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Local Anesthesia in Dentistry

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Mechanism and various contents of local anesthesia are covered here

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Local Anesthesia in Dentistry

  2. 2. CONTENTS  Introduction  Historical background  Definition  Methods of inducing local anesthesia  Desirable properties  Electrophysiology of nerve conduction  Impulse propagation and spread  Theories of mechanism of action of local anesthesia  Dissociation of local anesthesia 2
  3. 3. 3 Mode and site of action of local anesthesia Classification of local anesthetic according to biological site and mode of action Mechanism of action of local anesthesia Local anesthetics description Armamentarium Injection techniques Local & Systemic complications  Special care groups Recent advancements Conclusion References
  4. 4. Historical background • COCAINE -first local anesthetic agent-isolated by Nieman -1860 -from the leaves of the coca tree. • Its anesthetic action was demonstrated by Karl Koller in 1884. • First effective and widely used synthetic local anesthetic -PROCAINE -produced by Einhorn in 1905 from benzoic acid and diethyl amino ethanol. 4
  5. 5. 5 •It anesthetic properties were identified by Biberfield and the agent was introduced into clinical practice by Braun. •LIDOCAINE- Lofgren in 1948. •The discovery of its anesthetic properties was followed in 1949 by its clinical use by T. Gordh
  6. 6. 6 DEFINITION: Local anesthesia is defined as a loss of sensation in a circumscribed area of the body caused by depression of excitation in nerve endings or an inhibition of the conduction process in peripheral nerves. An important feature of local anesthesia is that it produces: LOSS OF SENSATION WITHOUT INDUCING LOSS OF CONSCIOUSNESS..
  7. 7. 7 METHODS OF INDUCING LOCAL ANESTHESIA:  Low temperature  Mechanical trauma  Anoxia  Neurolytic agents such as alcohol & phenol  Chemical agents such as local anesthetics
  8. 8. PROPERTIES OF LOCAL ANESTHESIA I==It should not be irritating to tissue to which it is applied N==It should not cause any permanent alteration of nerve structure S==Its systemic toxicity should be low T==Time of onset of anesthesia should be short E== It should be effective regardless of whether it is injected into the tissue or applied locally to mucous membranes D==The duration of action should be long enough to permit the completion of procedure 8
  9. 9. 9  It should have the potency sufficient to give complete anesthesia with out the use of harmful concentration solutions  It should be free from producing allergic reactions  It should be free in solution and relatively undergo biotransformation in the body  It should be either sterile or be capable of being sterilized by heat with out deterioration.
  10. 10. ELETROPHYSIOLOGY OF NERVE CONDUCTION • There is an electrical charge across the membrane. • This is the membrane potential. • The resting potential (when the cell is not firing) is a negative electrical potential of -70mv that exists across the nerve membrane, produced by different concentrations of either side of the membrane. • The interior of nerve is NEGATIVE in relation to exterior. 10
  11. 11. outside inside 11 + - + - + - + - + - Resting potential of neuron = -70mV
  12. 12. Action Potentials • At rest: Na+& K+ channels closed. -70mV • Fibre stimulated: Na+channel opens, Na+ enters cell. Potential rising • Cell depolarised, Na+ channel closes. +20mV • K+ channel opens, K+ exits cell, potential falling • Fibre repolarised, Na+& K+ channels closed. Na/K pump restores balance. -70mV • Result is a voltage gradient along axon, causing a current. This causes configurational change in Na-channels in the next segmentconduction 12
  13. 13. 13
  14. 14. SLOW DEPOLARIRIZATION RAPID DEPOLARIZATION: The interior of nerve is POSITIVE in relation to exterior. 14
  15. 15. REPOLARIZATION: . SODIUM PUMP energy comes from the oxidative metabolism of ATP • Depolarization takes 0.3 msec • Repolarization takes 0.7 msec • The entire process require 1 msec 15
