Anaesthesia /certified fixed orthodontic courses by Indian dental academy

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Anaesthesia /certified fixed orthodontic courses by Indian dental academy

  1. 1. INDIAN DENTAL ACADEMY Leader in continuing dental education www.indiandentalacademy.com www.indiandentalacademy.com
  2. 2. CONTENTS  INTRODUCTION  GENERAL ANAESTHESIA -HISTORY -CLASSIFICATION -IDEAL REQUIREMENTS -MECHANISM OF ACTION -STAGES OF ANAESTHESIA - COMMONLY USED ANAESTHETICS www.indiandentalacademy.com
  3. 3.  LOCAL ANAESTHESIA -HISTORY -CLASSIFICATION -MECHANISM OF ACTION -COMPOSITION -COMMONLY USED ANAESTHETICS -NERVE BLOCKS -COMPLICATIONS  NEWER ADVANCES  CONCLUSION  REFERENCES www.indiandentalacademy.com
  4. 4. www.indiandentalacademy.com
  5. 5. ANAESTHESIA (greek word) An aesthesis CLASSIFICATION General Local www.indiandentalacademy.com
  6. 6. GENERAL ANAESTHESIA A state of unconsciousness produced by an anesthetic agent,with absence of pain sensation over the entire body and a greater or lesser degree of muscle relaxation www.indiandentalacademy.com
  7. 7. CARDINAL SIGNS Loss of all sensations Unconsciousness (sleep) Muscle relaxation Abolition of reflexes www.indiandentalacademy.com
  8. 8. HistoryBefore 1846 - physical methods(packing the limb in ice) - drugs like alcohol,opium 1776 - Priestley - 1st anesthetic nitrous oxide 1844 - Horace Wells - nitrous oxide - extraction 1846 - William Morton – ether After 1846 1847 - James Simpson – chloroform 1868 - Edmond Andrews – N2O + O2 1929 – Cyclopropane 1935 – Thiopentone 1956 - Halothane www.indiandentalacademy.com
  9. 9. CLASSIFICATION INTRAVENOUS INHALATIONAL NITROUS OXIDE ETHER HALOTHANE SEVOFLURANE ENFLURANE DISSOCIATIVE ANESTHESIA INDUCING AGENTS KETAMINE BENZODIAZEPINES www.indiandentalacademy.com PROPOFOL THIOPENTONE DIAZEPAM
  10. 10. IDEAL REQUIREMENTS :  Smooth & rapid induction  Produce unconsciousness  Produce amnesia  Maintain essential physiological functions while blocking the reflexes  Produce skeletal muscle relaxation  Adequate analgesia  Smooth,rapid & uneventful recovery www.indiandentalacademy.com
  11. 11. MECHANISM OF ACTION  Inhibit reticular activating system      OVERTON & MEYOR(1901) potency---------lipid solubility Ligand gated ion channels—target I.V. anesthetics – GABA receptors N2O & ketamine – NMDA receptors www.indiandentalacademy.com
  12. 12. STAGES OF ANAESTHESIA : Guedel (1920) – i. Stage of analgesia ii. Stage of delirium iii. Stage of surgical anesthesia iv. Medullary paralysis www.indiandentalacademy.com
  13. 13. Pharmacokinetics of inhalalational anaesthetics alveoli blood brain Factors affecting the transfer of anesthetic agent :  Solubility of the agent in blood  Rate of blood flow through lungs & tissues  Partial pressure of the agent Elimination : Halothane – 20% in liver www.indiandentalacademy.com
  14. 14. METHODS OF ADMINISTRATION  Open drop method  Through anesthetic machines - open system - closed system Closed system Open system www.indiandentalacademy.com
  15. 15. PREANESTHETIC MEDICATION Need for :  Rapid & smooth induction  Sedation  Counteract adverse effects  Relieve pain DRUGS USED:  Chronic medication  Anticholinergics – atropine  H2 receptor antagonist – ranitidine  Sedative – hypnotics – diazepam  Opoids  Anti-emetics – metachlopromide www.indiandentalacademy.com
  16. 16. INHALATIONAL ANESTHETICS  NITROUS OXIDE – colorless / odorless / non irritating / non inflammable / sweet taste good analgesic poor anesthetic 70% N2O + 25- 30% O2+ 0.2 – 2% ether – anesthesia (G- O –E Technique)  METABOLISM : rapidly eliminated unchanged – lungs www.indiandentalacademy.com
  17. 17. ADVANTAGES :  rapid induction & recovery  No deleterious effects on heart ,kidney ,liver  Nausea, vomiting uncommon DISADVANTAGES :  Not a potent anesthetic  Co2 accumulation or hypoxia – prolonged administration  Special apparatus required CONTRAINDICATION :  Patients with collection of air in pericardial, pleural and peritoneal cavities, COPD. www.indiandentalacademy.com
