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Anesthesiology
Prepared By: Dr. Mostafa Lee Mehrafsha

Review on Local Anesthesiology

Topic: Pain

Pain
• It is perhaps the most commonly experienced symptom in dentistry.
• Yet, a precise definition of pain does not exist as pain has a subjective/ psychophysiological aspect (a painful stimuli
for one individual may not be painful for another)
• Arbitrarily, pain can be defined as any unpleasant experiences may it be emotional, mechanical/physical or chemical
with or without tissue damage.
Dual nature of Pain
• Pain like other sensations (touch, hot, cold, etc.) has a physioanatomical aspect which explains the physiological
processes and anatomical parts involved in Pain Perception.
• In addition pain also has a Psychophysiological aspect that is unique to each individual. it explains the
psychological factors associated with Pain Reaction.
Dual nature of Pain

Theories of pain
1. Specific theory:
• Developed by Descarets in 1644
• Describes pain systems as a straight-through channel from the skin to the brain
• Presence of specific nerve ending for pain perception called Nociceptors.
• These nociceptors once activated carry the unpleasant experience to “Pain Center” within the brain

2. Pattern Theory
• Developed by Goldscheider
• Pain are produced by the summation of sensory input

3. Gate control theory

• – Proposed by Melzack and Wall
• Claims the existence of a so called “gate” in the spinal cord that controls the passage of information from
periphery to brain
• The information that travel faster have higher priority to pass the gate and arrive at brain

4. Hydrodynamic Theory
• Provides explanation for dentinal pain and sensitivity
• Dentinal Sensitive is caused by direct stimulation of sensory nerve ending in the dentin which are primarily
located near the pulp
• Yet the most sensitive part of the tooth is at DEJ where no nerve endings exist
• Hydrodynamic theory suggest that the nerve endings near the pulp are stimulated due to the movement of
dentinal fluids present in dentinal tubules
Classification of Pain
• Acute pain:
• Sudden onset, 1st pain
• Sharp, localized and throbbing
• Information carried through A delta fibers which are large and thinly myelinated neurons (100m/s)
• Chronic Pain:
• Long lasting pain
• Dull and aching pain
• Information carried through C – fibers which are small and unmyelinated neurons ( 0.5-2m/s)

Pathway of Pain
• Describes how a certain stimuli can travel from periphery ( skin or tooth) to brain and be interpreted as pain
• Most of painful stimuli in dentistry are mechanical (a stimuli that causes physical injury to tissue) and can be
further aggravated by inflammation and its chemical modifiers

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• Explains the Physioanatomical aspect of pain

• Encompasses all theories of pain

Pathway of Acute Pain

Pathway of pain explains the anatomical and the physiological processes involved in pain perception. This
process of pain perception is similar in all individuals and all throughout the body.
Most dental pains are caused by mechanical stimuli which cause physical injury to tissue and inflammation.
A mechanical stimulus will cause tissue injury, excitation of nociceptors and inflammation. This mechanical
stimulus will be converted to an electrical impulse through a process called Mechanotransduction. The electrical
impulse travels along the 1st order neuron (A-delta fibres) and enter the dorsal horn of spinal cord. All sensory
information enter the spinal cord from the dorsal side. Here the 1st order neuron terminates and its axon
forms a Synapse with the dendrite of the 2nd neuron.
The information which was traveling in form of an electrical impulse through the 1st order neuron has to be
converted into chemical information to traverse the synapse and converted back to an electrical impulse to travel
along the 2nd order neuron. This is done by release of neurotransmitters from the 1st order neuron specifically
glutamate for a-delta fibres.
The 2nd order neuron then crosses to the contralateral side of the spinal cord and travels through the
Spinothalamic canal to the thalamus of the brain. Here in thalamus the brain will interpret the information and
generate “PAIN”. However, Thalamus fails to specify where the pain is coming from. Thus, 3rd order neuron will
carry the impulse to the cortex of the brain. In cortex, “Pain Localization” occurs and the brain can specify the
exact location of the painful stimulus.

