Local Anesthesia - Boynton Oral and Maxillofacial Surgery and

Local Anesthesia
GARY J. WAYNE DMD
DIPLOMATE AMERICAN BOARD OF
ORAL/MAXILLOFACIAL SURGERY
BOYNTON ORAL & MAXILLOFACIAL
SURGERY AND DENTAL IMPLANT CENTER
BOYNTON BEACH, FLORIDA
Review of Neurophysiology
HOW DO LOCAL ANESTHETICS WORK?
WHAT ARE THE IMPLICATIONS IN MY
CHOICE OF ANESTHETICS?
Summary
 Local anesthetics dissociate into the ionic form in order to
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penetrate the nerve membrane. Anesthetics are available as
salts clinical use.
Pka-the ability to dissociate into the ionic form in a given
ph
The ph of a nerve is quite stable. The ph of the extracellular
fluid is variable
The ph of a local anesthetic (and the surrounding tissue
into which it is injected) greatly influences its nerve
blocking action.
Ph of normal tissue is 7.4, ph of an inflamed area is 5 to 6
Summary
 Local anesthetics containing epinephrine or other
vasoconstrictors are acidified by manufacturers to
inhibit oxidation of the vasopressor
 The acidification causes more “burning” on injection
 Ph of solutions without epinephrine are around 5.5,
with epinephrine 3.3
 Clinically this lower ph is more likely to produce a
burning sensation, as well as a slightly slower onset
of action
Summary
 Increasing the ph (alkalinization) of a local
anesthetic solution speeds the onset of its action,
increases its clinical effectiveness, and makes its
injection more comfortable
 However, the local anesthetic base, because it is
unstable, precipitates out of alkanized solutions, and
this makes these solutions ill suited for clinical use
 Adding sodium bicarb to the anesthetic solution
immediately prior to injection provides greater
comfort and a more rapid onset of anesthesia
Local Anesthetics
Amides
Esters
 Articaine
 Butacaine
 Bupivacaine
 Cocaine
 Dibucaine
 Benzocaine
 Etidocaine
 Hexylcaine
 Lidocaine
 Piperocaine
 Mepivacaine
 Tetracaine
 Prilocaine
Local Anesthetics
Esters
Others
 PABA Type
 Quinoline
Chloroprocaine
Procaine
Propoxycaine
Centbucridine
 Diphenhydramine
 Saline
Amide Local Anesthetics
 Lidocaine “Xylocaine”
 Mepivacaine “Carbocaine”
 Prilocaine “Citanest”
 Articaine “Septocaine”
 Bupivacaine “Marcaine”
Lidocaine
 Available since 1943, most common
 Available with/without vasoconstrictor
 With 1:100,000 Epi
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Max dose 7mg/kg not to exceed 500mg
Pulpal Anesthesia 60min
Soft Tissue Anesthesia 3-5hr
Pka 7.9
Onset of action 2-3 minutes
Mepivacaine 3 %
 Common for non-surgical procedures
 Used in pediatrics and geriatrics
 Onset of action 1.5-2 minutes
 Slight Vasodilation < Lidocaine
 Pulpal Anesthesia 20-40 minutes
 Soft Tissue Anesthesia 2-3 hours
 Pka 7.6
 Maximum dose 6.6mg/kg not to exceed 400mg
Mepivacaine 2% with vasoconstrictor
 1:20,000 Neo-Cobefrin/Levonordefrin
 1/5 Vasoconstrictor Activity
 Rapid onset 1.5-2 minutes
 Soft Tissue/Pulpal Anesthesia Similar to Lidocaine
with vasoconstrictor
 Maximum Dose 6.6mg/kg not to exceed 400mg
 Is available with 1:100,000 epi (documented
lidocaine allergy)
4% Prilocaine
 Vasodilation >Mepivacaine,<Lidocaine
 Pka 7.9
 Onset 2-4 minutes
 Duration Pulpal 10min infiltration, 60 min block
 Maximum Dose 6mg/kg not to exceed 400mg
4% Prilocaine with 1:200,000 epi
 Rapid Biotransformation
Safest of all amides
Good for “epi sensitive” patients requiring prolonged
pulpal anesthesia >60min
 Duration of action pulpal 60-90min, soft tissue 38hrs
 Maximum Dose 6mg/kg not to exceed 400mg
4% Articaine with 1:100,000 epi
 Newest “wonder anesthetic” in U.S.
