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Local anesthetics

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LOCAL ANESTHETICS WITH TECHNIQUE AND COMPLICATION

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Local anesthetics

  1. 1. Dr.Shalini Singh 1 LOCAL ANESTHETICS
  2. 2. 2 CONTENTS • Definition • History • Classification • Pain propagation and mechanism of action • Important properties of local anesthetics • Undesired effects of local anesthetics • Specific local anesthetics • Local aanesthetic techniques • Maxillary • mandibular • Complication • Local • systemic • Advances
  3. 3. 3 DEFINITION : • Drugs that cause reversible loss of sensory perception specially of pain in a restricted area of the body, when applied topically or local injection. • LA if applied to a mixed nerve—sensory and motor impulses are interrupted—resulting in muscular paralysis and loss of autonomic control.
  4. 4. 4 Common Uses Of Local Anaesthetics: Dentistry Excision Dermatology Spinal Anaesthesia
  5. 5. 5 HISTORY
  6. 6. Early History Of Regional Anesthesia  Koller and Gartner report local anesthesia (1884) Carl Koller 1857 -1944 6
  7. 7. Early History Of Regional Anesthesia  Koller and Gartner report local anesthesia (1884)  1884 Halsted injects cocaine directly into mandibular nerve and brachial plexus William S. Halsted 7
  8. 8. Early History Of Regional Anesthesia  Koller and Gartner report local anesthesia (1884)  1884 Halsted injects cocaine directly into mandibular nerve and brachial plexus  1904 Einhorn discovers procaine (Novocaine) Procaine 8
  9. 9. Early History Of Regional Anesthesia  Koller and Gartner report local anesthesia (1884)  1884 Halsted injects cocaine directly into mandibular nerve and brachial plexus  1904 Einhorn discovers procaine (Novocaine)  1943 Lofgren discovers lidocaine (Xylocaine) Lidocaine 9
  10. 10. Chronology Of Local Anesthetics Cocaine Niemann 1860 Ester Benzocaine Salkowski 1895 Ester Procaine Einhorn 1904 Ester Tetracaine Eisler 1928 Ester Lidocaine Lofgren 1943 Amide Chloroprocaine Marks, Rubin 1949 Ester Mepivacaine Ekenstam 1956 Amide Bupivacaine Ekenstam 1957 Amide Ropivacaine Sandberg 1989 Amide After: Cartwright & Fyhr. Reg Anesth 1988;13:1-12 10
  11. 11. 11 CLASSIFICATION
  12. 12. 12 BASED ON SITE Cocaine, Prilocaine, Lignocaine Topical Lignocaine, MepivacaineInjectable
  13. 13. 13 BASED ON CHEMICAL STRUCTURE ESTERS • Esters of benzoic acid • Cocaine • Procaine • Benzocaine • Butacaine • Esters of PABA • Chlorprocaine • Propoxycaine • Tetracaine AMIDES • Articaine • Bupivacaine • Dibucaine • Etidocaine • Lidocaine • Mepivacaine • Prilocaine • Ropivacaine QUINOLONE Centbrucidine KETONE Dyclonine
  14. 14. 14 BASED ON DURATION OF ACTION • 2% lignocane without vasoconstrictor Ultra Short Duration • Procaine, • 2 % Lignocaine with 1:1,00,000 Epinephrine Short duration • Articaine • Mepivacaine • Prilocaine • 2 % Lignocaine with 1:2,00,000 Epinephrine Intermediate duration • Bupivacaine (400-450 min) • Etidocaine • 5 % Lignocaine with 1:2,00,000 Epinephrine Long duration
  15. 15. 15 B A S E D O N O R I G I N •cocaineNATURAL •Amino esters of PABA- procaine •Alkyl esters of PABA- benzocaine •Amino esters of MABA- unacaine •Amino amides- xylocaine , bupivacaine SYNTHETIC NITROGENOUS COMPOUND • benzyl alcohol SYNTHETIC NON NITROGENOUS COMPOUND MISCLLANEOUS DRUGS ------- Clove Oil, Phenol
  16. 16. 16 DIFFERENCES A M I D E S •longer lasting analgesia. •Produce more intense analgesia. •Rarely cause hypersensitivity reactions- no cross reactivity with ESTER L A s. •Bind to alpha1 acid glycoprotein in plasma •Not hydrolyzed by Plasma Cholinesterase, more slowly destroyed by liver microsomal P450 enzymes. E S T E R S •Short duration of action •Less intense analgesia •Higher risk of hypersensitivity ESTER linked LA s are rarely used. •Hydrolyzed by Plasma Cholinesterase in blood. •Rarely used for Infiltration anesthesia •But useful for topical ana on mucous membranes.
