Local anaesthesia

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Local Anaesthesia

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Local anaesthesia

  1. 1. DEPT.OF ORAL &MAXILLOFACIAL SURGERY Presented By Dr Haneef
  2. 2.  History  Armamentarium  Definition &Classification  Composition  Different Agents , Vasoconstrictors  Mechanism of Action  Bio Transformation  Systemic Action
  3. 3.  Ancient time – dental treatment associated with pain  Earliest pain relief – Coca shrub  mood elevator  Incas  Cocoa shrub – foot hills of Andes  Introduced by  Europeans to South America  Cocaine
  4. 4.  1855 – Gaedicke extracted alkaloid Erythroxylin  1860 – Dr. Scherzer  cocaine from this alkaloid  1844 – Francis Rynd (Dublin)   Acetate of morphine + Creosote  Skin incision  TGN treatment  First time liquid used - intradermally  1884 – marks birth of LA
  5. 5.  Sigmund Freud  Carl Koller  Cocaine for eye operation  William Steward Halsted  Cocaine for inferior dental nerve  1886 – BDJ  William Alfred Hunt et al  Cocaine - dental anesthetic documented  1901 – E Mayers   Vasoconstrictor + cocaine
  6. 6.  1905  13 lives claimed – addiction  A Einhorn & E Uhlfelder(Sweden)  Synthesized  Procaine hydrochloride  Procaine  sterilizable, non-additive, non-toxic  1943  N Lofgren(Sweden)  Synthesized  Anilide called Lignocaine  Lignocaine – amide linked synthetic derivative
  7. 7.  1946 – Lignocaine introduced  Dental practice  1948 – Lignocaine ; published in BDJ – Lofgren  Sweden – Birth place of newer LA agents  Bupivacaine  Ropivacaine
  8. 8.  DEFINITION --  It is defined as an unpleasant emotional experience usually initiated by a noxious stimulus and transmitted over a specific neural pathway to the central nervous system where it is interpreted as such.
  9. 9.  Accupuncture Analgesia --  Originated-CHINA,between600BC to 200AD  Hypnotism –  Still employed—susceptible patients,  Time consuming, lasts for less time  Audio Analgesia –  1959 Gardner and licklider  Loud noise used to produce analgesia  Electric analgesia -- Peripheral nerve- Direct electric current  Elos-1,powered by 18v battery- Siemens  Never more than 30 ma
  10. 10.  Syringe-  Breech loading, metallic cartridge-aspirating Advantage Visible cartridge Aspiration- 1 hand Autoclavable Rust resistance, Long lasting Disadvantage Weight Size-Too big Possibility of infection
  11. 11. PISTON WITH HARPOON FINGER GRIP THUMB RING SYRINGE BARREL NEEDLE ADAPTOR
  12. 12.  Breech loading plastic cartridge-aspirating Advantage Light weight Cartridge visible Rust resistance, Long lasting Low cost Disadvantage Size – Too big / small Possibility of infection Repeated autoclaving – Plastic looses its properties
  13. 13. PLASTIC REUSABLE SYRINGE
  14. 14.  Breech loading metallic cartridge-Self aspirating Advantage Cartridge visible Autoclavable Easier to aspirate Piston is scored – Qty Known Disadvantage Weight Possibility of infection Finger has to be moved from thumb ring to disc-Aspiration Takes time to accustom
  15. 15. SELF ASPIRATING SYRINGE
  16. 16.  Pressure syringe -- Advantage Measured dose Overcomes tissue resistance Non threatening – Cartridge protected Disadvantage Cost Inject too rapidly -Possibility
  17. 17. PRESSURE SYRINGE
  18. 18. WILCOX- JEWETT OBTUNDER
  19. 19.  Jet injectors Advantage Does not require – needle Very small volume – Delivered Topical anesthesia-effective Disadvantage Inadequate – Pulpal / Regional block Patient disturbed by jolt of jet. Cost PDL damage – common
  20. 20. JET INJECTOR
  21. 21.  Disposable syringe Advantage Single use Sterile-Till opened Light weight Disadvantage Does not accept – Dental cartridge Aspiration – Difficult – 2 hands
  22. 22.  Needle  Type – Stainless steel – Disposable Platinum Iridium platinum Ruthenium platinum  Parts – Bevel Shank Hub-Leur lock, Friction grip.
  23. 23. Rubber diaphragm Aluminum cap NECK GLASS TUBE RUBBER PLUNGER
  24. 24.  Additional Armamentarium –  Topical antiseptic  Topical anesthetic  Cotton Gauge  Hemostat  Applicator Stick.
  25. 25. It is defined as a transient loss of sensation to a painful or potentially painful stimulus, resulting from a reversible interruption of peripheral conduction along a specific neural pathway to its central integration and perception in the brain.
  26. 26. Its action must be reversible It must be nonirritating to the tissues and produce no secondary local reaction It should have a low degree of systemic toxicity It should have a potency sufficient duration to be advantageous. It should have a potency sufficient to give complete anesthesia without the use of harmful concentrated solutions It should have sufficient penetrating properties to be effective as a topical anesthetic. It should be relatively free from producing allergic reactions. It should be stable in solution and undergo biotransformation readily within the body It should be either sterile or capable of being sterlized by heat without deterioration.
