Final Revision Flashcards
What is the difference between anaesthesia and analgesia?
Analgesia is only loss of pain perception
Anaesthesia is the loss of perception of pain, touch, pressure and temperature and abolition of motor function
-you can’t move anything
What are the methods of pain control and anxiety and what are the types of sedation?
1.Pharmacological
-Surface Anaesthesia
• Refrigeration
• Topical anaesthetics
-Local Anaesthesia
-Sedation
• Oral (valium, semi sedated, night before or morning)
• Transmucosal
- Intranasal (in kids, hurts a lot, its like a shot)
- Inhalational (ex: nitrous oxide, only up to 70%, no leaking gas from it - it leaves the room, needs a specific room, used for kids with fillings, done by anesthetist)
- Intravenous (BEST WAY, propofol - short acting, sleep w/in 15sec, lasts from 5-10min)
-General Anaesthesia
• Inhalation
• Intravenous
-Out patient drugs
2.Non-pharmacological
• hypnosis
• phasic sensory inputs
-acupuncture (controls pre-dental anxiety and fear, pain and anxiety management during procedure, alleviation of gagging reflex)
-transcutaneous electronic nerve stimulation (TENS)
•patient management techniques
What is a Local Anaesthesic?
=drug used to prevent the transmission of nerve impulses in the area where it is applied, without affecting consciousness
/ =chemical that reversibly blocks action potentials in all excitable membranes
- stops nerve conduction
- is a weak base
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How are Local Anaesthetic Drugs classified as?
according to their chemical structure:
Amides – e.g. Lidocaine, Prilociane, Mepivicaine, Articaine, Bupivicaine
Esters – e.g. Procaine, Benzocaine, Amethocaine, Cocaine (only one that causes vasocontsriction)
-Local anaesthetic usually causes vasodilatation
What are the three main components of local anaesthetics?
- lipophilic/hydrophobic aromatic compound
- intermediate chain (ester or amide)
- hydrophilic amine
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What properties the ideal anaesthetic should have?
A specific and reversible action Good shelf life Non-irritant Produces no permanent damage No systemic toxicity High therapeutic ratio Active topically and by injection Rapid onset Suitable duration of action Chemically stable and sterilizable Combinable with other agents Non-allergenic Non- addictive
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What do local anaesthetic cartridges contain?
Local anaesthetic
Vasoconstrictor (+/-) – adrenaline or octapressin !!!!
Reducing agent (used to stabilize the vasoconstrictor so it doesn’t get oxidized – SODIUM METABISULPHITE) !!!!
Preservatives
?Fungicide
Vehicle - Ringer’s solution (Isotonic solution) - Sodium Chloride
Methylparaben – bacteriostatic agent and antioxidant
• only found in multi-dose drugs, ointments , creams
• bacteriostatic, fungistatic and antioxidant
• removed due to single use and paraben allergies
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How does Local Anaesthetic work?
Inhibits sodium influx through sodium- specific channels in nerve cell membrane
LA binds to Na+ channels when channel is open
Works by inhibiting passage of Na+ into the cell in 2 ways:
• Non specific expansion of nerve cell membrane
• LA binds to receptors in Na+ channel and maintains cell in the REFRACTORY PERIOD
Binding site for Na+ is intracellular
To cross membrane LA molecule must be uncharged/lipophilic
To bind to Na+ channel LA molecule must be charged
The quicker LA crosses cell membrane the more effective it is
LA with high proportion of uncharged molecules most effective
Absorption of Local Anaesthetics depends upon:
Dose
The drug used (is it a vasodilator?)
Presence of vasoconstrictors
Site of deposition
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How is ester metabolized?
- in plasma by pseudocholinesterase !!!!
- hydrolysis in liver
- excreted in urine
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How is amide metabolized?
hydrolysis in liver apart from prilocaine and articaine
- Lidocaine in liver
- Prilocaine partly in lung
- Articaine undergoes hydrolysis in plasma by pseudocholinesterase
- excretion in urine
Benefit of Vasoconstrictor in LA?