  17. 17. 17 PAIN PROPAGATION AND MECHANISM OF ACTION
  18. 18. Resting Membrane Potential • There is an electrical charge across the membrane. • The resting potential (when the cell is not firing) is a 70mV difference between the inside and the outside. 18 inside outside Resting potential of neuron = -70mV + - + - + - + - + -
  19. 19. 19
  20. 20. 20
  21. 21. 21
  22. 22. CONDUCTION of a NERVE IMPULSE 22 Voltage gradient along axon, causing a current. This causes configurational change in Na- channels in the next segmentconduction
  23. 23. 23
  24. 24. 24
  25. 25. 25 L A - MODE OF ACTION •Blockage of membrane depolarisation in all excitable tissues, usually intended on peripheral nerve  Membranestabilizer
  26. 26. THEORY OF ACTION OF L.A  Specific receptor theory by strichartz 1987  Drug molecules bind to specific receptors present on the external or internal axoplasmic surface of sodium channels & by acting directly on them, decrease or eliminate permeability to Na2+ leading to interruption of nerve conduction.
  27. 27. STRUCTURE OF LA R INTERMEDIATE CHAIN N R2 R3 INTERMEDIATE CHAIN:AMIDE C O O ESTER NH C O Drug should reach Nerve through tissue HYDROPHILLIC Drug should enter Neuron ( Nerve ) LIPOPHILLIC 27
  28. 28. 28 Conduction Blockade LAH+ LA Ionized Nonionized
  29. 29. 29 SEQUENCE OF EVENTS WHICH RESULT IN CONDUCTION BLOCKADE • Diffusion of the base (nonionized) form across the nerve sheath and nerve membrane • Re-equilibration between the base and cationic forms in the axoplasm • Penetration of the cation into and attachment to a receptor site within the sodium channel. • Blockade of the sodium channel • Inhibition of sodium conduction
  30. 30. 30 SEQUENCE OF EVENTS WHICH RESULT IN CONDUCTION BLOCKADE •Decrease in the rate and degree of the depolarization phase of the action potential •Failure to achieve the threshold potential •Lack of development of a propagated action potential •Blockade of impulse conduction
  31. 31. Ionized 31
  32. 32. Na +Na + 32
  33. 33. 33 IMPORTANT CLINICAL PROPERTIES OF LOCAL ANESTHETICS
  34. 34. pKa • ONSET = pKa • pKa = pH at which 50% of drug is ionized • LA’s <50% exists in the lipid soluble nonionized form • Only the nonionized form crosses into the nerve cell 34
  35. 35. 35 pH influence • Usually at range 7.4 -8.5 • Decrease in pH shifts equilibrium toward the ionized form, delaying the onset action. • Lower pH, solution more acidic, gives slower onset of action Presence of Pus and inflammation will retard the action of LA. ( probably low acidic pH) therefore • LA are more ionized - don’t penetrate very well • Blood flow • Decreased ability of LA to produce effects
  36. 36. ROLE of pH and pKa in LOCAL ANESTHETICS 36
  37. 37. LIPID SOLUBILITY Anesthetic Potency • Potency <=> lipid solubility • Higher solubility <=> can use a lower concentration and reduce potential for toxicity [LA] 37
  38. 38. 38 •Lipid solubility is an important characteristic. Potency is related to lipid solubility, because 90% of the nerve cell membrane is composed of lipid. This improve transit into the cell membrane
  39. 39. PROTEIN BINDING DURATION OF ACTION • Duration <=> protein binding • Bupivacaine 95% Lidocaine 65% Procaine 6% 39
  40. 40. 40 INCREASED DOASGE • Intensity & Duration <=> INCREASED • Increase dose via increased volume or concentration of LA
  41. 41. 41 VASODILATOR ACTIVITY • Affects Anesthetic potency and duration • Greater vasodilator activity = increased blood flow to region =rapid removal of anesthetic molecule from injection site ; thus decreased anesthetic potency and duration.