  27. 27.  ROOT CANAL TREATMENT FOR PULPAL ANESTHESIA  PERIODONTAL SURGERY  ORTHODONTIC EXTRACTIONS  EXTRACTION OF CARIOUS ,PRE PROSTHETIC EXTRACTIONS,MALPOSED AND IMPACTED TEETH.  PREPROSTHETIC SURGERY  SURGICAL EXCISION AND INSICION OF PATHOLOGICAL LESIONS.  ORTHOGNATHIC SURGERY  MAXILLARY ND MANDIBULAR # REDUCTIONS OPEN/CLOSED
  28. 28. ABSOLUTE:  DRUG ALLERGY OR HYPERSENSTIVITY REACTION
  29. 29.  IN HEPATIC FAILURE PATIENTS Amides are metabolized in the liver. Patients with significant liver disease who have poor hepatic blood flow will have trouble metabolizing amides and other agents.  Patients administered prilocaine may develop methemoglobinemia.  HEART FAILURE (ASA IV OR VI)  LIDOCAINE is used as an ACLS drug for patients with ventricular dysrythmias. However high levels of lidocaine will decrease contractility and cardiac output and can lead to circulatory collapse. Systemic actions on the central nervous system include CNS depression, seizures and analgesia.  In addition, one of the metabolites of lidocaine may actually cause some sedation. These metabolites are excreted in the kidney.IN RENAL FAILURE PATIENTS HAS TO BE USED WITH CAUTION.  ATYPICAL PSEUDOCHOLINESTERASE.  BLEEDING DISORDERS PERTICULARLY REGIONAL BLOCKS
  30. 30. Topical Surface contact. Paste, ethyl chloride. May be adequate for simple incision and drainage, preinjection, Infiltration Deposition of solution at or close to site of surgery. a) Sub mucous - for simple soft tissue surgery - includes long buccal infiltration. Not suitable for pulpal anaesthesia. b) Supraperiosteal - the commonest technique - solution diffuses through cortical bone into apical area. Usually adequate especially in maxilla but adult mandibles to thick in posterior buccal cortex. c) Subperiosteal - painful! - use if (b) fails. d) Intraosseous - very painful! again use if (b) fails. Drill small access hole over appropriate tooth apex and deposit 0.25ml of local anaesthetic.
  31. 31. e) Intraseptal - variation of (d) - similar indications but inject through softer crestal bone to reach apex. f) Intraligamentous - painful but occasionally very useful especially for acute pulpitis where regional block fails to give adequate depth of anaesthesia. Must use special syringe to avoid breaking cartridge. Push needle along root surface to apex - inject small volume of solution - effect is rapid so proceed with surgery C.FIELD BLOCKS D.NERVE BLOCKS E.Regional Block: Remote from site of surgery. Contraindicated in patients with bleeding diatheses even if controlled!Success depends on knowledge of local anatomy and good technique.
  32. 32.  Based on composition –  A) Natural – eg – cocaine.  B) synthetic nitrogenous compd – para amino benzoic acid-procaine, benzocaine. acetanilide - lignocaine quinoline - cinchocoline  C) non Nitrogenous compounds - benzyl alcohol  D) miscellaneous – clove oil , phenol .
  33. 33.  Based on intermediate group -- Esters – Benzoic acid Para Amino benzoic Acid Butane Chloroprocaine Cocaine Procaine Benzocaine Propoxycaine Hexylcaine Tetracaine Amides – Articaine Bupivacaine Dibucaine Lignocaine Mepivacaine Prilocaine
  34. 34.  According to biological site and mode of action—  Class A  Class B  Class C  Class D Agents acting at receptor site –external surface. Agents acting at receptor site- internal surface.. Agents acting at receptor independent physico chemical mechanism. Agents acting in combn of receptor and independent mechanism. Biotoxin -eg tetrodotoxin Quaternary amonium- scorpion venom Benzocaine Clinically useful agents –Lignocaine etc
  35. 35.  Injectables -- Surface --  Ultra short acting *Soluble - eg <80 min eg Lignocaine Cocaine Lignocaine  Short acting 45-50 *Insoluble- eg Min 2% ligno with Benzocaine 1:1 lakh VC  Medium acting 90-150 2% ligno with Vc or 4% prilocaine with 1:2 epin  Long acting > 180 Bupivacaine with 1:2 epin
  36. 36.  Local anesthetic agent  This is the active ingredient in the solution, but despite the constant development of new drugs, the ideal L.A. agent is yet to be introduced into clinical practice.  Vasoconstrictor  Merits  Reduces toxic effects by retarding the absorption of the constituents  By confining the anesthetic agent to a localized area it increases the depth and duration of anesthesia.  It produces a relatively blood less field of operation for surgical procedures.
  37. 37.  Demerits  In higher doses can cause systemic effects that are undesirable, practically in individuals suffering from cardiovascular disease.  Vasoconstrictor may also cause a delay in wound healing, edema and tissue necrosis. This is because sympathomimetic amines may increase O2 consumption of tissues. This, together with vaso constriction leads to hypoxia and local tissue damage.  The vasoconstrictors in general uses are  Adrenaline.  Noradrenaline  Felypressin
  38. 38.  Anti oxidant  Most often is sodium meta-bi sulphite  Amount varies from 0.0065 to 0.002 mg/CC.  Since this substance is more readily oxidized than adrenaline or noradrenaline it protects their stability.  Preservative  Modern LA solutions are very stable and have a shelf – life of 2 years or more.  Most frequently used bacteriostatic agents are methylparaben, propylparaben and chlorobutanol.  Fungicide Thymol is added.  Vehicle  The anaesthetic agent and the additives are dissolved in modified Ringer’s solution. This automatic vehicle minimizes the discomfort during injection.
  39. 39. Anesthetic pKa Onset Duration (with Epinephrine) in minutes Max Dose (with Epinephrine) Procaine 9.1 Slow 45 - 90 8mg/kg – 10mg/kg Lidocaine 7.9 Rapid 120 - 240 4.5mg/kg – 7mg/kg Bupivacaine 8.1 Slow 4 hours – 8 hours 2.5mg/kg – 3mg/kg Prilocaine 7.9 Medium 90 - 360 5mg/kg – 7.5mg/kg Articaine 7.8 Rapid 140 - 270 4.0mg/kg – 7mg/kg
  40. 40. Lignocaine-- Classified under – Amide  2-diethylamino 2,6 acetoxylidide hcl  1943 – Nils Lofgrens- intro 1948(dentistry)  Metabolised- Liver by microsomal fixed function oxidases to monoethyl glycerine and xylidide  Excretion -<10% unchanged, >80%-metab  Vasodilaton ->Procaine, <Mepivacaine  Pka –7.9 , ph(plain)-6.5,ph(with Vc)5 –5.5,Onset of action 2-3 min,Anesthetic half life 1.6hrs,topical anesthetic -yes
  41. 41. NH.CO.CH2.N CH3 CH3 C2H5 C2H5 LIGNOCAINE
  42. 42.  Recommended dose – 7mg/kg not>500mg with VC 4.4mg/kg not>300mg  For children with VC 3.2 mg/kg  Council for dental therapeutics- ADA 4.4mg/kg  It is non allergic available in three formulations Ligno2% with out Vc Ligno2% with VC 1:80,000 Ligno2% with VC 1:100,000  Adverse reactions- CNS stimulation then Depression,Overdose causes unconsciousness and respiratory arrest.
