Applied: Local Anaesthesia

CNV branches

• V1 - opthalmic nerve

• V2 - maxillary nerve

• V3 - mandibular nerve

Where does the Opthalmic Nerve V1 exit?

superior orbital fissure

Where does the Maxillary Nerve V2 exit?

Foramen rotundum

Where does the Mandibular Nerve V3 exit?

Foramen ovale

Pterygopalatine nerves of CN5 maxillary division

• nasopalatine

• greater palatine

• lesser palatine

Infraorbital nerves of CN5 maxillary division

• posterior superior alveolar

• middle superior alveolar

• anterior superior alveolar

What does the nasopalatine nerve supply?

palatal mucosa, gingivae, and alveolar bone anteriorly behind 2 1/1 2

What does the greater palatine nerve supply?

palatal mucosa, palatal alveolar bone and gingivae of the posterior region - 8 7 6 5 4 3/3 4 5 6 7 8

What does the lesser palatine nerve supply?

mucous membrane of the soft palate

What does the posterior superior alveolar nerve supply?

• buccal mucosa, gingivae, alveolar bone, and PDL of 8 7 6/6 7 8 (may not supply MB root of 6/6)

• maxillary sinus lining

What does the middle superior alveolar nerve supply?

• buccal mucosa, gingivae, alveolar bone, and PDL of MB root of 6/6 and 5 4/4 5

• maxillary sinus lining

What does the anterior superior alveolar nerve supply?

• buccal mucosa, gingivae, alveolar bone, and PDL of 3 2 1/1 2 3

• maxillary sinus lining

Anterior trunk nerves of CNV mandibular division

• buccal nerve (sensory)

• multiple motor nerves to muscles

Posterior trunk nerves of CNV mandibular division

• auriculotemporal nerve (sensory)

• lingual nerve (sensory)

• inferior alveolar nerve (sensory and motor)

What does the buccal nerve supply?

cheek, mucous membrane of buccal sulcus and buccal gingivae

What does the lingual nerve supply?

lingual gingivae and lingual alveolar bone adjacent to lower teeth, floor of mouth, sensation to anterior 2/3 of tongue

What does the inferior alveolar nerve supply?

• all lower teeth

• incisive nerve supplies lower anterior teeth

• mental nerve supplies labial gingivae and labial alveolar bone of anterior teeth, buccal gingiva and mucosa of the premolars, skin and mucosa of lower lip of chin

components of a nerve cell

• cell body

• dendrites

• axon

• myelin sheath

Define ‘Action Potential’

a sudden, fast, transitory, and propagatingg change of the resting membrane potential

Describe the Hypopolarisation phase

• initial increase of the membrane potential to the value of the threshold potential

• the threshold potential opens voltage-gated Na channels and causes a large influx of Na ions

Describe the Depolarisation phase

• the inside of the cell becomes more and more electropositive due to influx of Na+, until the potential gets closer to the electrochemical equilibrium for Na

• this phase of extreme positivity is the overshoot phase

Describe the Repolarisation phase

• Na permeability suddenly decreases due to the closing of its channels

• the overshoot value of the cell potential opens voltage-gated K channels - large K+ efflux decreases cell’s electropositivity

• repolarisation phase has purpose of restoring resting membrane

Describe the Hyperpolarisation phase

• membrane potential is more negative than resting membrane potential

• membrane will eventually establish again the values of membrane potential

Describe the Absolute Refractory Period

• occurs once the sodium channels close after an AP

• sodium channels then enter an inactive state during which they cannot be reopened, regardless of the membrane potential

Describe the Relative Refractory Period

• occurs when sodium channels slowly come out of inactivation

• the neurone can be excited with stronger stimuli than the one normally needed to initiate an AP

• early on in the relative refractory period, the strength of the stimulus required is very high

• gradually, the required stimulus strength becomes smaller as more sodium channels recover from inactivation

Define ‘Synapse’

gap between two neurones

Describe the process of neurotransmission across the synapse

1. AP arrives at synaptic knob and depolarises presynaptic membrane

2. voltage-gated Ca2+ channels open - influx of Ca2+ ions

3. influx causes vesticles containing various neurotransmitters to move and fuse with presynaptic membrane