Pathway of Chronic Pain

The pathway of chronic pain is almost similar with acute pain with few differences.
First, the neural fibres involve in impulse propagation are C-fibres.
Second, 1st order neuron synapses with an interneuron (located at a part of the dorsal horn of spinal cord called
Substantia Gelatinosa) and then the 2nd order neuron.
Third, the neurotransmitter released at the synaptic joint is Substance P and lastly, the 3rd order neuron carries
information not only to cortex but also to limbic system where the experience is remembered for the psychological
and emotional aspect of pain.
• Opioid Analgesics have a Supraspinal mode of action where they depress the cortex so the brain cannot localize the
pain.
( cortex= pain localization center)
• Patients taking opioid usually describe it as “the pain is still there but it is not that bad”; this is due to them not knowing
where the pain is coming from.
Pathway of Pain
• How does an impulse travel along the neuron? Watch the video below on Impulse Propagation and action potential
[Link]

Modulatory Pathways of Pain

• Pain is necessary for survival but there are instances that feeling pain can actually lead to worse consequences.
• For example twisting one’s ankle while being chased by a wild animal. Feeling pain at that instance can lead to animal
bite or death.
• Therefore body needs internal processes to control pain and these are called “Modulatory Pathways of Pain”

Ascending Modulatory Pathway

• Recall that all sensory information enter the spinal cord at the dorsal horn ( this includes pain, touch, hot, cold
and etc.)
• All their 1st order neurons synapse with their corresponding 2nd order neuron at Substantia Gelatinosa
• All 1st order neurons produce their own neurotransmitters and saturate the synaptic region.
• Therefore, if two sensory information (for instance pain and touch) compete with each other, the impulse that
travels faster (touch) can produce its neurotransmitter and saturate the synaptic region.
• Thus the second sensory information(pain) that has arrived late at the synaptic region cannot activate its
corresponding 2nd order neuron and information never reaches the brain and is not interpreted
• Ascending Modulatory So, Ascending modulatory pathway entails creating faster impulses than pain
impulses to overload the synaptic region.
• This is the reason you rub your hand when it is scratched or injured to lessen the intensity of pain
• The synaptic region located in Substantia Gelatinosa of Spinal cord is the “Gate” in Gate control theory

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• Since the information to modulate pain originates from periphery and travels toward CNS, it is named
ASCENDING MODULATORY PATHWAY.

• Descending Modulatory Pathway

• Interneuron in return releases its own neurotransmitter to saturate the synaptic region
• Endogenous opioids ( Enkephalin, morphine like substances produced inside the body) saturate the region
and
• A) inhibit neurotransmitter production in the 1st order neuron and
• b) Prevent depolarization of the 2nd order neuron
• Therefore, painful stimulus travelling through the 1st order neuron does not reach the brain

• Opioid Analgesics have a Spinal mode of action which is considered Indirect.

• Opioids cause activation of the Descending Modulatory Pathway.
• Tissue injury and inflammation leads to production of numerous chemicals at the site of injury.
• Prostaglandin is one of the chemicals produced that causes sensitization of free nerve endings (nociceptors)
• Therefore a weak stimulus which under normal circumstances would not be painful will now be interpreted as pain
since the nerve endings are at a state of Hypersensitivity
• For instance a sun-burned skin is painful to touch because it is inflamed, PGs are present and nociceptors are
hypersensitive.

• Opioid have a Peripheral mode of action where they cause desensitization of afferent sensory neurons. Opposite to
the effect of Prostaglandins and other pain modifiers (i.e prostglandins, histamines and bradykinins)

Psychophysiological Nature of Pain

• Pain Reaction depends on ff. psychological factors

1. age ( the younger the patient, the more pain reaction)

2. Gender (women have lower pain threshold)
3. Race (southern Europeans show more pain reaction than northern Europeans)
4. Fatigue
5. Emotional Stability
6. Fear and Apprehension

Methods of Pain Control

1. Removal of the cause
• Restorative treatment, extraction, periodontal treatment and etc
2. Blocking the Pathway of painful impulses
• Local anesthesia
3. Raising the pain threshold
• Non-opioid analgesics
4. Preventing pain reaction by cortical depression
• Opioid analgesic, General Anesthesia, Tranquilizers
5. Using Psychosomatic Method (placebo, patient reassurance and etc.