  16. 16. IMPULSE PROPOGATION DEPOLARIZED SEGMENT ADJACENT RESTING AREA IMPULSE SPREAD The propagated impulse travels along the nerve membrane towards CNS. The spread of impulse differs in myelinated and unmyelinated nerve fibers. UNMYELINATED NERVES: The high resistance cell membrane and extra cellular media produce a rapid decrease in density of current with in a short distance of depolarized segment. The spread of the impulse is characterized as a slow forward-creeping process. Conduction rate is 1.2m/sec
  17. 17. MYLINATED NERVES: Impulse conduction in myelinated nerves occurs by means of current leaps from nodes to node this process is called as SALTATORY CONDUCTION. It is more rapid in thicker nerves because of increase in thickness of myelin sheath and increase in distance between adjacent nodes of ranvier. If conduction of impulse is blocked at one node the local current will skip over that node and prove adequate to raise that membrane potential at next node to its firing potential and produce depolarization. Conduction rate of myelinated fibers is 120m/sec. 17
  18. 18. 18
  19. 19. MODE AND SITE OF ACTION OF LOCAL ANESTHETICS Local anesthetic agent interferes with excitation process in a nerve membrane in one of the following ways:  Altering the basic resting potential of nerve membrane  Altering the threshold potential  Decreasing the rate of depolarization  Prolonging the rate of repolarization 19
  20. 20. THEORIES MECHANISM OF ACTION OF LOCAL ANESTHETICS Many theories have been promulgated over the years to explain the mechanism of action of local anesthetics. ACETYLECHOLINE THEORY: Stated that acetylcholine was involved in nerve conduction in addition to its role as a neurotransmitter at nerve synapses. There is no evidence that acetylcholine is involved in neural transmission. 20
  21. 21. CALCIUM DISPLACEMENT THEORY: States that local anesthetic nerve block was produced by displacement of calcium from some membrane site that controlled permeability of sodium. 21
  22. 22. SURFACE CHARGE (REPULSION) THEORY: Proposed that local anesthetic acted by binding to nerve membrane and changing the electrical potential at the membrane surface. Cationic drug molecule were aligned at the membrane water interface, and since some of the local anesthetic molecule carried a net positive charge, they made the electrical potential at the membrane surface more positive, thus decreasing the excitability of nerve by increasing the threshold potential. Current evidence indicate that resting potential of nerve membrane is unaltered by local anesthetic. 22
  23. 23. MEMBRANE EXPANSION THEORY • It states that local anesthetic molecule diffuse to hydrophobic regions of excitable membranes, producing a general disturbance of bulk membrane structure, expanding membrane, and thus preventing an increase in permeability to sodium ions. Lipid soluble LA can easily penetrate the lipid portion of cell membrane changing the configuration of lipoprotein matrix of nerve membrane. This results in decreased diameter of sodium channel, which leads to inhibition of sodium conduction and neural excitation. 23
  25. 25. SPECIFIC RECEPTOR THEORY: The most favored today, proposed that local anesthetics act by binding to specific receptors on sodium channel the action of the drug is direct, not mediated by some change in general properties of cell membrane. Biochemical and electrophysiological studies have indicated that specific receptor sites for local anesthetic agents exists in sodium channel either on its external surface or on internal axoplasmic surface. Once the LA has gained access to receptors, permeability to sodium ion is decreased or eliminated and nerve conduction is interrupted. 25
  26. 26. CLASSIFICATION OF LOCAL ANESTHETIC SUBSTANCES ACCORDING TO BIOLOGICAL SITE AND MODE OF ACTION CLASS A: Agents acting at receptor site on external surface of nerve membrane Chemical substance: Biotoxins (e.g., tetrodotoxin and saxitoxin) CLASS B: Agents acting on receptor sites on internal surface of nerve membrane Chemical substance: Quaternary ammonium analogues of lidocaine, scorpion venom 26
  27. 27. CLASS C: Agents acting by receptor independent of physiochemical mechanism Chemical substance: Benzocaine CLASS D: Agents acting by combination of receptors and receptor independent mechanisms Chemical substance: most clinically useful anesthetic agents (e.g., lidocaine, mepivacaine, prilocaine) 27
