4. LOCAL ANAESTHESIA
HISTORY
1842 - Ether- Dr. Morton
1844 - Nitrous Oxide- Dr. Horace Wells
1884 - Cocaine- Dr.Carl koller
1894 - Ethyl chloride-Dr.H.J.Carlson
SYNTHETIC AGENT-
1943- Lidocaine
1956- Halothane
1967- Pancuronium
1990- Propofol
1992- Desflurane
5. LOCAL ANAESTHESIA
DEFINITION-
A loss of sensation in circumscribed area of the body
caused by a depression of excitation in nerve endings
or an inhibition of the conduction process in peripheral
nerves.
Stanley F.Malamed
.
6. LOCAL ANAESTHETIC AGENT
DEFINITION
A therapeutic modality which brings about a reversible
loss of conduction from periphery to its interpretation in
the central nervous system.
7. IDEAL PROPERTIES-
Action-
Potent-
Rapid onset-
Easily biotransformable-
Does not interfere with healing of tissue-
Stable and sterile as A solution-
9. PERIOD OF ACTION
Ultra short-<30min
Short acting-45 to75min
Medium acting-90to150min
Long acting-180min or more.
WITHOUT VASOCONSTRICTOR
2%lignocaine
Procaine
0.5% bupivacaine 1:200000 adrenalin
0.5%etidocain 1:200000 adrenalin
15. Ph(plain)-6.5 , ph(with Vc)4.5 –5.5
Onset Of Action 2-3 Min
Half Life 90 min
Recommended Dose – 7mg/Kg ( 500mg )
with vc 4.4mg/Kg ( 300mg)
Children with vc 3.2 mg/Kg
16. BUPIVACAINE
Classified under amide
1-butyl 2,6 pipecoloxylidide
Toxicity <4 times – Lignocaine, Mepivacaine
Metabolism –Liver by Amidases
Excretion by kidney (16% unchanged)
17. Onset of action –6-10 min
half life-2.7hrs
1.3mg/kg ,Maximum dose-not >40mg
Absolute maximum dose-not> 90mg
18. Indicaton-
pulpal anesthesia.
Full mouth recontruction.
Extensive perio surgery.
management of post op pain.
Duration –Pulpal- 90- 180 min
Soft tissue-4-12 hrs
Contra indication- burning sensation at site of injecton
24. CENTBUCRIDINE
Synthesized at the Centre for Drug Research of
India at Lucknow, India in the year 1983
A quinolone derivative with local anesthetic action .
It has intrinsic vasoconstricting and anti-histaminic
properties.
Concentration of 0.5% can be used effectively for
infiltration, nerve blocks and spinal anesthesia
25. Potency - 4-5 times Of 2% Lignocaine.
Action - Quicker
Duration - Longer
It does not require simultaneous administration of
adrenaline
It does not effect the CVS parameter due to its moderate
antihistaminic activity and is not likely to show skin sensitivity.
Can be used in patient hypersensitive to lignocaine.
27. PAIN DURING INJECTION
PRESSURE OF SOLUTION PH OF SOLUTION
LIGNOCAINE IS UNSTABLE AT PH 7.9
THEREFORE, IT IS PREPARED IN ACIDIC
FORMULATIONS TO INCREASE ITS STABILITY AND SHELF LIFE(4.7)
ACIDITY CAN CAUSE TISSUE IRRITATION
29. LIGNOCAINE
lidocaine stabilizes the neuronal membrane by inhibiting
ionic fluxes, required for initiation and conduction of nerve
impulses, thereby effecting local anesthetic action.
32. Catecholamines non catecholamines
Epinephrine Amphetamine
Norepinephrine Methamphetamine
Levonordefrin Ephedrine
Isoproterenol Mephentermine
Epinephrin reaction-palpitation,apprehension,sweating and chest
pain.Subsides in few minutes by reassurance only
33. Contraindication-
Uncontrolled hyperthyroidism
200/115 mmhg hypertension
>6 months for MI,cerebrovascular accident,bypass surgery
Unstable angina
Felypressin-
Indication- thyrotoxicosis ,antidepressant drugs
Only arteriolar constriction ,no effect on myocardium
o.o3 IU/ML(1:2000000)
34. Reducing Agent: Sodium Metabisulphite 0.5 mg -
This act's as a preservative for the vasoconstrictor.
