Title Page
Copyright Page
Foreword
Acknowledgements
Chapter 1 Basic Pharmacology and Anatomy: A Whistle-stop Tour
Aim
Outcome
Introduction and Terminology
How is Local Anaesthesia Achieved?
Metabolism
Practical Points
The Anatomy of Dental Local Anaesthesia
The maxillary division of the trigeminal nerve
The mandibular division of the trigeminal nerve
Conclusions
Further Reading
Chapter 2 Instrumentation
Aim
Outcome
Introduction and Terminology
Needles
Cartridges
The Syringe
Conventional dental local anaesthetic cartridge syringes
Single-use syringes
Intraligamentary syringes
Computerised Delivery Systems
Powered injectors
Medical Syringes
Conclusions
Further Reading
Chapter 3 Local Anaesthetic Drugs
Aim
Outcome
Introduction and Terminology
Amide Local Anaesthetics
Lidocaine
Prilocaine
Mepivacaine
Articaine
Bupivacaine and levobupivacaine
Ropivacaine
Ester Local Anaesthetics
Procaine
Benzocaine
Amethocaine
Cocaine
Vasoconstrictors
Epinephrine
Felypressin
Which Local Anaesthetic Solutions Should I Have in My Surgery?
Method of Anaesthesia
Patient Factors
Type of Treatment
Conclusions
Further Reading
Chapter 4 Techniques for Maxillary Anaesthesia
Aim
Outcome
Introduction and Terminology
Buccal Infiltration Anaesthesia
Technique
Problems with buccal infiltration anaesthesia
Palatal Infiltration
Regional block methods in the maxilla
Posterior superior alveolar nerve block
Maxillary molar nerve block
Middle superior alveolar nerve block
Anterior superior alveolar nerve block
Infraorbital nerve block
Palatal anterior superior alveolar nerve block
Anterior middle superior alveolar nerve block
Greater palatine nerve block
Nasopalatine (long sphenopalatine nerve) block
Maxillary nerve block
Tuberosity approach
Greater palatine canal approach
Conclusions
Further Reading
Chapter 5 Techniques for Mandibular Anaesthesia
Aim
Outcome
Introduction and Terminology
Infiltration Methods
Age of the patient
Tooth of interest
Regional Block Methods
Regional block methods in the mandible
The inferior alveolar and lingual nerve block
1. The direct technique
2. The indirect technique
3. Anterior ramus technique
Problems with inferior alveolar nerve block anaesthesia
Gow-Gates mandibular nerve block
Akinosi-Vazirani block
Incisive and mental nerve block
Long buccal nerve anaesthesia
Mylohyoid nerve block
Conclusions
Further Reading
Chapter 6 Supplementary Techniques
Aim
Outcome
Introduction and Terminology
Topical Anesthesia
The agent
Duration of application
Site
Uses
Jet Injection
Intrapapillary Anaesthesia
Technique
Intraosseous Anaesthesia
Technique
Duration and spread of anaesthesia
Factors governing success
Advantages of intraosseous anaesthesia
Disadvantages of intraosseous anesthesia
Intraligamentary (Periodontal Ligament) Anaesthesia
Technique
Duration and spread of intraligamentary anaesthesia
Factors influencing efficacy
Advantages of intraligamentary anaesthesia
Disadvantages of intraligamentary anaesthesia
Intraseptal Anaesthesia
Intrapulpal Anaesthesia
Technique
Spread of intrapulpal anaesthesia
Factors influencing efficacy
Advantages of intrapulpal anaesthesia
Disadvantages of intrapulpal anaesthesia
Transcutaneous Electronic Nerve Stimulation
Conclusions
Further Reading
Chapter 7 Safety
Aim
Outcome
Introduction and Terminology
Physical Trauma
Chemical Trauma
Inappropriate Site of Deposition
Intravascular injection
Injection into parotid gland
Toxicity
Intravascular injection
Overdose
Metabolic disorders
Methaemoglobinaemia
Allergy
Medically Compromised Patients
Underlying medical conditions
Drug interactions
Local anaesthetics
Anticonvulsants
Antimicrobials
Benzodiazepines
Beta-adrenergic blockers
Calcium-channel blockers
Vasoconstrictors
Beta-adrenergic blockers
Diuretics
Calcium-channel blockers
Anti-Parkinson drugs
Antidepressant drugs
General anaesthetics
Drugs of abuse
Staff Safety
Conclusions
Further Reading
Chapter 8 Trouble-shooting
Aim
Outcome
Introduction
Pre-anaesthetic Problems
Patient anxiety
1. Fainting
2. Reduced anaesthetic efficacy
Inability to deliver the solution at the appropriate site
Failure of Local Anaesthesia
Anatomical Causes of Failure
Bony barriers to diffusion
Variations in the position of nerves and foramina
Collateral nerve supply
1. Maxilla
2. Mandible
1. Additional fibres from the ipsilateral inferior alveolar nerve
2. Fibres from the contralateral inferior alveolar nerve
3. Lingual nerve
4. The long buccal nerve
5. The mylohyoid nerve
6. The auriculotemporal nerve
7. Cervical nerves
Use of supplementary techniques to overcome failure due to collateral supply
Pathological Causes of Failure
Trismus
Inflammation
Pharmaceutical Causes of Failure
Pharmacological Causes of Failure
Psychological Causes of Failure
Technical Causes of Failure
The Approach to the Failed Case
Post-anaesthetic Problems
Bleeding
Pain
Prolonged altered sensation
Trismus
Infection
Conclusions
Further Reading
Chapter 9 Painless Local Anaesthesia: Is It Possible?