  43. 43.  Bupivacaine –Classified under amide  1-butyl 2,6 pipecoloxylidide  Toxicity <4 times – Lignocaine, Mepivacaine  Metabolism –Liver by Amidases  Excretion by kidney (16% unchanged)  Vasodilation- relatively significant  Pka-8.1,ph(plain)- 4.5-6, ph(vc)- 3-4.5 Onset of action –6-10 min,Anesthetic half life-2.7hrs,Dose 1.3mg/kg ,Maximum dose-not >40mg,Absolute maximum dose-not> 90mg
  44. 44. N NH.CO C4H9 CH3 CH3 BUPIVACAINE
  45. 45.  Available as 0.5% soln 1:2,00,000 (vc)  Indicaton- pulpal anesthesia->90- min. 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, in children- anticipating self trauma .
  46. 46.  Procaine- Classified under –Esters  2Diethylamino ethyl 4aminobenzoate hcl  Metabolised-in Plasma by plasma pseudocholine esterases  Excretion >2%unchanged, 90% -PABA,8% diethyl aminoethanol in urine.  Pka-9.1,High degree of vasodilation, 2% procaine 15-30min soft tissue LA no pulpal anesthesia , > incidence allergy, drug of choice for intra arterial injection and accidents.
  47. 47.  Mepivacine- classified -amide type  1 Methyl 2,6 pipecoloxylidide hcl  Metabolism-microsomal fixed funcn oxidasea in liver.  Maximum dose 4.4 mg/kg , absolute max dose-300mg.  Excretion-1-10% unchanged urine.  Pka-7.6,Anesthetic half life-90min,  Mild vasodilator, 3% mepivacaine used in patients with vc contraindicaton. Low reported cases-allergy.over dose CNS stimulation followed by depression.
  48. 48. Articaine- classified- Amide  2 Carboxymethoxy 4 methylthiophene hcl  Metabolised- Liver  Excretion – Kidney 10% - unchanged.  Pka 7.8, Anesthetic half life-1.2-2 hrs,  Maximum dose – 1mg/kg , Absolute maximum dose – 500mg  first LAAgent with thiophene ring,little potential to diffuse through soft tissue.  Adverse reaction-methymoglobinemia-Rx by using methylene blue 1mg/kg.
  49. 49. Etidocaine- classified –Amide  Metabolism –Liver  Excretion –urine- Kidney  Pka 7.7 ,Anesthetic half life-56 min.  Maximum dose 8mg /kg, Absolute max dose 400 mg  Employed mainly in epidural or caudal regional block.
  50. 50.  Added – to counteract vasodilation effect of injectable L.A  Decreases rate of absorption  Reduces the risk of overdose reaction  Increases duration of action  Reduces bleeding at the site
  51. 51. Catecholamines Epinephrine Nor epinephrine Dopamine Non catecholamines Amphetamine Meta amphetamine Based on chemical stc  (Catechol nucleus) Based on mode of action Direct acting Epinephrine Nor epinephrine Indirect acting Amphetamine Tyramine Mixed acting Ephedrine
  52. 52. Proprietar y name Mode of action Systemic 1) CVS EPINEPHRINE Adrenaline α1& β receptors Systolic & Diastolic pressure Heart rate Oxygen consumption Stroke volume FELYPRESSIN Octopressin Direct stimulation of vasculature No direct effect on Myocardium Non-arrythmagenic High doses – impaired coronary flow
  53. 53. 2) CNS 3) RS 4) Vasculature 5)Metabolism CNS stimulation Bronchodilator α1 – vasoconstriction β 2 – vasodilation oxygen consumption blood sugar level Adrenergic nerve – no effect Vasoconstriction – coronary blood vessels Anti-diuretic action Oxytocin like action – uterus
  54. 54. 6) Clinical application 7) Max dose 8) Side effect Allergy, hemostasis 0.2 mg – healthy 0.04mg – CVS impaired CVS & CNS symptoms Cerebral hemorrhage As vaso-constrictor in L.A 0.04mg
  55. 55.  Rate  Non-myelinated 1.2m/s  Myelinated 14.8 – 120m/s  Site of action  Outer bimolecular lipoprotein layer in nerve membrane
  56. 56.  Altering the basic RMP of nerve  Altering the threshold potential  Decreasing the rate of depolarization  Prolonging rate of repolarization
  57. 57.  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
  58. 58.  SURFACE CHARGE THEORY:  Action by binding to nerve membrane and changing its electric potential.  Cationic molecules aligned at membrane water interface –surface elec potn more positively charged - electric potn , threshold potn.  Demerits- RMP not altered by LA. LA act on nerve channel rather than surface –cannot explain how uncharged LA molecule causes nerve blockage.
  59. 59. Membrane expansion theory-  LA lipid soluble – enters nerve membr and changes configuration of membr. 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.
  60. 60. Specific receptor theory—  LA act by binding to specific receptors- sodium channel-on external/ axoplasmic surface.  Once it binds there is no permeability of sodium- no conduction. LA molecule replace calcium molecule at calcium gate – thus prevent sodium entry. This is by far the most accepted theory.