More profound anaesthesia
More prolonged anaesthesia
Reduced operative haemorrhage
Produce vasoconstrictor of blood vessels and control tissue perfusion by:
• Decreasing blood flow to the site of drug administration
• Absorption of LA into CVS is slowed so decreased toxicity
• More LA enters the nerve and remains for longer periods thus increasing duration of action
• Decrease bleeding at the site
Routes of administration/Uptake Local Anaesthetic Drugs
Oral
• Poorly absorbed by tissues except cocaine
• Undergo significant hepatic first- pass metabolism
Topical
• Absorbed at different rates after application to mucous membranes
Injection
• Absorption related to vascularity of injection site and vasoactivity of drug
• IV (parenteral) provides most rapid elevation of blood levels – used clinically in the primary management of ventricular dysrhythmias
How is anesthesia distributed in the body?
Absorbed in the blood and distributed throughout the body to all tissues
Plasma conc of LA influenced by:
• Rate of absorption into CVS
• Rate of distribution of drug from vascular compartments to the tissues
• Elimination of the drug through metabolic or excretory pathways
Elimination half- life !!!
• The time necessary for a 50% reduction in the blood level
1st: 50%
2nd: 75%
All LA cross the blood-brain barrier and placenta (enter circulatory system of the developing fetus)
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Which local anaesthetic can be used for pregnant women?
Which local anaesthetic cannot be used for pregnant women?
Articaine
Prilocaine
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Biotransformation products of Amides:
- methemoglobin responsible for methemoglobinemia – Prilocaine
- Monoethylglycinexylidide and glycine xylidide produce Sedation - Lidocaine
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Lidocaine:
Gold standard !!
2% concentration with 1:80 000 adrenaline/epinephrine (used with adrenaline in dentistry)
Pulpal anaesthesia lasts 45 min
Soft tissue anaesthesia lasts longer
< 3% excretion
rarely has contraindications
if allergic to lidocaine (not adrenaline) better to use Mepivacaine than lidocaine plain - anything plain; so adrenaline is not good
Mepivacaine:
2% concentration with 1:100,000 adrenaline/epinephrine
Has similar effect to lidocaine
3% plain
Better anaesthesia than 2% lidocaine vasoconstrictor – free solution
1% excretion
Prilocaine:
3% with vasoconstrictor felypressin/octapressin (synthetic analog of vasopressin)
4% plain
Produces less vasodilation than lidocaine
Is one of the constituents of EMLA (eutectic mix of lidocaine and prilocaine)
3% formulation useful alternative to 2% lidocaine with epinephrine if a vasoconstrictor-free solution is indicated
Excreted in urine as o-toluidine
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Articaine:
4% concentration
1:100,000 (surgical - more constricted) or 1:200,000 (restorative - more diluted) adrenaline
Fast metabolism – low toxicity
Half life 20 minutes
Partly metabolized in the plasma
Increased risk of nerve injury in IDB (higher risk than Lidocaine)
Evidence of buccal infiltration of 4% articaine as effective as IDB with 2% lidocaine in anaesthesia of mandibular molar teeth
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Bupivacaine:
Long acting LA !!!
lasts for: 6hr plain, 8hr with adrenaline
0.25 – 0.75%
Reduced the number of analgesics required for post-operative pain when used as supplementary infiltration during general anaesthesia
With/out epinephrine 1:200,000
Ability to bind to proteins – 96% of it is protein bound
What are the systemic effects of LA on:
- Central Nervous System
- Cardiovascular System
- Local Tissue Toxicity
- Respiratory System
- Drug Interactions
1. Central Nervous System: • Depression • Anticonvulsant properties • Analgesia • Mood elevation
- Cardiovascular System: (action it has on the heart)
• Myocardial depression
• Therapeutic advantage in cardiac dysrhythmias
• Hypotension - Local Tissue Toxicity:
• Skeletal muscle more sensitive – produces skeletal muscle alterations – muscle regeneration within 2 weeks - Respiratory System:
• Dual effect on respiration
• At therapeutic levels – direct relaxant action on bronchial smooth muscle
• At overdose – may produce respiratory arrest (unable to breath) - Drug Interactions:
• Potentiate CNS- depressant effects of LA if used in combination with other CNS depressants e.g. opioids, antianxiety drugs
• Ester LA and use of muscle relaxant succinylcholine lead to prolong apnea as they share same metabolic pathway
• Drugs that induce production of hepatic microsomal enzymes e.g barbiturates can lead to increase rate of metabolism of amide LA
Which are Catecholamines?
