DEPT.

OF ORAL &MAXILLOFACIAL SURGERY
Presented By Dr Haneef

 History

 Armamentarium
 Definition &Classification  Composition

 Different Agents , Vasoconstrictors
 Mechanism of Action  Bio Transformation

 Systemic Action

 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

intradermally  1884 – marks birth of LA . 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 .

 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 .

non-additive. 1905  13 lives claimed – addiction  A Einhorn & E Uhlfelder(Sweden)  Synthesized  Procaine hydrochloride  Procaine  sterilizable. non-toxic  1943  N Lofgren(Sweden)  Synthesized  Anilide called Lignocaine  Lignocaine – amide linked synthetic derivative .

published in BDJ – Lofgren  Sweden – Birth place of newer LA agents  Bupivacaine  Ropivacaine . 1946 – Lignocaine introduced  Dental practice  1948 – Lignocaine .

 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. .

 Accupuncture Analgesia - Originated-CHINA.  Time consuming.Direct electric current  Elos-1. lasts for less time  Audio Analgesia –  1959 Gardner and licklider  Loud noise used to produce analgesia  Electric analgesia -- Peripheral nerve.between600BC to 200AD  Hypnotism –  Still employed—susceptible patients.powered by 18v battery.Siemens  Never more than 30 ma .

 Syringe Breech loading. metallic cartridge-aspirating Advantage Visible cartridge Aspiration. Long lasting Disadvantage Weight Size-Too big Possibility of infection .1 hand Autoclavable Rust resistance.

PISTON WITH HARPOON FINGER GRIP NEEDLE ADAPTOR SYRINGE BARREL THUMB RING .

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 Breech loading plastic cartridge-aspirating Advantage Light weight Cartridge visible Rust resistance. Long lasting Disadvantage Size – Too big / small Possibility of infection Repeated autoclaving – Plastic looses its properties Low cost .

PLASTIC REUSABLE SYRINGE .

 Breech loading metallic cartridge-Self aspirating Advantage Cartridge visible Autoclavable Easier to aspirate Disadvantage Weight Possibility of infection Finger has to be moved from thumb ring to disc-Aspiration Takes time to accustom Piston is scored – Qty Known .

SELF ASPIRATING SYRINGE .

 Pressure syringe -- Advantage Measured dose Overcomes tissue resistance Non threatening – Cartridge protected Disadvantage Cost Inject too rapidly -Possibility .

PRESSURE SYRINGE .

JEWETT OBTUNDER .WILCOX.

Cost PDL damage – common . 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.

JET INJECTOR .

 Disposable syringe Advantage Single use Sterile-Till opened Light weight Disadvantage Does not accept – Dental cartridge Aspiration – Difficult – 2 hands .

. Friction grip. Needle  Type – Stainless steel – Disposable Platinum Iridium platinum Ruthenium platinum  Parts – Bevel Shank Hub-Leur lock.

Aluminum cap GLASS TUBE NECK Rubber diaphragm RUBBER PLUNGER .

 Additional Armamentarium –  Topical antiseptic  Topical anesthetic  Cotton Gauge  Hemostat  Applicator Stick. .

resulting from a reversible interruption of peripheral conduction along a specific neural pathway to its central integration and perception in the brain.It is defined as a transient loss of sensation to a painful or potentially painful stimulus. .

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 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. . It should be relatively free from producing allergic reactions. 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.

ORTHOGNATHIC SURGERY MAXILLARY ND MANDIBULAR # REDUCTIONS OPEN/CLOSED . ROOT CANAL TREATMENT FOR PULPAL        ANESTHESIA PERIODONTAL SURGERY ORTHODONTIC EXTRACTIONS EXTRACTION OF CARIOUS . PREPROSTHETIC SURGERY SURGICAL EXCISION AND INSICION OF PATHOLOGICAL LESIONS.PRE PROSTHETIC EXTRACTIONS.MALPOSED AND IMPACTED TEETH.

ABSOLUTE:  DRUG ALLERGY OR HYPERSENSTIVITY REACTION .