Preservative: Methylparaben 0.1% (1mg)
Isotonic Solution: Sodium Chloride 6 mg
35. Fungicide: Thymol
Vehicle: Ringer’s Solution - Minimises discomfort during
injection
Diluting Agent: Distilled water
To adjust pH: Sodium Hydroxide
Nitrogen Bubble: 1-2mm in diameter and is present to
prevent Oxygen from being trapped in solution.
36.
37.
38.
39.
40.
41. RECENT LA DELIVERY SYSTEM
VIBROTACTILE DIVICES
gate control theory of pain management, which suggests that
pain can be reduced by simultaneous activation of nerve
fibers through the use of vibration
42. VIBROTACTILE DIVICES
VibraJect DentalVibe Accupal
Delivers A High-frequency Vibration To The Needle That Is Strong
Enough For The Patient To Feel
44. DENTALVIBE
U-shaped vibrating tip attached to a microprocessor.
Vibra-Puls motor gently stimulates the sensory receptors at
the injection site, effectively closing the neural pain
gate,blocking the painful sensation of injections
45. It also lights the injection area and has an attachment to retract the
lip or cheek.
47. Computer-controlled Local Anesthetic
Delivery Systems
In the mid-1990s, work began on the development of local
anesthetic delivery systems that incorporated computer technology
to control the rate of flow of the anesthetic solution through the
needle.
The first of these CCLAD devices,the Wand™ (Milestone
Scientific, Inc., Livingston, N.J.),was introduced in 1997.
48. Base unit - microproccesor
Foot padal -regulate flow of solution.
Handpiece - held in a pen-like grasp that provides
the user with greater tactile sensation and control compared to a traditional syringe.
49. Rate of Injection: foot pedal controls the rate of injection.
1. Slow: 0.005ml/s –PDL injection, Palatal administration
2. Fast: 0.03ml/s – buccal infiltrations, nerve block
3. Turbo: 0.06ml/s
50. base unit and syringe
Rate of injection: Five different basic injection rate settings
for specific applications: block, infiltration, PDL, IO and
Palatal regions.
The unit uses two stage delivery rates for every injection.
It initially expresses the LA solution at an extremely low rate and
after 10 seconds the rate slowly increases to the preprogramed
value for the selected injection technique
COMFIRT CONTROLED SYRYNGES
53. TRANSCUTANEOUS ELECTRIC NERVE STIMULATION
Principle of Trans cutaneous Electrical Nerve Stimulation (TENS)
which has been used for the relief of pain.
Some limitations are increased salivary flow and inability to use metal
instruments freely.
54. Advantage
No need of needle
No need for injections of drugs
Patient is in control of the anesthesia
No residual anesthetic effect at the end of procedure
Residual analgesic effect remains for several hours
55. Disadvantage
Cost of the unit Training & ‘Learning curve‘ initial success may be
low but increases with experience
It is contraindicated in several conditions
1.Heart disease, 2.Seizures,
3.Neurological disorders, 4.Brain tumors,
5.Patients wearing pacemakers and cochlear implants
56. Devices for intra-osseous anesthesia
Aim to inject local anesthetic solution into the cancellous
bone adjacent to the apex of the tooth.These systems are
Stabident x-tip intraflow
59. If the penetration zone is located in alveolar mucosa that moves once
the perforator is withdrawn, it can be extremely difficult to locate the
perforation site with the anesthetic needle.
