Plasma Concentration:
Age and weight
Presence of other drugs
Lipid solubility and protein binding
Metabolism and excretion rates
Metabolism: Liver function
Elimination: Significant kidney impairment
The Chemistry of LA
Two functional groups based on intermediate chain: Amides and Esters.
Functional Groups
Amides:
Metabolized primarily in the liver.
Rate of breakdown depends on hepatic blood flow.
Conditions affecting hepatic blood flow increase toxicity potential (hypotension, congestive heart failure, liver dysfunction).
Esters:
Rapidly hydrolyzed in plasma by pseudocholinesterase.
Metabolite para-aminobenzoic acid related to allergic reactions.
Atypical pseudocholinesterase can prolong higher levels of L.A potentially increasing toxicity
Factors affecting LA properties
Potency: Concentration, lipid solubility.
Onset: Speed, proximity to nerve, nerve fiber diameter.
Duration: Diffusion rate, protein binding, vasoconstrictor presence.
Tissue effects: Excitable tissues (cardiovascular, nervous systems).
Degradation and elimination: Liver (amides), kidneys; disease/drugs affect rate.
Topical Anaesthetics
Onset: 2-5 mins
Duration: 15-20 mins
Indications: Anesthetize mucous membranes, surface anesthesia before injections.
Contraindications: Known allergy.
Precautions: Overdose.
Examples:
Xylocaine®
Num ®
Oroqix ® (periodontal gel), thermosetting abilities, thus retained in pockets
Composition of Local Anaesthetics
Anaesthetic Agent (weak organic base- insoluble in water)
Stabilisers/salts (converts agent so it is water soluble)
Usually hydrochlorides
Vasoconstrictors (increase duration of action of L.A)
Antioxidants (prevents oxidation of stabiliser)
Sodium metabisulphite
Preservatives:
Fungicides, antibacterials
Methylparaben
Water:
Distilled water, increases volume of solution
Vasoconstrictors
Added for:
Longer lasting LA
More profound LA
Reduced operative haemorrhage
Reduced systemic effects
Types: Sympathomimetics (adrenaline) or Synthetic polypeptides (octapressin/felypressin).
Adrenaline
Naturally occurs; binds to adrenoreceptors.
Effects:
Heart: Increases HR and contractility, dilates coronary arteries.
Blood vessels: Vasoconstriction of skin/mucous membranes, vasodilation of skeletal muscle.
Lungs: Bronchiolar muscle relaxation.
GI Tract: Reduces gut contractility, decreases saliva flow.
Metabolism: Inhibits insulin release, increases glucose.
Felypressin
Causes vasoconstriction in smooth muscle of vascular beds.
More effective on venous side of peripheral circulation.
Appropriate when adrenaline is contraindicated.
Common Local Anaesthetics
Lidocaine/Lignocaine
Prilocaine
Articaine
Mepivacaine
Bupivacaine
Articaine
*is considered the safest local anaesthetic drug for use in patients with hepatic and renal impairments.
Scope of Practice
Dental hygienists are authorized to possess and use (administer) benzocaine, lidocaine (lignocaine), mepivacaine, prilocaine, procaine and any Schedule 2, 3 or 4 synthetic local anaesthetic.
Dental therapists and oral health therapists are authorized to possess and use (administer) tetracycline and triamcinolone in preparations for treatment of dental pulp, benzocaine, lidocaine (lignocaine), mepivacaine, prilocaine, procaine and any Schedule 2, 3 or 4 synthetic local anaesthetic.
CSU Used Anaesthetics:
Articaine (Septanest) (Schedule 4)
Felypressin (Schedule 4)
Lignospan/Lignocaine/Lidocaine (Schedule 2, 4)
Scandonest (Mepivacaine) (Schedule 4)
Oraqix (lidocaine and prilocaine periodontal gel)
Terminology
Contraindication: Use inadvisable.
Precautions: Use less; use different agent.