Review on Local Anesthesiology

Topic: Local Anesthetic Agent

Characteristics of an Ideal local Anesthetic Agent

1. Potent Local anesthesia
2. Reversible
3. Non-irritating
4. Low degree of systemic toxicity
5. Low allergic reaction
6. Rapid onset and sufficient duration
7. Adequate tissue penetration
8. Stable in solution
9. Sterile or capable of sterilization

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Classification of L.A. Agents
• Based on Chemistry
• Ester Anesthetics
• First injectable anesthetics (procaine)
• High rate of allergy reported in patients
• Generally used as topical anesthesia (benzocaine)

• Amide Anesthetics
• Commonly used injectable anesthetics (Lidocaine)

Classification of L.A. Solutions

• Based on Duration of Action
1. Ultra-short acting L.A
• 2% lidocaine without vasoconstrictor
2. Short acting L.A.
• 2% lidocaine with 1:100,000 epinephrine
• Mepivacaine without vasoconstrictor
3. Medium acting L.A.
• 2 %Mepivacaine with 1:20,000 levonoderfin
4. Long acting L.A.
• 0.5% Bupivacaine with 1:200,000 epinephrin

Contents of Local anesthetic Solution

Component Function
L.A. Agent Blockade of nerve conduction
Sodium chloride Isotonocity of solution
Sterile water Volume
Vasoconstricotor vasoconstriction (Increase depth and duration, decreases absorption, haemostasis)
Sodium bisulifit Antioxidant
Mehtylparaben Bacteriostatic

Pharmacodynamics
• Local anesthetics (LAs) reduce the amplitude and conduction velocity of action potentials in a reversible, dose-
dependent manner
• LAs’ sites of action are the voltage-gated sodium channels.
• The following sequence is the proposed mechanism of action of L.A. Agents
• Displacement of calcium ions from the sodium channel receptor site, which permits …
• Binding of the local anesthetic molecule to this receptor site, which produces …
• Blockade of the sodium channel, and a …
• Decrease in sodium conductance, which leads to …
• Depression of the rate of electrical depolarization, and …
• Failure to achieve the threshold potential level, along with …
• Lack of development of propagated action potentials, which is called …
• Conduction blockade

• Mode of Action of L.A. Agents

1. Altering the basic resting potential of the nerve membrane
2. Altering the threshold potential (firing level)
3. Decreasing the rate of depolarization (primary mode of Action)
4. Prolonging the rate of repolarization

Pharmacokinetics of L.A. Agents

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• Recall compartmental model of pharmacokinetics

• Body consists of many compartments which are separated from each other by membranes (i.e. capillary membrane,
stomach lining, cell membrane, neural membrane and etc.)
• Drugs can move from one compartment to another (recall movement of drugs through a permeable membrane)
• In local anesthetic agents, these compartments are

1. Absorption:
• Movement of drug from site of injection into blood is called absorption and in case of locally administered
drugs is disadvantageous
• High absorption is a disadvantage since it decreases the local effect of Local anesthesia (unlike drugs
administered systemically where higher absorption is beneficial
• Higher absorption= faster movement of drug into blood= lesser drug concentration at injection site= lesser
local effect
• Local anesthetic agents can pass thru membrane by passive diffusion
• All anesthetic agents are vasodilators (except cocaine which is a vasoconstrictor)
• Vasodilation= increase blood supply= increase absorption= Shorter duration of local anesthesia
• Therefor vasoconstrictor (epinephrine or levonordefrin) are added to the anesthetic solution
• Higher absorption in [Link] also mean higher risk of toxicity
• Mepivacain has the lowest coefficient of vasodilation (least vasodilator among all anesthetic agents)

2. Distribution
• LAs cross biological membranes by passive diffusion
• Movement of drug from site of injection into plasma membrane (specifically binding to Na+ channel receptors)
is therapeutic and leads to anesthesia

a. Distribution ( non-therapeutic)
• Movement of drug from blood into non-specific tissues (specifically brain and myocardium) lead to adverse
effects of Local Anesthetics
• Fast absorption, fast movement from blood to brain myocardium and slow elimination are factors contributing
to toxicity of a local anesthetic agent

b. Distribution( therapeutic)
• Movement of local anesthetic agent molecules thru membranes between compartments (specifically injection
site into plasma membrane) depends on their charge (ionized or unionized)
• Only unionized drug molecule can pass membrane
• Local anesthetic agent in each compartment exist in two forms (ionized and non-ionized) and equilibrates
itself in each compartment depending on the pKa of the Local anesthetic agent and pH of the environment
(compartment)

