Clinical Problem Solving in Dentistry (PDF) 3rd Edition

1 ( LINICAI PROBLEM SOLVING N DENTISTRY THIRD EDITION Clinical Problem Solving in Dentistry CHURCHII I U\ INGS'IT )NI IIMMIK  Clinical Problem Solvi...

1 ( LINICAI PROBLEM SOLVING N DENTISTRY THIRD EDITION Clinical Problem Solving in Dentistry CHURCHII I U\ INGS'IT )NI IIMMIK  Clinical Problem Solving in Dentistry Commissioning Editor: Alison Taylor Development Editor: Janice Urquhart, Louisa Welch Project Manager: Shereen Jameel Designer/Design Direction: Stewart Larking Illustration Manager: Bruce Hogarth Illustrator: Robert Britton  C l i n i c a l p r o b l e m so l v i n g i n d ent i st r SERIES y Third Edition Clinical Problem Solving in Dentistry Edited by Edward W. Odell Professor and Honorary Consultant in Oral Pathology and Medicine, King’s College London Dental Institute, Guy’s Hospital, London, UK CHURCHILL LIVINGSTONE ELSEVIER Edinburgh London New York Oxford Philadelphia St Louis Sydney Toronto 2010  CHURCHILL LIVINGSTONE ELSEVIER Third edition © 2010, Elsevier Limited. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Permissions may be sought directly from Elsevier’s Rights Department: phone: (+1) 215 239 3804 (US) or (+44) 1865 843830 (UK); fax: (+44) 1865 853333; e-mail: [email protected]. You may also complete your request online via the Elsevier website at http://www.elsevier.com/permissions. First published 2000 Second edition 2004 Third edition 2010 ISBN 978-0-443-06784-6 British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Cataloging in Publication Data A catalog record for this book is available from the Library of Congress Notice Knowledge and best practice in this field are constantly changing. As new research and experience broaden our knowledge, changes in practice, treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on their own experience and knowledge of the patient, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the Editor assumes any liability for any injury and/or damage to persons or property arising out of or related to any use of the material contained in this book. The Publisher your source for books, ELSEVIER journals and multimedia in the health sciences www.elsevierhealth.com Working together to grow libraries in developing countries www.elsevier.com | www.bookaid.org | www.sabre.org ELSEVIER Sabre Foundation The publisher’s policy is to use paper manufactured from sustainable forests Printed in China  Contents 1 A high caries rate 1 19 Troublesome mouth ulcers 87 David W. Bartlett and David Ricketts Penelope J. Shirlaw and Edward W. Odell 2 A multilocular radiolucency 7 Eric Whaites and Edward W. Odell 20 A lump in the neck 91 Nicholas M. Goodger and 3 An unpleasant surprise 13 Edward W. Odell Michael Escudier 21 Trauma to an immature incisor 95 4 Gingival recession 19 Mike G. Harrison Richard M. Palmer 22 Hypoglycaemia 99 5 A missing incisor 23 Michael Escudier Robert M. Mordecai 23 A tooth lost at teatime 103 6 Down’s syndrome 27 Alexander Crighton Emma K. Mahoney 24 A problem overdenture 109 7 A dry mouth 33 David R. Radford Penelope J. Shirlaw and Edward W. Odell 25 Impacted lower third molars 113 Tara F. Renton 8 Painful trismus 37 Paul D. Robinson 26 A phone call from school 119 Mike G. Harrison and 9 A large carious lesion 43 Evelyn Sheehy (Edward W. Odell) Avijit Banerjee 27 Discoloured anterior teeth 125 10 A lump on the gingiva 49 David W. Bartlett and David Ricketts Anwar R. Tappuni 28 A very painful mouth 131 11 Pain on biting 53 Penelope J. Shirlaw and David W. Bartlett and David Ricketts Edward W. Odell 12 A defective denture base 57 29 Caution – X-rays 135 Martyn Sherriff Eric Whaites 13 Sudden collapse 59 30 Whose fault this time? 139 David C. Craig David R. Radford 14 A difficult child 61 31 Ouch! 145 Wendy Bellis Guy D. Palmer 15 Pain after extraction 67 32 A swollen face and Tara F. Renton pericoronitis 151 16 A numb lip 71 Tara F. Renton Nicholas M. Goodger and Edward W. Odell 33 First permanent molars 155 Mike G. Harrison and Anna Gibilaro 17 A loose tooth 77 David W. Bartlett and David Ricketts 34 A sore mouth 159 Shahid I. Chaudhry and 18 Oroantral fistula 81 Edward W. Odell Tara F. Renton and Edward W. Odell  vi contents 35 A failed bridge 163 52 Refractory periodontitis? 243 Richard M. Palmer Edward W. Odell 36 Skateboarding accident? 