  30. 30. DISSOCIATION OF LOCAL ANESTHETICS • Local anesthetics are available as salts (usually hydrochlorides) for clinical use. • The salts, both water soluble and stable, is dissolved in either sterile water or saline. • In this solution it exists simultaneously as unchanged molecule (RN), also called base and positively charged molecules (RNH+) called cations. RNH+ ==== RN+ H+ 30
  31. 31. • The relative concentration of each ionic form in the solution varies in the pH of the solution or surrounding tissue. • In the presence of high concentration of hydrogen ion (low pH) the equilibrium shifts to left and most of the anesthetic solution exists in cationic form. RNH+ > RN+ + H+ • As hydrogen ion concentration decreases (higher pH) the equilibrium shifts towards the free base form. RNH+ < RN + H+ 31
  32. 32. • The relative proportion of ionic form also depends on pKa or DISSOCIATION CONSTANT, of the specific local anesthetic. • The pKa is a measure of molecules affinity for H+ ions. • When the pH of the solution has the same value as pKa of the local anesthetic, exactly half the drug will exists in the RNH+ form and exactly half in RN form. • The percentage of drug existing in either form can be determined by Henderson Hasselbalch equation Log base/acid = pH - pKa 32
  33. 33. • Henderson hasselbach equation Determines how much of a local anesthetic will be in a non-ionized vs ionized form . Based on tissue pH and anesthetic Pka . • Injectable local anesthetics are weak bases (pka=7.5-9.5) When a local anesthetic is injected into tissue it is neutralized and part of the ionized form is converted to non-ionized The non-ionized base is what diffuses into the nerve. 33
  34. 34. • Hence if the tissue is infected, the pH is lower (more acidic) and according to the HH equation; there will be less of the non-ionized form of the drug to cross into the nerve (rendering the LA less effective) • Once some of the drug does cross; the pH in the nerve will be normal and therefore the LA re-equilibrates to both the ionized and nonionized forms; but there are fewer cations which may cause incomplete anesthesia. 34
  35. 35. MECHANISM OF ACTION OF LOCAL ANESTHETICS The following sequence is proposed mechanism of action of LA:  Displacement of calcium ions from the sodium channel receptor site  Binding of local anesthetic molecule to this receptor site  Blockade of sodium channel 35
  36. 36.  Decrease in sodium conductance  Depression of rate of electrical depolarization  Failure to achieve the threshold potential level  Lack of development of propagated action potential  Conduction blockade… 36
  37. 37. 37 Na + Na +
  39. 39. 39 COMERCIALLY PREPARED LOCAL ANESTHESIA CONSISTS OF: Local anesthetic agent (xylocaine, lignocaine 2%) Vasoconstrictor (adrenaline 1: 80,000) Reducing agent (sodium metabisulphite) Preservative (methylparaben,capryl hydrocuprienotoxin) Fungicide (thymol) Vehicle (distillde water,NaCl)
  40. 40. 40
  41. 41. REDUCING AGENT • Vasoconstrictors are unstable in solution and may oxidize especially on prolong exposure to sunlight this results in turning of the solution brown and this discoloration is an indication that such a solution must be discarded. • To overcome this problem a small quantity of sodium metabisulphite is added - competes for the available oxygen. • SHELF LIFE INCRESES 41
  42. 42. PRESERVATIVE • Modern local anesthetic solution are very stable and often have a shelf of two years or more. Their sterility is maintained by the inclusion of small amount of a preservative such as capryl hydrocuprienotoxin. • Some preservative such as methylparaben have been shown to allergic reaction in sensitized subjects. 42
  43. 43. FUNGICIDE • In the past some solutions tended to become cloudy due to the proliferation of minute fungi. • In several modern solutions a small quantity of thymol is added to serve as fungicide and prevent this occurrence. 43
  44. 44. VEHICLE • The anesthetic agent and the additives referred to above are dissolved in distilled water & sodium chloride. • This isotonic solution minimizes discomfort during injection. 44
  45. 45. 45 . The chemical characteristics are so balanced that they have both lipophilic and hydrophilic properties. If hydrophilic group predominates, the ability to diffuse into lipid rich nerves is diminished. If the molecule is too lipophilic it is of little clinical value as an injectable anesthetic, since it is insoluble in water and unable to diffuse through interstitial tissue.