  18. 18. ETHER :  Oldest anesthetic  Not used – highly inflammable , pungent odor post operational nausea & vomiting HALOTHANE :  Fluorinated ,volatile anesthetic  non irritating / non inflammable / colorless liquid with sweet odor  potent anesthetic : 2 - 4% -induction 0.5 – 1% - maintenance METABOLISM :  60 – 80% -eliminated unchanged  Rest – liver www.indiandentalacademy.com
  19. 19. ADVANTAGES :  Quick & pleasant induction  Quick recovery  No post op nausea & vomiting DISADVANTAGES :  Inadequate muscle relaxation  Hypotension  Sensitizes heart to Adrenaline – arrhythmias  Expensive & special apparatus www.indiandentalacademy.com
  20. 20. INDICATIONS :  Bronchial asthma  Plastic surgery – bloodless field CONTRAINDICATIONS :  Intracranial lesions  Hepatic diseases www.indiandentalacademy.com
  21. 21. INTRAVENOUS ANESTHESIA THIOPENTAL :  Ultra short acting barbiturates  Induction dose : neonates – 5 – 8 mg / kg adults – 3-5 mg / kg elderly – 1 - 3 mg / kg METABOLISM :  Metabolized in liver USES :  For induction of GA  Anesthetic for short duration surgery  As an anti convulsant www.indiandentalacademy.com
  22. 22. ADVANTAGES : 1. Ease of administration 2. Rapid & pleasant induction 3. Low incidence of nausea & vomiting 4. Quick recovery DISADVANTAGES : 1. Depth of anesthesia cant be judged 2. Apnea , coughing , laryngospasm ( occasional ) 3. Shivering & delirium during recovery 4. Depresses vasomotor centre & myocardium 5. Poor analgesic & muscle relaxant www.indiandentalacademy.com
  23. 23. PROPOFOL : Oily liquid – 1% emulsion Unconsciousness – 15 -45 sec Rapidly metabolised in liver USES :  Induction  Short duration surgeries  Day care surgery www.indiandentalacademy.com
  24. 24. ADVANTAGES :  rapid induction & recovery  no bronchospasm  low post op nausea & vomiting  safe during pregnancy DISADVANTAGES :  Induction apnea  Respiratory depression – higher doses  Bradycardia  Pain during injection www.indiandentalacademy.com
  25. 25. KETAMINE :  Non – barbiturate anesthetic  Induces dissociative anesthesia  Primary site of action – cortex ( limbic system)  Dose – 1-3 mg / kg / IV - 5 – 10 mg /kg / IM DISADVANTAGES :  Delirium / hallucination  Poor muscle relaxant  Laryngospasm rare USES :  Children – induction & maintainence of anesthesia  Adults – short surgical procedures www.indiandentalacademy.com
  26. 26. CONTRAINDICATIONS :  Hypertensive patients  Thyrotoxic patients  Abdominal surgery  Ocular surgery www.indiandentalacademy.com
  27. 27. COMPLICATIONS : During Anaesthesia :  Respiratory depression  Salivation  Hypotension  Cardiac arrhythmias  Aspiration of gastric contents  Delirium , convulsions After anesthesia :  Nausea , vomiting  Organ toxicity  Emergence delirium www.indiandentalacademy.com
  28. 28. POST ANESTHETIC MEDICATION Need for:  Relief of pain  Post op nausea & vomiting DRUGS USED:  Opioids  Anti-emetics www.indiandentalacademy.com
  29. 29. LOCAL ANAESTHESIA Reversible loss of sensation in a area of the body caused by a depression of excitation in nerve endings or an inhibition of the conduction process in peripheral nerves. History : 1860 – Neimann isolated cocaine 1884 – Sigmond Frued – cocaine induced localised numbness 1884 – Koller introduced cocaine as LA 1884 – Nash used cocaine for extraction 1905 – Einhorn developed procaine 1943 – Lofgren synthesized lignocaine 1948 – Gordh usedwww.indiandentalacademy.com lignocaine
  30. 30. CLASIFICATION : I. BASED ON APPLICATION : INJECTABLE Low potency/short duration procaine, chloroprocaine SURFACE ANAESTHETICS Soluble cocaine, lignocaine Intermediate potency/duration lignocaine, prilocaine High potency/long duration tetracaine, bupivacaine www.indiandentalacademy.com Insoluble benzocaine
  31. 31. II. BASED ON CHEMICAL STRUCTURE : Esters Amides Benzioc acid esters lignocaine cocaine prilocaine Para-amino benzoic esters mepivacaine procaine / tetracaine bupivacaine benzocaine / chloroprocaine III. BASED ON ORIGIN : a. Natural : Cocaine b. Synthetic: PABA derivatives – procaine / tetracaine Acetanilide derivatives – lignocaine Quinolone derivatives – cinchocaine Acrinide derivatives – bucricaine www.indiandentalacademy.com