 Pka 7.8
 Onset of action 2-2.5 minutes block,1-2 minutes
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infiltration
Claim is that can diffuse more readily, controlled
comparisons failed to corroborate
Duration of action pulp 60-70 min, soft tissue 3-6hrs
Maximum dose 7mg/kg not to exceed 500mg
Available 1:200,000 epi
.5% Bupivacaine
 1:200,000 epi
 Good for lengthy procedures as an adjunct/post
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operative analgesia
“Weak” anesthetic
Pka 8.1
Onset of action 6-10 minutes
Maximum dose 1.3mg/kg not to exceed 90mg
Duration pulpal 90-180 min, soft tissue 4-9hrs (12hr
reported)
Esters
 Can Use with documented allergy to Amides
 Procaine+Propoxycaine
 “2 %” Procaine
Provides 30-60 min of pulpal
2-3 hours of soft tissue
each cartridge 7.2 mg of Propoxycaine
36mg of Procaine
 Maximum dose 6.6mg/kg
Vasoconstrictors
 Epinephrine
 Neo Cobefrin
 Levonordefrin
 Levophed
When to use/not use
Discussion:
 Cardiovascular disease
 “allergy”
 Pediatrics
 Elderly
 Post operative analgesia
 Hemostasis
Vasoconstrictors
“Vasoconstrictors should be included in local
anesthetic solutions unless specifically
contraindicated by the medical status of the patient
or by the duration of the planned treatment”
S.Malamed
Local Complications
 Needle Breakage
 Pain on Injection
 Burning on Injection
 Persistent Anesthesia or Paresthesia
 Trismus
 Hematoma
 Infection
 Edema
 Sloughing of Tissues
 Soft Tissue Injury
 Facial Nerve Paralysis
 Post Anesthetic Intraoral Lesions
Systemic Complications
 Overdose
Overdose
 Patient Factors
Age
Weight
Other Drugs
Sex (pregnancy)
Presence of Disease
Genetics
Mental Attitude and enviroment
Overdose
 Drug Factors
Vasoactivity
Concentration
Dose
Route of Administration
Rate of Injection
Vascularity of the Injection Site
Presence of Vasoconstrictors
Overdose
“Many local anesthetic overdose reactions occur as a
result of the combination of inadvertant
intravascular injection and too rapid rate of
injection, both of which are virtually 100%
preventable”
S. Malamed
Minima/Moderate Overdose Levels
 Signs
Talkativeness
Excitability
Generalized Stutter
Dysarthria
Sweating
Failure to follow commands
Loss of response to pain
^Heart Rate
Apprehension
Slurred Speech
Euphoria
Nystagmus
Vomiting
Disorientation
^Blood Pressure
^Respiratory Rate
Minimal/Moderate Overdose Levels
 Symptoms (progressive with increasing blood levels)
Light-Headedness and dizziness
Nervousness
Sensation of twitching, before observed
Visual Disturbances
Drowsiness and disorientation
Restlessness
Numbness
Metallic Taste
Auditory Disturbances
Loss of consciousness
Moderate/High Overdose Levels
 Tonic-Clonic seizure activity followed by
 Generalized CNS Depression
 Depressed blood pressure, heart rate, and
respiratory rate
Management of Mild Overdosage>5min
 Reassure patient
 O2 via nasal cannula or hood
 Monitor and record vital signs
 IV if able
 Self Limiting, discharge when recovered
Mild Overdose-Slower Onset>15min
 Biotransformation trouble
All of the previous methods plus
 Anticonvulsant
 Summon medical assistance