65. TECHNIQUES OF NERVE BLOCK
A.MAXILLARY NERVE
BLOCK
PSA
INFRA ORBITAL
NASOPALATINE
GP
B.MANDIBULAR NERVE
BLOCK
IANB
MENTAL NB
MANDIBULAR NB
66. POSTERIOR SUPERIOR ALVEOLAR NERVE BLOCK
Mucobuccal fold & its concavity,,zygomatic process of maxilla, infratemporal surface of
maxilla ,anterior border of coronoid process,maxillary tuberocity
67. Other common name –tuberocity block ,zygommatic block
Area anaesthetised-pulps of the 3rd
2nd 1st Molars,Buccal periodontium
and bone overlyning These teeth
Indication-tt involving two or more
molars
-when supraperiosteal injection is
contraindicated
Contraindication-in haemophillia as
The risk of haemorrhage is high
Advantage-atraumatic,
High success rate,minimumm
injection Requred,less volume
68. Technique à PSA Nerve Block
1) 25 gauge short needle is recommended
2) Insert needle at the height of the mucobuccal
fold above the maxillary 2nd molar
3) Target area is the PSA nerve which is
posterior, superior and medial to the posterior
border of the maxilla
4) Apply topical anesthetic for at least one minute
5) Have patient open their mouth half way which
makes more room
6) Retract the patient’s cheek with mirror
7) Pull the tissues taut
69. 8) Orient bevel toward bone
9) Insert needle at height of mucobuccal fold over the
2nd maxillary molarcartridge)
15) Wait 3 to 5 minutes to start treatment
10) Advance needle upward, inward and backward
direction
11) Odd feeling of having no resistance whatsoever
12) Penetrating to an average depth of 10-14 mm is
adequate
13) Aspirate in two planes by rotating bevel one
quarter turn
14) Deposit 0.9 ml of a cartridge
70. DISADVANTAGES-
Risk of haematoma,
Does not anaesthetised maxillary first molar completely
No bony land mark
NEEDLE PATHWAY DURING INSERTION
Needle penetrate the mucosa,alveolar tissue,and possibly the
buccal pad of fat it penetrates the posterior fiber of buccinator
muscle
APPROXIMATING STRUCTURE WHEN NEEDLE IS IN
POSITION
1. posterior to the posterior surface of maxilla
2. anterior and lateral to the anterior margin of the external
pterigoid plexus of veins
3. Anterior to pterigoid plexus of vein
71. Sign n symptoms-
1 subjective;none
2 objective-instrumentation is necessary to
demonstrate absence of pain
Safety measures
Slow injection ,repeated aspiration
Precaution
The depth of the needle penetration should be
checked
Overinsertion increase the risk of haematoma
72. INFRA ORBITAL NERVE BLOCK
Approach: . Insert the needle
into the mucobuccal fold at
junction of premolars 1 and 2.
Direct the needle parallel to the
long axis of premolar 2, palpating
its location as the needle is
advanced until it is adjacent to
the infraorbital foramen
(approximately 1.5-2 cm). If the
needle is directed at an angle that
is too acute, it will hit the
maxillary eminence; if directed at
an angle that is too superior, the
needle will enter the orbit
Inject .9 to1.2 mL of local anesthetic while holding
firm pressure with the index finger over infraorbital
ridge to prevent ballooning of lower eyelid. Massage
for 10-20 seconds.
73. An infraorbital nerve block, which
branches from the maxillary nerve,
anesthetizes the lower eyelid, upper
cheek, part of the nose, and upper lip
Maxillary central incisor up to premolar,
Mesiobuccal root of first molar
74. Landmarks:
Mucobuccal fold
Infraorbital notch
Infraorital foramen
Angle of mouth
Pupil of eye
75.
76. Extra oral approach
Insert the needle through the skin, subcutaneous
tissue, and muscle. Before injecting the anesthetic,
aspirate to ensure the needle is not within a vessel.
Inject the anesthetic.
The overlying tissues should appear edematous.
Massage the area for 10 to 15 seconds after removing
the needle.
79. NASO PALATINE
The nasopalatine nerve block anesthetizes
the anterior hard palate and associated soft
tissues
1 Insertion point: palatal mucosa just lateral to the incisive papilla
2) Approach the injection site at a 45 degree angle
3) Apply considerable pressure to the incisive papilla until ischemia
4) Continue to apply pressure to the cotton applicator tip while injecting
5) Advance the needle until bone is gently contacted
6) Depth of needle penetration is usually 5 mm
7) Slowly deposit ¼ cartridge over a 30 second interval
80.
81. MIDDLE SUPERIOR ALVEOLAR (MSA) NERVE BLOCK
anesthetizes the maxillary premolars with
occasional overlap to the canine and first
molar
Landmarks: Locate the mucobuccal fold
maxillary premolar 2
.