Patients administered prilocaine may develop methemoglobinemia. However high levels of lidocaine will decrease contractility and cardiac output and can lead to circulatory collapse. ATYPICAL PSEUDOCHOLINESTERASE. IN HEPATIC FAILURE PATIENTS Amides are metabolized in       the liver. These metabolites are excreted in the kidney.IN RENAL FAILURE PATIENTS HAS TO BE USED WITH CAUTION. BLEEDING DISORDERS PERTICULARLY REGIONAL BLOCKS . Patients with significant liver disease who have poor hepatic blood flow will have trouble metabolizing amides and other agents. seizures and analgesia. one of the metabolites of lidocaine may actually cause some sedation. Systemic actions on the central nervous system include CNS depression. HEART FAILURE (ASA IV OR VI) LIDOCAINE is used as an ACLS drug for patients with ventricular dysrythmias. In addition.

very painful! again use if (b) fails.includes long buccal infiltration. d) Intraosseous .Topical Surface contact. Infiltration Deposition of solution at or close to site of surgery.solution diffuses through cortical bone into apical area. Usually adequate especially in maxilla but adult mandibles to thick in posterior buccal cortex. Paste. . c) Subperiosteal .use if (b) fails. May be adequate for simple incision and drainage. Drill small access hole over appropriate tooth apex and deposit 0. preinjection. a) Sub mucous .painful! .25ml of local anaesthetic. b) Supraperiosteal . Not suitable for pulpal anaesthesia.for simple soft tissue surgery . ethyl chloride.the commonest technique .

effect is rapid so proceed with surgery C. Contraindicated in patients with bleeding diatheses even if controlled!Success depends on knowledge of local anatomy and good technique.painful but occasionally very useful especially for acute pulpitis where regional block fails to give adequate depth of anaesthesia.variation of (d) .FIELD BLOCKS D.Regional Block: Remote from site of surgery.inject small volume of solution .e) Intraseptal .NERVE BLOCKS E. Must use special syringe to avoid breaking cartridge. Push needle along root surface to apex . f) Intraligamentous . .similar indications but inject through softer crestal bone to reach apex.

 B) synthetic nitrogenous compd – para amino benzoic acid-procaine. . phenol . acetanilide lignocaine quinoline cinchocoline  C) non Nitrogenous compounds benzyl alcohol  D) miscellaneous – clove oil . benzocaine. Based on composition –  A) Natural – eg – cocaine.

 Based on intermediate group -- Esters – Benzoic acid Butane Cocaine Benzocaine Para Amino benzoic Acid Chloroprocaine Procaine Propoxycaine Amides – Articaine Bupivacaine Dibucaine Lignocaine Mepivacaine Prilocaine Hexylcaine Tetracaine .

internal surface.. tetrodotoxin Agents acting at receptor Quaternary amoniumsite.  Class C  Class D . According to biological site and mode of action—  Class A  Class B Agents acting at receptor Biotoxin -eg site –external surface. scorpion venom Agents acting at receptor Benzocaine independent physico chemical mechanism. Agents acting in combn Clinically useful agents –Lignocaine etc of receptor and independent mechanism.

 Injectables - Ultra short acting <80 min eg Lignocaine  Short acting 45-50 Surface -*Soluble .eg Cocaine Lignocaine *Insoluble.eg Benzocaine Min 2% ligno with 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 .

. agent is yet to be introduced into clinical practice. It produces a relatively blood less field of operation for surgical procedures. the ideal L. Local anesthetic agent  This is the active ingredient in the solution. 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.A. but despite the      constant development of new drugs.

edema and tissue necrosis. This is because sympathomimetic amines may increase O2 consumption of tissues. Noradrenaline Felypressin . This. together with vaso constriction leads to hypoxia and local tissue damage. The vasoconstrictors in general uses are Adrenaline. Demerits  In higher doses can cause systemic effects that are undesirable. Vasoconstrictor may also cause a delay in wound healing.      practically in individuals suffering from cardiovascular disease.

 Anti oxidant  Most often is sodium meta-bi sulphite  Amount varies from 0. propylparaben and chlorobutanol.  Vehicle  The anaesthetic agent and the additives are dissolved in modified Ringer’s solution.002 mg/CC.  Fungicide Thymol is added.  Preservative  Modern LA solutions are very stable and have a shelf – life of 2 years or more.  Most frequently used bacteriostatic agents are methylparaben.  Since this substance is more readily oxidized than adrenaline or noradrenaline it protects their stability.0065 to 0. This automatic vehicle minimizes the discomfort during injection. .