167 53 Unexpected findings 249 Jennifer C. Harris Eric Whaites 37 An adverse reaction 173 54 A gap between the front teeth 255 Chris Dickinson David R. Radford 38 Advanced periodontitis 177 55 A lump in the palate 261 David W. Bartlett and David Ricketts Tara F. Renton and Edward W. Odell 39 Fractured incisors 183 56 Rapid breakdown of first David W. Bartlett and David Ricketts permanent molars 265 Mike G. Harrison 40 An anxious patient 187 David C. Craig 57 Oral cancer 269 Nicholas M. Goodger and 41 A blister on the cheek 191 Edward W. Odell Michael J. Twitchen and Edward W. Odell 58 A complicated extraction 277 Guy D. Palmer 42 Will you see my son? 195 Wendy Bellis 59 Difficulty in opening the 43 Bridge design 199 mouth 281 David W. Bartlett and David Ricketts Wanninayaka M. Tilakaratne and Edward W. Odell 44 Management of anticoagulation 203 60 Toothwear 285 David W. Bartlett and David Ricketts Nicholas M. Goodger 45 A white patch on the tongue 209 61 Worn front teeth 289 David W. Bartlett and David Ricketts Michael J. Twitchen and Edward W. Odell 62 A case of toothache 293 Edward W. Odell and Eric Whaites 46 Another white patch on the tongue 215 63 A child with a swollen face 297 Edward W. Odell Eric Whaites and Edward W. Odell 47 Molar endodontic treatment 219 64 A pain in the neck 301 David Ricketts and Carol Tait Michael Escudier, Jackie Brown and Edward W. Odell 48 An endodontic problem 223 David Ricketts and Carol Tait 65 Failed endodontic treatment 307 David W. Bartlett and David Ricketts 49 A swollen face 229 Tara F. Renton and Paul D. Robinson 66 A pain in the head 311 Tara F. Renton 50 Missing upper lateral incisors 235 David W. Bartlett and David Ricketts Index 317 51 Anterior crossbite 239 Robert M. Mordecai  Preface The fact that a third edition of this book has been produced guidance, changes in legislation and advances in treatment. so soon after the last is testimony to the appeal of the Topics of the new sections range through basic dentistry, problem solving format. I said in the preface to both previ- special care topics and child protection to name a few. We ous editions that problem solving is a practical skill that hope you enjoy them and find them useful. cannot be learnt from textbooks. This book is designed to I am indebted to the many friends and colleagues who help the reader reorganize their knowledge into a clinically have contributed. As before, many of these chapters are useful format. It cannot teach you to solve problems unless team efforts with input from people who are not acknowl- you supplement it with clinical experience, for which there edged. It is difficult for a reader to appreciate how much is no substitute. effort the many authors have expended and the time they This third edition includes ten completely new problems, have given up to produce this book. Without them, and the making it almost twice as long as the first edition. All the patience and support of my wife Wendy and children, this chapters have been completely revised. Despite the short book would never have been written. interval since the last edition it is surprising how many have had to be extensively rewritten to account for new national EW Odell This page intentionally left blank  Contributors Dr Avijit Banerjee bds fds msc phd Dr Michael Escudier bds fdsrcs fdsrcs Senior Lecturer and Hon Consultant in (oral med) md ffgdp Restorative Dentistry, King’s College London Lecturer/Hon Consultant in Medicine in Dental Institute, London, UK Relation to Oral Disease, King’s College London Dental Institute, London, UK Professor David W. Bartlett, bds phd mrd fdsrcs (rest. dent.) Dr Anna Gibilaro bds dds msc dorth morth Professor of Prosthodontics, King’s College fdscrcs fdsrcs (orthodontics) London Dental Institute, London, UK Consultant in Orthodontics, Guy’s and St Thomas’ NHS Foundation Trust, London, UK Ms Wendy Bellis bds msc Senior Dental Officer in Paediatric Dentistry, Mr Nicholas M. Goodger phd frcs (Omfs) Islington & Camden Primary Care Trust, fdsrcs ffd dlorcs London, UK Consultant Oral and Maxillofacial Surgeon, East Kent Hospitals NHS Trust and Honorary Mrs Jackie Brown bdS msc fdsrcps ddrrcr Senior Lecturer in Maxillofacial Surgery, Consultant and Honorary Senior Lecturer in University of Kent, Canterbury, UK Dental Radiology, King’s College London Dental Institute, London, UK Mrs Jennifer C. Harris bds msc fdsrcs Specialist in Paediatric Dentistry, Sheffield Dr Shahid I. Chaudhry bds mbbs fds Salaried Primary Dental Care Service, Sheffield, mrcp(uk) UK Specialist Registrar/Honorary Lecturer in Oral Medicine, UCL