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The document comprehensively outlines local anesthesia, detailing its historical background, definition, desirable properties, mechanisms of action, classifications, and various administration techniques. It describes the physiological basis of nerve conduction and the interaction of anesthetics with nerve membranes, alongside the types of local anesthetics categorized as esters or amides. Additionally, the document covers potential complications and important considerations for special care groups, ensuring a clear understanding of local anesthetic practices within medical and dental contexts.

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By Dr. Lasya LOCAL ANESTHESIA
Contents *Historical Background *Definition *Desirable Properties of Local Anesthesia *Electrophysiology of Nerve conduction *Mechanism of Action *Theories *Classification of Local Anesthetics *Composition of Local Anesthetics *Administration of Local Anesthesia
*Techniques of Local Anesthesia *Local Complications *Systemic complications *Special Care Groups *Newer Local Anesthetic Drugs and Delivery Systems *Public Health Significance *Conclusion *References
Historical Background *COCAINE – First local anesthetic agent - isolated by NIEMAN 1860 – from the leaves of the coca tree *Its anesthetic action was demonstrated by KARL KOLLER – 1884 *First effective and widely used synthetic local anesthetic – PROCAINE – developed by EINHORN – 1904 - from benzoic acid and diethyl amino ethanol *Agent was introduced into clinical practice by BRAWN 1905 *LIDOCAINE - LOFGREN - 1943
Definition *Local anesthesia is defined as a loss of sensation in a circumscribed area of the body caused by depression of excitation in nerve endings or inhibition of the conduction process in peripheral nerves. Important feature of LA *Loss of sensation without inducing a loss of consciousness
Desirable properties of Local anesthesia *It should not be irritating *It should not cause any permanent alteration of nerve structure *Its systemic toxicity should be low *Time of onset of anaesthesia should be short *It must be effective regardless of whether it is injected into the tissue or is applied locally to mucous membrane *The duration of action must be long enough to permit the completion of procedure.
*It should have potency sufficient to give complete anesthesia without the use of harmful concentrated solutions *It should be relatively free from producing allergic reactions *It should be stable in solution and should readily undergo biotransformation in the body *It should be sterile or capable of being sterilized by heat without deterioration
Electrophysiology of Nerve Conduction *In Resting state, nerve possess negative membrane potential of -70mV *Na+ /K+ pump acts by transporting the Na+ ions out of the cell and k+ ions into the cell *Na+/K+ pump creates a conc. gradient by which it favors the transport of K+ out of the cell *Negatively charged ions accumulate within the cell Depolarization *When nerve is stimulated, it gets depolarized Impulse propagation Na+ K+
*Nerve membrane becomes permeable to Na+ ions also Entry of Na+ into the cell Threshold potential is achieved (-55mV) Permeability to Na+ increases rapid influx of Na+ *At the end of depolarization, the potential is around +35mV *Alterations in nerve membrane potentials Action potential
Repolarization *Nerve membrane permeability to Na+ ions decreases Along the conc. gradient, K+ moves into the cell and Na+ out of the cell Activation of Na+/K+ pump restores the resting membrane potential of -70mV *Entire process – 1 millisecond *Depolarization – 0.3 msec *Repolarization – 0.7 msec K+ Na+
Mechanism of Action *LA basically block the influx of Na+ ions *Weak bases, easily injectable, water soluble *In aq. solution – salt dissociates into ionized and non ionized forms *For LA to be effective – it should diffuse into nerve cell membrane *Non ionized form – lipophilic – responsible for the diffusion into nerve cell membrane *Ionized form – responsible for binding to the Na+ channel receptors – blocks Na+ channel – prevent Depolarization
*More than 90% of the nerve membrane is made of lipids *Proportion of ionized and non ionized forms depends on the ph of surrounding tissue *Decrease in ph of surrounding tissue shifts the equilibrium towards ionized form onset of LA is delayed *In case of infection or inflammation – acidic environment increases ionized form – LA is less effective
Theories 1) Acetylcholine Theory *Acetylcholine involved in nerve conduction *Acts as Neurotransmitter at nerve synapses 2) Calcium Displacement Theory *Calcium which is present at the sodium channel was responsible for the transport of Na+ through the channel *LA said to displace the calcium – prevent sodium influx 3) Surface Charge Repulsion Theory *Charged LA molecules bind to nerve membrane - alter electrical potential
4) Membrane Expansion Theory *LA is absorbed into the cell membrane and causes an expansion of the membrane itself – causes narrowing of Na+ channels – prevents Na+ influx 5) Specific Receptor Theory *Specific receptors present at the opening of the Na+ channels *LA diffuses across the nerve membrane and binds to these receptors – leads to an alteration in the structure and functioning of the Na+ channel – prevent Na+ influx
Classification of Local Anesthetics *Classified whether the intermediate chain is an Amide or an Ester Local Anesthetics Esters Amides Cocaine Tetracaine Benzocaine Butacaine Procaine Chlorprocaine Lidocaine Prilocaine Mepivacaine Bupivacaine Etidocaine Para-amino benzoic acid Benzoic acid
1) Esters *Metabolized by hydrolysis by Plasma Cholinesterase *One of the products of hydrolysis of this drug is PABA *Eg – Cocaine, Procaine, Chlorprocaine, Tetracaine 2) Amides *Metabolized in the liver by microsomal enzymes *Lidocaine is metabolized by a specific microsomal enzyme P – 450 3A4 *Eg – Lidocaine, Prilocaine, Mepivacaine, Bupivacaine, Etidocaine
* According to Biological site and Mode of Action Agents acting at receptor site on external surface of nerve membrane Eg: Biotoxins like tetrodoxin, saxitoxin Agents acting at receptor site on internal surface of nerve membrane Eg: Quaternary ammonium analogs of lidocaine Scorpion venom Agents acting by a receptor – independent physico–chemical mechanism Eg: Benzocaine Agents acting by combination of receptor and receptor independent mechanisms Eg: articaine, lidocaine, mepivacaine, prilocaine Class A Class B Class C Class D
Composition of Local Anesthetic Solution 1) Local Anesthetic 2) Vasoconstrictor 3) Antioxidant 4) Preservative 5) Fungicide 6) Salt 7) Vehicle *Local anesthetic – Amide or Ester *Vasoconstrictor – Epinephrine (1:1,00,000)
*Local anesthetics are Vasodilators – Vasodilatation of the peripheral arterioles – LA to be rapidly absorbed into the blood stream *Epinephrine is added to the LA – Vasoconstriction – prevents rapid absorption into the blood stream *Also reduces systemic toxicity *Increases the duration of action – as it delays absorption from the local site *Also causes hemostasis in the injected area – helps in creating a blood - free field for operation
*Epinephrine has toxic effects *May produce cardiac arrhythmias in patients with previous heart disease *May induce hypertension – Hypertensive and in Hyperthyroid patients *May induce arrhythmias when used along with Halothane *May hamper the healing of a flap *LA with epinephrine should not be injected in the ala of the nose or in the helix of the ear
*Antioxidant – Sodium Metabisulphite – prolongs shelf life *Preservative – Methyl Paraben or Capryl hydro cuprinotoxin *Fungicide – Thymol *Salt – Bicarbonate – isotonic *Vehicle – Distilled Water or Ringer’s Lactate solution – dissolves all the contents of LA to make it injectable
