Local anaesthesia - Basics in dentistry

Local anaesthesia - Basics in dentistry, conventional local anesthesia techniques and complications

1. DR.K.PRASHANT III YEAR MDS

2. Introduction Historical background Definition Ideal properties Electrophysiology of nerve conduction & Impulse propagation Theories of mechanism of action of local anesthesia Classification of LA Dissociation of local anesthesia 2 CONTENTS

3. 3 Local Anesthetic agent Types of Local Anesthetics B iokinetics Metabolism MRD Armamentarium Injection techniques Local & Systemic complications References

4. 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 Historical background LIDOCAINE- Lofgren in 1948 . The discovery of its anesthetic properties was followed in 1949 by its clinical use by T. Gordh

5. 5 DEFINITION: Local anesthesia is defined as a reversible 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. LOSS OF SENSATION WITHOUT INDUCING LOSS OF CONSCIOUSNESS..

6. 6 METHODS OF INDUCING LOCAL ANESTHESIA : Low temperature Mechanical trauma Anoxia Neurolytic agents such as alcohol & phenol Chemical agents such as local anesthetics

7. 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 7 PROPERTIES OF LOCAL ANESTHESIA

8. 8 inside outside Resting potential of neuron = -70mV + - + - + - + - + - ELETROPHYSIOLOGY OF NERVE CONDUCTION

9. 9 DEPOLARIZATION DEPOLARIZATION : REPOLARIZATION: 0.3 msec 0.7 msec Result is a voltage gradient along axon, causing a current i.e sequential configurational change in Na-channels in the next segment  CONDUCTION .

10. Local anesthetic agent achieves interference 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. 10 MECHANISM OF ACTION OF LOCAL ANESTHETICS

11. ACETYLECHOLINE THEORY : There is no evidence that acetylcholine is involved in neural transmission. 11 THEORIES MECHANISM OF ACTION OF LOCAL ANESTHETICS

12. CALCIUM DISPLACEMENT THEORY: . 12 SURFACE CHARGE (REPULSION) THEORY:

13. 13 MEMBRANE EXPANSION THEORY Lipid soluble LA can easily penetrate the lipid portion of cell membrane decreasing the diameter of sodium channel.

14. The most favored today, proposed that local anesthetics act by binding to specific receptors on sodium channel ; the action of the drug is direct, 14 SPECIFIC RECEPTOR THEORY:

15. Local anesthetics are available as salts (usually hydrochlorides) for clinical use. In this solution it exists simultaneously as unchanged molecule (RN), also called base and positively charged molecules (RNH + ) called cations. RNH + == ==  RN+ H + 15 DISSOCIATION OF LOCAL ANESTHETICS

16. In the presence of high concentration of hydrogen ion (low pH) the equilibrium shifts to left 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 + 16

17. 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 hasselbach equation which d etermines how much of a local anesthetic will be in a non-ionized vs ionized form . Based on tissue pH and anesthetic Pka . Log base/acid = pH - pKa 17

18. 18 LOCAL ANESTHETIC AGENT

19. 19 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 (distilled water, NaCl )

20. 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 20 REDUCING AGENT

21. 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. 21 PRESERVATIVE

22. 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 . 22 FUNGICIDE

23. The anesthetic agent and the additives referred to above are dissolved in distilled water & sodium chloride. This isotonic solution minimizes discomfort during injection. 23 VEHICLE

24. 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. Max dose of vasoconstrictors Healthy patient approximately 0.2mg Patient with significant cardiovascular history: 0.04mg 24 VASOCONSTRICTORS

25. The local anesthetics used in dentistry are divided into two groups: ESTER GROUP AMIDE GROUP 25 LOCAL ANESTHETIC AGENT

26. 26 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

27. 27 CLASSIFICATION OF LOCAL ANESTHETICS ESTERS Esters of benzoic acid Butacaine Cocaine Benzocaine Hexylcaine Piperocaine Tetracaine Esters of Para-amino benzoic acid Chloroprocain Procaine Propoxycain e

28. 28 AMIDES Articaine Bupivacaine Dibucaine Etidocaine Lidocaine Mepivacaine Prilocaine Ropivacaine QUINOLINE Centbucridine AB C DE LMPR

29. NATUAL SYNTHETIC OTHERS BASED ON MODE OF APPLICATION INJECTABLE TOPICAL BASED ON DURATION OF ACTION ULTRA SHORT( < 30min) SHORT( 45-75min) MEDIUM( 90- 150min) LONG( 180 min) 29 BASED ON THE SOURCE BASED ON ONSET OF ACTION SHORT INTERMEDIATE LONG Classifications:

30. 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 ) 30 Classifications: 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

31. 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 . 31 PHARMACOKINETICS OF LOCAL ANESTHETICS

32. 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 32

33. 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 .( Lidocaine 2.5% + Prilocaine 2.5%) 33

34. 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. ROUTE TIME TO PEAK LEVEL (MIN) INTRAVENOUS 1 TOPICAL 5 INTRAMUSCULAR 5-10 SUBCUTANEOUS 30 - 90 34 RATES AT WHICH LOCAL ANESTHETICS ARE ABSORBED AND REACH THEIR PEAK BLOOD LEVEL

35. 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. 35

36. 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. 36 METABOLISM (BIOTRANSFORMATION )

37. 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. 37

38. 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. Amides are present in the urine as a parent compound in a greater percentage then are esters. 38 EXCRETION

39. 39 MRD

40. 40

41. 1.) The Syringe 2.) The Needle 3.) The Cartridge 4.) Other Armamentarium Topical Anesthetic (strongly recommended) -ointments, gels, pastes, sprays Applicator sticks Cotton gauze 41 Local Anesthesia Armanterium

42. 42 TYPES OF SYRINGES

43. 43 Plastic disposable syringe

44. 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. 44 Needle

45. 45 Components of needle

46. Supraperiosteal PDL injection Intraseptal Injection Intracrestal Injection Intraosseous Injection PSA Nerve Block MSA Nerve Block ASA Nerve Block Infra-Orbital Nerve Block MaxillaryNerve Block 46 INJECTION TECHNIQUES Infra-Alveolar Nerve Block Greater Palatine Nerve Block Nasopalatine Nerve Block Inferior Alveolar Nerve Block Mental Nerve Block LingualNerve Block Incisive Nerve Block Gow Gates Nerve Block Vzrani-Akinosi Nerve Block

47. 47

48. 48 Types of blocks

49. 49 Supraperiosteal injection

50. 50 Posterior superior alveolar nerve block

51. 51 Posterior superior alveolar nerve block

52. 52 Anterior superior alveolar nerve block

53. 53 MIDDLE superior alveolar nerve block

54. 54 INFRA- orbital nerve block

55. Greater palatine nerve block Nasopalatine nerve block 55 Palatal Anasthesia

56. 56 Other maxillary Anasthesia High Tuberosity technique Greater palatine Canal Technique

57. MANDIBULAR INJECTION TECHNIQUES: IANB Nerve block Buccal Nerve Block Mandibular nerve block techniques: Gow Gates technique Vazirani Akinosi closed mouth mandibular block 4) Mental Nerve block 5) Incisive nerve block 57

58. 58 Inferior alveolar nerve block

59. 59 Inferior alveolar nerve block

60. 60 Buccal nerve block

61. 61 Gow gates technique

62. 62 Vazirani-Akinosi technique

63. 63 Mental nerve block INCISIVE NERVE BLOCK

64. 64

65. 1) Needle breakage : Prevention 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. 65 Local Complications

66. 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 . Examination every 2 months 66

67. 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. 67

68. 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 68

69. 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. 69

70. 6) Hematoma : When swelling becomes evident during or immediately after a local anesthetic injection, direct pressure should be applied to the site of bleeding. Ice may be applied to the region immediately on recognition of a developing hematoma. 70

71. 7) Pain on injection 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 71

72. 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 72

73. 9) Infection : Use sterile disposable needles. Use sterile local anesthetic solutions. 73

74. 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., 108) is summoned. 74

75. 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) Histamine blocker is administered IM or IV. Corticosteroid is administered IM or IV. 75

76. 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 76

77. 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 ) Orabase , a protective paste can provide a degree of pain relief. 77

78. Overdose reactions: Allergic reaction: More common with ester based local anesthetics Most allergies are to preservatives in pre- made local anesthetic carpules Methylparaben Sodium bisulfite metabisulfite 78 Systemic complications

79. 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 79 CLINICAL MANIFESTATION OF LOCAL ANESTHETIC OVERDOSE

80. 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 80

81. 81

82. Handbook of local anesthesia – Stanley F Malamed – 6 th edition Netter , F . Atlas of Human Anatomy . CIBA. 1989. 82

83. THANK YOU 83