  42. 42. Composition of LA Solution  Lignocaine Hcl --- (Anesthetic) 24.64 mg (2 %)  Adrenaline --- (Vasoconstrictor) 0.0125 mg (1:80,000)  Sodium metabisulphite (Reducing Agent) 0.5 mg  Methyl paraben --- (Preservative) 1 mg OR Cupryl hydrocuprinotoxin 1 mg  Thymol --- (Fungicide)  Salts (NaCl) --- (Isotonicity) 5-6 mg  Distilled Water --- (Vehicle) 100 ml OR Ringer’s Lactate 42
  43. 43. NEED FOR VASOCONSTRICTOR • All clinically effective injectable L.A have some degree of vasodialating activity • ↑ absorption of L.A into CVS → removal from injection site • Rapid diffusion of L.A from inj site → ↓ duration of action & depth of anesthesia. • Higher plasma level of L.A → ↑ risk of toxicity • ↑ bleeding at inj site. • Addition of vasoconstrictor to L.A.. • Constriction of blood vessels → ↓ tissue perfusion • Slow absorption into CVS → low anesthetic blood level → ↓ risk of toxicity. • Higher volume of L.A around nerve → ↑ duration of action • ↓ bleeding at inj site 43
  44. 44. Classification  Pyrocatechin derivatives - Epinephrine & Norepinephrine  Benzol derivatives - Levonordefrin  Phenol derivatives - Phenylephrine • Catecholamines • Epinephrine, Dopamine, Isoproterenol • Noncatecholamines • Amphetamine, Ephedrine, Methoxamine 44
  45. 45. ADDITION of Sodium Bicarbonate • NaHCO3 - é pH & nonionized base • Speeds onset of block • 1 mEq NaHCO3 per 10 ml Lido/Mepiv • .1 mEq NaHCO3 per 10 ml Bupiv 45
  46. 46. 46 ACTIONS OF LA - LOCAL • All LAs have effects on nerves acting via Na+ channel – sensory endings, nerve trunks, NM junctions, ganglion and receptors • Sensory and Motor fibres are equally sensitive – depends on diameter and types of fibres • Smaller fibers are more sensitive than larger ones • Myelinated nerves are blocked earlier than non-myelinated ones • Autonomic fibres are more susceptible than somatic ones • Order of blockade in general: Pain – temperature – touch – deep pressure
  47. 47. 47 UNDESIRED EFFECTS OF LOCAL ANESTHETICS
  48. 48. • CNS – biphasic (stimulation then depression) • CVS – depression • Respiratory system – mild bronchodilation Clinical situation Blood level (ug/ml) Anticonvulsive 0.5 - 4 Preseizure signs 4.5 - 7 Tonic – clonic seizures > 7.5 Clinical situation Blood level (ug/ml) Antiarrhythmic 1.5 - 5 Myocardial depression 5 - 10 Cardio-vascular collapse > 10
  49. 49. CENTRAL NERVOUS SYSTEM • CNS Stimulation: • (More sensitive than cardiac) • Dose-related spectrum of effects and All effects are due to depression of neurons • First an apparent CNS stimulation (convulsions most serious) • Followed by CNS depression (death due to respiratory depression) • Premonitory signs include: ringing in ears, metallic taste, numbness around lips • Cocaine - euphoria (unique in its ability to stimulate CNS) • Lidocaine - sedation even at non-toxic doses 49
  50. 50. 50 CARDIOVASCULAR SYSTEM • ARRHYTHMIAS: direct effect (More resistant than CNS) • Decrease cardiac excitability and contractility • Decreased conduction rate • Increased refractory rate (bupivicaine) • ALL can cause arrhythmias if conc. is high enough Note: cocaine is exception......it stimulates heart • HYPOTENSION: Arteriolar dilation is a result of: • Direct effect (procaine and lidocaine have most effect) • Block of postganglionic sympathetic fiber function • CNS depression • Avoid by adding vasoconstrictor to the preparation • Cocaine is exception: produces vasoconstriction, blocks catecholamine reuptake
  51. 51. 51 METHEMOGLOBINEMIA • Some LA metabolites have significant oxidizing properties • This may cause a significant conversion of hemoglobin to methemoglobin and compromise ability to carry oxygen • May be a problem if cardiopulmonary reserve is limited • Treat with oxygen and methylene blue (converts methemoglobin to hemoglobin) • prilocaine benzocaine lidocaine have been implicated
  52. 52. 52 •Hypersensitivity: • Common with ester-linked LA • Rashes, angio-edema, dermatitis and rare anaphylaxis • Sometimes typical asthmatic attack •Neurotoxicity: • LA can cause concentration-dependent nerve damage to central and peripheral NS • Mechanism(s) not clear • Permanent neurological injury is rare • May account for transient neurological symptoms.