ADMINISTRATION OF LOCAL ANESTHESIA
Nerve Block Field Block Submucosal Injection Paraperiosteal Injection Intraosseous Injection Interseptal Injection Periodontal Ligament Injection Local Infiltration Administration of LA Topical Anesthesia
TECHNIQUES OF LOCAL ANESTHESIA
Maxillary Nerve Blocks Anterior Superior Alveolar Block Greater Palatine Block Techniques of LA Mandibular Nerve Blocks Posterior Superior Alveolar Block Middle Superior Alveolar Block Naso Palatine Block Anterior Superior Alveolar Block Inferior Alveolar Block Lingual Block Incisive Block Mental Block Buccal Block
Anterior Superior Alveolar Nerve Block *Infraorbital nerve block *Simple technique and Safe Indications *Dental procedures involving more than 2 maxillary teeth and their overlying buccal tissues *When supraperiosteal injection are ineffective Contraindications *Discrete treatment areas *Hemostasis of localized areas
Nerves anesthetized 1) Anterior superior alveolar nerve 2) Middle superior alveolar nerve 3) Infraorbital nerve A) Inferior palpebral B) Lateral nasal C) superior labial Areas Anesthetized *Pulps of max. central incisor through the canine on the injected side
*Pulps of max. premolar and mesiobuccal root of the 1st molar *Buccal periodontium and bone *Lower eye, lat. Aspect of nose, upper lip Target Area – Infraorbital Foramen Landmarks *Mucobuccal fold *Infraorbital Notch *Infraorbital Foramen
Technique *2 Extra oral Intra oral Intraoral Technique *Infraorbital ridge is palpated and 1cm inferior to it, the infraorbital foramen is palpated with middle finger. *The needle is inserted at the apex of the canine fossa or along the long axis of the first premolar
Extra oral Technique *Infraorbital rim is palpated and infraorbital depression is felt 1cm inferior to it *A needle is inserted cutaneously near the foramen Symptoms *Numbness – Infraorbital region Lateral aspect of the nose Upper lip
*On instrumentation – Upper labial mucosa Maxillary anterior teeth Gingiva on buccal side Complications *Hematoma – rarely *Diplopia *Exophthalmos *Blindness - rarely Orbit
Middle Superior Alveolar Nerve Block *Minimizes the number of injections and vol. of solution Indications *Dental procedures involving only max. premolars *Where ASA nerve block fails to provide pulpal anesthesia distal to max. canine Contraindications *Infection or Inflammation *When MSA is absent
Nerves Anesthetized *Middle superior alveolar nerve and terminal branches Areas Anesthetized *Pulps of max. premolars, mesiobuccal root of max.1st molar *Buccal periodontal tissues and bone Target area *Maxillary bone above the apex of max. 2nd premolar Landmarks *Mucobuccal fold above max 2nd premolar
Technique
Posterior Superior Alveolar Nerve Block *Tuberosity Block , Zygomatic Block *Commonly used dental nerve block *Atraumatic *High success rate *Minimizes the no. of injections *Minimizes total vol. of solution Indications *Treatment involving 2 or more max. molars *When supraperiosteal injection is contraindicated
Contraindications *When risk of haemorrhage is too great Nerves Anesthetized *Posterior superior alveolar nerve and its branches Areas Anesthetized *Pulps of max. 3rd , 2nd , and 1st molars *Buccal periodontium and bone Target area *PSA nerve – posterior, superior, and medial to the posterior border of the maxilla
Landmarks *MB fold *Maxillary tuberosity *Zygomatic process of maxilla Technique *Short needle Complications *Haematoma *Chances of mandibular nerve anesthesia
Greater Palatine Nerve Block *Anterior palatine nerve block *Minimizes needle penetrations and vol. of solution Indications *When palatal soft tissue anesthesia is necessary *For pain control during periodontal or oral surgical procedures involving hard and soft tissues Contraindications *Infection or inflammation at injection site *Procedure involving 1 or 2 teeth
Nerves Anesthetized - Greater palatine Areas Anesthetized *Posterior portion of hard palate and its overlying tissues Target Area *Greater palatine nerve as it passes anteriorly between soft tissues and bone of the hard palate Technique Complications *Ischemia of palate *Anesthesia of soft palate – leads to gagging
Nasopalatine Nerve Block *Incisive nerve block, sphenopalatine nerve block *Minimizes needle penetrations and vol. of solution *Minimizes patient discomfort from multiple needle penetrations Indications *When palatal soft tissue anesthesia is necessary *For pain control during periodontal or oral surgical procedures involving hard and soft tissues Contraindications *Infection or inflammation at injection site *Procedure involving 1 or 2 teeth
Nerves Anesthetized - Nasopalatine nerve bilaterally Areas Anesthetized *Anterior portion of hard palate bilaterally Target Area *Incisive foramen (beneath incisive papilla) Landmarks *Central incisors *Incisive papilla
*Technique Complications *Ischemia and necrosis of the palatal tissues *Inability to deposit enough solution due to excessive density of palatal gingiva
Inferior Alveolar Nerve Block *Mandibular nerve block *Wide area of anesthesia Indications *Procedures on mand. teeth in one quadrant *When buccal and lingual soft tissue anesthesia is necessary Contraindications *Infection or acute inflammation *Very young child *Mentally or physically handicapped
Nerves anesthetized *Inferior alveolar nerve *Lingual nerve *Incisive *Mental Areas Anesthetized *Mand. teeth to the midline *Body of the mandible, inferior portion of the ramus *Buccal mucoperiosteum, mucous membrane anterior to the mental foramen
*Ant 2/3rd of the tongue and floor of the oral cavity *Lingual soft tissues and periosteum Target area *Inferior alveolar nerve ( near Mandibular foramen) Landmarks *Coronoid Notch *Pterygopalatine raphe *Occlusal plane of the mand. posterior teeth
Technique *Anterior border of the ramus is palpated as sharp edge lateral to the molars. *Deepest part on anterior border – Coronoid notch *Pterygomandibular raphe - ‘S’ shape curve - runs from max. tuberosity to retromolar fossa *The thumb is still placed on the coronoid notch *The needle is placed from the opposite side premolar – it bisects the nail of the thumb *The needle is inserted around 3/4th till bony resistance is encountered
*Aspirate and 1.5 ml of solution is deposited Symptoms *Tingling and numbness – lower lip, tongue *On instrumentation – labial gingiva anterior to 1st premolar Complications *Transient facial nerve paralysis *Trismus – spasm of Medial Pterygoid *Hematoma
Lingual Nerve Block Technique *Similar to an IANB *After the inferior alveolar nerve block is given , the needle is withdrawn less than 1cm. *The remaining solution, around 1cc, is deposited Symptoms *Tingling and numbness – ant. 2/3rd of the tongue *On instrumentation – lingual gingiva
Buccal Nerve Block *Long buccal nerve block, Buccinator nerve block Indications *Buccal soft tissue anesthesia (Mandibular molar region) Contraindications *Infection or inflammation Nerves anesthetized - Buccal nerve Areas anesthetized *Soft tissues and periosteum – buccal to mand. molar teeth
Target Area *Buccal Nerve – anterior border of the ramus Landmarks *Mandibular molars *Mucobuccal fold Technique Complications *Swelling - superficial mucosal injection
Mental Nerve Block *Atraumatic Indications *Buccal soft tissue anesthesia (ant. to mental foramen) *Soft tissue biopsies *Suturing of soft tissues Nerves anesthetized - Mental nerve Areas Anesthetized *Buccal mucosa ant. to mental foramen to the midline *Skin of the lower lip
Target area – mental foramen usually between the apices of 1st and 2nd premolars Landmarks *Mandibular premolars *Mucobuccal fold Technique Symptoms *Numbness – lower lip and labial mucosa