Conditions that contraindicate local anesthetics
Hypersensitivity to any components
Serious IV conduction defects
Severe hypotension
Severe liver and renal disease
Conditions where cartridges containing adrenaline is contraindicated
Adrenal tumors
Uncontrolled hyperthyroidism/not on HRT
Uncontrolled diabetes/elevated blood glucose
Cardiovascular disease:\ unstable angina, recent myocardial infarct and refractory cardiac dysrhythmias, uncontrolled HBP (>200mmHg systolic >115 mmHg diastolic)
Conditions Requiring Precautions
Impaired renal/liver function (reduce dose).
Cardiovascular disease (reduce adrenaline dose).
Atypical pseudocholinesterase (avoid articaine and esters).
Existing anemia (avoid prilocaine and articaine).
Pregnancy (avoid certain medication categories).
Coronary artery disease (avoid high doses felypressin).
Children/elderly (dose reduction).
Certain medications (interactions).
Drug Interactions
Many drug interactions are theoretical
More associated with combined use of adrenaline:
Exogenous drugs effect or compete with the pathways responsible for the metabolism of adrenaline in the body
Precautions Required
Non selective Beta Blockers
Tricyclic Antidepressants and SNRIs.
MAOI?
Phenothiazines
CNS Depressants: Sedatives, Opiods, Halothenes
Drugs of abuse: Cocaine, inhalants and cannabis can exacerbate effects adrenaline
Diuretics
Calculating Maximum Doses
Anaesthetic Dosage
CNS and CVS are very susceptible to actions of L.A.
Systemic actions are related to the blood or plasma level of the L.A agent
This is determined by amount injected and site of injection
Do not exceed maximum recommended doses, otherwise patient may overdose
Know amount of Local in preparation (2.2mls/1.8mls)
Calculating Maximum Recommended Dose
Determine amount (in mg) of the local anesthetic present in the cartridge
= Volume of cartridge (ml) x Concentration of active agent (mg/ml)
(Calculate the mg/mL using the basic formula mg=% x 10 x ml)Identify maximum dose in mg/kg for a specific Local Anaesthetic
(manufacturers recommendations) and multiply by pt's weightDetermine how many cartridges this is equivalent to:
= maximum dose for the clients weight/ Amount in mg in cartridge
Local Complications
Failure to achieve L.A
Pain during Injection
Sensitivity Disorders
Needle Breakage
Needle Track Infection
Trismus
Haematoma
Facial Nerve Paralysis
Soft Tissue Lesion
Mucous Membrane Lesion
Other intraoral lesion
Failure to Achieve Anaesthesia
Inadequate dose
Acute Inflammation- may require a course of antibiotics
Injection into blood vessel
Inadequate patience
Incorrect technique/unusual anatomy
Expired L.A or not stored adequately
Volume of Solution
Increasgin volume has shown to improve success rates in patients who have symptoms of pulpitis
Pain on Injection
Causes
Careless technique
Too rapid injection- torn tissues
Subperiosteal injection
Solution is too warm or too cold
Pronounced- needle unintentionally pricks an anatomical structure ({electric shock- nerve}, tendon, periosteum, muscle)
Prevention
Know your landmarks, have a good technique, inject solution SLOWLY
Bevel facing bone
Make Sure L.A is room temp when injecting
Sensitivity Disorders
Effects
* Burning or tingling
* Persistent/permanent anaesthesia
* Tingling or pins and needles: paraesthesia
* Increased sensitivity to noxious stimuli: hyperesthesia
* Pain to non- noxious stimuli: dysesthesia
*Causes
* Very rarely is sensitivity disorder a result of local anaesthesia type
* Trauma to nerve impairs nerve conduction
* Direct trauma by needle or indirect
* Administration of L.A from a cartridge contaminated by alcohol orsterilisation🡪 irritation🡪 oedema
* Haemorrhage into or around nerve sheath🡪 intraneural hematoma🡪↑ pressure
* Risk of nerve damage is greater if repeated injections are given into a previously partially anaesthetised site