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• Two forms are free base form(unionized) and salt form (ionized)
• pKa or dissociation constant is the pH of a compartment where half of the drug is ionized and half unionized
(balanced)
• All local anesthetic agents are weak bases (for example lidocaine has pKa of 7.9)
• Anesthetic agents are added with HCl to make them stable and water-soluble therefor all anesthetic solutions
are acidic (pH of around 3.5)
c. Potency
• The structural domain of LAs responsible for their lipophilicity is the aromatic group
• The lipid solubility or partition coefficient of a LA determines its ability to pass through biological membranes
and reach their receptor sites
• Therefore, the primary determinant of a LA’s potency is its partition coefficient

d. Onset of Action
• Only the unionized or neutral forms of LA molecules can translocate across neuronal membranes.
• The ratio of ionized to unionized forms is predicated on the drugs’ dissociation constant (pKa) and the pH at
the site of injection
• The closer is a LA’s pKa to the pH at the site of its injection (physiologic pH of 7.4), greater is its fraction of
unionized molecules (free base) that can translocate across neuronal membranes
• Therefore, the primary determinant of a LA’s onset of action is its dissociation constant

e. Duration of Action
• Receptor site for LAs, i.e., the voltage-gated sodium channels which integral membrane proteins.
• LAs with high protein-binding capacity bind more tightly
• The lower is the protein-binding capacity of a LA, the weaker is the drug-receptor bond.
• Therefore, the primary determinant of a LA’s duration of action is its protein-binding capacity
• Other modulation factors
• Lipophilic [Link] have higher duraion
• Dosage of anesthetic agent at the site of injection
• Vascularity of site of injection
• Presence or absence of vasoconstrictor

f. Clinical importance
• This shifting between ionized and non-ionized L.A. drug molecules makes movement of the drug possible and
leads to a successful anesthesia
• Changes in the pH of each compartment can hinder drug movement and lower the success of anesthetic
injections.
• An example is when L.A. is injected into an infected or inflamed tissue.

3. Metabolism and Excretion

• Ester-type local anesthetic agents are metabolized in blood plasma by cholinesterase enzyme
• Amide type local anesthetics are metabolized in the liver by cytochrome P450
• Excretion happens in the kidney
• Articaine is metabolized rapidly in plasma and around 5-10% by the hepatic CYP450

4. Toxicology
• Local reactions
• Edema, desquamation, and ischemic necrosis
• Mytotoxicity and vasoconstrictor-associated necrosis\
• Neurologic effect ; paresthesia

• CNS effects
• Excitory effects: lightheadedness, restlessness, anxiety, euphoria, blurred vision and dizziness (
they are brief and progress to.
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• Depressant effects: unconsciousness, respiratory depression and finally respiratory arrest

• CVS effects
• Depressed CV function ( conduction, excitability and contractility) which can lead to
• Reduced cardiac output, ventricular arrhythmias and cardiac arrest

• Hypersensitivity reaction
• may manifest as pruritus, erythema, rash, urticaria, angioedema, wheezing, and, rarely, anaphylaxis
• Allergic reactions to ester-type is due to a breakdown products para-aminobenzoic acid (PABA)
• True allergy to amide are rare
• However, LAs formulated with a vasoconstrictor contain metabisulfite may precipitate an allergic
reaction
• Cross sensitivity among memebers of amide type have not been reported
• Idiosyncratic
• Methemoglobinemia : caused by tolouidine which is a metabolite of prilocaine and benzocaine
breakdown

• Sympathetic reactions
• Anesthetic solutions may contain epinephrine or levonordefrin
• Healthy adults can safely receive up to 0.2 mg of epinephrine or 1.0 mg of levonordefrin per visit
Special Mentions
Cocaine
• 1st discovered
• Only natural
• Only vasoconstrictor
Prociane
• 1st synthetic
• 1st injectable
• Longest used in practice
• Baseline for comparison
Lidocaine
• Most Commonly used LA agent

Tetracaine
• Most toxic
• Longest elimination time
Prilocaine
• Can lead to Methemoglobinemia due to its metabolite Toluidine

Review on Local Anesthesiology

Topic: Armamentarium
Syringe

ADA Criteria for acceptance of L.A. syringes

1. They must be durable and able to withstand repeated sterilization without damage. (If the unit is disposable, it
should be packaged in a sterile container.)
2. They should be capable of accepting a wide variety of cartridges and needles of different manufacture, and
should permit repeated use.
3. They should be inexpensive, self-contained, lightweight, and simple to use with one hand
4. They should provide for effective aspiration and be constructed so that blood may be easily observed in the
cartridge