Approach: While retracting the cheek,
insert the needle into the intersection
point at a 45-degree angle, and advance 1-
1.5 cm.
Slowly inject 0.9 to 1.2 mL of local
anesthetic
82. The anterior superior alveolar (ASA)
The anterior superior alveolar (ASA) nerve block anesthetizes the maxillary
canine, the central and lateral incisors, and the mucosa above these teeth,
with occasional crossover to the contralateral maxillary incisors
83. Landmarks: Locate the mucobuccal fold where it
intersects with the apex of the canine (cuspid) tooth
by retracting the membrane with gauze and pulling
out and down.
Approach: insert the needle apex/center of the canine
at a 45-degree angle, advancing the needle
approximately 1-1.5 cm.
Slowly inject 1 mL of local anesthetic and massage for
10-20 seconds
84.
85. GRETER PALATINE NERVE BLOCK
Blocking the greater palatine nerve anesthetizes
the posterior two thirds of the hard palate
Landmarks: The greater palatine foramen can
be identified by finding the junction of molars 2
and 3 and then moving the needle 1 cm medially.
Approach: Insert the needle adjacent to the
greater palatine foramen, at a 90-degree angle to
the curvature of the hard palate. Do not advance
further.
Inject 0.3-0.5 mL of anesthetic. Do not inject
more than this because it can cause separation of
the mucosa from the palate and subsequent
tissue necrosis
86. MENTAL N INSICIVE NERVE BLOCK
Landmarks: junction of mandibular
premolars 1 and 2 and down 1 cm inferior to
the gum line (just medial to the midline
pupil). this is in the same line as the
infraorbital foramen.
Approach: Insert the needle in to the
mucolabial fold , at a 45-degree angle.
Advance until the needle contacts the
mandible. Withdraw the needle slightly.
Inject 0.5-1 mL of solution anterior to apex
of second premolar.
87. A mental nerve block anesthetizes the
ipsilateral lower lip and skin of the chin
For blocking incisive nerve the
Same technique is followed and needle
Is directed in medial ,inferior and
Anterrior direction to enter the mental
foramen
This procedure blocks both mental
And incisive nerve at the same time
90. Landmarks: Start by standing contralateral to the side to be anesthetized. Place the
thumb in the mouth, and place the index finger externally and posterior to the
ramus (angle of the jaw). Retract cheek laterally and palpate the retromolar fossa
to find the greatest depth of the anterior border of the ramus; this is the coronoid
notch
91.
92. Buccal nerve block
The buccal nerve block anesthetizes the mucous
membrane of the cheek and vestibule and, to a lesser
extent, a small patch of skin on the face
Landmarks: Locate the buccal nerve 1 mm lateral to
mandibular molar 3 at the anterior border of the ramus in
the occlusive plane.
Approach: With the thumb of the nondominant hand,
pull the cheek laterally. Insert the needle into the anterior
border of the ramus 1 mm lateral to the third mandibular
molar and in line with the occlusive plane. Advance the
needle 3-4 mm.
Slowly inject o.5 ml to 1 mL of local anesthetic
93.
94. ERRORS IN IANB
High injection
1.Numbness of the ear
Injection near to the auriculo temporal nerve
2.Trismus
Injection into the lateral pterigoid muscle
3Toxicity
Pterigoid plexus
95. Low injection
1 .Trismus
Injection to medial pterigoid
2.Toxicity
Posterior facial vein
Low n deep
1.Facial paralysis
Facial nerve
97. FAILURE OF IANB
all the nerve blocks which may be administered in the human body the
IANB has the highest failure rate (Malamed, 2012).
Accessory or supplementary nerve supply to the mandibular teeth, in
addition to that from the inferior alveolar nerve, may be a plausible
explanation for failed anaesthesia in mandibular teeth.
In addition to the inferior alveolar nerve in the mandible, the lingual
nerve, the long buccal nerve, the nerve to mylohyoid, and the cervical
nerves have been implicated as possible accessory suppliers of sensation
to the mandibular teeth.
98.
99.
100.