  46. 46. LOCAL ANESTHETIC AGENT The local anesthetics used in dentistry are divided into two groups:  ESTER GROUP  AMIDE GROUP 46
  47. 47. 47 ESTER GROUP: It is composed of the following An aromatic lipophilic group An intermediate chain containing an ester linkage A hydrophilic secondary or tertiary amino group AMIDE GROUP: It is composed of the following An aromatic, lipophilic group An intermediate chain containing amide linkage A hydrophilic secondary or tertiary amino group
  48. 48. 48 CLASSIFICATION OF LOCAL ANESTHETICS ESTERS Esters of benzoic acid Butacaine Cocaine Benzocaine Hexylcaine Piperocaine Tetracaine Esters of Para-amino benzoic acid Chloroprocain Procaine Propoxycaine
  49. 49. 49 AMIDES Articaine Bupivacaine Dibucaine Etidocaine Lidocaine Mepivacaine Prilocaine Ropivacaine QUINOLINE Centbucridine ABCDE LMPR
  50. 50. PHARMACOKINETICS OF LOCAL ANESTHETICS UPTAKE: When injected into soft tissue most local anesthetics produce dilation of vascular bed.  Cocaine is the only local anesthetic that produces vasoconstriction, initially it produces vasodilation which is followed by prolonged vasoconstriction.  Vasodilation is due to increase in the rate of absorption of the local anesthetic into the blood, thus decreasing the duration of pain control while increasing the anesthetic blood level and potential for over dose. 50
  51. 51. ORAL ROUTE: Except cocaine, local anesthetics are poorly absorbed from GIT Most local anesthetics undergo hepatic first-pass effect following oral administration. 72% of dose is biotransformed into inactive metabolites TOCAINIDE HYDROCHLORIDE an analogue of lidocaine is effective orally 51
  52. 52. TOPICAL ROUTE: Local anesthetics are absorbed at different rates after application to mucous membranes, in the tracheal mucosa uptake is as rapid as with intravenous administration. In pharyngeal mucosa uptake is slow In bladder mucosa uptake is even slower Eutectic mixture of local anesthesia (EMLA) has been developed to provide surface anesthesia for intact skin. 52
  53. 53. INJECTION: The rate of uptake of local anesthetics after injection is related to both the vascularity of the injection site and the vasoactivity of the drug. IV administration of local anesthetics provide the most rapid elevation of blood levels and is used for primary treatment of ventricular dysrhythmias. RATES AT WHICH LOCAL ANESTHETICS ARE ABSORBED AND REACH THEIR PEAK BLOOD LEVEL ROUTE TIME TO PEAK LEVEL (MIN) INTRAVENOUS 1 TOPICAL 5 INTRAMUSCULA R 5-10 SUBCUTANEOUS 30 - 90 53
  54. 54. DISTRIBUTION  Once absorbed in the blood stream local anesthetics are distributed through out the body to all tissues.  Highly perfused organs such as brain, head, liver, kidney, lungs have higher blood levels of anesthetic than do less higher perfused organs. 54
  55. 55. The blood level is influenced by the following factors: Rate of absorption into the blood stream. Rate of distribution of the agent from the vascular compartment to the tissues. Elimination of drug through metabolic and/or excretory pathways. All local anesthetic agents readily cross the blood-brain barrier, they also readily cross the placenta. 55
  56. 56. METABOLISM (BIOTRANSFORMATION) ESTER LOCAL ANESTHETICS: • Ester local anesthetics are hydrolyzed in the plasma by the enzyme pseudocholinesterase. • Chloroprocaine the most rapidly hydrolyzed, is the least toxic. • Tertracaine hydrolyzed 16 times more slowly than Chloroprocaine ,hence it has the greatest potential toxicity. 56
  57. 57. AMIDE LOCAL ANESTHETICS The metabolism of amide local anesthetics is more complicated then esters. The primary site of biotransformation of amide drugs is liver. Entire metabolic process occurs in the liver for lidocaine, articaine, etidocaine, and bupivacaine. Prilocaine undergoes more rapid biotransformation then the other amides. 57
  58. 58. EXCREATION Kidneys are the primary excretory organs for both the local anesthetic and its metabolites A percentage of given dose of local anesthetic drug is excreted unchanged in the urine. Esters appear in only very small concentration as the parent compound in urine. Procaine appears in the urine as PABA (90%) and 2% unchanged. 10% of cocaine dose is found in the urine unchanged. Amides are present in the urine as a parent compound in a greater percentage then are esters. 58