=Catechols and if have an amine group (NH2)
naturals: -Epinephrine -Norepinephrine -Dopamine synthetics: -Isoproterenol -Levonordefrin
Which are Noncatecholamines?
Amphetamine Methamphetamine Hydroxyamphetamine Ephedrine (nasal congestant) Mephentermine
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Mode of action of vasoconstrictors:
Three categories of sympathomimetic amines:
• Direct-acting drugs:
epinephrine, norepinephrine, levonordefrin
• Indirect-acting drugs:
tyramine, amphetamine, hydroxyamphetamine
• Mixed-acting drugs:
ephedrine, metaraminol
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Mode of action of vasoconstrictors:
Adrenergic receptors:
α and β receptors based on inhibitory or excitatory actions of catecholamines on smooth muscle
Activation of α receptors – contraction of smooth muscle – vasoconstriction
• α 1 – excitatory postsynaptic
• α 2 – inhibitory postsynaptic
Activation of β receptors – smooth muscle relaxation
• β 1 – in the heart and small intestine causing cardiac stimulation and increased heart rate and lipolysis
• β 2 – brochi, vascular beds and uterus producing brochodilation and vasodilation
Systemic Actions of Epinephrine:
Myocardium
• Stimulates β1 – positive inotropic (force of contraction) and positive chronotropic (rate of contraction) effect
Pacemaker cells
• Stimulates β1 – increase irritability of pacemaker cells leading to increase incidence of dysrhythmias – e.g ventricular tachycardia and premature ventricular contractions
Blood Pressure
• Increased systolic blood pressure, diastolic pressure is decreased
• Diastolic pressure is increased at larger doses due to α receptor stimulation
Cardiovascular System
• Increased blood pressure, cardiac output, stroke volume, heart rate, strength of contraction, myocardial oxygen consumption (OPPOSITE EFFECT ON HR FROM NOREPINEPHRINE)
Vasculature
• Constriction in the vessels – small arterioles supplying skin, mucous membranes and kidneys
• Small dose of epinephrine produces dilatation due to stimulation of β2 receptors, higher doses produce vasoconstriction due to stimulation of α receptors
Haemostasis
• α receptor stimulation causing vasoconstriction at site
• As levels of epinephrine decrease action on blood vessels revert to vasodilation due to β2 receptors stimulation- therefore is common to notice bleeding at about 6hrs postoperative
Respiratory system
• brochodilation due to β2 effect
Central Nervous System
• No effect at therapeutic doses
Termination of action
• Reuptake by adrenergic nerves
• If escaped reuptake is rapidly absorbed in the blood by the enzyme catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) both present in liver
• Only 1% unchanged in urine
Site effects and Overdose of Epinephrine:
- Increased fear, anxiety, tension, restlessness, trembling, throbbing headache, tremor, weakness, pallor, dizziness, palpitations, pallor, respiratory difficulty – CNS
- Cardiac dysrhythmias
- Dramatic increase in BP - Angina episodes in patients with coronary artery insufficiency
Systemic Actions of Norepinephrine:
Mode of action
• Almost exclusively on α receptors (90%)
• Stimulates β actions in the heart(10%)
• ¼ as potent as epinephrine
Myocardium
• +ve inotropic action through β1
Pacemaker cells
• Stimulates β1 – increase irritability of pacemaker cells leading to increase incidence of dysrhythmias
Coronary Arteries
• Increased coronary artery blood flow
Heart rate
• Decrease in heart rate due to reflex actions on carotid and aortic baroreceptors and vagus nerve after a marked increased in blood pressure (OPPOSITE EFFECT ON HR FROM EPINEPHRINE)
Blood Pressure
• Increased blood pressure – both systolic and diastolic due to α-stimulating actions
Cardiovascular Dynamics • Increase blood pressure • Decrease heart rate (OPPOSITE TO EPI) • Slight or no effect on cardiac output • Increase stroke volume • Increase total peripheral resistance
Vasculature
• α-stimulating actions producing constriction and increased total peripheral resistance
Respiratory system
• α-stimulating actions producing constriction of lung arterioles
Central Nervous System
• No effect at therapeutic levels
Metabolism
• Increase blood sugar level
• Increase tissue oxygen level consumption
• Increase basal metabolic rate
Termination of Action and Elimination
• Reutake at adrenergic nerve terminals and its oxidation by MAO
• Exogenous norepinephrine is inactivated y COMT
Side effect and Overdose of Norepinephrine:
- Similar to epinephrine but less frequent and severe !!!