  61. 61.  All LA are available as acid salt of weak bases.  Weak base(BNHOH) combined with acid (HCL) to give acid salt(BNHCL)& water.  In mucosa BNHCL dissociates into BNH and CL . Normal tissue PH 7.4 is necessary for conversion of acid salt to free base.  BNH which is hydrophilic further dissociates to BN and H. BN is now lipophilic.
  62. 62.  Lipophilic BN diffuses through nerve membrane (lipid). Inside the nerve it combines with intrinsic H. (H in nerve formed by buffering action.)  Newly formed ionised BNH displaces calcium from the sodium channel receptor site to cause conduction blockade.
  63. 63. LA Solution .
  64. 64.  Esters- eg- Procaine- hydrolyzed to pseudo cholinesterase's Para amino benzoic acid Diethyl amino alcohol Excreted unchanged urine further transformed-urine Atypical cholinesterase's --- increase toxicity
  65. 65.  Amide eg lidocaine -- Mono ethyl xylidide Glycine xylidide xylidide Xylidide Hydroxy xylidide. Excreted kidney . Significant renal diseases – contra indication.
  66. 66. CNS – Low levels – no action Toxic dose – tonic clonic convulsions Blood- 0.5-4.0 mg/ml-no complication 4.5-7.0 mg/ml-pre seizure sign/ symptom >7.5mg/ml-tonic clonic seizures. Anti convulsive property – As it causes depression of CNS. Seizure threshold- excitability nerve
  67. 67. CVS-  Action on Heart  Electrical excitability of myocardium .  conduction rate  Tone of contraction. clinically effective level-1.8-5mg/ml –anti arrhythmic used in premature ventricular contractures , arrhythmias.
  68. 68.  Action on vasculature- normal value no change. over dose- hypo tension.( myocardial contractility) Lethal dose- cardio vascular collapse ( myocardial contractility, massive peripheral vaso dilatation )
  69. 69. Action on Respiratory system–  Normal levels- no over dose- bronchial muscles relaxation .  Over dose – Respiratory arrest due to CNS depression.
  70. 70. DEPT.OF ORAL &MAXILLOFACIAL SURGERY Presented By Dr Haneef
  71. 71.  Anatomical considerations  Local anaesthesia technique- Maxilla  Local anaesthesia technique- Mandible  Complications  Future trends
  72. 72.  The right and left trigeminal nerves provide among other functions, the overwhelming majority of sensory innervation from the teeth, bone, soft tissues of the oral cavity.  Two parts:- i. Motor:- a. Masseter b. temporalis c. lateral/medial pterygoid d. Mylohyoid e. Anterior belly of digastric f. Tensor tympani g. Tensor veli palatini ii. Sensory: V1 Opthalmic nerve V2 Maxillary division V3 mandibular division
  73. 73.  Use a Sterile Sharp Needle  Check The flow of Solution  Determine Whether to Warm solution before use or not.  Position the patient  Dry the tissue/ wipe once.  Apply topical anesthetic
  74. 74.  Communicate with patient apply firm hand rest  Inject few drops of soln, communicate with patient,  Advance to the target slowly ,aspirate , inject  Withdraw the needle slowly  Observe the patient & check for anesthetic symptoms
  75. 75. Intra Oral injection techniques  Supraperiosteal injection  Intralegimentry injection  Intraspetal injection  Intraosseus injection  Posterior superior alveolar nerve block  Middle superior alveolar nerve block  Anterior superior alveolar nerve block  Maxillary nerve block  Greater palatine nerve block  Nasopalatine nerve block Exta oral injection techniques  Ifraorbital nerve block – anterior, middle superior alveolar nerve block  Maxillary nerve block
  76. 76.  Supra periosteal injection:  Anaesthetize buccal soft tissue & hard tissue  Nerves anaesthetized – large terminal branches  Indication :  1 or 2 teeth need to be anaesthetized / small area
  77. 77.  Contra-indication :  Infection  Dense bone covering  Target area :  Behind apices of tooth  Landmarks :  Muco-buccal fold  Crown & root length
  78. 78.  Area anaesthetized:  Maxillary 3rd, 2nd & 1st molar (except mesio-buccal root of 1st molar  Bone & periodontium over these  Indication:  Treatment of 2 or more molars required  Supra-periosteal injection – ineffective  Acute inflammation
  79. 79.  Contra-indication:  Pt with bleeding disorders  Disadvantage:  More of soft tissue landmarks used  2nd injection for 1st molar  Landmarks:  Mucobuccal fold  Zygomatic process of maxilla  Infratemporal surface of maxilla  Anterior border and coronoid process of mandible  Tuberosity of maxilla
  80. 80.  Complications:  Hematoma –  Non visible - pterygoid plexus posteriorly  Visible – buccal aspect  Accidental mandibular Anaesthesia  Orbital contents – anaesthetized accidentally  Accidental - parotid gland  facial nerve affected
  81. 81. Only in present in about 20% of the poplation thereby limiting its clinical usefulness of this block.  Area anaesthetized:  Mesiobuccal root of the 1st molar, pulps of maxillary first 1st and 2nd premolar  Buccal periodontal tissues  Indication:  When ifra orbital block fails to provide anaesthesia to maxillary canine  Dental procedures involving both maxillary premolars  contraindication:  When infection or inflammation
  82. 82.  Areas anaesthetized  Pulp of maxillary C.Is – Canine  Buccal periodontium, lower eyelid, lateral aspect of nose  Upper lip  Indications  More than 2 anterior teeth  Contraindications  Discreet treatment areas  Hemostasis of localized area – not adequately achieved
  83. 83.  Landmarks  Mucobuccal fold,lforamen supra –orbital notch infra-orbital notch, infra-orbital foramen, mental foramen  2 methods:  Intra-oral  Premolar approach  Incisal approach
  84. 84. 1.Nasopalatine nerve block/spenopalatine nerve block/ incisive nerve block  Areas anaesthetized  Anterior portion of Hard palate and over lying structures back to the bicuspid area.  Indications  Anterior palatal procedures supplementing infraorbital nerve blocks  Anaesthesia of nasal septum  Landmarks  Central incisor & incisive papilla