  59. 59. MRD 59
  60. 60. VASOCONSTRICTORS • Constrict vessels and decrease blood flow to the site of injection. • Absorption of LA into bloodstream is slowed, producing lower levels in the blood. • Lower blood levels lead to decreased risk of overdose (toxic) reaction. • Higher LA concentration remains around the nerve increasing the LA's duration of action. 60
  61. 61. • Minimize bleeding at the site of administration. • Naturally Occurring Vasoconstrictors: - Epinephrine - Norepinephrine • Vasoconstrictors should be included unless contraindicated. • Mode of Action - Attach to and directly stimulate adrenergic receptors . Act indirectly by provoking the release of endogenous catecholamine from intraneuronal storage sites. 61
  62. 62. • Concentrations of Vasoconstrictor in Local Anesthetics - 1:50,000 ,1:100,000, 1:200,000 - 0.020mg/ml ,0.010mg/ml, 0.005 mg/ml • Calculation 1:50,000= 1gram/50,000ml= 1000mg/50,000ml= 1mg/50ml= 0.02mg/ml • Levonordefrin - One fifth as active as epinephrine • Vasoconstrictors - Unstable in Solution Sodium metabisulfite added Known allergen 62
  63. 63. • Max dose of vasoconstrictors - Healthy patient approximately 0.2mg - Patient with significant cardiovascular history: 0.04mg • Max Dose for Vasoconstrictors (CV patient) 1 carpule = 1.8cc 1:100,000=.01mg/cc 0.01 X 1.8cc= 0.018mg 0.04/0.018=2.22 carpules • In a healthy adult patient 0.2/0.018=11.1 carpules 63
  64. 64. Local Anesthesia Armanterium 1.) The Syringe 2.) The Needle 3.) The Cartridge 4.) Other Armamentarium - Topical Anesthetic (strongly recommended) -ointments, gels, pastes, sprays - Applicator sticks - Cotton gauze 64
  65. 65. TYPES OF SYRINGES 65
  66. 66. Plastic disposable syringe 66
  67. 67. Syringe Components 1.) Needle adapter 2.) Piston with harpoon 3.) Syringe barrel 4.) Finger grip 5.) Thumb ring 67
  68. 68. • American Dental Association (ADA) criteria for acceptance of LA syringes: 1-Durable and re-sterilzable or packaged in a sterile container (if disposable). 2-Accept a wide variety of cartridges and needles of different manufactures (universal use) 3-Inexpensive, light weight, and simple to use with one hand. 4-Provide effective aspiration and the blood be easily observed in the cartridge. The incidence of positive aspiration may be as high as 10%-15% in some injection techniques. 68
  69. 69. Needle • The Needle Gauge: the larger the gauge the smaller the internal diameter of the needle Usual dental needle gauges are 25,27, & 30 Length: 1-Long(approximately 40 mm "32-40 mm"), for NB. 2-Short(20-25 mm). 3-Extra-short(approximately 15 mm), for PDL. 69
  70. 70. Components of needle 70
  71. 71. Cartridge • The Cartridge Components: - Cylinder, plunger, diaphragm - Types: Standard – Self aspirating, plastic, Glass - Contents: LA, VC, Vehicle, preservative. - Volume: 1.8, 2.00 & 2.2 ML. 71
  72. 72. • The Cartridge: - Should not be autoclaved Stored at room temperature (21°C to 22°C (70°F to 72°F) - Should not soak in alcohol - Should not be exposed to direct sunlight 72
  73. 73. INJECTION TECHNIQUES • MAXILLARY : 1) Supraperiosteal 2) PDL 3) Intraseptal Injection 4) Intracrestal Injection 5) Intraosseous Injection 6) PSA Nerve Block 7) MSA Nerve Block 8) ASA Nerve Block 9) Maxillary Nerve Block 10) Greater Palatine Nerve Block 11) Nasopalatine Nerve Block 12) AMSA Nerve Block 13) P-ASA Nerve Block 73
  74. 74. Supraperiosteal injection 74
  75. 75. Posterior superior alveolar nerve block 75
  76. 76. Anterior superior alveolar nerve block 76
  77. 77. Palatal Anasthesia • Greater palatine nerve block • Nasopalatine nerve block 77
  78. 78. • MANDIBULAR INJECTION TECHNIQUES: 1) IANB Nerve block 2) Buccal Nerve Block 3) Mandibular nerve block techniques: - Gow Gates technique - Vazirani Akinosi closed mouth mandibular block 4) Mental Nerve block 5) Incisive nerve block 78
  79. 79. Inferior alveolar nerve block 79
  80. 80. Buccal nerve block 80
  81. 81. Gow gates technique 81
  82. 82. Vazirani-Akinosi technique 82
  83. 83. Mental nerve block 83 INCISIVE NERVE BLOCK
  84. 84. 84