- Stimulation of CNS
- Marked increased in blood pressure – increasing risk of haemorrhagic stroke, angina episode in susceptible patients and cardiac dysrhythmias
- Extravascular injections into soft tissues can cause necrosis and sloughing – to be avoided for vasoconstrictive purposes in hard palate – some authorities grounded its use in LA
Felypressin (Octapressin):
• Synthetic analog of vasopressin
• A nonsympathomimetic amine
Mode of action
• Direct stimulant of smooth muscle
Myocardium – no direct effects noted
Pacemaker cells
• Nondysrhythmogenic
Coronary Arteries - No effect at therapeutic levels
Vasculature – facial pallor in high doses
Central Nervous System – no effect on adrenergic nerve transmission
Uterus
• Antidiuretic and oxytocic actions, the latter CONTRAINDICATED IN PREGNANT patients !!!!!!!!!
Side Effects and Overdose
• Wide margin of safety
3% Prilocaine and 0.03 IU/mL
What is ASA?
American Society of Anaesthesiologist
What ASA III means?
A patient with severe systemic disease
-poorly controlled DM, morbid obesity, active hepatitis, alcohol dependence, implanted pacemaker
What ASA I means?
A normal healthy patient
-non smoking, no or minimal alcohol use
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What ASA II means?
A patient with mild systemic disease
-controlled DM, current smoker, social alcohol drinker, pregnancy, obesity, mild lung disease, asthma, epileptic, thyroid conditions, active allergies
What ASA IV means?
A patient with severe systemic disease that is a constant threat to life
-cardiac ishemia, severe valve dysfunction, sepsis
What ASA V means?
A moribund patient who is not expected to survive without the operation
-abdominal/thoracic aneurysm, massive trauma, intracranial bleed, ischemic bowel, cardiac pathology, multiple organ/system dysfunction
What ASA VI means?
A declared dead patient whose organs being removed for donor purposes
Trigeminal Nerve - Sensory innervations to:
- Dentition, mucosa of mouth
- Skin of face
- Nose and paranasal sinuses
• Except base of tongue and pharynx
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Trigeminal Nerve - Motor innervations to:
- Muscles of mastication !!!
- Tensor ville palatini, Tensor tympany
- Anterior belly of digastric
- Mylohyoid
Origin of Trigeminal Nerve:
- EMERGES FROM the middle of the PONS
- Run to the front of petrous part of temporal bone
- Trigeminal ganglion (Semilunar or Gasserian ganglion)
- Trigeminal ganglion formed by aggregation of cell bodies of sensory neurons
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three main branches which emerge from trigeminal ganglion:
What is the name of the foramen of each division that exits the skull?
V1 – superior orbital fissure
opthalmic
V2 – foramen rotundum
maxillary
V3 – foramen ovale
mandibular
Which are the motor and sensory nucleus within brainstem?
Mesenchephalic, Principal and Spinal Trigeminal nucleus
Ophthalmic V1 innervation:
Caries sensory information from the skin of the forehead, the upper eyelids, cornea and nose ridge, frontal sinus, parts of the meninges and nasal mucosa
• Supplies eyeballs, conjunctiva, lacrimal gland, mucosa of nose and paranasal sinus, skin of forehead eyelid and nose
Smallest division
Sensory only
Maxillary V2 innervation:
Innervates the skin of the middle facial area, the side of the nose, lower eyelids, maxillary dentition and associated gingival tissues, part of nasal mucosa (including the maxillary sinus), cheek, upper lip and the palate, ethmoid, sphenoid sinuses and part of meninges
Pure Sensory
Nasal and nasopalatine nerves – innervate back of nasal mucosa, anterior part of palatal mucosa, gingiva and maxillary incisors
Greater palatine nerve – innervates hard palate and palatal gingiva of alveolar process
Lesser palatine nerve – innervates soft palate
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Mandibular V3 innervation:
Innervates skin of lower facial area, mandibular dentition and associated gingival tissues, mucosa of lower lip, cheeks, and floor of mouth, chin, jaw, tongue, parts of meninges and external ear
Two main branches:
-Anterior trunk !!!!!