0mg/kg – 7mg/kg Procaine Lidocaine Bupivacaine Prilocaine Articaine 9.Anesthetic pKa Onset Duration (with Epinephrine) in minutes 45 .1 7.5mg/kg – 3mg/kg 5mg/kg – 7.8 Slow Rapid Slow Medium Rapid .5mg/kg – 7mg/kg 2.240 4 hours – 8 hours 90 .5mg/kg 4.9 8.1 7.270 Max Dose (with Epinephrine) 8mg/kg – 10mg/kg 4.360 140 .90 120 .9 7.

 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

CH3 NH.CO.CH2.N

C2H5 C2H5

CH3

LIGNOCAINE

 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.

Absolute maximum dose-not> 90mg .Dose 1.3mg/kg .7hrs.5 Onset of action –6-10 min. Bupivacaine –Classified under amide  1-butyl 2.Anesthetic half life-2.relatively significant  Pka-8.Maximum dose-not >40mg.4.ph(plain). Mepivacaine  Metabolism –Liver by Amidases  Excretion by kidney (16% unchanged)  Vasodilation.5-6.3-4.1.6 pipecoloxylidide  Toxicity <4 times – Lignocaine. ph(vc).

CH3 NH.CO CH3 N C4H9 BUPIVACAINE .

burning sensation at site of injecton.min.  Duration –Pulpal. Full mouth recontruction.00. Extensive perio surgery.pulpal anesthesia->90. in children- anticipating self trauma .5% soln 1:2. management of post op pain. Available as 0. .180 min Soft tissue-4-12 hrs  Contra indication.90.000 (vc)  Indicaton.

Classified under –Esters  2Diethylamino ethyl 4aminobenzoate hcl  Metabolised-in Plasma by plasma pseudocholine esterases  Excretion >2%unchanged. 2% procaine 15-30min soft tissue LA no pulpal anesthesia .  Pka-9. drug of choice for intra arterial injection and accidents.High degree of vasodilation. Procaine.8% diethyl aminoethanol in urine.1. . 90% -PABA. > incidence allergy.

4 mg/kg .  Excretion-1-10% unchanged urine. 3% mepivacaine used in patients with vc contraindicaton. .over dose CNS stimulation followed by depression.  Maximum dose 4. Mepivacine. Low reported cases-allergy.6 pipecoloxylidide hcl  Metabolism-microsomal fixed funcn oxidasea in liver.  Mild vasodilator.Anesthetic half life-90min.6. absolute max dose-300mg.classified -amide type  1 Methyl 2.  Pka-7.

unchanged.  Adverse reaction-methymoglobinemia-Rx by using methylene blue 1mg/kg.classified. Absolute maximum dose – 500mg  first LA Agent with thiophene ring. . Pka 7.8.little potential to diffuse through soft tissue. Maximum dose – 1mg/kg .Liver Excretion – Kidney 10% . Articaine. Anesthetic half life-1.Amide      2 Carboxymethoxy 4 methylthiophene hcl Metabolised.2-2 hrs.

 Maximum dose 8mg /kg.Anesthetic half life-56 min.Kidney  Pka 7. .classified –Amide  Metabolism –Liver  Excretion –urine. Etidocaine. Absolute max dose 400 mg  Employed mainly in epidural or caudal regional block.7 .

 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 .

Based on chemical stc  (Catechol nucleus) Catecholamines Epinephrine Nor epinephrine Dopamine Non catecholamines Amphetamine Meta amphetamine Based on mode of action Direct acting Epinephrine Nor epinephrine Indirect acting Amphetamine Tyramine Mixed acting Ephedrine .

EPINEPHRINE Proprietar Adrenaline y name α1& β receptors Mode of action Systolic & Systemic Diastolic pressure 1) CVS Heart rate FELYPRESSIN Octopressin Direct stimulation of vasculature No direct effect on Myocardium Non-arrythmagenic High doses – impaired coronary flow Oxygen consumption Stroke volume .

2) CNS CNS stimulation Adrenergic nerve – no effect Vasoconstriction – coronary blood vessels Anti-diuretic action Oxytocin like action – uterus 3) RS Bronchodilator 4) Vasculature α1 – vasoconstriction β 2 – vasodilation oxygen 5)Metabolism consumption blood sugar level .