Types
1. Nondisposable syringes:

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• Breech-loading, metallic, cartridge-type, aspirating

• Breech-loading, plastic, cartridge-type, aspirating
• Breech-loading, metallic, cartridge-type, self-aspirating
• Pressure syringe for periodontal ligament injection
• Jet injector (“needle-less” syringe)
2. Disposable syringes
3. “Safety” syringes
4. Computer-controlled local anesthetic delivery systems

Jet injector (“needle-less” syringe)

• liquids forced through very small openings, called jets, at very high pressure can penetrate intact skin or mucous
membrane
• primary purpose of the jet injector is to obtain topical anesthesia before insertion of a needle
• Regional nerve blocks or supraperiosteal injections are still necessary for complete anesthesia.
• Only nasopalatine and greater palatine nerves can be blocked by jet inkectors

Disposable syringes
• Advantages
• Disposable, single use
• Sterile until open
• Lightweight

• Disadvantages
• Does not accept pre-filled dental cartridges
• Aspiration difficult

Problems Associate with Syringe

• Leakage during Injection (due to off-centric penetration of rubber diaphragm of cartridge by the needle)
• Broken Cartridge ( too much force during injection)
• Bent Harpoon
• Disengagement of the Harpoon from the Plunger during Aspiration
• Surface Deposits

Needle
• Is the vehicle that permits local anesthetic solution to travel from the dental cartridge into the tissues surrounding the
needle tip.
• Most commonly made of stainless steel

Gauge
• Diameter of the lumen
• Smaller the number the greater the diameter of the lumen
• Gauge 25 needle is recommended
• Most common used are gauge 27(long) and 30( short)
• 25 gauge is the needle of choice for injections that have a high potential for a positive aspiration

Length
• From hub to tip
• Average length of short needles: 20 mm
• Average length of long needles: 32 mm
• Needles should not be inserted to the hub unless absolutely necessary for the success of the injection

Problems associated with needles

• Pain on Insertion (after multiple use)
• Breakage (shifting during injection)
• Pain on Withdrawal ( hooked needle)
• Injury to the Patient or Administrator (keep needle in sight at all times)

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Cartridge
• Glass cylinder containing the local anesthetic drug, among other ingredients
• Most commonly contain 1.8ml of solution

Problems associated with Cartridge

• Bubble in the cartridge (<0.5mm is normal, nitrogen)
• Extruded stopper
• Burning on injection (due to acidity is normal due to cold solution is not normal)
• Sticky stopper
• Corroded cap
• “Rust” on the cap
• Leakage during injection
• Broken cartridges

Review on Local Anesthesiology

Topic: Maxillary Injection Techniques
Basic Injection Techniques
• Local Infiltration
• Nerves anesthetized: Small terminal nerve endings
• Area of treatment: same as injection area
• Filed Block
• NA: Larger terminal nerve branches
• AT: an area away from the site of injection
• Nerve Block
• NA: Main nerve Trunk
• AT: Distant from the site of injection

Maxillary Injection Techniques

Supraperosteal Injection
• commonly (but incorrectly) called local infiltration
• Most frequently used technique for obtaining pulpal anesthesia in maxillary teeth
• Nerves Anesthetized: Large terminal branches of the dental plexus
• Area Anesthetized: The entire region innervated by the large terminal branches of this plexus: pulp and root area
of the tooth, buccal periosteum, connective tissue, and mucous membrane
• Indication:
o Pulpal anesthesia of the maxillary teeth when treatment is limited to one or two teeth
o Soft tissue anesthesia when indicated for surgical procedures in a circumscribed area
• Contraindications:
• Infection or acute inflammation in the area of injection.
• Dense bone covering the apices of teeth
• Advantages:
• High success rate (>95%)
• Technically easy injection
• Usually entirely atraumatic
• Disadvantages:
• Large areas: because of the need for multiple needle insertions and the necessity to administer larger total
volumes of local anesthetic.
• Landmarks:
• Mucobuccal fold
• Crown of the tooth
• Root contour of the tooth
• Failure of Anesthesia
• Needle tip lies below the apex
• Needle tip lies too far from the bone
• Complications
• Pain on needle insertion