101. GOW GATES TECHNIQUE
Anatomic landmarks include the
following:
Corner of the mouth
The intertragic notch
Distolingual cusp of the second
maxillary molar tooth
1.8 mL of local anesthetic is injected
slowly over 1 minute. This blocks the
IAN and its branches and the lingual,
mylohyoid, auriculotemporal, and
buccal nerves.
102.
103. Vazirani-Akinosi (closed-mouth) technique
It is useful in trismatic patients
and those with ankylotic
temporomandibular joint; in
addition, it is less traumatic
and has a lower complication
rate. However, the Vazirani-
Akinosi technique is less
effective than the Gow-Gates
technique. Recent studies have
not shown any difference in the
quality of pain relief with
either of the approaches.
104. Anatomic landmarks
include the following:
Gingival margin over
the second and third
maxillary molars
Pterygomandibular
raphe
The aim is to enter the pterygomandibular space where the IAN,
lingual nerve, and mylohyoid nerve are present. This space is
bordered laterally by the ramus of mandible, medially and
inferiorly by the medial pterygoid muscle, posteriorly by the
parotid gland, and anteriorly by buccinators muscle.
105. Extra oral technique
The needle is inserted perpendicular to the skin into
the sigmoid notch below the zygomatic arch anterior
to condyle.
The tip of the needle is then withdrawn slightly and
redirected posteriorly and inferiorly so that it goes
beyond the lateral pterygoid plate.
After redirection of the needle, paresthesias in the
mandibular region are elicited at a depth of about 1
cm. After aspiration, 3-5 mL of local anesthetic
solution is slowly injected.
106.
107. ANTERIOR MIDDLE SUPERIOR ALVEOLAR NERVE BLOCK
Facial n palatal gingiva as
well as pulp in the region of
maxillary 1---5
Without any collateral facial
anaesthesia
Operator Fatigue
1.Ischhemia
2.Supplimental Anesthesia
3.Flap reflection should not beyond the
mucogingival junction3 to 5mm penetrating depth
1.5ml ,in 3to 4 min
108. Periodontal ligament injection
The PDL
injection provides pulpal anesthesia to the tooth, with
only localized soft tissue anesthesia developing. When
administered in the mandible, there is no associated
extraoral or lingual anesthesia like traditional inferior
alveolar nerve block.
109. THEORIES OF ACTION OF L.A
ACTEYLCHOLINE THEORY: –
Involved in nerve conduction in addition to its role as a
neurotransmitter at nerve synapses • No such evidence •
CALCIUM DISPLACEMENT THEORY: –
L.A causes nerve block by displacement of Ca from some
membrane site that controls entry of Na
Varying conc. Of Ca in nerve – not seen
110. SURFACE CHARGE THEORY: –
Action by binding to nerve membrane and changing its
electric potential.
LA act on nerve channel rather than surface –It cannot
explained how uncharged LA molecule causes nerve
blockage.
111. NON SPECIFIC MEMBRANE EXPANSION THEORY-
– LA are lipid soluble – enters nerve membrane and changes
configuration of membrane.
There by reduced space for sodium to enter and thus cause
inhibition. •
Explains how non ionised drug causes- blockade, nerve membrane
do expand and become more fluid when exposed to LA .
• No evidence to tell that the whole blockade is due to this
phenomenon.
112. SPECIFIC RECEPTOR THEORY:
The hydrophilic charged amino terminal binds to
specific receptors of the sodium gates to block the
passage of sodium ions.
113.
114.
115. EFFECT OF PH
Local anesthetics are weak bases and are usually formulated as the
hydrochloride salt to render them water-soluble.
At the chemical's pKa the protonated (ionized) and unprotonated
(unionized) forms of the molecule exist in an equilibrium but only
the unprotonated molecule diffuses readily across cell membranes.
Once inside the cell the local anesthetic will be in equilibrium,
with the formation of the protonated (ionized form), which does not
readily pass back out of the cell. This is referred to as "ion-
trapping"
116. Acidosis caused by inflammation at a wound partly
reduces the action of local anesthetics. This is partly
because most of the anesthetic is ionized and therefore
unable to cross the cell membrane to reach its cytoplasmic-
facing site of action on the sodium channel.
117. Small nerve fibres are more sensitive than large nerve fibres
• Myelinated fibres are blocked before non-myelinated
fibres of the same diameter.