• Sensory- Buccal nerve
• Motor – lateral pterygoid, deep temporal and masseteric nerves
-Posterior trunk
• Sensory – auriculotemporal and lingual
• Mixed sensory and motor – inferior alveolar nerve
Course of Opthalmic Nerve:
- Emerges from Trigeminal ganglion
- Lateral wall cavernous sinus
- 3 branches in anterior part of cavernous sinus Lacrimal, Nasocilliary, Frontal !!!
- Superior orbital fissure
- Orbit
Course of Maxillary Nerve:
- Emerges from Trigeminal ganglion
- Lateral wall cavernous sinus
- Foramen rotundum
- Pterygopalatine fossa
- Through inferior orbital fissure reaches floor of the orbit as infraorbital nerve
- Reaches the face through infraorbital foramen
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Innervation of Tongue:
Sensory - pain, touch, temperature - to anterior 2/3 is supplied by lingual nerve (branch of V3)
Taste- to anterior 2/3 is supplied by chorda tympani (branch of VII) - sensory as well but not one of the mains
Sensory to posterior 1/3 tongue is supplied by glossopharyngeal (IX)
MOTOR innervation of tongue is supplied by hypoglossal (XII)
Ganglia Associated with Trigeminal Nerve:
Cilliary Ganglion
Pterygopalatine Ganglion
Otic Ganglion
Submandibular Gaglion
Injection Syringes must be:
- durable
- able to withstand repeated sterilization without damage
- capable of accepting a wide variety of cartridges and needles from different manufacturers and permit repeated use
- inexpensive
- self-contained
- lightweight and simple to use with one hand
- provide aspiration so blood can be seen through the glass cartridge
Syringe Components:
needle adaptor piston with harpoon finger grip syringe barrel thumb ring
Advantages and Disadvantages of the Metallic, Breech-loading Aspirating Syringe:
Advantages: Visible cartridge Aspiration with one hand Autoclavable Rust resistant Long lasting with proper maintenance
Disadvantages:
Weight – heavier than plastic syringe
Syringe may be too big for small operators
Possibility of infection with improper care
Non-disposable
Self- Aspirating Syringes:
The syringe use the elasticity of the rubber diaphragm in the anaesthetic cartridge to obtain negative pressure
The diaphragm rests on a metal projection inside the syringe that directs the needle into the cartridge
Pressure acting directly on the cartridge through the thumb disk or indirectly through the plunger shaft distorts the rubber diaphragm producing positive pressure within the anaesthetic cartridge
Advantages and Disadvantages of Pressure Syringes (+their use):
for periodontal ligament injection
non-disposable
Advantages: Measured dose Overcomes tissue resistance Nonthreatening (new devices) Cartridges protected
Disadvantages:
Cost
Easy to inject too rapidly
Threatening (original device)
Jet injector – ‘needle-less syringe’:
For topical anaesthesia
Based on the principles that liquids forced through small openings called jets at very high pressures can penetrate intact skin and mucous membranes
Disposable Syringes:
Plastic disposable syringes are available in a variety of sizes with assortment of needle gauges
Commonly used for IM and IV injections but also can be use for intraoral injections
No aspirating tip
Cannot accept local cartridges
Safety Syringe:
Aspiration is possible
Some brands come with an autoclavable plunger and disposable self-contained injection unit
Made to be single use items
More expensive than reusable syringes
Minimize the risk of needle injuries by having a sheath that ‘locks’ over the needle
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Advantages of Larger-Gauge Needles Over Smaller-Gauge Needles:
Less deflection as needle advances through tissues
Greater accuracy in injection
Less chance of needle breakage
Easier aspiration
No perceptual difference in patient comfort
Rotational Insertion Technique:
Bi-Rotational Insertion Technique –BRIT
• the operator rotates the needle in a back-and-forth rotational movement while advancing the needle through soft tissue
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Components of the needle:
- Bevel: point or tip of the needle; long, medium and short
- Shaft: long portion of the needle (diameter of lumen)
- Hub: plastic/metal piece that attaches the needle to the syringe
- Cartridge penetrating end: perforates the diaphragm of cartridge