Aim
Outcome
Introduction
The expectation of pain
The needle
Needle gauge
Needle condition
Surface preparation
Refrigeration
Topical anaesthesia
Jet injection
Transcutaneous electronic nerve stimulation
Relative analgesia
The syringe
The area of the mouth injected
The technique
The anaesthetic solution
Temperature
pH
The order of the injection
Technique for Painless Anaesthesia
To Answer the Question
Conclusions
Further Reading
Quintessentials of Dental Practice – 6
Oral Surgery and Oral Medicine – 1
British Library Cataloguing in Publication Data
Meechan, J. G.
Practical dental local anaesthesia. - (The quintessentials of dental practice)
1. Anesthesia in dentistry 2. Local anesthesia
I. Title II. Wilson, Nairn H. F.
617.9'676
ISBN 1-85097-325-3
Copyright © 2002 Quintessence Publishing Co. Ltd., London
All rights reserved. This book or any part thereof may not be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, or otherwise, without the written permission of the publisher.
ISBN 1-85097-325-3
Painless, effective local anaesthesia is a real practice builder. Irrespective of how confident prospective readers may be about their knowledge and techniques in dental local anaesthesia, this volume in the Quintessentials for General Dental Practitioners Series is bound to provide new knowledge and understanding. Questions as to what best to do, where and when, notably in the presence of complicating factors and in the event of failed anaesthesia, are addressed in confidence-giving detail. The text, in the style of the Quintessentials Series, has been prepared primarily for the hard-pressed practitioner and the student seeking the benefit of experience tempered by authoritative insight.
Practical Dental Local Anaesthesia will give practitioners and students alike something to apply for the immediate benefit of their patients. Whether this benefit stems from a nugget of information or a stimulus to adopt a fresh approach to state-of-the-art dental local anaesthesia, Practical Dental Local Anaesthesia will undoubtedly prove to be a valuable addition to every dentist’s library.
Nairn Wilson
Editor-in-Chief
This book could not have been written without the help of a number of people. Janet Howarth, Jan Ledvinka, Carole Rose and David Rynn all helped with the photography in Newcastle. John Rout of the Birmingham Dental Hospital kindly provided Fig 9-1. Figs 7-1 and 9-4 are reproduced from Dental Update by permission of George Warman Publications (UK) Ltd. Fig 9-5 originally appeared in R R Welbury (ed.), Paediatric Dentistry, and is reproduced by permission of Oxford University Press.
The time invested in writing this book would not have been possible without the understanding and support of my family. So to Jan, Rob and Si – a big “Thank you”.
John G Meechan
The aim of this chapter is to describe the basic principles of dental local anaesthesia.
After reading this chapter you should have a basic understanding of the pharmacology and anatomy of dental local anaesthesia.
The main purpose of this book is to act as a practical guide to the use of local anaesthesia in dentistry. Before embarking on practical issues it is important to acquire a basic understanding of the pharmacology and anatomy of dental local anaesthesia. Anaesthesia is defined as a loss of sensation in a circumscribed area of the body by a depression of excitation in nerve endings or an inhibition of the conduction process in peripheral nerves. This definition includes all sensation. In dentistry it is pain sensation we want to eliminate. Loss of pain sensation is termed analgesia. The terms local anaesthesia and local analgesia are used almost synonymously in dental practice. As true anaesthesia may be produced on occasion following intra-oral injection, the former term is used in this book.