 Patient to be examined by physician or hospital
Severe Overdose
 BLS
 Anticonvulsant
 Terminate treatment
 Summon Help
Epinephrine Overdose
 More common in gingival retraction cord
 Symptoms
Fear,Anxiety
Tenseness
Restessness
Throbbing Headache
Tremor
Perspiration
Respiratory difficulty
Palpitations
Pallor
Dizziness
Weakness
Epinephrine Overdose
 Signs of epinephrine overdose
Sharp elevation in blood pressure, systolic
Elevated heart rate
Possible cardiac dysrhythmias (PVC,Vtach,Vfib)
Management of Epinephrine Overdose
 Terminate procedure
 Position patient –Semisitting or erect
Minimized CNS Effect
 Monitor Blood Pressure
 Administer O2 (except hyperventilation)
 Recover-Most are self limiting
Allergic Reactions
 Rare with amides
 Seen with topical anesthetics-esters
 Sodium metabisulfites-only with vasoconstrictors
 Treatment
BLS
Oral Histamine Blocker
Sub Q epi
IM Histamine Blocker
Bronchial Treatment
Laryngeal Treatment
Maxillary Anesthesia
 Field Block
 Infiltration
 Nerve Block
 Intraseptal
 Intraosseous
 Periodontal Ligament
Infiltration
Area of treatment is flooded with local anesthesia
Periodontal treatment
Selective restorative procedures
Field Block
 Anterior Superior
 Middle Superior
 Posterior Superior
Nerve Blocks
 Maxillary (Second Division)
Junction of Vertical/Horizontal Shelves
Second Molar
Long Needle
2cc of solution
 Greater Palatine
 Nasopalatine
 Infra-orbital
Infraorbital
Problems with Maxillary Anesthesia
 Few
 Related to inflammation/infection
 Posterior teeth
 Use Nerve Blocks
Infraorbital-Extra/Intra Oral
Nasopalatine
Secondary Division
Mandibular Anesthesia
Mandibular Anesthesia
Inferior Alveolar Block
 80-85% Successful
 Related to Greater Density of Bone
Limited Accessibility
Wide Variation of Anatomy
Solution Depot within 1mm
 Most Important Block
 Variations
 Accessory Innervation
Inferior Alveolar Block
 Deepest Part of Ascending Ramus
 Parallel to Occlusal Plane
 Lateral To Raphe
 Hit bone
 Pull Back?
 Bevel aimed away, assist in needle deflection and
direction of liquid
Accessory Innervation
 Determine Objective Anesthesia of IAN
 Mylohyoid
 Accessory Foramina
 Cervical Branches
Mental Nerve Block
 Does not anesthetize incisive branch
 Angle needle anterior
 Second Premolar
 High risk of nerve injury
Buccal Nerve Block
 Bevel Toward Bone
 Distal and buccal to most distal molar
Gow-Gates
 Anesthetizes all branches
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IAN,lingual,mylohyoid,mental, incisive
auriculotemporal and buccal
High Success >95%
Low Aspiration
Parallel tragus to anterior border of ramus
Mesiolingual cusp of maxillary second molar
Hit neck of condyle and back off 1mm
Stay open 1-2 minutes-bite block
Gow-Gates Target
Vazirani-Akinosi Closed Mouth Block
 IAN, Incisive, Mental, Lingual and Mylohyoid
 Mucogingival of Maxillary Third or Second Molar
 Parallel Maxillary Occlusal Plane
 Medial of Anterior Ramus
 Approximate 25mm (midway)
Supplemental Aids
 Ligamentary Injections
 Intraosseous Injections
 Intrapulpal
 Electronic
 Hypnosis
 Nitrous Oxide
 IV/General Anesthesia
Always reduces local anesthesia
 “Gizmos”