  85. 85. Local Complications 1) Needle breakage : Prevention • Do not use short needles for inferior alveolar nerve block in adults or larger children. • Do not use 30-gauge needles for inferior alveolar nerve block in adults or children. • Do not bend needles when inserting them into soft tissue. • Do not insert a needle into soft tissue to its hub, unless it is absolutely essential for the success of the injection. • Observe extra caution when inserting needles in younger children or in extremely phobic adult or child patients. 85
  86. 86. 2) Prolonged Anesthesia or Paresthesia • Strict adherence to injection protocol • Most paresthesias resolve within approximately 8 weeks to 2 months without treatment. • Determine the degree and extent of paresthesia. • Explain to the patient that paresthesia • Record all findings • Second opinion • Examination every 2 months • It would be prudent to contact your liability insurance carrier should the paresthesia persist without evident improvement beyond 1 to 2 months. 86
  87. 87. 3) Facial Nerve palsy • Reassure the patient • Contact lenses should be removed until muscular movement returns. • An eye patch should be applied to the affected eye until muscle tone returns • Record the incident on the patient's chart. • Although no contraindication is known to reanesthetizing the patient to achieve mandibular anesthesia, it may be prudent to forego further dental care at this appointment. 87
  88. 88. 4) Trismus • Prescribe heat therapy, warm saline rinses, analgesics (Aspirin 325 mg) • If necessary, muscle relaxants to manage the initial phase of muscle spasm - Diazepam (approximately 10 mg bid) • Initiate physiotherapy • Antibiotics should be added to the treatment regimen described and continued for 7 full days • Patients report improvement within 48 to 72 hours 88
  89. 89. 5) Soft tissues injury • Analgesics, antibiotics, lukewarn saline rinse, petroleum jelly • Cotton roll placed between lips and teeth, secured with dental floss, minimizes risk of accidental mechanical trauma to anesthetized tissues. 89
  90. 90. 6) Hematoma : • Hematoma is not always preventable. Whenever a needle is inserted into tissue, the risk of inadvertent puncturing of a blood vessel is present. • When swelling becomes evident during or immediately after a local anesthetic injection, direct pressure should be applied to the site of bleeding. • For most injections, the blood vessel is located between the surface of the mucous membrane and the bone; localized pressure should be applied for not less than 2 minutes. This effectively stops the bleeding. • Ice may be applied to the region immediately on recognition of a developing hematoma. 90
  91. 91. 7) Pain on injection • Adhere to proper techniques of injection, both anatomic and psychological. • Use sharp needles. • Use topical anesthetic properly before injection. • Use sterile local anesthetic solutions. • Inject local anesthetics slowly. • Make certain that the temperature of the solution is correct • Buffered local anesthetics, at a pH of approximately 7.4, have been demonstrated to be more comfortable on administration 91
  92. 92. 8) Burning on Injection • By buffering the local anesthetic solution to a pH of approximately 7.4 immediately before injection, it is possible to eliminate the burning sensation that some patients experience during injection of a local anesthetic solution containing a vasopressor. • Slowing the speed of injection also helps 92
  93. 93. 9) Infection : • Use sterile disposable needles. • Properly care for and handle needles. • Properly prepare the tissues before penetration. • Prescribe 29 (or 41, if 10 days) tablets of penicillin V (250-mg tablets). • Erythromycin may be substituted if the patient is allergic to penicillin. 93
  94. 94. 10) Edema If edema occurs in any area where it compromises breathing, treatment consists of the following: • P (position): if unconscious, the patient is placed supine. • A-B-C (airway, breathing, circulation): basic life support is administered, as needed. • D (definitive treatment): emergency medical services (e.g., 9-1-1) is summoned. • Epinephrine is administered: 0.3 mg (0.3 mL of a 1:1000 epinephrine solution) (adult), 0.15 mg (0.15 mL of a 1:1000 epinephrine solution) (child [15 to 30 kg]), intramuscularly (IM) or 3 mL of a 1:10,000 epinephrine solution intravenously (IV-adult), every 5 minutes until respiratory distress resolves. • Histamine blocker is administered IM or IV. • Corticosteroid is administered IM or IV. • Preparation is made for cricothyrotomy if total airway obstruction appears to be developing. This is • extremely rare but is the reason for summoning emergency medical services early. • The patient's condition is thoroughly evaluated before his or her next appointment to determine the cause of the reaction. 94