Incisive Nerve Block Indications *Dental procedures requiring pulpal anesthesia on mand. teeth *anterior to the mental foramen *When IANB is not indicated Contraindications *Infection or inflammation Nerves Anesthetized – Mental and Incisive
Areas Anesthetized *Buccal mucous membrane ant. to mental foramen *Lower lip and skin of chin Target Area – Mental foramen Landmarks *Mandibular premolars *Mucobuccal fold Technique
Mandibular Nerve Block : The Gow Gates Technique *Intraoral technique uses extra-oral landmarks Indications *Multiple procedures on mandibular teeth *When buccal soft tissue anesthesia, from 3rd molar to the midline is necessary *Lingual soft tissue anesthesia *When conventional inferior alveolar nerve block is unsuccessful
Contraindications *In young children, physically or mentally handicapped, adults *Patients who are unable to open their mouth wide(Trismus) Nerves Anesthetized *Inferior alveolar, Mental, Incisive, Lingual, Mylohyoid, Auriculotemporal, and Buccal nerves Areas Anesthetized *Mandibular teeth to the midline *Buccal mucous membrane *Ant. 2/3rd of the tongue, floor of the oral cavity
*Lingual soft tissues and periosteum *Body of the mandible, inferior portion of the ramus *Skin over the zygoma, posterior portion of the cheek, and temporal region Target Area *Lateral side of the condylar neck, just below the insertion of the lateral pterygoid muscle Technique *An imaginary line is drawn from the corner of the mouth to intertragic notch
*Open the mouth wide *Intraorally, the needle is penetrated just below the mesiopalatal cusp of the maxillary 2nd molar along the imaginary line *Depth of insertion of the needle will be at least 3/4th ( contact the bone) *Aspiration and deposition of 2cc solution Symptoms *Tingling and numbness along the distribution of the mandibular nerve
Akinosi Vazirani’s Closed Mouth Technique Indications *Limited mouth opening *Multiple procedures on mandibular teeth *Inability to visualize landmarks for IANB Contraindications *In young children, physically or mentally handicapped, adults *Poor access to the lingual aspect of the ramus Nerves Anesthetized *Inferior alveolar, Incisive, Mental, Lingual, Mylohyoid
Areas Anesthetized *Mandibular teeth to the midline *Buccal mucous membrane anterior to the mental foramen *Ant. 2/3rd of the tongue, floor of the oral cavity *Lingual soft tissues and periosteum *Body of the mandible, inferior portion of the ramus Target Area - Soft tissue on the medial border of the ramus Landmarks *Mucogingival junction of max.3rd molar *Maxillary tuberosity and coronoid notch
Technique *Patient is asked to close the mouth till the teeth occlude *Cheek retracted and needle is inserted parallel to the occlusal plane at the level of mucogingival junction of max. arch *Needle is inserted medial to the ramus. About 3/4th of the needle is inserted *Aspiration and deposition of 2cc solution Symptoms *Tingling and numbness – lower lip, anterior 2/3rd of the tongue *On instrumentation – labial gingiva Complications – Transient Facial nerve paralysis
Local Complications 1) Needle Breakage Cause *Use of very narrow gauge needle *Sudden movement of the patient when needle is within the tissues Management *If needle is visible – grasped with hemostat and removed immediately *Panoramic and 3D CT Scanning – identify the location of retained needle fragment
*Surgeon removes the needle fragment while patient is under GA Prevention *Do not use short needles , 25 gauge needles for IANB *Do not bend needle when inserting them into soft tissues
2) Prolonged Anesthesia /Paresthesia Cause *May be due to a) Direct injury to the nerve during injection b) Pressure on nerve from an expanding hematoma Management *Usually resolves within app. 8 weeks to 2 months without treatment *The patient should be reassured and the problem explained to them clearly
*Patient should be periodically recalled and the improvement in the nerve regeneration should be noted *Examination every 2 months Prevention *Strict adherence to injection protocol and proper care
3) Transient Facial nerve paralysis Cause *Introduction of LA into the capsule of parotid gland which is located at posterior border of the mand. ramus, clothed by Medial pterygoid and masseter Prevention *Strict adherence to injection protocol and proper care Management *Reassurance of the patient *Any eye patch should be applied to affected eye until muscle tone returns
4) Trismus Cause *Trauma to the muscles due to repeated needle punctures *Injury to IA vessels during injection Hematoma Compresses on the muscle Spasm and trismus
*Use of contaminated needles or infection in local region Management *Trismus - Analgesics + Muscle Relaxants *Infection – Antibiotics *To relieve muscle spasm in absence of infection *Physiotherapy – Gentle mouth opening and lateral excursions *If physiotherapy is unsuccessful – forceful mouth opening - Mouth gag Hot fomentation + Muscle Relaxants
Prevention *Use of sharp, sterile, disposable needle *Use aseptic technique *Practise Atraumatic insertion and injection technique *Avoid repeat injections and multiple insertions into same area
5) Soft Tissue Injury *Inadvertent biting or chewing of lips or tongue Management *Analgesics and Antibiotics *Petroleum jelly or other lubricant to cover lip lesions to minimize irritation Prevention *LA of appropriate duration should be selected *A cotton roll is placed between lips and teeth *Parents should be informed to take care that the child is prevented from lip biting or chewing
6) Hematoma *Effusion of blood into extravascular spaces Cause *Inadvertent nicking of a blood vessel during LA administration Management *Immediate treatment – pressure application in the region post. to max. tuberosity for PSA block *Ice packs – extra-orally *Hematoma resolves by itself within 7 – 14 days
7) Pain or Burning sensation on injection Cause *Use of blunt needle *Use of broader gauge needles *Rapid injection *Acidic LA – burning sensation Prevention *Use of sharp, narrow gauge disposable needles *Isotonic LA (addition of Bicarbonate)
8) Infection Cause *Contaminated needle *Use of improper technique Prevention *Use of sterile disposable needles *Proper technique Management *Antibiotics
Systemic Complications 1) Overdose Cause *Administration of excessive dose of LA *Inadvertent IV injection of the drug *Diminished activity of plasma pseudo cholinesterase
Minimal to Moderate Overdose Signs *Talkativeness *Elevated B.P, Heart rate, Respiratory rate *Loss of response to painful stimuli *Vomiting *Sweating *Apprehension *Slurred speech Symptoms *Lightheadedness *Dizziness *Restlessness *Nervousness *Numbness *Tinnitus *Inability to Focus *Metallic taste *Drowsiness and Disorientation *Loss of consciousness
Moderate to High Overdose levels Signs *Tonic – Clonic Seizures *Generalized CNS Depression *Depressed B.P, Heart Rate, Respiratory Rate Normal Maximum dose of Lidocaine *4.5 mg/kg body weight without vasoconstrictor *7 mg/kg body weight with vasoconstrictor
Management *P – A – B – C – D For CNS manifestations *Seizures – Benzodiazepines / Barbiturates Propofol/Thiopental For CVS Manifestations *Cardiac life support may be required which may be prolonged as the drug takes long time to be eliminated *IV fluids and Vasopressors like Ephedrine to counter Hypotension
2) Hypersensitivity/ Allergic reaction to LA *Rare *Esters of anaesthetics is metabolized by Plasma Pseudo cholinesterase *PABA is known to be antigenic and capable of inducing a humoral immune response *Amide anesthetics contain methyl paraben as preservative chemically similar to PABA and capable of initiating similar response systemically *Reactions of LA may be type 1 or type 4