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PSA nerve block

Advantages:
• Atraumatic;
• High success rate (>95%)
• Minimum number of necessary injections
• Minimizes the total volume of local anesthetic solution administered

Disadvantages:
• Risk of hematoma
• Technique somewhat arbitrary: no bony landmarks during insertion
• Second injection necessary for treatment of the first molar

Area of Insertion: height of the mucobuccal fold above the maxillary second molar

Target area: PSA nerve—posterior, superior, and medial to the posterior border of the maxilla

Landmarks:
• Mucobuccal fold
• Maxillary tuberosity
• Zygomatic process of the maxilla

Direction of needle
• Upward: superiorly at a 45-degree angle to the occlusal plane
• Inward: medially toward the midline at a 45-degree angle to the occlusal plane
• Backward: posteriorly at a 45-degree angle to the long axis of the second molar

Depth of insertion: 16mm

Two plane aspirations
Complications: hematoma, Mandibular Nerve anesthesia
MSA Nerve Block
Least used blocking technique

NA: Middle superior alveolar and terminal branches.

AA:
• Pulps of the maxillary first and second premolars, mesiobuccal root of the first molar
• Buccal periodontal tissues and bone over these same teeth
Indication:
• Where the ASA nerve block fails to provide pulpal anesthesia distal to the maxillary canine
• Dental procedures involving both maxillary premolars only

Contraindications
• Infection or inflammation in the area of injection or needle insertion or drug deposition
• Where the MSA nerve is absent
Advantages
• Minimizes the number of injections and the volume of solution.

Failure of Anesthesia:
• Anesthetic solution not deposited high above the apex of the second premolar
• Deposition of solution too far from the maxillary bone
• Bone of the zygomatic arch at the site of injection preventing the diffusion of anesthetic
Complications: Hematoma

ASA Nerve Block

Area of Insertion: Height of mucobuccal fold over 1st PM or CI or Canine or any tooth from 2nd PM anteriorly

Target Area: Infraorbital Foramen

Landmarks: Pupil of the eye, Infraorbital notch, Infraorbital Foramen

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Muscle pierced: Quadratus Labii Superioris/ Levator Anguli Oris

Failure: Needle below infraorbital foramen, needle medial/ lateral to foramen

ASA Nerve block Vs. Infraorbital N. Block

• Nerves Anesthetized in ASAN block: MSAN, ASAN, Infraorbital (inf. Palpebral, external nasal, sup. Labial)
• Nerves Anesthetized in Infraorbital block: Infraorbital (inf. Palpebral, external nasal, and sup. Labial)
GP Nerve Block
NA: Anterior Palatine Nerve
AA: post. Portion of hard plate and its overlying soft tissue anteriorly as far as 1st Pm and medially to the midline
Landmarks: Greater Palatine Foramen, Distal to the second molar 10mm away from gingival margin

Failure:
• needle to anteriorly positions
• Partial anesthesia at the area of 1st PM ( due to supplemental innervation from NP nerve)

Complications:
• Ischemia and Necrosis
• Hematoma
• Soft Palate anesthesia

NP Nerve Block
• A.k.a: Sphenopalatine Nerve Block
• AA: Palatal mucoperiosteum from canine to canine
• Only injection that leads to bimaxillary anesthesia (with the other one being the Palatal approach ASAN block)
• Most traumatic injection

Single penetration Technique

• Path of Insertion: 45 degrees to incisive papilla
Multiple penetration technique
• 1st injection at labial frenum to anesthetize interdental papilla
• 2nd injection at interdental papilla to ansthetize incisive papilla
• 3rd injection into incisive papilla

Complication:
• Hematoma
• Necrosis
• Inadequate hemostasis (at areas away from deposition)
• Solution can squirt back

Failure: Partial Anesthesia at the area of Canine ( supplementary innervation from GP

AMSA Nerve Block

• Needs CCLAD
• Injection into large nutrient canal between the two maxillary premolars
• NA: GP, NP, ASAN, MSAN
Palatal approach- ASA Nerve Block
A.k.a. : Palatal Approach Maxillary anterior field block
NA: Nasopalatine, ASAN (infraorbital not anesthetized)
Better done with CCLAD