  53. 53. 53 SPECIFIC LOCAL ANESTHETICS
  54. 54. 54 PROCAINE (NOVOCAINE) • First synthetic injectable local anesthetic. • Produce the greatest vasodilation of all currently used local anesthetics. • Slower clinical onset (6-10 mins.) • Used for • Soft tissue anesthesia for 15- 30 mins. • Systemic toxicity negligible because rapidly destroyed in plasma • Max. recommended dose for peripheral nerve block 1000mg
  55. 55. LIDOCAINE •The most popular contains epinephrine 1:100,000 and provides good anesthesia for healthy patients. •Lidocaine with epinephrine 1:50,000 is used for hemostasis, but because of the rebound effect noted earlier, it should be used sparingly. Gold standard 1:200000 conc. is safest As well as potent 55
  56. 56. 56 Lignocaine ( Xylocaine ) • Most widely used Amide linked LA and most versatile ana. • Has variety of applications like Local, nerve block, topical. • When used locally action starts within 3 mts, more profound anesthesia, has longer duration of action and greater potency. • Overdose causes muscle twitchings, convulsions, cardiac arrhythmias, fall in BP, coma, respiratory arrest. • Most popular anti arrhythmic drug
  57. 57. Maximum Dose of Lignocaine •Without Vasoconstrictor : 4.4 mg / kg of body wt = 300 mg in a 70 kg individual = 15 ml of solution •With Vasoconstrictor : 7.2 mg / kg of body wt = 500 mg in a 70 kg individual = 25 ml of solution • For children with VC 3.2 mg/kg • Council for dental therapeutics- ADA 4.4mg/kg
  58. 58. MEPIVACAINE • 3% Mepivacaine without a vasoconstrictor is used as anesthetic for patients who cannot take a vasoconstrictor or for short procedures. • It is appropriate for pedodontics and for use on geriatric patients. • 2% Mepivacaine with vasoconstrictor provides pulpal anesthesia that is similar to lidocaine with epinephrine, but hemostasis is not as intense. Cardiac patients 58
  59. 59. PRILOCAINE • The action of prilocaine plain varies with the area injected (longer with a nerve block). • Prilocaine with vasoconstrictor gives good anesthetic effect and uses a 1:200,000 concentration of epinephrine. Secondary amine Orthotoulidine Liver+kidney+lung CO2 methaglobinemia Biotransformation 59
  60. 60. ARTICAINE •Articaine is a newer anesthetic typically given in a 4% solution with 1:100,000 epinephrine. •Practitioners reported rarely missing a inferior alveolar nerve block with Articaine. •However, concern has arisen about its potential for tissue necrosis and persistent nerve parasthesia. Thiophene group Ester side chain Lipophilic,High penetrating Rare over dosage 60
  61. 61. BUPIVACAINE • Bupivacaine is used when pulpal anesthesia is desired for longer appointments and when postoperative pain is anticipated. • Bupivacaine is not recommended for children or handicapped patients because of the increased risk of postoperative injury (chewing on a numb lip). CVS symptoms first Preemptive analgesia High pKa Sensoricaine 61
  62. 62. • Available as 0.5% soln 1:2,00,000 (vc) • Indicaton- pulpal anesthesia->90- min. Full mouth recontruction. Extensive oral and maxillofacial surgery, 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, in children- anticipating self trauma .
  63. 63. POSTPROCEDURAL PAIN CONTROL •Prescribe nonsteroidal antiinflammatory agents prior to the appointment •Use an intermediate duration anesthetic for the procedure •Inject bupivacaine just prior to the patient's dismissal •Direct the patient to take oral analgesics for a certain number of days following the procedure. 63
  64. 64. ROPIVACAINE • It is prepared as an isomer rather than a racemic mixture • Greater margin of safety between convulsive and lethal doses. • A newer Bupivacaine congener, equally long acting but less cardio toxic. Sensory block is more compared to Motor. • Ropivacaine is being used for relief of postoperative pain. I t can also be used for nerve blocks. • It is available in USA not in India. 64
  65. 65. HYALURONIDASE • An enzyme that breaks down intracellular cement. • Advocated as an additive to local anesthetics as it permit as injected solutions to spread and penetrate tissues. • Available as Wydase in a lyophilized powder and a stabilized solution. • Added to the cartridge just before administration by removing approximately 1/8th of solution. • Allergic reactions have been demonstrated. 65
  66. 66. LOCAL ANAESTHESIA TECHNIQUE 66
  67. 67. 67 TOPICAL • The local anesthetic solution is applied on the mucous membrane or skin, through which it penetrates to anesthetize superficial nerve endings. • e.g. - Ointments containing 5% • lignocaine • -Viscous solution containing • lignocaine hydrochloride • -Ethyl chloride sprays
  68. 68. 68 INFILTRATION • Small terminal nerve endings in the area of dental treatment are flooded with local anesthetic. • The treatment is done in the same place where anesthetic is deposited.