Clinical signs Type Ⅰ 1) Pruritis 2) Utricaria 3) Facial swelling 4) Dyspnea 5) Cyanosis 6) Nausea, vomiting Type Ⅳ 1) Erythema 2) Plaques 3) Pruritis
Management *Stop the procedure immediately *Mild Allergy – Antihistamines / Corticosteroids *Severs reactions – 0.3 – 0.5 ml of 1: 1000 Epinephrine SC – every 20 – 30 minutes. Not more than 3 doses *If Anaphylaxis still continue – 5 ml of 1: 10,000 Epinephrine IV
Special Care Groups 1) Uncooperative Patients *Choose a shorter needle and/or a larger gauge needle which is less likely to bent or broken *Better to use general anesthesia 2) Bleeding Disorders *Oral procedures must be done at the beginning of the day & must be performed early in the week, allowing delayed re-bleeding episodes, usually occurring after 24-48 hrs., to be dealt with during the working weekdays
*Local anesthetic containing a vasoconstrictor should be administered by infiltration or by intra ligamentary injection * Regional nerve blocks should be avoided when possible. 3) Pregnancy *Lidocaine + Vasoconstrictor – most common LA used in dentistry extensively used in pregnancy with no proven ill effects. *Esters are better to be used *Accidental intravascular injections of lidocaine pass through the placenta but the conc. is too low to harm fetus
4) Geriatric Patients *When choosing an anesthetic, we are largely concerned with the effect of the anesthetic agent upon the patient's cardiovascular and respiratory systems. *Increased tissue sensitivity to drugs acting on the CNS *Decreased hepatic size and blood flow may reduce hepatic metabolism of drugs *Hypertension is common and can reduce renal function
5) Liver Disorders Potential complications: 1. Impaired drug detoxication eg., Sedative, analgesics, general anesthesia. 2. Bleeding disorders (decrease clotting factors, excess fibrinolysis, impaired vitamin K absorption). 3. Transmission of viral hepatitis. *Management – Amides (lidocaine, mepicaine) should be avoided. Esters should be used
Newer Local Anesthetic Drugs and Delivery Systems Articaine *New drug that have proved to be equal or more effective than lignocaine *Articaine was introduced clinically in 1976 and is used widely today *Amide LA Properties *Articaine has faster onset of action, longer duration of action, high success rate, greater potency *Systemic intoxication of Articaine is lower
*Very safe drug *Enhanced diffusion into the tissues than other Local anesthetics *Buccal infiltration of the mandibular molar with 1.8ml 0f 4% Articaine with 1:1,00,000 epinephrine is significantly better than similar infiltration of 2% Lidocaine with 1:1,00,000 epinephrine in achieving pulpal anesthesia in mandibular posterior teeth *4% articaine with 1:1,00,000 epinephrine possesses superior anesthetic efficiency relative to lidocaine for inferior alveolar nerve block during 3rd molar extraction
Centbucridine *Quinolone derivative with local anesthetic action *It has intrinsic vasoconstricting and anti-histaminic properties *0.5% centbucridine – used effectively for infiltration, nerve blocks, and spinal anesthesia with anesthetic potency 4-5 times greater than that of 2% lignocaine
Phentolamine Mesylate *Drug used for reversal of effects of local anesthetic solutions *Non–selective -adrenergic blocking agent and reverses the effects of epinephrine and nor – epinephrine on tissues containing the 1 and 2 adrenergic receptors *Clinical effects – Vasodilation and Tachycardia *Adverse effects – diarrhea, facial swelling, hypertension, jaw pain, oral pain, tenderness and vomiting
EMLA *Eutectic mixture of lignocaine and prilocaine in 1:1 by weight *Designed as topical anesthetic able to provide surface anesthesia for intact skin *Clarke et al in 1986 suggested the use of EMLA cream for anesthetizing the skin prior to needle insertion as this reduces the incidence of injection pain
Dentipatch *A patch that contains 10-20% lidocaine is placed on the dried mucosa for 15 minutes *Used for achieving topical anesthesia for both maxilla and mandible JET INJECTION *Effective for palatal injection *In this technique, a small amount of local anesthetic is propelled as a jet into the sub – mucosa without the use of a hypodermic syringe/ needle from a reservoir
*This takes place when the knob is pressed to release air pressure which produces a fine jet of solution which penetrates the mucosa through a small puncture wound to produce surface anesthesia COMPUTER CONTROLLED LOCAL ANESTHESIA DELIVERY SYSTEM (C-CLAD) *Milestone scientific – introduced the first C-CLAD System in 1997 and was termed the “WAND” and subsequent versions renamed as “WAND PLUS” and “COMPUDENT” *In 2001, DENTSPLY International introduced the Comfort Control Syringe, Anaeject and Orastar from Japan
Public Health Significance *Incidence of complications of local anesthesia – 4.5% *The incidence of systemic toxicity to local anesthesia has significantly reduced in the past 30 years, from 0.2% - 0.01% *Peripheral nerve blocks are associated with highest incidence of systemic toxicity – 7.5 per 10,000 *Incidence of IgE mediated (type 1 hypersensitivity) allergic reaction was 1%
Conclusion *Local Anesthesia remains the backbone of pain control in dentistry *Adapting local anesthetic techniques can overcome difficulties in access and limit soft tissue anesthesia. *Local anesthetic doses must be controlled *Research has been continued in both medicine and dentistry to seek new and better means of managing pain associated with many surgical treatments.
References *Stanley F. Malamed. Handbook of Local anesthesia. 6th Edition. Elseiver *Chitra Chakravarthy. Textbook of Oral and Maxillofacial Surgery: 2nd Edition. Hyderabad: Paras *Richard Bennett C. Monheim’s Local Anaesthesia and Pain Control in Dental practice: 7th edition, New Delhi: CBS publishers *Zhang A et al. Anesthetic efficiency of articaine versus lidocaine in the extraction of lower third molars: a meta-analysis and systematic review. Journal of Oral and Maxillofacial Surgery. 2019 Jan 1; 77(1): 18-28.
*Anil Kumar Karanam et al. Effects of lignocaine with adrenaline on blood pressure and pulse rate in normotensive and hypertensive patients undergoing extraction: A clinical study. International Editorial/Reviewer Board Prof. Raveendranath. Rajendran-Saudi Arabia. 2017; 3(4): 202-204 *Payal Saxena et al. Advances in dental Local Anesthesia techniques and devices: An update. National Journal of Maxillofacial Surgery. 2013 Jan - Jun; 4(1): 19-24 *Sharma S.S et al. Newer Local Anesthetic Drugs and Delivery Systems in Dentistry. An update. IOSR Journal of Dental and Medical Sciences. 2012 sep – oct; 1(4): 10-16
*Bhole MV et al. IgE-mediated allergy to local anaesthetics: separating fact from perception: a UK perspective. British journal of anaesthesia. 2012 Jun 1; 108(6): 903-11. *Robertson D et al. The anesthetic efficacy of articaine in buccal infiltration of mandibular posterior teeth. J Am Dent Assoc. 2007, Nov 138(11): 1418-1420 *Daublander M et al. The incidence of complications associated with local anesthesia in dentistry. The Journal of Sedation and Anesthesiology in Dentistry. 1997, 44(4): 132-141 *Faccenda KA et al. Complications of regional anaesthesia incidence and prevention. Drug safety. 2001 May 1;24(6):413-42.

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LOCAL ANESTHESIA.pptx

  • 1.
  • 2.
    Contents *Historical Background *Definition *Desirable Propertiesof Local Anesthesia *Electrophysiology of Nerve conduction *Mechanism of Action *Theories *Classification of Local Anesthetics *Composition of Local Anesthetics *Administration of Local Anesthesia
  • 3.
    *Techniques of LocalAnesthesia *Local Complications *Systemic complications *Special Care Groups *Newer Local Anesthetic Drugs and Delivery Systems *Public Health Significance *Conclusion *References
  • 4.