4. exocytosis of neurotransmitters which diffuse across synaptic cleft

5. neurotransmitters bind to specific receptors on postsynaptic membrane

6. binding causes Na channels to open - influx of Na+ ions

7. depolarisation of postsynaptic membrane - AP is sent down axon once threshold for AP is reached

8. when the presynaptic membrane is no longer depolarised, neurotransmitters bound to receptors are broken down by a specific enzyme and the products are recycled

Draw the basic structure of an LA agent

Which group in an LA agent determines its fat solubility?

R1 - lipophilic group

Which group in an LA agent determines its water solubility?

R3 and R4 - hydrophilic group

Describe LA agents which have their lipophilic form predominating

• unionised

• more fat soluble

• diffuse through lipid bilayer

Describe LA agents which have their hydrophilic form predominating

• ionised

• less fat soluble

• reduced diffusion through lipid bilayer

How to determine if an LA agent is more lipophilic or hydrophilic

Local anaesthetics are weak bases, so their form depends on pKa relative to physiological pH (~7.4):

• Lower pKa (closer to 7.4)
  → more non-ionised (lipophilic) form
  → crosses membranes easily

• Higher pKa
  → more ionised (hydrophilic) form
  → crosses membranes less easily

2 main theories for LA action

• Membrane Expansion Theory

• Specific Binding Theory

Describe the Membrane Expansion Theory

1. Anaesthetic enters the membrane

• Anaesthetic molecules are lipid-soluble

• They insert themselves between phospholipids in the membrane

2. Membrane expands and becomes more fluid

• This causes:

  • Increased membrane volume (expansion)

  • Increased fluidity

  • Slight thickening/disordering of the bilayer

3. Ion channel function is disrupted

• Membrane proteins (like ion channels) rely on precise structure

• Expansion alters their:

  • Shape

  • Conformation

  • Ability to open/close properly

➡ Especially affects ion movement (Na⁺, K⁺, Ca²⁺)

4. Nerve signalling is impaired

• Ion channels don’t function normally

• Action potentials cannot be generated or propagated effectively

➡ Leads to loss of sensation / anaesthesia

Describe the Specific Binding Theory

1. Anaesthetic binds to target proteins

• The drug binds to specific sites on:

  • Ion channels

  • Neurotransmitter receptors

This binding is selective and reversible.

2. Alters ion channel/receptor function

This can happen in two main ways:

🔹 Enhance inhibition

• Increase activity of inhibitory pathways

• Example: potentiation of GABA_A receptor
  ➡ More Cl⁻ enters neurons → hyperpolarisation → reduced excitability

🔹 Reduce excitation

• Inhibit excitatory receptors or channels
  ➡ Less depolarisation

3. Suppresses neuronal activity

• Reduced ability to generate and transmit action potentials

• Leads to:

  • Loss of consciousness (general anaesthetics)

  • Loss of sensation (depending on site)

Properties of an ideal local anaesthetic

• have a reversible action

• non-irritant and non-damaging to tissues

• rapid onset and appropriate duration

• effective in concentrations that are not harmful

• chemically stable in solution

• adequate shelf life

Examples of LA agents that are amides

• articaine

• bupivicaine

• lidocaine

• mepivicaine

• prilocaine

Examples of LA agents that are esters

• benzocaine

• cocaine

• procaine

• amethocaine

Proprietary name of Lidocaine/lignocaine

• lignospan

• xylocaine

• xylotox

• lignostab

Preparation of Lidocaine

2% lidocaine with 1:80,000 epinephrine

Proprietary name of Prilocaine

citanest

When is Prilocaine popularly used?