Local anaesthesia may be obtained by a number of mechanisms. Traumatic severance of a nerve will produce it. This may occur after damage to the lingual nerve during third molar surgery. This is not always reversible. In order to be acceptable for clinical use a reversible method is required. Local anaesthetic drugs achieve this goal. Although the mechanism of local anaesthetic action is complex it can be explained in a straightforward way. A nerve transmits information along its length by producing a change in the electrical gradient across the nerve cell membrane (Fig 1-1). At rest the inside of the nerve cell is negatively charged compared to the outside. When the nerve is excited to the so-called “firing” level this polarity changes. The reversal in electrical charge is the signal that is transmitted along the nerve. This change in polarity is principally due to the rapid entry of positively charged sodium ions into the cell. At rest the cell is impermeable to sodium ions. Stimulation causes a conformational change that permits the inward passage of these positive ions. Thus, transmission is dependent upon sodium ion entry. This occurs at the sodium channel. Local anaesthetics work by inhibiting the passage of sodium into the nerve cell. In simple terms they act as chemical roadblocks to the transmission of electrical impulses. They achieve this by a combination of two mechanisms. First, there is probably a contribution to the effect by a non-specific expansion of the nerve cell membrane. This causes physical obstruction of the sodium channel. Secondly, and more importantly, local anaesthetics bind reversibly to specific receptors in the sodium channel. The binding site for the local anaesthetic molecule is exposed during a conformational change that occurs to the sodium channel during the refractory period of the firing cycle. During this period further stimulation of the nerve is ineffective in producing a signal. When the local anaesthetic binds to its receptor the sodium channel is maintained in the refractory conformation. A simplified diagrammatic representation of this action is shown in Fig 1-2.
Fig 1-1 The major factor involved in nerve transmission is the differential concentration of sodium ions across the nerve membrane. Local anaesthetics block the entry of sodium into the cell and thus prevent “firing”.
Fig 1-2 At rest, ion passage through the sodium channel is inhibited by a gate known as the “m” (for “make”) gate. This gate is open during “firing”. During the refractory period, another gate, the “h” (for “halt”) gate, closes blocking further sodium entry. The local anaesthetic molecule binds to a receptor on or close to the “h” gate maintaining the channel in the refractory conformation.
Access to the local anaesthetic binding site is obtained from the inside of the nerve cell. This is important and represents an interesting pharmacological challenge. Why? In order to gain entry into the cell the anaesthetic must be soluble in fat, as the cell membrane contains much lipid. Non-charged molecules are fat-soluble. Therefore, to gain entry into the cell the local anaesthetic must be in a non-charged state. As specific binding to a receptor is important in achieving anaesthesia a material that recognises its receptor is needed. Receptor binding depends upon the molecule being charged. Thus, once in the cell, it is important that the molecule is in a charged form. This ability to exist in both lipid-soluble and charged states is achieved because local anaesthetics are weak bases. When the local anaesthetic is in solution some of the molecules are charged and some are uncharged (Fig 1-3). It is only the uncharged molecules that can penetrate the lipid nerve cell membrane to gain access to the inside of the cell. The uncharged portion enters the nerve cell and then re-equilibrates in this aqueous environment to a mixture of charged and uncharged molecules. Once in the cell it is the charged portion that binds to the specific receptor. If no material enters the cell the local anaesthetic will not function. The more rapidly a local anaesthetic enters the cell the more effective it is and the quicker it will act. Thus materials that have a high proportion of uncharged molecules present in tissue fluid after injection are the most effective. Two factors govern the proportion of charged to uncharged molecules following injection. These are:
the pH of the region
the dissociation constant (pKa) of the local anaesthetic molecule.
Fig 1-3 Local anaesthetics molecules are present in both charged and uncharged forms in solution. It is the uncharged moiety that enters the nerve cell. This then re-equilibrates to charged and uncharged forms and the charged portion binds to the specific receptor to block sodium entry.
The relationship of these factors to the proportion of charged and uncharged molecules in solution is explained in the Henderson Hasselbach equation:
Therefore, the lower the pH the less uncharged local anaesthetic molecules are present in solution. The lower the pKa the more uncharged molecules exist. Local anaesthetics vary in their pKas and thus differ in their onset of action. For example, the older dental local anaesthetic procaine had a pKa of 9.0 compared to the pKa of 7.9 for lidocaine. This is one reason why lidocaine is a much more effective local anaesthetic compared to procaine.