Prolonged Anaesthesia or Paraesthesia
Prevention
Adherence to injection protocol
Management
Duration determined by extent of damage to the nerve
* Reassure and advise pt that it is not uncommon after L.A administration
* Mostly transient and will resolve within 8 weeks
* Examine pt and determine degree and extent of paresthesia- DOCUMENT
* have pt reviewed by DO if necessary
* If transition from anaesthesia to paraesthesia good chance of recovery
* If unresolved after 8 weeks likely it is irreversible, pt will require a consult with a neurologist or oral surgeon, because if left longer without action, may be permanent
Needle Breakage
Causes
Smaller diameter needles (30gauge) are more likely to break (usually occurs at hub)
Strong indication in cases reported that needle had been bent first
Needle was inserted in its entire length
Prevention
Larger gauge needle
Don’t insert all way into hub
Management- Remain calm, If portion visible remove it, if not visible inform and refer. DOCUMENT
Needle Track Infection
Introducing infection into surrounding tissue
Direct: needle contamination
Trismus
Prolonged spasm of jaw muscles impairing mouth opening (painful).
Symptoms arise 1-6 days post injection.
Causes
Needle insertion into muscles
Haemorrhage
Injection directly into muscle leads to mild myotoxic response leads to necrosis of exposed muscle fibers
Prevention
Adherence to injection protocol
Avoid repeat injections
Use minimum volumes of L.A
*Management *heat saline rinse and analgesic
* DOCUMENT!!!!
Facial Nerve Paralysis
* Iatrogenic- introduction of L.A into capsule of parotid gland, results in unilateral paralysis of muscles of facial expression (bells palsy)
* Prevention-Adherence to injection protocol and Technique
Soft Tissue Injury
*bite lip or check because of lingering L.A
Prevention
*Select L.A of appropriate duration for the client
*Cotton role in mouth
*Post Operative Instructions to Pt and Parent- DOCUMENT!!!!
*Warning stickers
Haematoma
*Caused because Effusion of blood into an extravascular space, most likely from inadvertently nicking a blood vessel
*Direct pressure, ice and advise patient
Mucous Membrane Lesions
*Caused by Prolonged ischemia of tissues as a direct result of vasoconstrictor, or reaction on mucous tissues to anaesthetic agent
Other Intraoral Lesions
Cause Recurrent Apthous Stomatitis
*Herpes Simplex
*Management
Primarily manage pain, assure pt that not bacterial infection but the exacerbation of a process that was already present in latent form Refer to DO for scripts for topical agents to help relieve discomfort if required
Systemic Complications
Major causes of adverse systemic reactions to local anaesthetics
Psychogenic
Hypersensitivity
Toxicity
Psychogenic
*syncope, panic attack, nausea
*Emotional disturbances
*May be syncope, ensure pt lying down and elevate legs
*Always try and rouse pt via sound and pain
*Calm the patient once roused
Hypersensitivity
*skin itching, GIT, respiratory, CVS
Management of Allergies
*cease dental treatment and red bag depending on level
Toxicity
*predominantly neurological
*solution itself, and the vasoconstrictor
May arise after: Inadvertent intravascular injection
* Rapid systemic absorption
* Excessive dose administration
Toxicity
effects on excitable tissues heart, brain
may exert effects on these tissues CNS involvement
*CVS involvement
*increased plasma concentration of drug, effects usually seen in a continuum
Warning signs of Incr
CNS Initial Signs of elevated blood levels
Low levels= STIMULATION-Restlessness, tremor, confusion or agitation PRE- CONVULSIVE: drowsiness, loss of concentration, slurred speech, dizziness, disorientation, visual disturbances, bilateral tongue numbness, dream like state
*CONVULSIVE phase
Respiratory depression