• Thus the loss of nerve function proceeds as loss of pain,
temperature, touch, proprioception, and then skeletal
muscle tone.
This is why people may still feel touch but not pain when
using local anaesthesia.
118. COMPLICATION
Local or systemic
Mild or severe
Transient or permanent
Primary or secondary
Due to needle or due to solution
119. LOCAL COMPLICATION
Parasthesia.
Facial palcy
Trismus
Needle breakage
Soft tissue injury
Pain on injection
Hematoma
Infection edema n sloghing of tissue
120. Parasthesia.
There are many theories as to the cause of paresthesia
Following inferior alveolar nerve blocks. Needle
trauma, the volume of solution injected, repeated
injections, the type of local anesthesia administered,
and neurotoxicity are the most commonly reported
causes in the literature.
121. According to Pogrel and Thamby ,higher incidence of occurrences
with the lingual nerve (79%) than inferior alveolar nerve (21%).
122. Pogrel and colleagues23 believe that the lingual nerve may be predominantly
affected because of its fascicular pattern.
In their studies they found that just above the lingula, where an inferior
alveolar nerve block is normally deposited, the lingual nerve was
unifascicular in one-third of cases, and a unifascicular nerve may be injured
more easily and permanently than a multifascicular nerve, which may have
greater powers of recovery.
The lingual nerve is also more likely to be injured by a needle because of its
position (5–6 mm below the surface mucosa) and because it is exposed below
the mandibular foramen.
The mechanism of nerve damage is believed to be caused by direct needle
trauma.
123. If the patient feels an “electric shock” in the tongue, stopping the
injection,backing the needle out a few millimeters, and
repositioning it may minimize the incidence of permanent nerve
damage.
High-dose corticosteroids to reduce immune inflammatory reaction
may be considered.
Most paresthesias resolve within 10 to 14 days, but may take up to
6 months. On rare occasion, however, it may be permanent.
124. Hillerup and Jensen ,the sensation was not seen as an
indicator of nerve injury.
The volume of injection and repeated injections have not
been associated with the severity of nerve injury.
In 1995, Haas and Lennon
Parasthesia local anesthetics do have the potential
for neurotoxicity and that there was a higher incidence .
125. Occular Damage
Uncommon positive aspiration the
most common theory is back pressure from an inferior
alveolar nerve block traveling back into the maxillary
artery via retrograde flow and gaining access into the
midlemeningeal artery to the ophthalmic artery, which
causes the symptoms,such as diplopia, to appear.32
Furthermore
126. Wilke41 claimed that instantaneous blindness results from
the anesthetic agent being carried into the central artery of
the retina through the anastomosis of the ophthalmic and
middle meningeal arteries via the recurrent meningeal
branch of the lacrimal artery.
127. TRISMUS
Injection into the temporalis,masseter, or medial pterygoid muscles
may damage the muscle fibers and cause limitations in opening.
Muscle damage pain when they are stretched
resulting in loss of range of motion
Bleeding in to the muscle
Haematoma
128. MANAGMENT
NSAID –first 48 hour
Passive motion applied several times per day is significantly more
effective than static stretching in reducing inflammation.
musle relaxant-diazepam,10 mg bd
stacked tongue depressors
chewing gum
antibiotics
129. NEEDLE BREAKAGE
bending of the needle, unexpected patient movement, and defective
needles.
Do not deliberately bend the needle before inserting it into the
tissue
Avoid using a short or a 30-gauge needle to administer inferior
alveolar blocks
Do not bury the needle in the tissue all the way to the hub.
130. HEMATOMA
nicking of blood vessel
blood effuses
Until extra vascular pressure exceeds intravascular pressure
Prevantion- multidirection,short needle
Management- digital prssure,cold compression,warm compression
after 24 hour
132. Allergic reaction
When exposed to an antigen, the immune system is
triggered to produce a hypersensitivity reaction or an
allergic reaction.
Ester>amide ,methylparaben
skin prick test
the interdermal or subcutaneous placements test, and/or
the drug provocative challenge test.