  85. 85.  Complications  Hematoma  Necrosis  Technique  Single needle penetration  Multiple needle penetration Usually most discomforting block for patient – very painful
  86. 86. 2.Greater palatine nerve block/ anterior palatine nerve block  Areas anaesthetized  Palatal soft tissue – posterior aspect  Palatal hard tissue  Indication  Surgical procedures posterior portion of hard palate  Palatal Anaesthesia in conjunction with posterior superior alveolar nerve block.  Landmarks  Greater palatine foramen – junction of the maxillary alveolar process & palatine bone  Between the 2nd & 3rd molars – 1-1.5cms away from gingival margin
  87. 87.  First reported by freidman and hochman in 1997 during development of CCLAD system  Muscles of facial expression and upper lip anesthesized.  Nerves anesthetized  ASA and MSA  Areas anesthetized  Pulpal anesthesia of maxillary incisors,canines and premolars  Buccal and palatal attached gingiva  Indications  Performed with CCLAD  When anterior cosmetic procedures are performed  When anesthesia is desired from a single injection  contraindications  Patients with thin palatal tissues  Patients who cannot tolerate the 3-4 minute adminstration time  Long procedures >90 mins
  88. 88.  Advantage  Less amount of LA is deposited 0.5ml/min  Allows for accurate smile line assesment in case of aesthetic restorations  Disadvantage  Very slow adminstration  Can cause operator fatigue  Maybe uncomfortable for the patient  Technique sensitive
  89. 89.  Nerve anaesthetized  Maxillary division of trigeminal nerve  Areas anaesthetized  Pulpal Anaesthesia  Maxillary teeth – 1 side  Periodontium / soft tissue – 1 side  Indications  Extensive oral / periodontal / endodontal procedures  Other regional nerve blocks not possible  Therapeutic procedure to diagnose neuralgias
  90. 90.  Contra-indications  Pediatric patients  Inexperience operators  Infection / inflammation  Hemorrhage – anticipated  Greater palatine canal approach not possible – bony obstr.  Landmarks  Mucobuccal fold distal to maxillary 2nd molar  Maxillary tuberosity  Zygomatic process  Greater palatine foramen
  91. 91.  Complications  Hematoma  Penetration into orbit  Volume – displaces orbital structures, periorbital swelling, proptosis, 6th nr block – diplopia, transient loss of vision, optic nerve blocked, retrobulbar block producing mydriasis, corneal anesthesia / hemorrhage, opthalmoplegias (common)  Penetration into nasal cavity  Patient complains – LA running down the throat – to prevent keep mouth wide open  Technique  High tuberosity approach  Greater palatine canal approach
  92. 92. I. Anterior and middle superior alveolar nerve block –  Nerves anaesthetized  Infraorbital nerve  Inferior palpebral, lateral nasal and superior labial nerves  Area anaesthetized  Incisors and bicuspids on the effected side  Labial alveolar plate and associated tissues  Anatomical landmarks  Pupil of the eye  Infraorbital ridge  Infrorbital notch  Infraorbital depression  Indications  When Intra oral route is not feasable  When attempts of intra oral anaesthesia have been ineffective
  93. 93. II. Maxillary nerve block –  Areas anaesthetised  Anterior temporal & zygomatic region  Lower eyelid  Side of nose  Anterior cheek  Upper lip  Maxillary teeth / alveolar bone & overlying structures – 1side  Hard & soft palate  Tonsils – parts of pharynx  Nasal septum – floor of nose
  94. 94.  Indications  Extensive surgery – 1 half of maxilla  Others blocks not possible  Therapeutic purposes  Technique  mid point of zygomatic process  Needle gently contact lateral pterygoid plate  Maximum length of 4.5cms directed slightly upward & forward  Note:  In final position – internal maxillary artery – inferior to needle  Temporal vessels on either sides  Posteriorly foramen ovale with mandibular nerve & foramen spinosum with middle meningeal artery  Anteriorly pterygomaxillary fissure
  95. 95. INFERIOR ALVEOLAR NERVE BLOCK Other common name- Mandibular block Different techniques are:  DIRECT METHOD.  INDIRECT METHOD.  METHOD OF CLARKE & HOLMES  METHOD OF ANGELO SARGENTI  VAZIRANI- AKINOSI TECHNIQUE  GOW-GATE’S TECHNIQUE  KURT THOMA EXTERNAL APPROACH
  96. 96.  Classical inferior alveolar nerve block  Nerves anaesthetised- inferior alveolar nerve block and its subdivisions  Areas anaesthetised  Mandibular teeth upto midline  Body of mandible  Inferior portion of ramus  Buccal periosteum & mucous membrane  Lingual soft tissue  Anterior 2/3rd of tongue  Indications  Multiple mandibular teeth – procedures  Buccal / Lingual soft tissue anaesthesia
  97. 97.  Contraindications  Infection / acute inflammation  Young children / mentally handicapped  Landmarks  Coronoid notch  Mucobuccal fold  External oblique ridge  Retromolar triangle  Internal oblique ridge  Pterygomandibular raphe  Occlusal plane of posterior mandibular teeth  Complication  Hematoma  Trismus  Transient facial paralysis (parotid gland)
  98. 98.  Anatomical structures - final position  Disadvantages: • Rate of indequate anesthesia is high 10-20% • Intra oral landmarks are not consistently reliable • Highest positive aspiration of about 10-20% • Partial anesthesia where bifid inferior alveolar nerve and bifid mandibular canal are present
  99. 99. Stages in the indirect technique :- Initial insertion of the needle more laterally,thus immediately strikes the bone, needle is partially withdrawn after touching the bone, syringe is moved parallel to the lower molars on the other side, insertion of the needle beyond theinternal oblique ridge, the syringe is returned to it’s original direction, ie over the lower premolars and deposit 1.5ml of solution in the pterygomandibular space.