Another reason why local anaesthetics vary in their inherent activity is due to the fact that they differ in their effects on blood vessels. Most of the clinically useful local anaesthetic agents are vasodilators; an exception is cocaine, which has potent vasoconstrictive properties. The degree of vasodilatation varies between agents. Procaine is a potent vasodilator whereas mepivacaine has less vasodilator action. As local anaesthetics have a dilator effect on blood vessels they are often combined with vasoconstrictor drugs such as epinephrine to increase their efficacy. The addition of a vasoconstrictor increases both the depth and the duration of local anaesthesia as well as reducing blood loss during surgical procedures.
Eventually all of an injected dose of a local anaesthetic is absorbed into the blood stream to undergo metabolism prior to excretion in urine. The type of agent involved determines its metabolism. There are two classes of local anaesthetic agent:
esters
amides.
Esters are metabolised rapidly in plasma by pseudocholinesterases. An example of an ester is the topical anaesthetic agent benzocaine. The breakdown of amides is more complex and slower than that of the esters. All of the local anaesthetic drugs available in dental cartridges in the UK are amides. Most of these drugs have to be transported to the liver to begin their breakdown. Some metabolism of prilocaine also occurs in the lungs. An exception to the usual process occurs with articaine. This agent undergoes initial biotransformation in plasma by esterases, this means that articaine is metabolised more rapidly than the other amide agents used in dentistry. Very little of an administered local anaesthetic is excreted unchanged in urine.
In order to produce their effect local anaesthetics must be placed close to the nerve they are going to anaesthetise. In dentistry this is usually achieved by topical application or by injection. A sufficient amount must be used, as the effect is dose-dependent. One area where nerve conduction may be blocked is close to the nerve ending. Techniques such as infiltration, intra-osseous, intraligamentary and topical anaesthesia work this way. Alternatively, transmission may be blocked at any part of a nerve trunk proximal to the ending; this is the so-called regional block. In order to be competent in providing dental local anaesthesia, especially by regional block injection, it is essential to have an understanding of the anatomy of the sensory nerves that supply the teeth and associated structures.
The anatomy of dental local anaesthesia is not complex. For most purposes only two branches of the trigeminal (the fifth cranial) nerve need be considered. These are:
the maxillary division
the mandibular division.
The rider to this is that on occasion some “rogue” supply from other sources, such as the upper cervical nerves, may contribute to pulpal nerve supply. The consequences of this are discussed in Chapter 8.
Branches of the maxillary division of the trigeminal nerve supply the upper teeth and their supporting structures (Figs 1-4 and 1-5). The nerves of interest are:
posterior superior alveolar nerve
middle superior alveolar nerve
anterior superior alveolar nerve
greater palatine nerve
lesser palatine nerve
nasopalatine (long sphenopalatine) nerve.
Fig 1-4 The branches of the maxillary division of the trigeminal nerve that are important in dental local anaesthesia.
Fig 1-5 The nasopalatine, greater and lesser palatine nerves.
The maxillary division of the trigeminal nerve is best considered in two portions. The first is that part between the skull and the maxilla. This section of the nerve emerges from the skull through the foramen rotundum. It then enters the pterygopalatine fossa. A number of branches leave the main trunk in the pterygopalatine fossa; some of these subsequently enter the maxilla independent of the main nerve bundle. The nasopalatine, greater and lesser palatine nerves leave the main trunk to enter the sphenopalatine ganglion. The nasopalatine nerve continues along the nasal septum and exits the maxilla at the incisive papilla. The greater and lesser palatine nerves exit the greater palatine and lesser palatine foramina respectively (Fig 1-5). The former nerve passes anteriorly towards the region supplied by the nasopalatine nerve and the latter passes posteriorly into the soft palate and uvula. The zygomatic and posterior-superior alveolar nerves also leave the main trunk of the maxillary nerve in the pterygopalatine fossa. The posterior-superior alveolar nerve runs inferiorly along the posterior wall of the maxilla to enter that bone about a centimetre above and behind the third molar tooth.
The second part of the maxillary nerve comprises of that section of the main nerve bundle that enters the maxilla. The nerve passes through the inferior orbital fissure to enter the orbit. In the floor of the orbit it enters the infra-orbital canal. The middle superior alveolar nerve leaves the main trunk within this canal and travels inferiorly in the lateral wall of the maxillary antrum to the alveolus. At a more anterior part of the infra-orbital canal the main trunk supplies the anterior superior alveolar nerve that descends to the alveolus at the anterior maxilla. The remaining part of the maxillary nerves continues as the infraorbital nerve and exits the maxilla at the infra-orbital foramen. The structures of importance in dental local anaesthesia supplied by the maxillary nerve are given in Table 1-1.