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: 40mm40mm

    • Short: 25mm25mm

  • 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 (0.50.5 to 3mm3 mm).

  • 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 Na+Na^+ Channels

  • Resting membrane Potential is approx. 70mV-70mV

  • Nerve impulse increases membrane conductivity (x100\approx x100).

    • 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

  1. Displace calcium ions from the sodium channel receptor site

  2. Binding of the LA molecule to the receptor site

  3. Blockade of the sodium channel

  4. Decrease in sodium conductance

  5. Depression of the rate of electrical depolarization

  6. Failure to achieve the threshold potential level

  7. Lack of development of propagated action potentials

  8. 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 898-9. 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

  1. Anaesthetic Agent (weak organic base- insoluble in water)

  2. Stabilisers/salts (converts agent so it is water soluble)

  • Usually hydrochlorides

  1. Vasoconstrictors (increase duration of action of L.A)

  2. Antioxidants (prevents oxidation of stabiliser)

  • Sodium metabisulphite

  1. Preservatives:

  • Fungicides, antibacterials

  • Methylparaben

  1. 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

  1. 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)

  2. Identify maximum dose in mg/kg for a specific Local Anaesthetic
    (manufacturers recommendations) and multiply by pt's weight

  3. Determine 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 or

  • sterilisation🡪 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

  1. Psychogenic

  2. Hypersensitivity

  3. 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