Maxillary Nerve block

AA: complete hemi-maxillary Anesthesia

High tuberosity Approach : similar to PSAN block but with 30mm needle insertion

Greater palatine Approach: 30mm needle insertion into greater palatine canal

Complications:
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• Hematoma
• Penetration of orbit
• Volume displacement
• Diplopia ( Abducens,VI)
• Retrobulbar block, mydriasis, corneal anesthesia, opthamoplegia
• Amaurosis ( optic nerve)
• Retrobulbar Hemorrhage
• Penetration of nasal cavity

Review on Local Anesthesiology

Topic: Mandibular Injection Techniques

Mandibular Injection Techniques

Inferior Alveolar Nerve Block

• A.k.a:
• Mandibular Nerve block
• Halsted Approcah IAN Block
• NA:
• IAN
• Incisive
• Mental
• Lingual (commonly but not always)

• Landmarks
• Coronoid notch (EOR, IOR)
• Pterygomandibular Raphe
• Occuls al plane of Mand. Post. Teeth

• Parameters
• Height: coronoid notch or 1cm above mand. Occusal plane
• Anteroposterior: Point A: hotizontal line from coronoid notch to deepest part of pterygomandibular raphe,
Point B: ¾ distance from ant. Border of ramus
• Penetration Depth: until bone contact, atleast 3/4 to 2/3 of needle, 20-25mm

• Failure of anesthesia
• Too low deposition
• Too anteriorly deposition
• Accessory innervations ( incomplete anesthesia of post. Due to bifid IAN or supplementary innervation by
mylohyoid nerve)
• Incomplete anesthesia of incisors (supplementary innervation from contralateral IAN)

• Complications
• Hematoma
• Trismus
• Transient facial paralysis

Buccal Nerve block

• A.k.a.:
• Long buccal Nerve block
• Buccinator Nerve Block

V3 block- The Gow-Gates Technique

• NA:
• IAN, Mental, Incisive
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• Lingual
• Mylohyoid
• Auriculotemporal
• Buccal (75%)
• Lanmdarks
• Intraoral: Mesiopalatal cusp of maxillary second
• Landmarks
• Extraorla: Lower border of tragus, Corner of mouth
• Complications
• Hematoma
• Trismus
• Temporary paralysis of cranial nerves III, IV, and VI leading to diplopia, blepharoptosis, and complete
paralysis of the right eye
• Failure:
• Too little solution
• Anatomic difficulty

Vazirani-Akinosi
• A.k.a. : Akinosi technique, closed-mouth mandibular nerve block, tuberosity technique
• NA:
• Inferior alveolar
• Incisive
• Mental
• Lingual
• Mylohyoid
• Patient need not be able to open the mouth.
• Area of insertion: Soft tissue overlying the medial (lingual) border of the mandibular ramus directly adjacent to the
maxillary tuberosity at the height of the mucogingival junction adjacent to the maxillary third molar

• Target area: Soft tissue on the medial (lingual) border of the ramus in the region of the inferior alveolar, lingual, and
mylohyoid nerves as they run inferiorly from the foramen ovale toward the mandibular foramen
Landmarks:
• Mucogingival junction of the maxillary third (or second) molar
• Maxillary tuberosity
• Coronoid notch on the mandibular ramus
• Orientation of the bevel: away from the bone
• Depth of insertion: 25mm
• Motor nerve paralysis develops as quickly as or more quickly than sensory anesthesia
• Failure:
• flaring nature of the ramus
• Needle insertion point too low.

• Complications:
• Hematoma (<10%)
• Trismus (rare)
• Transient facial nerve (VII) paralysis
Mental Nerve Block
• NA:
• Mental, a terminal branch of the inferior alveolar
• Landmarks:
• Mucobuccal fold
• Mandibular Premolars
• Mental Foramen

• Depth: 5-6mm

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Incisive Nerve Block

• NA:
• Mental nerve
• Incisive nerve
• Similar to mental nerve block but with finger pressure.

PDL Injection
• A.k.a. :
• Peridental (original name) injection,
• intraligamentary injection (ILI).
• Bevel facing the tooth
• 0.2ml per root min of 20sec
Intraseptal Injection
• Needle orientation
• Frontal plane: 45 degrees to the long axis of the tooth
• Sagittal plane: At right angle to the soft tissue
Intraosseous Anesthesia
• Last resort
• Anesthetic solution deposited directly into bone
• Needs additional armamentarium for bone perforation
Intrapulpal Injection
• 0.2-0.3ml only
• Only injection technique that provides pressure anesthesia ( in addition to pharmacological anesthesia)

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