    Historical Background *COCAINE –First local anesthetic agent - isolated by NIEMAN 1860 – from the leaves of the coca tree *Its anesthetic action was demonstrated by KARL KOLLER – 1884 *First effective and widely used synthetic local anesthetic – PROCAINE – developed by EINHORN – 1904 - from benzoic acid and diethyl amino ethanol *Agent was introduced into clinical practice by BRAWN 1905 *LIDOCAINE - LOFGREN - 1943
  • 5.
    Definition *Local anesthesia isdefined as a loss of sensation in a circumscribed area of the body caused by depression of excitation in nerve endings or inhibition of the conduction process in peripheral nerves. Important feature of LA *Loss of sensation without inducing a loss of consciousness
  • 6.
    Desirable properties ofLocal anesthesia *It should not be irritating *It should not cause any permanent alteration of nerve structure *Its systemic toxicity should be low *Time of onset of anaesthesia should be short *It must be effective regardless of whether it is injected into the tissue or is applied locally to mucous membrane *The duration of action must be long enough to permit the completion of procedure.
  • 7.
    *It should havepotency sufficient to give complete anesthesia without the use of harmful concentrated solutions *It should be relatively free from producing allergic reactions *It should be stable in solution and should readily undergo biotransformation in the body *It should be sterile or capable of being sterilized by heat without deterioration
  • 8.
    Electrophysiology of NerveConduction *In Resting state, nerve possess negative membrane potential of -70mV *Na+ /K+ pump acts by transporting the Na+ ions out of the cell and k+ ions into the cell *Na+/K+ pump creates a conc. gradient by which it favors the transport of K+ out of the cell *Negatively charged ions accumulate within the cell Depolarization *When nerve is stimulated, it gets depolarized Impulse propagation Na+ K+
  • 9.
    *Nerve membrane becomespermeable to Na+ ions also Entry of Na+ into the cell Threshold potential is achieved (-55mV) Permeability to Na+ increases rapid influx of Na+ *At the end of depolarization, the potential is around +35mV *Alterations in nerve membrane potentials Action potential
  • 10.
    Repolarization *Nerve membrane permeabilityto Na+ ions decreases Along the conc. gradient, K+ moves into the cell and Na+ out of the cell Activation of Na+/K+ pump restores the resting membrane potential of -70mV *Entire process – 1 millisecond *Depolarization – 0.3 msec *Repolarization – 0.7 msec K+ Na+
  • 11.
    Mechanism of Action *LAbasically block the influx of Na+ ions *Weak bases, easily injectable, water soluble *In aq. solution – salt dissociates into ionized and non ionized forms *For LA to be effective – it should diffuse into nerve cell membrane *Non ionized form – lipophilic – responsible for the diffusion into nerve cell membrane *Ionized form – responsible for binding to the Na+ channel receptors – blocks Na+ channel – prevent Depolarization
  • 12.
    *More than 90%of the nerve membrane is made of lipids *Proportion of ionized and non ionized forms depends on the ph of surrounding tissue *Decrease in ph of surrounding tissue shifts the equilibrium towards ionized form onset of LA is delayed *In case of infection or inflammation – acidic environment increases ionized form – LA is less effective
  • 13.
    Theories 1) Acetylcholine Theory *Acetylcholineinvolved in nerve conduction *Acts as Neurotransmitter at nerve synapses 2) Calcium Displacement Theory *Calcium which is present at the sodium channel was responsible for the transport of Na+ through the channel *LA said to displace the calcium – prevent sodium influx 3) Surface Charge Repulsion Theory *Charged LA molecules bind to nerve membrane - alter electrical potential
  • 14.
    4) Membrane ExpansionTheory *LA is absorbed into the cell membrane and causes an expansion of the membrane itself – causes narrowing of Na+ channels – prevents Na+ influx 5) Specific Receptor Theory *Specific receptors present at the opening of the Na+ channels *LA diffuses across the nerve membrane and binds to these receptors – leads to an alteration in the structure and functioning of the Na+ channel – prevent Na+ influx
  • 15.
    Classification of LocalAnesthetics *Classified whether the intermediate chain is an Amide or an Ester Local Anesthetics Esters Amides Cocaine Tetracaine Benzocaine Butacaine Procaine Chlorprocaine Lidocaine Prilocaine Mepivacaine Bupivacaine Etidocaine Para-amino benzoic acid Benzoic acid
  • 16.
    1) Esters *Metabolized byhydrolysis by Plasma Cholinesterase *One of the products of hydrolysis of this drug is PABA *Eg – Cocaine, Procaine, Chlorprocaine, Tetracaine 2) Amides *Metabolized in the liver by microsomal enzymes *Lidocaine is metabolized by a specific microsomal enzyme P – 450 3A4 *Eg – Lidocaine, Prilocaine, Mepivacaine, Bupivacaine, Etidocaine
  • 17.
    * According toBiological site and Mode of Action Agents acting at receptor site on external surface of nerve membrane Eg: Biotoxins like tetrodoxin, saxitoxin Agents acting at receptor site on internal surface of nerve membrane Eg: Quaternary ammonium analogs of lidocaine Scorpion venom Agents acting by a receptor – independent physico–chemical mechanism Eg: Benzocaine Agents acting by combination of receptor and receptor independent mechanisms Eg: articaine, lidocaine, mepivacaine, prilocaine Class A Class B Class C Class D
  • 18.
    Composition of LocalAnesthetic Solution 1) Local Anesthetic 2) Vasoconstrictor 3) Antioxidant 4) Preservative 5) Fungicide 6) Salt 7) Vehicle *Local anesthetic – Amide or Ester *Vasoconstrictor – Epinephrine (1:1,00,000)
  • 19.
    *Local anesthetics areVasodilators – Vasodilatation of the peripheral arterioles – LA to be rapidly absorbed into the blood stream *Epinephrine is added to the LA – Vasoconstriction – prevents rapid absorption into the blood stream *Also reduces systemic toxicity *Increases the duration of action – as it delays absorption from the local site *Also causes hemostasis in the injected area – helps in creating a blood - free field for operation
  • 20.
    *Epinephrine has toxiceffects *May produce cardiac arrhythmias in patients with previous heart disease *May induce hypertension – Hypertensive and in Hyperthyroid patients *May induce arrhythmias when used along with Halothane *May hamper the healing of a flap *LA with epinephrine should not be injected in the ala of the nose or in the helix of the ear
  • 21.
    *Antioxidant – SodiumMetabisulphite – prolongs shelf life *Preservative – Methyl Paraben or Capryl hydro cuprinotoxin *Fungicide – Thymol *Salt – Bicarbonate – isotonic *Vehicle – Distilled Water or Ringer’s Lactate solution – dissolves all the contents of LA to make it injectable
  • 22.
  • 23.
    Nerve Block FieldBlock Submucosal Injection Paraperiosteal Injection Intraosseous Injection Interseptal Injection Periodontal Ligament Injection Local Infiltration Administration of LA Topical Anesthesia
  • 25.
  • 26.
    Maxillary Nerve Blocks Anterior SuperiorAlveolar Block Greater Palatine Block Techniques of LA Mandibular Nerve Blocks Posterior Superior Alveolar Block Middle Superior Alveolar Block Naso Palatine Block Anterior Superior Alveolar Block Inferior Alveolar Block Lingual Block Incisive Block Mental Block Buccal Block
  • 27.
    Anterior Superior AlveolarNerve Block *Infraorbital nerve block *Simple technique and Safe Indications *Dental procedures involving more than 2 maxillary teeth and their overlying buccal tissues *When supraperiosteal injection are ineffective Contraindications *Discrete treatment areas *Hemostasis of localized areas
  • 28.