  32. 32. CHEMISTRY : Amphiphilic in nature LA consists of : Hydrophobic group Aromatic residue Intermediate alkyl Intermediate alkyl www.indiandentalacademy.com Hydrophilic group Tertiary amine
  33. 33. R3 Ester: R 1—COO—R2 —N R 1 — Lipophilic aromatic residue. R4 R3 Amide: R 1—NHCO—R 2—N R4 R 2 — Aliphatic intermediate connector. R 3, R 4 — Alkyl groups, occasionally H. Constitute with N the hydrophilic terminus. www.indiandentalacademy.com
  34. 34. IDEAL REQUIREMENTS :           Non irritating to tissues Not cause permanent alteration in the nerve Low systemic toxicity Highly effective Rapid onset of anesthesia Long duration of action No allergic reactions Readily undergo biotransformation Should be stable in solution Should be sterile www.indiandentalacademy.com
  35. 35. MECHANISM OF ACTION : STRUCTURE OF A NERVE CELL – www.indiandentalacademy.com
  36. 36. Differential sensitivity of nerve fibre CLASS MYLENATION DIAMETER CONDUCTION VELOCITY FUNCTIONS Aα heavy 12-20 70-120 Motor and propioception Aβ Moderate 5-12 30-70 Touch and pressure Aχ Moderately 3-6 15-30 Motor to muscle spindle Aδ lightly 2-5 12-30 Pain, temperature, touch B lightly 1-3 3-15 Preganglionic autonomic C None none 0.4-1.2 0.3-1.3 0.7-1.3 0.7-1.3 Pain & reflex response Postganglionic sympathetics www.indiandentalacademy.com
  37. 37. PHYSIOLOGY OF NERVE CONDUCTION : www.indiandentalacademy.com
  38. 38. MECHANISM OF ACTION : THEORIES :  Acetylcholine theory  Calcium displacement theory  Surface charge theory  Membrane expansion theory  Specific receptor theory – most accepted www.indiandentalacademy.com
  39. 39. www.indiandentalacademy.com
  40. 40. HOW DOES LA WORK ?  Displacement of Ca2+ from Na channel receptor site which permits  Binding of LA to the receptor site which produces  Blockade of Na+ channel &  Decrease in Na conductance which leads to  Depression of rate of electrical depolarisation &  Failure to achieve threshold potential , along with a  Lack of development of propagated action potential which is called conduction blockade www.indiandentalacademy.com
  41. 41. R-NH+ R-N + + H acid base base pH = pKa + log acid www.indiandentalacademy.com
  42. 42. Factors Affecting the Reaction of Local Anesthetics Lipid solubility  Increase in the lipid solubility leads to faster nerve penetration, block sodium channels, and speed up the onset of action..  Local anesthetics have two forms, ionized and nonionized. The nonionized form can cross the nerve membranes and block the sodium channels.  So, the more nonionized present, the faster the onset of action. pH influence  Usually at range 7.6 – 8.9  Decrease in pH shifts equilibrium toward the ionized form, delaying the onset action. www.indiandentalacademy.com
  43. 43. Vasodilation  Affects the anesthetic potency & duration of action .  Lower vasodilator activity of a local anesthetic leads to a slower absorption and longer duration of action Protein binding  Protein binding regulate the duration of anaesthetic activity  Highly protein bound LA will remain for a long time Procaine  6% protein bound  Ropi, bupi, etidocaine  94-96% protein bound www.indiandentalacademy.com
  44. 44. Local anesthetic metabolism Ester Hydrolysis Hydrolysis CH 3 Amide Hydroxylation and conjugation O NHC CH R2 R3 N R1 www.indiandentalacademy.com R4 N-dealkylation (and cyclization)
  45. 45. LIGNOCAINE COMPOSITION:  Lignocaine – Local anesthetic agent  Adrenaline – Vasoconstrictor  Sodium metabisulfite – Antioxidant  Methyl paraben – Preservative  Thymol – Fungicide  Sodium chloride – Isotonicity of solution  Water - Diluent www.indiandentalacademy.com