When patients cannot have adrenaline as their vasoconstrctor

Preparation of Prilocaine

• prilocaine 3% with felypressin

• prilocaine 4% plain (no vasoconstrictor)

Why can Prilocaine not be administered to pregnant people?

vasoconstrictor (felypressin) is similar to a labour-inducing hormone - prilocaine plain is okay to administer

Proprietary name of Mepivicaine

Scandonest

When is Mepivicaine popularly used?

shorter duration - popularly used for short duration procedures

Preparation of Mepivicaine

• Mepivicaine 2% with 1:100,000 epinephrine

• Mepivicaine 3% plain

Proprietary name of Articaine

Septanest

Preparation of Articaine

4% articaine with 1:100,000 or 1:120,000 epinephrine

Constituents of an LA cartridge

• active anaesthetic agent

• vasoconstrictor

• reducing agent - prevent oxidation of vasoconstrictor

• preservative

• fungicide

• vehicle - sodium chloride, sodium hydrochloride, water

Why are vasoconstrictors used in local anaesthetic?

LAs cause vascular dilation which would take away the agent more freely

• prolongs duration of pulpal anaesthesia

• allows for more profound anaesthesia

• reduces local blood flow and hence bleeding

• reduces toxicity; slows rate of absorption (minor effect)

Types of vasoconstrictors

• epinephrine (adrenaline)

• felypressin (octapressin)

Describe epinephrine as a vasoconstrictor

• naturally occurring hormone

• acts on adrenoceptors in blood vessels

• has direct and indirect effects on the heart

  • increases heart rate and force of contraction, therefore C.O, pulse and potentially systolic BP

  • standard LA doses have little effect

• affects a number of the systems

• never use at extremities (ischaemia)

Describe felypressin as a vasoonstrictor

• synthetic

• analogue of vasopressin (labour induction)

• no effect on the heart

• less vasoconstrictor effect

• common conc in citanest: 0.03 units per ml

When should using LA containing epinephrine be avoided?

• unstable/severe hypertension or angina

• unstable cardiac rhythm

Duration of action of Lidocaine 2% (with epinephrine)

• Pulpal: 60 (infil) - 90 (block) mins

• Soft tissue: 2.5-3hrs

Duration of action of Prilocaine 3% (with felypressin)

• Pulpal: 60 (infil) - 90 (block) mins

• Soft tissue: 2.5-3hrs

Duration of action of Prilocaine 4% Plain

• Pulpal: 10mins (infil), 50mins (block)

• Soft tissue: 2-3hrs

Duration of action of Mepivicaine 3%

• Pulpal: 30 mins

• Soft tissue: 2-3hrs

Duration of action of Articaine 4% (with epinephrine)

• Pulpal: 60 (infil) - 90 (block) mins

• Soft tissue: 2.5-3hrs

similar to Lidocaine has the ability to diffuse widely

Recommended maximum dose of Lidocaine 2%

• 4.4mg/kg

• 300mg

• 6.8 cartridges

Recommended maximum dose of Prilocaine 3%

• 6mg/kg

• 400mg

• 6 cartridges

Recommended maximum dose of Articaine 4%

• 7mg/kg

• 5 cartridges

General contraindications of using LA

• uncooperative patient

• hypersensitivity to LA

• infection at injection site

  • absorption to blood stream may increase possibility of systemic side effects

  • altered local pH may decrease effect of LA

• haemorrhagic disorders

• anticoagulant therapy (depends on NR)

• significantly reduced vascularity

• severe liver dysfunction

• severe renal dysfunction

Types of LA delivery

• topical

• infiltration

• regional block

Systemic complications related to LA

• vasovagal faint

• drug interaction

• adverse reaction to drug

• psychogenic reaction

• toxicity

Local complications related to using LA (excluding those related to ID blocks)

• failure to achieve anaesthesia

• prolonged anaesthesia and paraesthesia - trauma to nerve itself

• bleeding at injection site

• blanching at injection site - caused by intrarterial injections if blanching remains

• needle and cartridge breakage

• pain on injection

• post-injection pain

• trauma to blood vessel - haematoma

Local complications related to using LA specifically for ID blocks

• restricted jaw opening (trismus)

• facial palsy

• visual disturbance (very rare)

• blanching of skin in cheek area (rare)

What can cause pain on injection?