- Syringe adaptor
Components of the Cartridge:
Latex rubber Diaphragm - through it the needle penetrates the cartridge
Aluminum Cap - holds the diaphragm in position
Neck
Cylindrical glass tube
Stopper (Plunger, Bang) -silicon rubber
Mylar plastic label surrounds glass with content information and colour coded band to identify anaesthetic
Care and Handling of Cartridges:
should not be permitted to soak in alcohol or other sterilizing solution because the diaphragm will allow diffusion
-CARTRIDGES SHOULDN’T BE AUTOCLAVED
Maxillary Injection Techniques:
Provide anaesthesia of teeth, soft and hard tissues
Type of anaesthesia is determined by type of procedure
Techniques include: • Supraperiosteal (infiltration) !!! • Periodontal ligament • Intraseptal injection • Intracrestal injection • Intraosseous injection • Superior Alveolar Nerve blocks • Nasopalatine and Greater palatine Nerve blocks
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Supraperiosteal Injection:
Most frequently used technique to obtain PULPAL anaesthesia in MAXILLARY teeth
– also known as local infiltration !!!!
Anaesthetises: pulp and root of tooth, buccal periosteum, CT and mucous membrane
Indicated when treatment is limited to 1-2 maxillary teeth and for soft tissue anaesthesia when surgical procedure is in a circumscribed area
Alternative supplemental techniques: PDL, intraosseous, regional blocks
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Posterior Superior Alveolar Nerve Block:
Effective for maxillary third, second and first molar
Known as tuberosity or zygomatic block
Note: mesiobuccal root of maxillary first molar is not consistently innervated by PSA but also can be by MSA therefore a second local/subperiosteal infiltration is needed !!!!!!
Area of insertion: height of mucobuccal fold above the maxillary second molar
Landmarks: mucobuccal fold, maxillary tuberosity and zygomatic process of maxilla
Complications:
temporary hematoma – if inserted too far posteriorly into pterygoid plexus of veins, also maxillary artery may be perforated
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Middle Superior Alveolar Nerve Block:
Present only in 28% of population
Limited clinical usefulness however IF ASA BLOCK FAILS to provide pulpal anaesthesia distal to the maxillary canine then MSA block is indicated
Anaesthetises: pulpal tissue of first and second premolars and mesiobuccal root of first molar
No contact with bone
Same as with PSA nerve
Area of insertion: height of the mucobuccal fold above UPPER SECOND PREMOLAR
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Anterior Superior Alveolar Nerve Block:
known as Infraorbital Nerve Block incorrectly
Profound pulpal and buccal soft tissue anaesthesia from maxillary central incisors through premolars in about 72% of patients
Area of insertion: height of mucobuccal fold directly over the first premolar
Landmarks: Mucobuccal fold, Infraorbital notch, Infraorbital foramen
Complications:
Hematoma may develop across eyelid and the tissues between it
-This is rare as pressure is routinely applied to the injection site during and after administration
•Hematoma can get infected: prescribe antibiotics OR can go away by its own
Anterior Middle Superior Alveolar Nerve Block Technique:
Areas anesthetised:
• Pulpal anaesthesia of the maxillary incisors, canines and premolars
• Buccal attached gingiva of the same teeth
• Attached palatal tissues form midline to free gingival margin on associated teeth
Palatal approach thus muscles of facial expression and upper lip are not anaesthetised
Described as field block of the terminal branches of the ASA block
Area of insertion: on hard palate halfway along an imaginary line connecting the midpalatal suture to the free gingiva margin ; the location between first and second premolars
45-degree angle with bevel facing bone – insert until in contact with bone
2 approaches of Maxillary Nerve Block:
Produces anaesthesia to hemimaxilla
Two approaches:
-High Tuberosity Approach
• Area of insertion: height of the mucobuccal fold above the distal aspect of the maxillary second molar
• Landmarks: mucobuccal fold at the distal aspect of maxillary second molar, maxillary tuberosity, zygomatic process of maxilla
-Greater Palatine Approach Technique:
Area of insertion: palatal soft tissue directly over greater palatine foramen
Landmark: greater palatine foramen, junction of the maxillary alveolar process and palatine bone
Same as greater palatine nerve block- once is complete proceed with very slow advancement into the greater palatine canal to a depth of 30 mm
Palatal Infiltration:
Necessary when manipulation of palatal soft or hard tissues
Topical anaesthesia at injection site – at least 2 minutes, using cotton roll/cotton applicator stick
Pressure anaesthesia can be produced at the site of injection by applying considerable pressure using a firm object such as cotton applicator stick/ handle of the dental mirror
This will produce ischemia (blanching) of normally pink tissues at the penetration site and a feeling of intense pressure (dull and tolerable, not sharp and painful)
Deposit anaesthetic solution slowly
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Greater Palatine Nerve Block:
Anaesthesia to the palatal soft tissues distal to the canine
Profound hard and soft tissue anaesthesia
Indicated when more than two maxillary teeth required periodontal/surgical treatment and sometimes for restorative treatment if subgingival restorations
Minimizes patient discomfort as no need for multiple injections on the palate
Technique:
Insertion of needle slightly anterior to the greater palatine foramen
Landmarks: greater palatine foramen and junction of the path of maxillary alveolar process and palatine bone
Advance the syringe from the opposite side of the mouth at right angle to the target area – bevel of needle should face palatal soft tissues
Position for Right greater palatine nerve block – administrator should be at 7-8 o’clock position
Position for Left greater palatine nerve block – administrator should be at 11 o’ clock – positions apply for right-handed administrator
Complications:
• Hematoma if maxillary artery is punctured
• Penetration of the orbit may occur if needle goes far
• Penetration of nasal cavity
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Nasopalatine Nerve Block:
Palatal anaesthesia achieved to anterior portion of the hard palate (soft and hard tissues) bilaterally from the mesial of the right first premolar to the mesial of the left first premolar
Tissue penetration lateral to incisive papilla on the palatal aspect of the maxillary central incisors
Technique:
Insertion on palatal mucosa lateral to incisive papilla
Target area the incisive foramen
Needle at 45- degree towards incisive papilla
Bevel of needle towards palatal mucosa
Administrator position- sit at 9 or 10 o’clock position and ask patient to extend neck
Pressure anaesthesia at site of needle insertion
Multiple Needle Penetrations
Palatal Approach- Anterior Superior Alveolar Nerve Block:
Shares several common elements with the nasopalatine nerve block
The P-ASA injection uses similar tissue point of entry (lateral aspect of incisive papilla) but differs in its final target – the needle is positioned within the incisive canal
Mandibular Injection Techniques:
Inferior Alveolar Nerve block Mandibular Nerve Block: • Gow-Gates Technique • Vazirani-Akinosi Closed Mouth Technique Mental Nerve block Buccal Nerve block Incisive Nerve block
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Inferior Alveolar Nerve Block Technique:
Area of insertion: Mucous membrane on the medial side of the mandibular ramus
Landmarks: Coronoid notch, Pterygomandibular raphe, occlusal plane of mandibular teeth
Depth of penetration: 20-25 mm (2/3rd to 3/4th ) the length of a long needle until contact with bone
Height of injection: Imaginary line- place thumb of your left hand in the coronoid notch !!!!!
Anteroposterior site of injection: Needle penetration occurs at the intersection of two points !!!!
•Point 1- horizontal line form coronoid notch to deepest part of the pterygomandibular raphe
•Point 2 – vertical line through point 1 about 3/4ths of the distance from the anterior border of ramus
Insert the needle, when bone is contacted withdraw approximately 1 mm and aspirate
If negative aspiration deposit slowly 2/3rds of cartridge over 1 minute
Three parameters should be considered during penetration of Inferior Alveolar Nerve Block Technique: the height of injection, depth of penetration and anterior posterior placement of the needle