A 0.04mg – CVS impaired CVS & CNS symptoms Cerebral hemorrhage effect .2 mg – healthy L.6) Clinical Allergy.04mg dose 8) Side 0. hemostasis As vaso-constrictor in application 7) Max 0.

2m/s  Myelinated 14.8 – 120m/s  Site of action  Outer bimolecular lipoprotein layer in nerve membrane . Rate  Non-myelinated 1.

 Altering the basic RMP of nerve  Altering the threshold potential  Decreasing the rate of depolarization  Prolonging rate of repolarization .

A causes nerve block by displacement of Ca from some membrane site that controls entry of Na  Varying conc. ACTEYLCHOLINE THEORY:  Involved in nerve conduction in addition to its role as a neurotransmitter at nerve synapses  No such evidence  CALCIUM DISPLACEMENT THEORY:  L. Of Ca in nerve – not seen .

 Demerits. SURFACE CHARGE THEORY:  Action by binding to nerve membrane and changing its electric potential.RMP not altered by LA.  Cationic molecules aligned at membrane water interface –surface elec potn more positively charged potn. . threshold LA act on nerve channel rather than surface –cannot explain how uncharged LA molecule causes nerve blockage. electric potn .

.  Explains how non ionised drug causes. Membrane expansion theory LA lipid soluble – enters nerve membr and changes configuration of membr.blockade. There by reduced space for sodium to enter and thus cause inhibition.  No evidence to tell that the whole blockade is due to this phenomenon. nerve membrane do expand and become more fluid when exposed to LA .

sodium channel-on external/ axoplasmic surface. This is by far the most accepted theory. Specific receptor theory—  LA act by binding to specific receptors.no conduction.  Once it binds there is no permeability of sodium. LA molecule replace calcium molecule at calcium gate – thus prevent sodium entry. .

4 is necessary for conversion of acid salt to free base. All LA are available as acid salt of weak bases.  Weak base(BNHOH) combined with acid (HCL) to give acid salt(BNHCL)& water. BN is now lipophilic. Normal tissue PH 7.  BNH which is hydrophilic further dissociates to BN and H.  In mucosa BNHCL dissociates into BNH and CL . .

(H in nerve formed by buffering action.)  Newly formed ionised BNH displaces calcium from the sodium channel receptor site to cause conduction blockade. Lipophilic BN diffuses through nerve membrane (lipid). . Inside the nerve it combines with intrinsic H.

LA Solution . .

increase toxicity .eg. Esters.Procaine- hydrolyzed to pseudo cholinesterase's Para amino benzoic acid Diethyl amino alcohol Excreted unchanged urine further transformed-urine Atypical cholinesterase's --.

Significant renal diseases – contra indication. . Amide eg lidocaine -- Mono ethyl xylidide Glycine xylidide Xylidide xylidide Hydroxy xylidide. Excreted kidney .

0.5-7.5mg/ml-tonic clonic seizures. CNS – Low levels – no action Toxic dose – tonic clonic convulsions Blood.5-4.0 mg/ml-no complication 4. Anti convulsive property – As it causes depression of CNS.excitability nerve .0 mg/ml-pre seizure sign/ symptom >7. Seizure threshold.

8-5mg/ml –anti arrhythmic used in premature ventricular contractures . CVS Action on Heart    Electrical excitability of myocardium . clinically effective level-1. conduction rate Tone of contraction. arrhythmias. .

hypo tension. Action on vasculaturenormal value no change.cardio vascular collapse ( myocardial contractility. massive peripheral vaso dilatation ) .( myocardial contractility) Lethal dose. over dose.

 Action on Respiratory system–  Normal levels.no over dose.  Over dose – Respiratory arrest due to CNS depression. .bronchial muscles relaxation .

DEPT.OF ORAL &MAXILLOFACIAL SURGERY Presented By Dr Haneef .

 Anatomical considerations  Local anaesthesia technique.Mandible  Complications  Future trends .Maxilla  Local anaesthesia technique.