  95. 95. 10) Sloughing of tissue • Usually, no formal management is necessary for epithelial desquamation or sterile abscess. Be certain to reassure the patient of this fact. • For pain, analgesics such as aspirin or other NSAIDs and a topically applied ointment (Orabase) • The course of a sterile abscess may run 7 to 10 days 95
  96. 96. 11) Postanesthetic Intra-oral lesion: • Primary management is symptomatic • No management is necessary if the pain is not severe • Topical anesthetic solutions (e.g., viscous lidocaine) • A mixture of equal amounts of diphenhydramine (Benadryl) and milk of magnesia rinsed in the mouth effectively coats the ulcerations and provides relief from pain. • Orabase, a protective paste, without Kenalog can provide a degree of pain relief. • A tannic acid preparation (Zilactin) can be applied topically to the lesions extraorally or intraorally (dry the tissues first). 96
  97. 97. Systemic complications  Adverse drug reaction • Toxicity Caused by Direct Extension of the Usual Pharmacologic Effects of the Drug: 1) Side effects 2) Overdose reactions 3) Local toxic effects • Toxicity Caused by Alteration in the Recipient of the Drug: 1) A disease process (hepatic dysfunction, heart failure, renal dysfunction) 2) Emotional disturbances 3) Genetic aberrations (atypical plasma cholinesterase, malignant hyperthermia) 4) Idiosyncrasy • Toxicity Caused by Allergic Responses to the Drug 97
  98. 98. CLINICAL MANIFESTATION OF LOCAL ANESTHETIC OVERDOSE SIGNS: LOW TO MODERATE OVERDOSE LEVELS:  Confusion  Talkativeness  Apprehension  Excitedness  Slurred speech  Generalized stutter  Muscular twitching, tremor of face and extremities  Elevated BP, heart rate and respiratory rate 98
  99. 99. MODERATE TO HIGH BLOOD LEVELS:  Generalized tonic clonic seizure, followed by  Generalized CNS depression  Depressed BP, heart rate and respiratory rate SYMPTOMS:  Headache  Light headedness  Auditory distrurbances  Dizziness  Blurred vision  Numbness of tongue and perioral tissues  Loss of consciousness 99
  100. 100. Management of systemic complications 1) Basic emergency management : A-B-C-D approach 2) Allergy : Medical history questionnaire is important. 3) Elective dental care 4) Emergency dental care: - Protocol no.1 : no treatment of an invasive nature - Protocol no.2 : use general anesthesia - Protocol no.3: Histamine blockers - Protocol no.4 : Electronic dental anesthesia/hypnosis 100
  101. 101. LA Management For Special Patients • Uncooperative child The maximum safe dose of lidocaine for a child is 4.5 mg/kg per dental appointment. Local infiltration of anesthesia is sufficient for all dental treatment procedures in 90% of cases even in the mandible. 101
  102. 102. • Handicapped Patient • retarded patients choose a shorter needle and/or a larger gauge needle which is less likely to be bent or broken. better to use general anesthesia 102
  103. 103. • Patients receiving anticoagulation or suffering from bleeding disorders  Oral procedures must be done at the beginning of the day & must be performed early in the week, allowing delayed re-bleeding episodes, usually occurring after 24-48 h, to be dealt with during the working weekdays.  Local anesthetic containing a vasoconstrictor should be administered by infiltration or by intraligamentary injection wherever practical. X Regional nerve blocks should be avoided when possible.  Local vasoconstriction may be encouraged by infiltrating a small amount of local anesthetic containing adrenaline (epinephrine) close to the site of surgery. 103
  104. 104. PREGNANCY 104 • Lidocaine + vasoconstrictor: most common local anesthetic used in dentistry extensively used in pregnancy with no proven ill effects, Esters are better to be used. • Accidental intravascular injections of lidocaine pass through the placenta but the concentrations are too low to harm fetus.
