Local Anaesthesia Part 1 PDF
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LSBU
Lucy Harrison
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This document provides an overview of local anesthesia, focusing on the theory behind its mechanism. It describes various local anesthetic agents, their properties, and explains how they work. It also briefly touches on the principles of pain and pain control, relevant for healthcare professionals and dental students.
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Local Anaesthesia Part 1 Lucy Harrison FCSP Key GDC learning outcomes 1.1.5 1.1.8 Describe relevant and 1.1.6 Describe the propertie...
Local Anaesthesia Part 1 Lucy Harrison FCSP Key GDC learning outcomes 1.1.5 1.1.8 Describe relevant and 1.1.6 Describe the properties of appropriate dental, oral, Describe relevant and relevant medicines and craniofacial and general appropriate physiology and therapeutic agents and anatomy and explain their explain its application to discuss their application to application to patient patient management patient management management 1.7.4 Manage patient anxiety and 1.7.5 pain through effective Manage patient pain communication, through the appropriate use reassurance and relevant of analgesia behavioural techniques Aims and Objec@ves By the end of this session students should be able to: Describe various types of pain control and jus56ca5on of using pain control agents Explain how LA agents work Explain the systemic e@ects of LA Discuss the contra-indica5ons and cau5ons of LA agents Terminology Analgesia – loss of pain sensa5on unaccompanied by loss of other forms of sensibility e.g. pressure Anaesthesia – loss of all forms of sensa5on; pain, touch, temperature, pressure percep5on Both may be local (only part of body a2ected) or general (all body a2ected) Pain in den@stry The aim of dental treatment is to contain ac2ve disease and prevent its recurrence Oral 5ssues are well supplied with nerves which carry sensa5ons to the brain Some dental treatment is perceived as painful How can we avoid this? Pain Reac@on The same s5mulus produces di@erent reac5ons in di@erent people Even the same pa5ent may react in a di@erent way to the same s5mulus at di@erent 5mes This is due to the apprecia5on of pain within the central nervous system Why? Di@erences in pain reac5on are partly explained by the Gate Control Theory Control of Pain Pain can be abolished by interrup5ng the neural pathways at various levels to produce a permanent or temporary result For dental treatment, removal of the s5mulus is not possible. We require reversible pain control at a local level This is achieved by the use of a local anaesthe@c which blocks painful impulses being conveyed Don’t forget that because of the gate control theory, the e2ect of local analgesia can be enhanced by the surgery environment, hypnosis and distrac;on Local anaesthesia Can be achieved by: 1. Applica@on of cold 2. Applica@on of pressure 3. Use of drugs How does LA Agent work? This is the headline LA agents work by blocking transmission of impulses in sensory nerves Ac@on poten@al revision Electrical impulse produced by a nerve cell Travels in one direc5on Can only send one message at one speed The frequency or number of pulses can vary Impulse transmission Res@ng poten@al High Na+ (extracellular) Low K+ (intracellular) Semi-permeable nerve cell membrane Res5ng poten5al (-70mV) Depolariza@on With a s5mulus… Increased permeability of nerve cell membrane to Na+ ions Na+ ions rush into nerve cell Membrane poten5al becomes +ve (+40mV) Repolariza@on Brings back the neuron cell to the membrane res@ng poten@al Sodium-potassium pump ac5vely moves Na+ and K+ ions across the nerve cell membrane to restore balance Membrane poten5al returns to approximately -70mV Blocks inward movement of sodium ions Blocking of nerve conduc@on LA agents set up a chemical roadblock between the source of the impulse and the brain LA agent acts in two ways: 1. Binds to speci6c receptors in the sodium channels in the nerve cell membrane blocking the inward movement of Na+ ions during the conduc5on of an impulse 2. Non-speci6c expansion of nerve cell membrane causing physical obstruc5on of the Na+ channels No ac5on poten5al generated so no impulse conducted to brain Channels are blocked so action potential cannot