Motor:. lateral/medial pterygoid d.  Two parts:i.a. soft tissues of the oral cavity. Sensory: V1 Opthalmic nerve V2 Maxillary division V3 mandibular division . Mylohyoid e. The right and left trigeminal nerves provide among other functions. the overwhelming majority of sensory innervation from the teeth. bone. Anterior belly of digastric f. Tensor veli palatini ii. Tensor tympani g. temporalis c. Masseter b.

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 Position the patient  Dry the tissue/ wipe once. Use a Sterile Sharp Needle  Check The flow of Solution  Determine Whether to Warm solution before use or not.  Apply topical anesthetic .

 Communicate with patient apply firm hand rest  Inject few drops of soln. communicate with patient.  Advance to the target slowly . inject  Withdraw the needle slowly  Observe the patient & check for anesthetic symptoms .aspirate .

middle superior alveolar nerve block  Maxillary nerve block .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.

 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 .

 Contra-indication :  Infection  Dense bone covering  Target area :  Behind apices of tooth  Landmarks :  Muco-buccal fold  Crown & root length .

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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 . Area anaesthetized:  Maxillary 3rd.

 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 .

parotid gland  facial nerve affected .pterygoid plexus posteriorly  Visible – buccal aspect  Accidental mandibular Anaesthesia  Orbital contents – anaesthetized accidentally  Accidental . Complications:  Hematoma –  Non visible .

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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 .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.

 Areas anaesthetized  Pulp of maxillary C.Is – Canine  Buccal periodontium. lateral aspect of nose  Upper lip  Indications  More than 2 anterior teeth  Contraindications  Discreet treatment areas  Hemostasis of localized area – not adequately achieved . lower eyelid.

lforamen supra –orbital notch infra-orbital notch. infra-orbital foramen. mental foramen  2 methods:  Intra-oral  Premolar approach  Incisal approach . Landmarks  Mucobuccal fold.

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 Indications  Anterior palatal procedures supplementing infraorbital nerve blocks  Anaesthesia of nasal septum  Landmarks  Central incisor & incisive papilla .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.1.

 Complications  Hematoma  Necrosis  Technique  Single needle penetration  Multiple needle penetration Usually most discomforting block for patient – very painful .

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 – 1-1.2.5cms away from gingival margin .

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 Nerves anesthetized  ASA and MSA  Areas anesthetized  Pulpal anesthesia of maxillary incisors. First reported by freidman and hochman in 1997 during development of CCLAD system  Muscles of facial expression and upper lip anesthesized.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 .

 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 .

 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 .

 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 .

periorbital swelling. 6th nr block – diplopia. optic nerve blocked. Complications  Hematoma  Penetration into orbit proptosis. retrobulbar block producing mydriasis. 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  Volume – displaces orbital structures. transient loss of vision. . corneal anesthesia / hemorrhage.

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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 .I. Anterior and middle superior alveolar nerve block –  Nerves anaesthetized  Infraorbital nerve  Inferior palpebral.

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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 .

 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 .

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AKINOSI TECHNIQUE  GOW-GATE’S TECHNIQUE  KURT THOMA EXTERNAL APPROACH .Mandibular block Different techniques are:  DIRECT METHOD .  INDIRECT METHOD.  METHOD OF CLARKE & HOLMES  METHOD OF ANGELO SARGENTI  VAZIRANI.INFERIOR ALVEOLAR NERVE BLOCK Other common name.

 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 .

 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) .

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 . Anatomical structures .

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.Initial insertion of the needle more laterally. the syringe is returned to it’s original direction. ie over the lower premolars and deposit 1. syringe is moved parallel to the lower molars on the other side. needle is partially withdrawn after touching the bone. insertion of the needle beyond theinternal oblique ridge.thus immediately strikes the bone.Stages in the indirect technique :.5ml of solution in the pterygomandibular space.

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Depositing the solution at a higher level causing complete anesthesia.It involves deposition of solutions @ a higher level than usual. the analgesic is placed immediately behind the mandibular foramen. It is a modification of indirect technique. . In the standard direct/indirect technique. which is 1cm above the occlusal plane of molar teeth. At this level the nerve is concealed by lingula & sphenomandibular ligament.