133. Type I or type IV hypersensitivity reactions
vasoconstrictors should be used cautiously
Sulfites
stablize the epinephrine
MANAGMENT
oral or intramuscular antihistamines
diphenhydramine, 25 to 50 ,
Hydrocortison sodium succinate 100mg
Aminophylline 0.5mg
cricothyrotomy
134. TOXICITY
Toxicity can be caused by excessive dosing of either the local
anesthetic or the vasoconstrictor.
Blood level of LA
intravascular injection, repeated injections excessive
volumes,without ephenephrin
135. Starts with an excitatory phase, which maybe be brief or may not occur
at all.
The excitatory phase, when it does occur, can manifest as tremors,
muscle twitching, shivering, and clonic tonic convulsions.
CNS CVS cardiac conduction decrease.
The cardiac manifestations include ectopic rhythms, bradycardia and
ensuing peripheral vasodilation, and significant hypotension.
136. Basic life support
Trendlenburg position
pulse<60, atropin 0.4-.6g iv
Stimulation-Diazepam 5-10mg iv
Convulsive-succinylcholine 20,40 mg
137. Methemoglobinemia
Amide LA
Ferros feric (Methemoglobinemia) oxyygen
capacity
Prilocain,benzocaine
Symptom after 3-4 hour
Methyleneblue 1 to 2 mg/kg intravenously is used for the treatment
of methemoglobinemia
138. Reversing local anesthesia
Prolonged facial and lingual anesthesia is an often unnecessary and
unwanted consequence of intra oral local anesthesia.
In May 2009, The FDA approved OraVerse (phentolamine
mesylate; Novalar Pharmaceuticals Inc, San Diego, CA,USA) for
the reversal of soft tissue anesthesia and the associated functional
deficits resulting from a local dental anesthetic.
139. Topical anaesthesia
Topical anesthetics are substances that can cause surface anesthesia
of skin or mucosa. 1 to 5 minutes of contact time is required for
topical anesthetics to reach their full effectiveness (up to 2–3 mm
from the surface)
The 20% benzocaine has virtually no systemic absorption.
Compound topical anesthetics are used to relieve pain
140. EMLA –EUTECTIC MIXTURE OF LA
As topical anesthetic in pediatric patient and
needle phobic patient
141. Composed of lidocaine 2.5% and prilocaine 2.5%Supplied as a 5g
or 30g tube or as an EMLA anesthetic disc.
should be applied 1 hr before the procedure.
Patient with congenital or idiopathic
methemoglobinemia
Infants younger than 12 month
Known sensitivity to amide type LA
142. ORAQIX(LIDOCAINE AND PRILOCANE
PERIODONTAL GEL)
Eutectic mixture of local anesthetics Solution at room
temperature; gel at body temperature
First topical anesthetic specifically designed for
scaling and root planing
143.
144. FUTURE TREND
An area of future interest is the possibility of development of newer
improved devices and techniques for achieving profound
anesthesia.
A nasal spray has shown to anesthetize maxillary anterior six teeth
is set to be tested in an FDA Phase 3 trial, which will assess the
spray’s effectiveness compared to the current “gold standard
”treatment - painful anesthesia injections.
Syringe micro vibrator (SMV), a new device being introduced in
dentistry to alleviate pain and anxiety of intraoral injections.
145. CONCLUSION
Local anesthetics have made a great advancement in dentistry and
have changed patients’ perspectives of dental procedures to a great
extent. There is still room for the improvement of painless
techniques in administrating local anesthetics. It is important for
clinicians to be familiar with all the local anesthesia devices and
techniques available for dental procedures to best exploit them.
146. References
1. Cumming s DR,et al . Complications of Local Anesthesia Used in
Oral and Maxillofacial Surgery Oral Maxillofacial Surg. Clin N
Am 23 (2011) 369–377
2.Ogle OE, Mahjoubi G. Local anesthesia: agents, techniques, and
complications. dent clin north am.2012 Jan;56(1):133-48, ix. doi:
10.1016/j.cden.2011.08.003.
3. Hand book of local anesthesia by Stanley F.Malamed
4. Hand book of exodontia and local anaesthesia in dental practice
Rishi k.bali
147. 5. Payal Saxena et al. Advances in dental local anesthesia techniques
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