    Nerves anesthetized 1) Anteriorsuperior alveolar nerve 2) Middle superior alveolar nerve 3) Infraorbital nerve A) Inferior palpebral B) Lateral nasal C) superior labial Areas Anesthetized *Pulps of max. central incisor through the canine on the injected side
  • 29.
    *Pulps of max.premolar and mesiobuccal root of the 1st molar *Buccal periodontium and bone *Lower eye, lat. Aspect of nose, upper lip Target Area – Infraorbital Foramen Landmarks *Mucobuccal fold *Infraorbital Notch *Infraorbital Foramen
  • 30.
    Technique *2 Extra oral Intraoral Intraoral Technique *Infraorbital ridge is palpated and 1cm inferior to it, the infraorbital foramen is palpated with middle finger. *The needle is inserted at the apex of the canine fossa or along the long axis of the first premolar
  • 31.
    Extra oral Technique *Infraorbitalrim is palpated and infraorbital depression is felt 1cm inferior to it *A needle is inserted cutaneously near the foramen Symptoms *Numbness – Infraorbital region Lateral aspect of the nose Upper lip
  • 32.
    *On instrumentation –Upper labial mucosa Maxillary anterior teeth Gingiva on buccal side Complications *Hematoma – rarely *Diplopia *Exophthalmos *Blindness - rarely Orbit
  • 33.
    Middle Superior AlveolarNerve Block *Minimizes the number of injections and vol. of solution Indications *Dental procedures involving only max. premolars *Where ASA nerve block fails to provide pulpal anesthesia distal to max. canine Contraindications *Infection or Inflammation *When MSA is absent
  • 34.
    Nerves Anesthetized *Middle superioralveolar nerve and terminal branches Areas Anesthetized *Pulps of max. premolars, mesiobuccal root of max.1st molar *Buccal periodontal tissues and bone Target area *Maxillary bone above the apex of max. 2nd premolar Landmarks *Mucobuccal fold above max 2nd premolar
  • 35.
  • 36.
    Posterior Superior AlveolarNerve Block *Tuberosity Block , Zygomatic Block *Commonly used dental nerve block *Atraumatic *High success rate *Minimizes the no. of injections *Minimizes total vol. of solution Indications *Treatment involving 2 or more max. molars *When supraperiosteal injection is contraindicated
  • 37.
    Contraindications *When risk ofhaemorrhage is too great Nerves Anesthetized *Posterior superior alveolar nerve and its branches Areas Anesthetized *Pulps of max. 3rd , 2nd , and 1st molars *Buccal periodontium and bone Target area *PSA nerve – posterior, superior, and medial to the posterior border of the maxilla
  • 38.
    Landmarks *MB fold *Maxillary tuberosity *Zygomaticprocess of maxilla Technique *Short needle Complications *Haematoma *Chances of mandibular nerve anesthesia
  • 39.
    Greater Palatine NerveBlock *Anterior palatine nerve block *Minimizes needle penetrations and vol. of solution Indications *When palatal soft tissue anesthesia is necessary *For pain control during periodontal or oral surgical procedures involving hard and soft tissues Contraindications *Infection or inflammation at injection site *Procedure involving 1 or 2 teeth
  • 40.
    Nerves Anesthetized -Greater palatine Areas Anesthetized *Posterior portion of hard palate and its overlying tissues Target Area *Greater palatine nerve as it passes anteriorly between soft tissues and bone of the hard palate Technique Complications *Ischemia of palate *Anesthesia of soft palate – leads to gagging
  • 41.
    Nasopalatine Nerve Block *Incisivenerve block, sphenopalatine nerve block *Minimizes needle penetrations and vol. of solution *Minimizes patient discomfort from multiple needle penetrations Indications *When palatal soft tissue anesthesia is necessary *For pain control during periodontal or oral surgical procedures involving hard and soft tissues Contraindications *Infection or inflammation at injection site *Procedure involving 1 or 2 teeth
  • 42.
    Nerves Anesthetized -Nasopalatine nerve bilaterally Areas Anesthetized *Anterior portion of hard palate bilaterally Target Area *Incisive foramen (beneath incisive papilla) Landmarks *Central incisors *Incisive papilla
  • 43.
    *Technique Complications *Ischemia and necrosisof the palatal tissues *Inability to deposit enough solution due to excessive density of palatal gingiva
  • 44.
    Inferior Alveolar NerveBlock *Mandibular nerve block *Wide area of anesthesia Indications *Procedures on mand. teeth in one quadrant *When buccal and lingual soft tissue anesthesia is necessary Contraindications *Infection or acute inflammation *Very young child *Mentally or physically handicapped
  • 45.
    Nerves anesthetized *Inferior alveolarnerve *Lingual nerve *Incisive *Mental Areas Anesthetized *Mand. teeth to the midline *Body of the mandible, inferior portion of the ramus *Buccal mucoperiosteum, mucous membrane anterior to the mental foramen
  • 46.
    *Ant 2/3rd ofthe tongue and floor of the oral cavity *Lingual soft tissues and periosteum Target area *Inferior alveolar nerve ( near Mandibular foramen) Landmarks *Coronoid Notch *Pterygopalatine raphe *Occlusal plane of the mand. posterior teeth
  • 47.
    Technique *Anterior border ofthe ramus is palpated as sharp edge lateral to the molars. *Deepest part on anterior border – Coronoid notch *Pterygomandibular raphe - ‘S’ shape curve - runs from max. tuberosity to retromolar fossa *The thumb is still placed on the coronoid notch *The needle is placed from the opposite side premolar – it bisects the nail of the thumb *The needle is inserted around 3/4th till bony resistance is encountered
  • 48.
    *Aspirate and 1.5ml of solution is deposited Symptoms *Tingling and numbness – lower lip, tongue *On instrumentation – labial gingiva anterior to 1st premolar Complications *Transient facial nerve paralysis *Trismus – spasm of Medial Pterygoid *Hematoma
  • 49.
    Lingual Nerve Block Technique *Similarto an IANB *After the inferior alveolar nerve block is given , the needle is withdrawn less than 1cm. *The remaining solution, around 1cc, is deposited Symptoms *Tingling and numbness – ant. 2/3rd of the tongue *On instrumentation – lingual gingiva
  • 50.
    Buccal Nerve Block *Longbuccal nerve block, Buccinator nerve block Indications *Buccal soft tissue anesthesia (Mandibular molar region) Contraindications *Infection or inflammation Nerves anesthetized - Buccal nerve Areas anesthetized *Soft tissues and periosteum – buccal to mand. molar teeth
  • 51.
    Target Area *Buccal Nerve– anterior border of the ramus Landmarks *Mandibular molars *Mucobuccal fold Technique Complications *Swelling - superficial mucosal injection
  • 52.
    Mental Nerve Block *Atraumatic Indications *Buccalsoft tissue anesthesia (ant. to mental foramen) *Soft tissue biopsies *Suturing of soft tissues Nerves anesthetized - Mental nerve Areas Anesthetized *Buccal mucosa ant. to mental foramen to the midline *Skin of the lower lip
  • 53.
    Target area –mental foramen usually between the apices of 1st and 2nd premolars Landmarks *Mandibular premolars *Mucobuccal fold Technique Symptoms *Numbness – lower lip and labial mucosa
  • 54.
    Incisive Nerve Block Indications *Dentalprocedures requiring pulpal anesthesia on mand. teeth *anterior to the mental foramen *When IANB is not indicated Contraindications *Infection or inflammation Nerves Anesthetized – Mental and Incisive
  • 55.
    Areas Anesthetized *Buccal mucousmembrane ant. to mental foramen *Lower lip and skin of chin Target Area – Mental foramen Landmarks *Mandibular premolars *Mucobuccal fold Technique
  • 56.