  100. 100. It involves deposition of solutions @ a higher level than usual. It is a modification of indirect technique. In the standard direct/indirect technique, the analgesic is placed immediately behind the mandibular foramen, which is 1cm above the occlusal plane of molar teeth. At this level the nerve is concealed by lingula & sphenomandibular ligament. Depositing the solution at a higher level causing complete anesthesia.
  101. 101. This technique is a modification of direct method. The difference is that the nerve is approached from a higher level than usual. TECHNIQUE: Syringe with 1 5/8 inch 26gauge needle is used.The index finger is placed in the retro molar fossa with nail facing lingually. The needle is inserted opposite to the mid point of the finger nail. The barrel of the syringe is now placed between and in contact with the upper premolars of the opposite side. Needle is slowly inserted in a downwards & backwards direction until it touches the bone, depth is 1cm. 1.5ml of solution is deposited.
  102. 102.  Nerves anesthetized – inferior alveolar nerve, lingual nerve buccinator nerves  Area anesthetized  one half of mandible upto mid line including lingual tissue and inferior portion of the ramus of the mandible.  Land mark-  occluding plane of the teeth.  Muco gingival junction maxillary teeth.  Antr border of ramus.  Orientation of bevel must be oriented away from the bone of mandibulaar ramus (bevel faces toward mid line).  More popular now  Land marks easy  One prick – mandibular, buccal, lingual n anesthetised.  Patient more comfortable.
  103. 103.  Advantages • Atraumatic, • pats. with restricted mouth opening. • fewer post op complications. • Disadvantages • Difficult to visualize the path of needle and depth of insertion. • Complications • hematoma, transient facial n. paralysis.
  104. 104. Nerves anaesthetised – inferior alveolar, mental, incisive, lingual, mylohyoid, auriculotemporal and buccal.  Area –all mandibular hard and soft tissue Upto mid line.  Indications- multiple procedures on mandibular teeth, buccal soft tissue anaesthesia from third molar to midline, conventional inf. alv. n. block is unsuccessful.  Contraindications – infection or acute inflammation in the area of infection, pats. with restricted mouth opening.
  105. 105.  Land marks-  Extraoral- corner of mouth, lower border of the tragus, intertragic notch  Intraoral – height of injection established by placement of needle tip just below the mesiolingual cusp of max. 2nd molar, penetration of soft tissue distal to 2nd molar at the same height.  Final position needle is just inferior to condyle and insertion of lateral pterygoid. Gained popularity – single needle penetration, relies on soft tissue landmarks – differ from patient to patient
  106. 106. OTHER NAME Buccal nerve block or buccinator nerve block. TARGET AREA Buccal nerve as it passes over the anterior border of the ramus LAND MARKS  External oblique ridge  Retromolar triangle  Distal to 3rd molar TECHNIQUE 1” 25 gauge needle is inserted in to the buccal mucosa just distal to the lower 3rd molar. 0.25 to 0.5ml of solution is deposited.
  107. 107.  Lingual nerve block –  Area anaesthetised –  Anterior 2/3rd tongue, floor of mouth, lingual mucoperiosteum Only used singly to operate on tongue, floor of mouth  Buccinator / long buccal nerve block  Area anaesthetised –  Buccal mucosa & mandibular molar – mucoperiosteum  Land marks  External oblique ridge, retromolar triangle
  108. 108.  Mental & Incisive nerve block  Area anaesthetised  Mandibular hard & soft tissue – labial aspect with lower lip  Landmarks  Bicuspid teeth, lower ridge of body of mandible  Supra & infra orbital notch  Pupil of the eye 2 inch 22 gauge needle used & introduced slightly anteriorly & downwards
  109. 109.  Mandibular nerve  Area anaesthetised  Temporal region with auricle of ear & external auditory meatus  TMJ, salivary glands  Anterior 2/3rd of tongue  Mandible – hard & soft tissue – midline  Landmarks  mid point of zygomatic arch  Zygomatic notch  Cornoid process of mandible  Lateral pterygoid plate
  110. 110.  Indications  When need to anaesthetise entire mandibular nerve  Infection / trauma – makes terminal anaestheisa not possible  Diagnostic / therapeutic The needle is pointed posteriorly & to a greater depth of 5 cms
  111. 111. This technique is used when there is severe limitation of opening of the jaws in case of ankylosis of TMJ. Anatomical land marks/ surface markings:  Lowest point on the anterior border of the masseter  Tragus  Posterior border of the ascending ramus Anterior border of masseter is located by clenching the teeth.The point is marked and a line drawn connecting this with the tragus of the ear.The mid point of this line shows the position of the mandibular foramen. Needle Used 21 gauge,7 to 8cm long.