continue Nerve conduc@on blocked Stops sodium and potassium going in and out (blocks channels) Local Anaesthe@c Agents Local anaesthe@c agent May be described as a drug which brings about a temporary loss of pain sensa@on in a limited area of the body The drug acts by making the nerve 6bres incapable of transmi`ng an impulse on s5mula5on Proper@es of an ideal LA agent Effective and Diffuse through the reversible action on Not irritate or injure Produce rapid onset lipid membrane of the nerves and nerve the tissues of numbness nerve fibre endings Allow combination Adequate working Isotonic (same pH as High safety margin with a time body) vasoconstrictor Capable of Adequate shelf life sterilization Contents of a dental LA cartridge Analgesic agent For blockade of nerve conduction E.G. Lidocaine, Prilocaine, Articaine, Mepivacaine Vasoconstrictor To increase depth and duration of analgesia E.G. Epinephrine, Felypressin - ↓ (LIDOCAINE] Reducing agent To prevent oxidation of the vasoconstrictor E.G. Sodium metabisulphite Vehicle To carry the above agents and ensure solution isotonic E.G. Sterile saline ↓SuR Ester VS Amide Benzocaine Lidocaine Cocaine Prilocaine Procaine Amethocaine Mepivacaine Ar@caine Bupivacaine Ropivacaine Levobupivacaine General features Organic weak bases which are insoluble in water Converted into soluble salts (hydrochlorides) for clinical use 2 chemical forms: un-ionized and ionized forms (weak base) Un-ionized form Lipid soluble Able to cross the faby sheath around the nerve to gain access to nerve 6bres Ionized form Actually blocks nerve conduc5on Once solu5on inside nerve 6bres Amides - Lidocaine Lidocaine 2% with epinephrine 1:80,000 is the gold standard for most dental procedures E@ec5ve Rapid onset Useful dura5on of pulpal and sof 5ssue analgesia Low toxicity Good topical e@ect Gold standard for most dental procedures Lidocaine topical prepara@ons Xylocaine spray 10mg Lidocaine per spray Xylonor gel Lidocaine 5%, cetrimide 0.15% Onset of ac5on 2-5 min Amides - Prilocaine As potent as lidocaine Shorter dura5on of ac5on Less vasodila5on than lidocaine so can be Citanest 3% + Octapressin (Felypressin) (0.03iu/ml) delivered without a vasoconstrictor Some5mes combined with felypressin but less vasoconstric5on than epinephrine Citanest 4% plain Rapidly dispersed and cleared (No vasoconstrictor) Very low incidence of side e@ects DO NOT USE ON PREGNANT WOMEN OR CHILDREN UNDER 4 Amides - Mepivacaine Similar proper5es to prilocaine Shorter analgesia if used as in6ltra5on (15-30 minutes) Scandonest 3% Plain Scandonest 2% with epinephrine 1:100,000 Amides - Ar@caine Powerful analgesic agent Rapid onset of ac5on Longer dura5on of sof 5ssue analgesia Rapidly metabolized in plasma and liver CAN NOT BE GIVEN AS A INFERIOR DENTAL BLOCK Cautious using during pregnancy and breast feeding Septanest 1:100,000 Benefits must outweigh risks!! 4% ar5caine hydrochloride with epinephrine 1:100,000 Septanest 1:200,000 Amides - Bupivacaine Very long las5ng (6-8 hours) Depresses cardiac ac5vity and causes dysrhythmias Useful for post-surgery Not available in dental use cartridges- given with standard medical type syringe Form: Marcaine + epinephrine Vasoconstrictors Increase depth and dura@on of anaesthesia < Adrenaline 6 Epinephrine (1:80,000, 1:100,000 or 1:200,000) Occurs naturally in the body More profound analgesia Haemorrhage control Bleeding. Felypressin (0.03 IU/mL) Synthe5c octapep5de Not such a profound vasoconstrictor Dura@on of anaesthesia Restoration PMPR Prepara@on Pulpal anaesthesia SoW @ssue anaesthesia Lidocaine 2% + 45 minutes 3 + hours epinephrine 1:80,000 Prilocaine 3% + 30–45 min 2 hours felypressin 0.03iu/ml Ar5caine 4% + 75 min 3-4 + hours epinephrine 1:100,000 Mepivacaine 3% plain 20 min 1 hour Bupivacaine 4 hours 6 –8 hours Maximum safe dosages EYec@veness of L.A. depends on… Analgesic potency of the agent Concentration of the agent Solubility of the agent in (a) water (b) lipid How long it stays at the injection site (concentration of agent and vasoconstrictor) Rate at which agent is metabolized at injection site Accuracy of technique Amount of spread and diffusion of agent Presence of inflammation and infection General Contraindica@ons and cau@ons Latex allergy All LA cartridges at Eastman have latex-free bungs Need to check in other dental prac;ces