    Mandibular Nerve Block: The Gow Gates Technique *Intraoral technique uses extra-oral landmarks Indications *Multiple procedures on mandibular teeth *When buccal soft tissue anesthesia, from 3rd molar to the midline is necessary *Lingual soft tissue anesthesia *When conventional inferior alveolar nerve block is unsuccessful
  • 57.
    Contraindications *In young children,physically or mentally handicapped, adults *Patients who are unable to open their mouth wide(Trismus) Nerves Anesthetized *Inferior alveolar, Mental, Incisive, Lingual, Mylohyoid, Auriculotemporal, and Buccal nerves Areas Anesthetized *Mandibular teeth to the midline *Buccal mucous membrane *Ant. 2/3rd of the tongue, floor of the oral cavity
  • 58.
    *Lingual soft tissuesand periosteum *Body of the mandible, inferior portion of the ramus *Skin over the zygoma, posterior portion of the cheek, and temporal region Target Area *Lateral side of the condylar neck, just below the insertion of the lateral pterygoid muscle Technique *An imaginary line is drawn from the corner of the mouth to intertragic notch
  • 59.
    *Open the mouthwide *Intraorally, the needle is penetrated just below the mesiopalatal cusp of the maxillary 2nd molar along the imaginary line *Depth of insertion of the needle will be at least 3/4th ( contact the bone) *Aspiration and deposition of 2cc solution Symptoms *Tingling and numbness along the distribution of the mandibular nerve
  • 60.
    Akinosi Vazirani’s ClosedMouth Technique Indications *Limited mouth opening *Multiple procedures on mandibular teeth *Inability to visualize landmarks for IANB Contraindications *In young children, physically or mentally handicapped, adults *Poor access to the lingual aspect of the ramus Nerves Anesthetized *Inferior alveolar, Incisive, Mental, Lingual, Mylohyoid
  • 61.
    Areas Anesthetized *Mandibular teethto the midline *Buccal mucous membrane anterior to the mental foramen *Ant. 2/3rd of the tongue, floor of the oral cavity *Lingual soft tissues and periosteum *Body of the mandible, inferior portion of the ramus Target Area - Soft tissue on the medial border of the ramus Landmarks *Mucogingival junction of max.3rd molar *Maxillary tuberosity and coronoid notch
  • 62.
    Technique *Patient is askedto close the mouth till the teeth occlude *Cheek retracted and needle is inserted parallel to the occlusal plane at the level of mucogingival junction of max. arch *Needle is inserted medial to the ramus. About 3/4th of the needle is inserted *Aspiration and deposition of 2cc solution Symptoms *Tingling and numbness – lower lip, anterior 2/3rd of the tongue *On instrumentation – labial gingiva Complications – Transient Facial nerve paralysis
  • 63.
    Local Complications 1) NeedleBreakage Cause *Use of very narrow gauge needle *Sudden movement of the patient when needle is within the tissues Management *If needle is visible – grasped with hemostat and removed immediately *Panoramic and 3D CT Scanning – identify the location of retained needle fragment
  • 64.
    *Surgeon removes theneedle fragment while patient is under GA Prevention *Do not use short needles , 25 gauge needles for IANB *Do not bend needle when inserting them into soft tissues
  • 65.
    2) Prolonged Anesthesia/Paresthesia Cause *May be due to a) Direct injury to the nerve during injection b) Pressure on nerve from an expanding hematoma Management *Usually resolves within app. 8 weeks to 2 months without treatment *The patient should be reassured and the problem explained to them clearly
  • 66.
    *Patient should beperiodically recalled and the improvement in the nerve regeneration should be noted *Examination every 2 months Prevention *Strict adherence to injection protocol and proper care
  • 67.
    3) Transient Facialnerve paralysis Cause *Introduction of LA into the capsule of parotid gland which is located at posterior border of the mand. ramus, clothed by Medial pterygoid and masseter Prevention *Strict adherence to injection protocol and proper care Management *Reassurance of the patient *Any eye patch should be applied to affected eye until muscle tone returns
  • 68.
    4) Trismus Cause *Trauma tothe muscles due to repeated needle punctures *Injury to IA vessels during injection Hematoma Compresses on the muscle Spasm and trismus
  • 69.
    *Use of contaminatedneedles or infection in local region Management *Trismus - Analgesics + Muscle Relaxants *Infection – Antibiotics *To relieve muscle spasm in absence of infection *Physiotherapy – Gentle mouth opening and lateral excursions *If physiotherapy is unsuccessful – forceful mouth opening - Mouth gag Hot fomentation + Muscle Relaxants
  • 70.
    Prevention *Use of sharp,sterile, disposable needle *Use aseptic technique *Practise Atraumatic insertion and injection technique *Avoid repeat injections and multiple insertions into same area
  • 71.
    5) Soft TissueInjury *Inadvertent biting or chewing of lips or tongue Management *Analgesics and Antibiotics *Petroleum jelly or other lubricant to cover lip lesions to minimize irritation Prevention *LA of appropriate duration should be selected *A cotton roll is placed between lips and teeth *Parents should be informed to take care that the child is prevented from lip biting or chewing
  • 72.
    6) Hematoma *Effusion ofblood into extravascular spaces Cause *Inadvertent nicking of a blood vessel during LA administration Management *Immediate treatment – pressure application in the region post. to max. tuberosity for PSA block *Ice packs – extra-orally *Hematoma resolves by itself within 7 – 14 days
  • 73.
    7) Pain orBurning sensation on injection Cause *Use of blunt needle *Use of broader gauge needles *Rapid injection *Acidic LA – burning sensation Prevention *Use of sharp, narrow gauge disposable needles *Isotonic LA (addition of Bicarbonate)
  • 74.
    8) Infection Cause *Contaminated needle *Useof improper technique Prevention *Use of sterile disposable needles *Proper technique Management *Antibiotics
  • 75.
    Systemic Complications 1) Overdose Cause *Administrationof excessive dose of LA *Inadvertent IV injection of the drug *Diminished activity of plasma pseudo cholinesterase
  • 76.
    Minimal to ModerateOverdose Signs *Talkativeness *Elevated B.P, Heart rate, Respiratory rate *Loss of response to painful stimuli *Vomiting *Sweating *Apprehension *Slurred speech Symptoms *Lightheadedness *Dizziness *Restlessness *Nervousness *Numbness *Tinnitus *Inability to Focus *Metallic taste *Drowsiness and Disorientation *Loss of consciousness
  • 77.
    Moderate to HighOverdose levels Signs *Tonic – Clonic Seizures *Generalized CNS Depression *Depressed B.P, Heart Rate, Respiratory Rate Normal Maximum dose of Lidocaine *4.5 mg/kg body weight without vasoconstrictor *7 mg/kg body weight with vasoconstrictor
  • 78.
    Management *P – A– B – C – D For CNS manifestations *Seizures – Benzodiazepines / Barbiturates Propofol/Thiopental For CVS Manifestations *Cardiac life support may be required which may be prolonged as the drug takes long time to be eliminated *IV fluids and Vasopressors like Ephedrine to counter Hypotension
  • 79.
    2) Hypersensitivity/ Allergicreaction to LA *Rare *Esters of anaesthetics is metabolized by Plasma Pseudo cholinesterase *PABA is known to be antigenic and capable of inducing a humoral immune response *Amide anesthetics contain methyl paraben as preservative chemically similar to PABA and capable of initiating similar response systemically *Reactions of LA may be type 1 or type 4
  • 80.