  112. 112.  Definition  An anaesthetic complication may be defined as any deviation from the normal expected pattern during or after securing regional anaesthesia  2 types  Local  Systemic
  113. 113.  LOCAL COMPLICATIONS  Needle breakage  Pain on injection  Burning on injection  Persistent anaesthesia or paresthesia  Trismus  Hematoma  Sloughing of the tissue / soft tissue injury  Facial nerve paralysis
  114. 114.  SYSTEMIC COMPLICATIONS  Toxicity  Idiosyncracy  Allergy  Anaphylactoid reaction  Syncope
  115. 115.  Classification  Primary / secondary  Primary – caused & manifested at time of anaesthesia  Secondary – manifested later  Mild / severe  Mild – exhibit slight change from normal expected pattern - reverses itself without treatment  Severe – manifests itself – pronounced deviation - requires specific treatment
  116. 116.  Transient / permanent  Transient – is one that is severe at occurrence – no residual effects  Permanent – residual effect; lasts for a life time even though it is mild Complications could be a combination of any of the above mentioned types Majority are either Primary Mild & Transient or Secondary Mild & Transient
  117. 117.  Complications  Attributed to solutions – toxicity, allergy, idiosyncrasy, anaphylactoid reaction, local irritation  Attributed to technique / needle – syncope, muscle trismus, pain, edema, hematoma
  118. 118.  Cause –  Unexpected movement – patient (if patient movement is opposite to path of needle insertion)  Multiple used needle  Defective manufacture of needles/barbed needles  smaller gauge – more likely to break
  119. 119.  Prevention  Correct gauge – 25 gauge  Long needles – prevent penetration till hub  Not to redirect when in tissue  Management  Patient – not to move – hand in the mouth – mouth open  Fragment visible – remove it  Fragment not visible – inform patient – not necessary for intervention immediately – Radiograph suggested
  120. 120.  Precautions  Avoid bony contact  Avoid heavy pressure  Avoid movement of needle and patient
  121. 121.  Causes –  Careless injection technique  Multiple used needle  Rapid deposition  Problems –  Pain – patient anxiety – unexpected movements  Prevention –  Proper technique – sharp needles  Enter topical anaesthetics  Inject slowly – solution sterilized  Check temperature of solution
  122. 122.  Causes  Due to pH of solution  5 (LA) – 3 (LA+VC)  Rapid injection  Contamination  Warm solution  Problems  pH  disappears upon LA action – no residual effect  Contaminated solution  other complications – trismus, edema, paraesthesia
  123. 123.  Prevention  Slow injection – 1ml / minute  Cartridge stored at room temperature – away from containers with alcohol / other agents
  124. 124.  Causes  Direct trauma to nerve – bevel of needle  LA solution containing neurotoxic substance – alcohol  Injection of wrong solution  Hemorrhage / infection – near to nerve  Problem  Persistent anaesthesia – usually rare  Biting / thermal / chemical insult – without patient awareness  When lingual nerve is involved – taste impaired
  125. 125.  Prevention  Proper care & handling of dental cartridge  Adherence to injection protocol  Management  Usually resolve in 8 weeks  Periodic recall & check up of patients  Persistence – consult neurosurgeon  TENS  Recall patient every 2 months for check up
  126. 126.  Definition  “difficulty in opening the jaws due to muscle spasm”  Causes  Trauma – muscle / blood vessel  Irritating solution  hemorrhage  Infection  Multiple needle punctures  LA have been known to have slight myotoxicity  Excessive volume – distension of tissues  Problems  Pain / hypomobility
  127. 127.  Prevention  Use of sharp, sterile, disposable needle  Aseptic technique  Practice atraumatic methods  Avoid repeated injections  Use minimum volume  Control infection
  128. 128. Management  Heat therapy  Warm saline rinses, moist hot packs  Analgesics  Aspirin, Codeine (30-60mg), muscle relaxants  Initial physiotherapy  Thrice a day  Antibiotic regime  Possibility of infection
  129. 129.  “effusion of blood into extra-vascular spaces”  Causes  Arterial & venous puncture – common in PSA & Inf. Alv. nerve blocks  Patients with bleeding disorders  Problem  Bruise – may / may not be visible extra-orally  Complications – pain & trismus  Swelling & discoloration  Prevention  Knowledge of normal anatomy – proper technique  Shorter needle – PSA, minimize the number of penetration  Discard defective needles- barbed needles
  130. 130.  Management  Immediate – apply firm pressure  5-10minutes  Inf. Alv. Nr. Block – medial aspect of ramus  Infra orbital, Mental, Incisive block – directly over foramen  PSA – pressure on soft tissue with finger as posteriorly as tolerated by patient – medial superior direction  Patient to be reviewed after 24 hours, advice analgesics, cold application upto 4-6 hours, warm- pack application next day
  131. 131.  Comparitively rare complication  Instrument needle solution to be as aseptic as possible  Area & operative hands – cleaned  Avoid passing needle through infected area  Use disposable syringes
  132. 132.  Causes  Trauma during injection  Infection, hemorrhage  Allergy (Angioedema)  Injection of irritating solution  Problems  Pain & dysfunction  Airway obstruction
  133. 133.  Prevention  Proper care & handling of armamentarium  Atraumatic injection technique  Complete medical evaluation prior to injection  Management  Trauma – resolve in few days without therapy  Hemorrhage – resolve slowly 7-14 days  Allergy – life threatening, airway impairment – basic life support, call medical help, Epinephrine – 0.3mg, Antihistamine, Corticosteroids  Total airway obstruction – Tracheostomy / Cricothyroidectomy
  134. 134.  Causes  Epithelial desquamation – topical anaesthesia – long time, heightened sensitivity to LA  Sterile abscess – secondary to prolonged ischemia – VC in LA  site – hard palate  Problems  Pain & infection  Prevention  Topical – for not more than 1-2 minutes  VC – minimal concentration in solution
  135. 135.  Management  Symptomatic – pain – analgesia  Epithelial desquamation – resolve few days  Sterile abscess resolve  7-10 days
  136. 136.  Causes  Trauma occurs – frequently mentally / physically challenged children  Primary cause – significantly longer duration of action  Problem  Pain & swelling  Infection of soft tissue  Prevention  Cotton roll between lip & teeth  Patient – guarded against eating / drinking  Warning sticker
  137. 137.  Cause  LA solution into parotid gland – usually while giving Inf Alv Nr. Block, Akinosis technique  Problem  Ipsilateral loss of motor control – Buccinator muscle  Inability to raise the corner of Mouth, close Eye lid  Prevention  Needle tip to contact bone, redirection of needle to be done only after complete withdrawal
  138. 138.  Management  Reassure the patient  Resolves after action of LA is over  Eye patches to the affected – eye drops  Contact lenses if any – removed