  105. 105. GERIATRIC PATIENT – When choosing an anesthetic, we are largely concerned with the effect of the anesthetic agent upon the patient's cardiovascular and respiratory systems. – increased tissue sensitivity to drugs acting on the CNS – Decreased hepatic size and blood flow may reduce hepatic metabolism of drugs – hypertension is common and can reduce renal function – Same prevention procedures used with children 105
  106. 106. LIVER DISORDERS – Advanced liver diseases include:  Liver cirrhosis - Jaundice - Potential complications: 1 . Impaired drug detoxication e.g. sedative, analgesics, general anesthesia. 2. Bleeding disorders ( decrease clotting factors, excess fibrinolysis, impaired vitamin K absorption). 3. Transmission of viral hepatitis. Management – Avoid LA metabolized in liver: Amides (Lidocaine, Mepicaine), esters should be used 106
  109. 109. Recent developments in local anesthesia and oral sedation. 2003 Journal of anesthesia • Yagiela JA. Abstract • This article reviews 3 recent developments in anxiety and pain control with significant potential for altering dental practice. First is the introduction of articaine hydrochloride as an injectable local anesthetic. Although articaine is an amide, its unique structure allows the drug to be quickly metabolized, reducing toxicity associated with repeated injections over time. The second development is the formulation of a lidocaine and prilocaine dental gel for topical anesthesia of the periodontal pocket. This product may significantly reduce the need for anesthetic injections during scaling and root planing. Finally, the use of triazolam as an oral sedative/anxiolytic is reviewed. The recent administration of triazolam in multiple doses has extended the availability of anxiety control to many dental patients, but unknowns about the safety of the technique as practiced by some dentists remains a concern. 109
  110. 110. Eutectic mixture of local anesthesia (EMLA) 110 surface anesthesia for intact skin.
  111. 111. • DentiPatch (lidocaine transoral delivery system) Preinjection – 10- 15 minutes exposure prior to injection - Root scaling/planing – apply 5-10 minutes prior to beginning procedure. 111
  112. 112. • PRESSURE SYRINGE : Used in IL injection techniques, especially in mandibular teeth (types: pistol-grip, pen-grip). 112
  113. 113. 113
  114. 114. 114
  115. 115. 115
  116. 116. 116
  117. 117. CONCLUSION • Please Remember !!! - Principle 1- No drug ever exerts a single action - Principle 2- No clinically useful drug is entirely devoid of toxicity - Principle 3- The potential toxicity of a drug rests in the hands of the user 117
  118. 118. References • Handbook of local anesthesia – Stanley F Malamed – 6th edition • Essentials of Local Anesthetic Pharmacology : Daniel E Becker : Anesth Prog. 2006 Fall; 53(3): 98– 109. • Vasoconstrictors in local anesthesia for dentistry: A. L. Sisk; Anesth Prog. 1992; 39(6): 187–193. 118
  119. 119. • Local anesthetic failure associated with inflammation: verification of the acidosis mechanism and the hypothetic participation of inflammatory peroxynitrite : Takahiro Ueno et al ; Journal of Inflammation Research; November 2008 Volume 2008:1 Pages 41 - 48 • Advanced techniques and armamentarium for dental local anesthesia; Clark TM; Dent Clin North Am. 2010 Oct;54(4):757-68 119
  120. 120. • Advances in dental local anesthesia techniques and devices: An update ; Payal Saxena et al: National Journal of Maxillofacial Surgery | Vol 4 | Issue 1 | Jan-Jun 2013. 120
  121. 121. THANK YOU! 121