  46. 46. PROPERTIES:  Amide type of anesthetic  Potency = 2  Toxicity = 2  Metabolism: in liver (microsomal enzymes)  Excretion: via kidney  Vasodilating property less than procaine  pH = 6.5 (plain solution) 5.0 – 5.5 (with vasoconstrictor)  8.Onset of action – rapid (2 –3 mins)  9.Effective dental concentration is 2%  10.Maximum recommended dose (with vasoconstrictor) - 7.0 mg/kg; not to exceed a dose of 500 mg - 4.4 mg/kg; not to exceed a dose of 300 mg (without vasoconstrictor) www.indiandentalacademy.com
  47. 47. ARTICAINE :  Classification : Amide  Potency : 1.5 times lignocaine , 1.9 times procaine  Toxicity :same as lignocaine  Metabolism :partially in liver &plasma  Half-life :shorter than lignocaine (30 min) articaine  Excretion :via kidneys  Onset of action : 2-3 min (nerve block) 1-2 min (infiltration)  Effective dental conc. :4%  Maximum recommended dose :7.0mg/kg body wt www.indiandentalacademy.com lignocaine
  48. 48. NERVE BLOCKS www.indiandentalacademy.com
  49. 49. INFRA-ORBITAL NERVE BLOCK www.indiandentalacademy.com
  50. 50. NASOPALATINE NERVE BLOCK www.indiandentalacademy.com
  51. 51. GREATER PALATINE NERVE BLOCK www.indiandentalacademy.com
  52. 52. POSTERIOR SUPERIOR NERVE BLOCK www.indiandentalacademy.com
  53. 53. INFERIOR ALVEOLAR NERVE BLOCK www.indiandentalacademy.com
  54. 54. MENTAL NERVE BLOCK www.indiandentalacademy.com
  55. 55. LONG BUCCAL NERVE BLOCK www.indiandentalacademy.com
  56. 56. COMPLICATIONS LOCAL COMPLICATIONS :  Paresthesia  Facial nerve paralysis  Trismus  Hematoma  Pain on injection  Infection  Edema  Soft tissue injury  Sloughing of tissues www.indiandentalacademy.com
  57. 57. Systemic Complications :  Overdose reactions  Allergy  Syncope www.indiandentalacademy.com
  58. 58. OVERDOSE REACTIONS :  Slow biotransformation  Slow elimination  Too large a total dose  Rapid injection CLINICAL MANIFESTATIONS : CNS ACTIONS : Concentration(µg/ml) Effect 0.5 – 4.0 Anticonvulsant action 4.5 – 7.0 Excitation, agitation, talkativeness 7.5 – 10.0 Tonic-clonic seizures Above 10 Generalized CNS depression www.indiandentalacademy.com
  59. 59. Basic Emergency Management  P – position unconscious – supine with feet elevated slightly conscious – based upon patients comfort  A – airway unconscious – assess and maintain the airway conscious – assess the airway  B – breathing unconscious – assess and ventilate if necessary conscious – assess breathing  C – circulation unconscious – assess and provide external cardiac compression if necessary conscious – assess circulation  D – Definitive care Diagnosis Management:www.indiandentalacademy.com and/or assistance Emergency drugs
  60. 60. CVS actions Concentration(µg/ml) Effect 1.8-5.0 Antidysrhythmic actions 5.0-10.0 ECG alterations, Myocardial depression, Peripheral vasodilation. Above 10.0 Massive peripheral vasodilation, Intensive myocardial depression, Cardiac arrest. www.indiandentalacademy.com
  61. 61. ALLERGY Hypersensitive state due to exposure to a particular allergen, reexposure to which produces a heightened capacity to react. • Causes –  Methyl paraben  Sodium bisulfite  Epinephrine • Signs and symptoms –  Skin reactions Urticaria, Angioedema  Respiratory reactions Respiratory distress, Wheezing, Dyspnea, Cyanosis  Generalized anaphylaxis www.indiandentalacademy.com
  62. 62. MANAGEMENT  ELECTIVE DENTAL CARE -treatment postponed  EMERGENCY DENTAL CARE -no treatment of invasive nature -use GA -histamine blockers as local anesthetics -electronic dental anesthesia www.indiandentalacademy.com
  63. 63. Newer advances Wand Comfort control syringe www.indiandentalacademy.com
  64. 64. www.indiandentalacademy.com
  65. 65. REFERENCES :  The pharmacological basis of therapeutics : Goodman & Gillman 10th ed.  Pharmacology & pharmacotherapeutics : Satoskar – 18th ed.  Essentials of medical pharmacology : Tripathi – 5th ed.  Local anesthesia & pain control in dental practice : Monheim’s – 7th ed.  Handbook of LA : Malamed – 5th ed.  Dental update 2005, (32) , 8 – 14  Dental update 2005 , 32 , 66 - 72 . www.indiandentalacademy.com
  66. 66. www.indiandentalacademy.com
  67. 67. Thank you www.indiandentalacademy.com Leader in continuing dental education www.indiandentalacademy.com

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