• subperiosteal injection

• injecting too quickly - liquid is being forced into area

• touching nerve when giving ID block will translate to ‘electric shock’ - rapid anaesthesia

• injecting large amounts into dense tissues

What can cause post-injection pain?

• rapid injection

• large volumes of LA

• lip and cheek trauma

What causes temporary facial palsy after administering ID block?

• incorrect placement of needle

• penetration of parotid gland capsule during injection (facial nerve)

• causes short duration paralysis of face

POI after temporary facial palsy

• reassure pt that palsy will subside in a few hours

• if pt cannot blink, offer eye patches or eye drops

• offer pt to wait in reception until anaesthesia wears off for monitoring

Causes for LA failure

• pharmaceutical reasons - expired/incorrect storage

• poor technique/inappropriate placement

• inadequate volume of LA

• anatomical variation

• injection into infected or inflamed area

• patient anxiety

Nerve supply for upper teeth

• upper teeth - maxillary nerve

  • posterior superior alveolar nerve - molars (and part of first molar)

  • middle superior alveolar nerve - premolars (sometimes first molar)

  • anterior superior alveolar nerve - incisors and canines

Nerve supply for lower teeth

• lower teeth - mandibular nerve

  • mandibular nerve - main nerve

  • inferior alveolar nerve - travels through mandible to supply all lower teeth then gives off branches to incisors and canines

Nerve supply for buccal/labial gingivae

buccal nerve

Nerve supply for palatal gingivae

greater palatine nerve

Nerve supply for lingual gingivae

lingual nerve

Infiltration technique

1. Retract tissues taut to allow good visibility

2. place bevel towards tooth and insert needle at point of reflection of alveolar and vestibular mucosa

3. ensure needle is parallel to long axes of tooth and angle needle towards bone surface

4. advance needle forward (3-5mm) so that the needle tip is opposite the apex of tooth

5. aspirate, check cartridge

6. deliver solution at slow and steady pace

7. withdraw smoothly and rub area gently

Post-operative advice

• avoid smoking

• avoid hot foods and drinks

• avoid biting cheek and lip

• assure them that their face is not swollen and the numbness will pass in a few hours

• give contact number for any concerns

Which teeth and surfaces does the IDN not cover?

• mandibular incisors - cross-innervation

• buccal gingiva of mandibular molars - long buccal nerve

• lingual gingiva - depends on lingual nerve

Where should you aim to deposit the LA in an IDB?

as close to the mandibular foramen as possible

Height of injection in IDB

• adults: approx 1cm above the occlusal surfaces of the molars

• children: approx 0.5cm above the occlusal plane

• very young children: approx the height of the occlusal plane

Key landmarks for IDB

• external oblique ridge

• coronoid notch

• pterygomandibular raphe

IDB Technique

1. position patient and position of mandibular foramen estimated using landmarks

   • parallel to occlusal plane, approx 1cm above occlusal surfaces of molars

2. place thumb of opposing hand onto external oblique ridge (at anterior aspect of ascending ramus) - do not move

3. roll tip of thumb forward onto coronoid notch

4. identify pterygomandibular raphae (attached to internal oblique ridge)

   • buccinator muscle and the superior constrictor muscle of the pharynx

5. insert needle from left side of mouth with syringe barrel lying across contralateral premolars (direct technique)

6. needle enters tissues at midpoint of tip of palpating finger or thumb (about 0.5cm medial to it) and lateral to pterygomandibular raphe

7. insert slowly until bone is contacted (about 2-2.5cm) and then withdraw ~1mm (prevents subperiosteal injection) and aspirate

8. slowly deposit almost a full cartridge

9. deposit remaining 0.5ml solution as you pull out - anaesthetise lingual nerve

Common positioning mistakes when administering IDB

• inject too posteriorly - early bone contact

• inject too anteriorly - no bone contact

Importance of aspiration

prevent intravascular injection:

• avoids systemic toxicity - dizziness, increased heart rate, tinnitus

• prevents failed anaesthesia - LA is taken away in blood quicker

• less risk of haematoma formation