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1. Needle is slowly inserted in a downwards & backwards direction until it touches the bone. The difference is that the nerve is approached from a higher level than usual. The barrel of the syringe is now placed between and in contact with the upper premolars of the opposite side. The needle is inserted opposite to the mid point of the finger nail.This technique is a modification of direct method. .The index finger is placed in the retro molar fossa with nail facing lingually.5ml of solution is deposited. depth is 1cm. TECHNIQUE: Syringe with 1 5/8 inch 26gauge needle is used.

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lingual n anesthetised. Nerves anesthetized – inferior alveolar nerve. .  Muco gingival junction maxillary teeth.  Orientation of bevel must be oriented away from the bone of mandibulaar ramus (bevel faces toward mid line). 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.  Patient more comfortable.  Land mark occluding plane of the teeth.  Antr border of ramus.  More popular now  Land marks easy  One prick – mandibular. buccal.

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 Advantages

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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.

multiple procedures on mandibular teeth. pats. n. block is unsuccessful. . mental.  Area –all mandibular hard and soft tissue Upto mid line. mylohyoid.Nerves anaesthetised – inferior alveolar. alv. with restricted mouth opening. conventional inf.  Contraindications – infection or acute inflammation in the area of infection. lingual. auriculotemporal and buccal. incisive.  Indications. buccal soft tissue anaesthesia from third molar to midline.

penetration of soft tissue distal to 2nd molar at the same height. Gained popularity – single needle penetration. Land marks-  Extraoral. 2nd molar.  Final position needle is just inferior to condyle and insertion of lateral pterygoid. intertragic notch  Intraoral – height of injection established by placement of needle tip just below the mesiolingual cusp of max. relies on soft tissue landmarks – differ from patient to patient .corner of mouth. lower border of the tragus.

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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.OTHER NAME Buccal nerve block or buccinator nerve block.25 to 0.5ml of solution is deposited.

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lingual mucoperiosteum Only used singly to operate on tongue. Lingual nerve block –  Area anaesthetised –  Anterior 2/3rd tongue. retromolar triangle . floor of mouth. floor of mouth  Buccinator / long buccal nerve block  Area anaesthetised –  Buccal mucosa & mandibular molar – mucoperiosteum  Land marks  External oblique ridge.

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 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 .

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 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 .

 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

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.

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 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

 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

 SYSTEMIC COMPLICATIONS  Toxicity  Idiosyncracy  Allergy  Anaphylactoid reaction  Syncope .

requires specific treatment .reverses itself without treatment  Severe – manifests itself – pronounced deviation . Classification  Primary / secondary  Primary – caused & manifested at time of anaesthesia  Secondary – manifested later  Mild / severe  Mild – exhibit slight change from normal expected pattern .

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 . Transient / permanent  Transient – is one that is severe at occurrence – no residual effects  Permanent – residual effect.

 Complications  Attributed to solutions – toxicity. local irritation  Attributed to technique / needle – syncope. anaphylactoid reaction. muscle trismus. pain. allergy. idiosyncrasy. hematoma . edema.

 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 .

 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 .

 Precautions  Avoid bony contact  Avoid heavy pressure  Avoid movement of needle and patient .

 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 .

edema. paraesthesia . 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.

 Prevention  Slow injection – 1ml / minute  Cartridge stored at room temperature – away from containers with alcohol / other agents .

 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 .

 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 .

 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 .

sterile. Prevention  Use of sharp. disposable needle  Aseptic technique  Practice atraumatic methods  Avoid repeated injections  Use minimum volume  Control infection .

Codeine (30-60mg). moist hot packs  Analgesics  Aspirin. muscle relaxants  Initial physiotherapy  Thrice a day  Antibiotic regime  Possibility of infection . Management  Heat therapy  Warm saline rinses.

barbed needles . ―effusion of blood into extra-vascular spaces‖  Causes  Arterial & venous puncture – common in PSA & Inf. 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. Alv. minimize the number of penetration  Discard defective needles.

advice analgesics. 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.pack application next day . Management  Immediate – apply firm pressure  5-10minutes  Inf. Mental. warm. Nr. cold application upto 4-6 hours. Alv. Block – medial aspect of ramus  Infra orbital.

 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 .

 Causes  Trauma during injection  Infection. hemorrhage  Allergy (Angioedema)  Injection of irritating solution  Problems  Pain & dysfunction  Airway obstruction .

3mg. airway impairment – basic life support. Antihistamine. call medical help. Corticosteroids  Total airway obstruction – Tracheostomy / Cricothyroidectomy . 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. Epinephrine – 0.