  139. 139.  Toxicity / toxic overdose  “Signs and symptoms that result from an overly high blood level of a drug in various target organs and tissues”  Predisposing factors  Age – any age  Weight – greater the body weight greater is the amount of dose tolerated before overdose reaction  Sex – during pregnancy – renal function disturbed – females more affected at this time  Diseases – hepatic & renal dysfunction reduced breakdown  Congestive heart failure – less liver perfusion  Genetics – pseudocholinesterase deficient – toxicity - Ester LA
  140. 140.  Drug factors – Vasoactivity – vasodilation – increase in blood concentration  More concentration – greater risk  Dose- smaller dose should always be preferred  Route of Administration – Intravascular – increased toxicity  Rate of injection – slower rate preferred  Vascularity of injection site – more vascular – greater absorption  Presence of Vasoconstrictor – with VC less absorption
  141. 141.  Causes of toxicity –  Biotransformation usually slow  Drug – slowly eliminated by kidney  Too large a total dose  Absorption from injection site - rapid  Accidental intra-vascular injection  Symptoms –  CNS – cerebral cortical stimulation – talkative, restless, apprehensiveness, convulsions  Cerebral cortical depression – lethargy, sleepiness, unconsciousness  Medullary stimulation – increased B.P, Pulse rate, Respiration
  142. 142.  Medullary depression – mild fall in B.P– severe cases drops to 0 , Pulse , Respiration – similar effect  Treatment  Mild overdose reaction – slow onset reaction – > 5 mins administer Oxygen (prevent acidosis), monitor vital signs, in case of convulsions – anti-convulsants (diazepam/midazolam infusion)  Slower onset - >15 mins – same procedure  Severe overdose reaction – rapid onset – 1 minute – unconsciousness with or without convulsion, patient in supine position, convulsions – protect hand, leg, tongue, BLS, administer anti-convulsant,use of vasopressor(phenyl ephrine) i.m if hypotensiom presists.  post seizure – CNS depression usually present
  143. 143.  “It is an adverse response that is neither an overdose nor an allergic reaction”  Common cause – some underlying pathology/psychological /genetic mechanism  Psychotherapy may be helpful  Treatment – symptomatic ..ABC
  144. 144.  “transient loss of consciousness that is caused due to cerebral ischemia (neurogenic shock)”  Anxiety – increased blood supply to muscles, sitting position 2mm Hg, less pressure – cerebral arteries  Clinically pallor, light headedness, dizziness, tachycardia & palpitation – may further lead to Unconsciousness  Treatment – discontinue procedure, supine position- (trendelenburg position), deep breathing, O2 administration if required, BLS
  145. 145.  “hypersensitive state acquired through exposure to a particular allergen reexposure to which produces a heightened capacity to react”  1 % of all reaction in LA is allergy  Predisposing factors  Hyper sensitivity to ester more common-procaine  Most of patients allergic to methyl paraben  Recently allergy to sodium meta bi sulfide is also increasing Precautions--- Ho of allergy to be recorded Ho any asthmatic attack to be noted. Always better to test the patient for allergy before treatment.
  146. 146.  Consultation and allergy testing  Refer doubtful cases for allergic skin test – sub cutaneous test most sensitive.  Informed consent that includes cardiac arest end death to be included.  Signs and symptoms of allergy.  Dermatological------ urticaria –wheal and smooth elevated patch seen, --- ---angio oedema—localised swelling – face hands, common  Respiratory– broncho spasm, respiratory distress,  dysnea, wheezing, flushing, tachycardia etc.
  147. 147.  Laryngeal edema – type of angio neurotic oedema- life threating.  Edema upper air way – laryngeal edema  Lower air way affect broncioles- small.
  148. 148. Management skin reactions-  Delayed – non life threatening - oral histamine blockers- 50 mg diphenhidramine,10 mg chlorpheniramine 3-4 days.  Immediate reaction—with conjunctivitis rhinitis- vigorous management.  0.3 mg epinephrine. IM  50 mg diphenhydramine Im  medical help summoned.
  149. 149.  Observe patient for minimum of 60 min  Oral histamine blockers for 5 days.  Respiratory reaction –  patient in comfortable position.  administer - oxygen  Admn epinephrine- bronchodilator  Observe for 60 min , advise anti histamines to prevent relapse.  Histamine blockers Im  Laryngeal edema-  Patient position ,oxygen, broncho-dilator, iv anti histamines.  If condition not improving cricothyrotomy - achieve patent air way if necessary give artificial ventilation.
  150. 150.  Patient with confirmed allergy status-  if patient allergic to any one type of anesthetic ester / amide use the other.  Use histamine blocker like diphenhydramine as anesthetic.  General anesthesia  alternative method of pain control –  electric anesthesia / hypnosis.
  151. 151.  Efforts have been made to improve to increase the ability of the anesthetic to cross intact skin  Attempts at making the experience more comfortable for the patients  The addition of hyalurodinase for deeper penetration than plain solutions  Local anaesthesia without the use of needles  Exploring the possibility of reversing local anaesthesia at the conclusion of dental procedure
  152. 152. Centbucridine-  5-8 time potency of lidocaine  Doesn’t effect CNS or CVS except in large doses  When adminstered in overdose the drug acts as a true stimulant of nervous system  0.5% concentratio effective to 2% lignocaine Ropivacaine  Amide anaesthetic similar to mepivicaine and bupvicaine  Has greater margin of safety  Decrease cardiotoxicity as compared to others
  153. 153.  Its an oil in water emulsion containing high concentrations of lidocaine and prilocaine in base form  Provides enouh anaesthesia of intact skin to permit a venipuncture  Consists of 5% cream containing 25mg/g lidocaine and prilocaine respectively
  154. 154.  The adminsteration of local anaesthetic is usually uncomfortable for the patient due to difference in PH  Addition of sodium bicarbonate provides more rapid onset of block, but it has decreased stability  CO2 enhances diffusion, as it increase intracellular PH. Unstable solution, has short life
  155. 155.  First used described in 1949  Provides more rapid onset of anaesthesia  Decrease duration of action  Possibility for allergic reactions
  156. 156.  Precursor for TENS  It acts by working at low frequency of 2 Hz  It serotonin, endomorphin levels in blood  It takes about 10 minutes for sufficient rise of blood levels  It causes dilation of vessels  It can be used to reverse partially of totally the effects of local anaesthesia  Can be used in patients who have needle phobia  Its being used with increasing success in chronic TMJ pain  Its contraindicated in patients having cardiac pacemakers, pregnancy, young and old age patients
  157. 157. THANK YOU

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