  69. 69. 69 FIELD BLOCK •Local anesthetic solution is deposited near the larger terminal branches so the anesthetized area is well circumscribed. •Incision or treatment is done at an area away from the site of injection of local anesthetic.
  70. 70. 70 NERVE BLOCK •Local anesthetic solution is deposited close to the main nerve trunk, usually at a distance from the site of operative intervention
  71. 71. SUPRA PERIOSTEAL INJECTION 71
  72. 72. POSTERIOR SUPERIOR ALVEOLAR NERVE BLOCK 72
  73. 73. 74
  74. 74. 75 MIDDLE SUPERIOR ALVEOLAR NERVE BLOCK
  75. 75. Middle Superior Alveolar Nerve Block
  76. 76. INFRAORBITAL NERVE BLOCK 77
  77. 77. GREATER PALATINE NERVE BLOCK 81
  78. 78. NASOPALATINE NERVE BLOCK 83
  79. 79. 84
  80. 80. 85 PALATAL APPROACH ANTERIOR SUPERIOR ALVEOLAR
  81. 81. 87 MAXILLARY NERVE BLOCK
  82. 82. 90 MAXILLARY NERVE BLOCK
  83. 83. INFERIOR ALVEOLAR NERVE BLOCK 91
  84. 84. March 5, 2007 Faisal A. Quereshy, MD, DDS, FACS
  85. 85. March 5, 2007 Faisal A. Quereshy, MD, DDS, FACS
  86. 86. March 5, 2007 Faisal A. Quereshy, MD, DDS, FACS
  87. 87. March 5, 2007 Faisal A. Quereshy, MD, DDS, FACS
  88. 88. March 5, 2007 Faisal A. Quereshy, MD, DDS, FACS
  89. 89. BUCCINATOR / LONG BUCCAL NERVE BLOCK 97
  90. 90. March 5, 2007 Faisal A. Quereshy, MD, DDS, FACS
  91. 91. March 5, 2007 Faisal A. Quereshy, MD, DDS, FACS
  92. 92. MENTAL NERVE BLOCK 100
  93. 93. March 5, 2007 Faisal A. Quereshy, MD, DDS, FACS
  94. 94. GOW GATES TECHNIQUE– 1973 (MANDIBULAR N. BLOCK) 102
  95. 95. COMPLICATIONS OF LOCAL ANESTHETICS 105
  96. 96. DEFINITION “any deviation from the normally expected pattern during or after the securing of regional analgesia” 106
  97. 97. 107 CLASSIFICATION 1 •Primary or Secondary •Mild or Severe •Transient or permanent CLASSIFICATION 2 •Solution used •Insertion of needle CLASSIFICATION 3 •Local •Systemic
  98. 98. LOCAL COMPLICATIONS • Needle Breakage • Prolonged anesthesia • Facial nerve paralysis • Trismus • Soft- tissue injury • Hematoma • Pain on injection • Burning on injection • Infection • Edema • Sloughing of tissues • Postanesthetic intra- oral lesions 108
  99. 99. SYSTEMIC COMPLICATIONS •Toxicity or Overdosage •Allergy •Idiosyncrasy •Syncope •Hyperventilation syndrome 109
  100. 100. 110 EMLA = eutectic mixture of local anesthetics • Eutectic = two solid substances mixed together in equal quantities by weight form a eutectic mixture • the melting point of the mixture is lower than the melting points of the individual components • EMLA = lidocaine and prilocaine becomes an oily mixture
  101. 101. 111 TAC: (LET) •tetracaine 0.5%, adrenaline1 in 2000 and cocaine 10% •topical anesthetic mixture found to be effective for nonmucosal skin lacerations to the face and scalp •applied directly to the wound using a cotton-tipped applicator with firm pressure that is maintained for 20 to 40 minutes •maximum dose for children-0.05ml/Kg •toxicity due to cocaine
  102. 102. 112 Thank You
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