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 . Causes  Epithelial desquamation – topical anaesthesia – long time.

 Management  Symptomatic – pain – analgesia  Epithelial desquamation – resolve few days  Sterile abscess resolve  7-10 days .

 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 .

redirection of needle to be done only after complete withdrawal . 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. Cause  LA solution into parotid gland – usually while giving Inf Alv Nr.

 Management  Reassure the patient  Resolves after action of LA is over  Eye patches to the affected – eye drops  Contact lenses if any – removed .

 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 .

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 . Drug factors – Vasoactivity – vasodilation – increase in blood concentration  More concentration – greater risk  Dose.

Pulse rate. Respiration . convulsions  Cerebral cortical depression – lethargy. Causes of toxicity –  Biotransformation usually slow  Drug – slowly eliminated by kidney  Too large a total dose  Absorption from injection site .P. sleepiness. restless. unconsciousness  Medullary stimulation – increased B. apprehensiveness.rapid  Accidental intra-vascular injection  Symptoms –  CNS – cerebral cortical stimulation – talkative.

administer anti-convulsant. Pulse . leg. monitor vital signs. Medullary depression – mild fall in B.use of vasopressor(phenyl ephrine) i.m if hypotensiom presists.  post seizure – CNS depression usually present . BLS.>15 mins – same procedure  Severe overdose reaction – rapid onset – 1 minute – unconsciousness with or without convulsion.P– severe cases drops to 0 . in case of convulsions – anti-convulsants (diazepam/midazolam infusion)  Slower onset . tongue. convulsions – protect hand. patient in supine position. Respiration – similar effect  Treatment  Mild overdose reaction – slow onset reaction – > 5 mins administer Oxygen (prevent acidosis).

 ―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 ..

supine position- (trendelenburg position). light headedness. ―transient loss of consciousness that is caused due to cerebral ischemia (neurogenic shock)‖  Anxiety – increased blood supply to muscles. tachycardia & palpitation – may further lead to Unconsciousness  Treatment – discontinue procedure. deep breathing. O2 administration if required. BLS . dizziness. sitting position 2mm Hg. less pressure – cerebral arteries  Clinically pallor.

 ―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.

 dysnea.  Signs and symptoms of allergy.  Dermatological-----. tachycardia etc.  Informed consent that includes cardiac arest end death to be included. Consultation and allergy testing  Refer doubtful cases for allergic skin test – sub cutaneous test most sensitive. common  Respiratory– broncho spasm.urticaria –wheal and smooth elevated patch seen. flushing. --- ---angio oedema—localised swelling – face hands. respiratory distress. wheezing. .

.  Edema upper air way – laryngeal edema  Lower air way affect broncioles.small. Laryngeal edema – type of angio neurotic oedema- life threating.

IM  50 mg diphenhydramine Im  medical help summoned. . Management  skin reactions Delayed – non life threatening .oral histamine blockers.3 mg epinephrine.  Immediate reaction—with conjunctivitis rhinitisvigorous management.  0.50 mg diphenhidramine.10 mg chlorpheniramine 3-4 days.

oxygen  Admn epinephrine. Observe patient for minimum of 60 min  Oral histamine blockers for 5 days.  If condition not improving cricothyrotomy .bronchodilator  Observe for 60 min .achieve patent air way if necessary give artificial ventilation.  administer . . iv anti histamines.  Histamine blockers Im  Laryngeal edema Patient position .  Respiratory reaction –  patient in comfortable position. advise anti histamines to prevent relapse.oxygen. broncho-dilator.

 Patient with confirmed allergy status if patient allergic to any one type of anesthetic ester / amide use the other.  General anesthesia  alternative method of pain control –  electric anesthesia / hypnosis.  Use histamine blocker like diphenhydramine as anesthetic. .

 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 .

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 .

 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 .

has short life . 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. Unstable solution. but it has decreased stability  CO2 enhances diffusion. as it increase intracellular PH.

 First used described in 1949  Provides more rapid onset of anaesthesia  Decrease duration of action  Possibility for allergic reactions .

young and old age patients . pregnancy. 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. Precursor for TENS  It acts by working at low frequency of 2 Hz  It serotonin.

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