    Clinical signs Type Ⅰ 1)Pruritis 2) Utricaria 3) Facial swelling 4) Dyspnea 5) Cyanosis 6) Nausea, vomiting Type Ⅳ 1) Erythema 2) Plaques 3) Pruritis
  • 81.
    Management *Stop the procedureimmediately *Mild Allergy – Antihistamines / Corticosteroids *Severs reactions – 0.3 – 0.5 ml of 1: 1000 Epinephrine SC – every 20 – 30 minutes. Not more than 3 doses *If Anaphylaxis still continue – 5 ml of 1: 10,000 Epinephrine IV
  • 82.
    Special Care Groups 1)Uncooperative Patients *Choose a shorter needle and/or a larger gauge needle which is less likely to bent or broken *Better to use general anesthesia 2) Bleeding Disorders *Oral procedures must be done at the beginning of the day & must be performed early in the week, allowing delayed re-bleeding episodes, usually occurring after 24-48 hrs., to be dealt with during the working weekdays
  • 83.
    *Local anesthetic containinga vasoconstrictor should be administered by infiltration or by intra ligamentary injection * Regional nerve blocks should be avoided when possible. 3) Pregnancy *Lidocaine + Vasoconstrictor – most common LA used in dentistry extensively used in pregnancy with no proven ill effects. *Esters are better to be used *Accidental intravascular injections of lidocaine pass through the placenta but the conc. is too low to harm fetus
  • 84.
    4) Geriatric Patients *Whenchoosing an anesthetic, we are largely concerned with the effect of the anesthetic agent upon the patient's cardiovascular and respiratory systems. *Increased tissue sensitivity to drugs acting on the CNS *Decreased hepatic size and blood flow may reduce hepatic metabolism of drugs *Hypertension is common and can reduce renal function
  • 85.
    5) Liver Disorders Potentialcomplications: 1. Impaired drug detoxication eg., Sedative, analgesics, general anesthesia. 2. Bleeding disorders (decrease clotting factors, excess fibrinolysis, impaired vitamin K absorption). 3. Transmission of viral hepatitis. *Management – Amides (lidocaine, mepicaine) should be avoided. Esters should be used
  • 86.
    Newer Local AnestheticDrugs and Delivery Systems Articaine *New drug that have proved to be equal or more effective than lignocaine *Articaine was introduced clinically in 1976 and is used widely today *Amide LA Properties *Articaine has faster onset of action, longer duration of action, high success rate, greater potency *Systemic intoxication of Articaine is lower
  • 87.
    *Very safe drug *Enhanceddiffusion into the tissues than other Local anesthetics *Buccal infiltration of the mandibular molar with 1.8ml 0f 4% Articaine with 1:1,00,000 epinephrine is significantly better than similar infiltration of 2% Lidocaine with 1:1,00,000 epinephrine in achieving pulpal anesthesia in mandibular posterior teeth *4% articaine with 1:1,00,000 epinephrine possesses superior anesthetic efficiency relative to lidocaine for inferior alveolar nerve block during 3rd molar extraction
  • 88.
    Centbucridine *Quinolone derivative withlocal anesthetic action *It has intrinsic vasoconstricting and anti-histaminic properties *0.5% centbucridine – used effectively for infiltration, nerve blocks, and spinal anesthesia with anesthetic potency 4-5 times greater than that of 2% lignocaine
  • 89.
    Phentolamine Mesylate *Drug usedfor reversal of effects of local anesthetic solutions *Non–selective -adrenergic blocking agent and reverses the effects of epinephrine and nor – epinephrine on tissues containing the 1 and 2 adrenergic receptors *Clinical effects – Vasodilation and Tachycardia *Adverse effects – diarrhea, facial swelling, hypertension, jaw pain, oral pain, tenderness and vomiting
  • 90.
    EMLA *Eutectic mixture oflignocaine and prilocaine in 1:1 by weight *Designed as topical anesthetic able to provide surface anesthesia for intact skin *Clarke et al in 1986 suggested the use of EMLA cream for anesthetizing the skin prior to needle insertion as this reduces the incidence of injection pain
  • 91.
    Dentipatch *A patch thatcontains 10-20% lidocaine is placed on the dried mucosa for 15 minutes *Used for achieving topical anesthesia for both maxilla and mandible JET INJECTION *Effective for palatal injection *In this technique, a small amount of local anesthetic is propelled as a jet into the sub – mucosa without the use of a hypodermic syringe/ needle from a reservoir
  • 92.
    *This takes placewhen the knob is pressed to release air pressure which produces a fine jet of solution which penetrates the mucosa through a small puncture wound to produce surface anesthesia COMPUTER CONTROLLED LOCAL ANESTHESIA DELIVERY SYSTEM (C-CLAD) *Milestone scientific – introduced the first C-CLAD System in 1997 and was termed the “WAND” and subsequent versions renamed as “WAND PLUS” and “COMPUDENT” *In 2001, DENTSPLY International introduced the Comfort Control Syringe, Anaeject and Orastar from Japan
  • 93.
    Public Health Significance *Incidenceof complications of local anesthesia – 4.5% *The incidence of systemic toxicity to local anesthesia has significantly reduced in the past 30 years, from 0.2% - 0.01% *Peripheral nerve blocks are associated with highest incidence of systemic toxicity – 7.5 per 10,000 *Incidence of IgE mediated (type 1 hypersensitivity) allergic reaction was 1%
  • 94.
    Conclusion *Local Anesthesia remainsthe backbone of pain control in dentistry *Adapting local anesthetic techniques can overcome difficulties in access and limit soft tissue anesthesia. *Local anesthetic doses must be controlled *Research has been continued in both medicine and dentistry to seek new and better means of managing pain associated with many surgical treatments.
  • 95.
    References *Stanley F. Malamed.Handbook of Local anesthesia. 6th Edition. Elseiver *Chitra Chakravarthy. Textbook of Oral and Maxillofacial Surgery: 2nd Edition. Hyderabad: Paras *Richard Bennett C. Monheim’s Local Anaesthesia and Pain Control in Dental practice: 7th edition, New Delhi: CBS publishers *Zhang A et al. Anesthetic efficiency of articaine versus lidocaine in the extraction of lower third molars: a meta-analysis and systematic review. Journal of Oral and Maxillofacial Surgery. 2019 Jan 1; 77(1): 18-28.
  • 96.
    *Anil Kumar Karanamet al. Effects of lignocaine with adrenaline on blood pressure and pulse rate in normotensive and hypertensive patients undergoing extraction: A clinical study. International Editorial/Reviewer Board Prof. Raveendranath. Rajendran-Saudi Arabia. 2017; 3(4): 202-204 *Payal Saxena et al. Advances in dental Local Anesthesia techniques and devices: An update. National Journal of Maxillofacial Surgery. 2013 Jan - Jun; 4(1): 19-24 *Sharma S.S et al. Newer Local Anesthetic Drugs and Delivery Systems in Dentistry. An update. IOSR Journal of Dental and Medical Sciences. 2012 sep – oct; 1(4): 10-16
  • 97.
    *Bhole MV etal. IgE-mediated allergy to local anaesthetics: separating fact from perception: a UK perspective. British journal of anaesthesia. 2012 Jun 1; 108(6): 903-11. *Robertson D et al. The anesthetic efficacy of articaine in buccal infiltration of mandibular posterior teeth. J Am Dent Assoc. 2007, Nov 138(11): 1418-1420 *Daublander M et al. The incidence of complications associated with local anesthesia in dentistry. The Journal of Sedation and Anesthesiology in Dentistry. 1997, 44(4): 132-141 *Faccenda KA et al. Complications of regional anaesthesia incidence and prevention. Drug safety. 2001 May 1;24(6):413-42.