Eastman Dental Institute, Mr Mike G. Harrison bds fdsrcs London, UK (paed. dent) mphil mscd Consultant in Paediatric Dentistry, Guy’s and Dr David C. Craig ba bds mmedsci mfgdp St Thomas’ NHS Foundation Trust, London, Consultant in Sedation and Special Care UK Dentistry, King’s College London Dental Institute, London, UK Miss Emma K. Mahoney bds msc snd, msnd rcs Dr Alexander Crighton bds mbchb fdsrcs Senior Dental Officer in Special Care Dentistry, (oral med) fdsrcps Islington and Camden Primary Care Trust, Consultant in Oral Medicine, Hon Clinical London, UK Senior Lecturer in Medicine in Relation to Dentistry, Glasgow Dental Hospital & School, Mr Robert M. Mordecai bds fdsrcs dorth Glasgow, UK morth Formerly Senior Lecturer and Honorary Mr Chris Dickinson bds msc mfds ddph Consultant in Orthodontics, King’s College rcs dipdsed London Dental Institute, London, UK Consultant in Special Care Dentistry, Guy’s and St Thomas’ NHS Foundation Trust, London, Professor Edward W. Odell bds fdsrcs UK msc phd frcpath Professor of Oral Pathology and Medicine, King’s College London Dental Institute, London, UK  x co n t r i b u to r s Mr Guy D. Palmer bds msc mrd Dr Martyn Sherriff bsc phd mrsc mimmm Consultant in Special Care Dentistry, King’s ancrt fss College Hospital NHS Foundation Trust, Reader in Dental Materials Science, King’s London, UK College London Dental Institute, London, UK Professor Richard M. Palmer bds fdsrcs Mrs Penelope J. Shirlaw bds fdsrcs phd Consultant in Oral Medicine, Guy’s and St Professor of Implant Dentistry and Thomas’ Hospitals NHS Foundation Trust, Periodontology, King’s College London Dental London, UK Institute, London, UK Carol Tait bds msc mfds mrd Dr David R. Radford bds phd fdsrcs mrd Senior Clinical Teacher in Endodontology, Senior Lecturer and Honorary Consultant, Dundee Dental Hospital and School, Dundee, King’s College London Dental Institute, UK London, UK Dr Anwar R. Tappuni ldsrcs mracds(om) Professor Tara F. Renton bds fdsrcs phd fracds (oms) phd Clinical Senior Lecturer in Oral Medicine, Bart’s Professor of Oral Surgery, King’s College and the London School of Medicine and London Dental Institute, London, UK Dentistry, London, UK Professor David Ricketts bds msc phd Professor Wanninayaka M. Tilakaratne fdsrcs fds (rest. dent.) bds ms fdsrcs frcpath Professor of Cariology and Conservative Professor and Consultant in Oral Pathology, Dentistry and Honorary Consultant in University of Peradeniya, Sri Lanka Restorative Dentistry, Dundee Dental Hospital and School, Dundee, UK Dr Michael J. Twitchen ffd lmssa General Medical Practitioner, West Sussex, UK Mr Paul D. Robinson mbbs bds fdsrcs phd Specialist Oral Surgeon, Formerly Department Mr Eric Whaites msc bds fds rcs frcr of Oral and Maxillofacial Surgery, Guy’s ddrrcr Hospital, London, UK Senior Lecturer and Honorary Consultant in Dental Radiology, King’s College London Dr Evelyn Sheehy bdsc phd fdsrcs Dental Institute, London, UK (paed. dent.) Consultant in Paediatric Dentistry, Guy’s and St Thomas’ Hospitals NHS Foundation Trust, London, UK  Case 1 Examination Extraoral examination He is a fit and healthy-looking adolescent. No submental, submandibular or other cervical lymph nodes are palpable and the temporomandibular joints appear normal. Intraoral examination A high caries rate The lower right quadrant is shown in Figure 1.1. The oral mucosa is healthy and the oral hygiene is reasonable. There is gingivitis in areas but no calculus is visible and probing depths are 3 mm or less. The mandibular right first molar is grossly carious and a sinus is discharging buccally. There are no other restorations in any teeth. No teeth have been extracted and the third molars are not visible. A small cavity is present on the occlusal surface of the mandibular right second molar. What further examination would you carry out? SUMMARY Test of tooth vitality of the teeth in the region of the sinus. A 17-year-old sixth-form college student presents at Even though the first molar is the most likely cause, the your general dental surgery with several carious adjacent teeth should be tested because more than one lesions, one of which is very large. How should you tooth might be nonvital. The results should be compared stabilize his condition? with those of the teeth on the opposite side. Both hot/cold methods and electric pulp testing could be used because extensive reactionary dentine may moderate the response. The first molar fails to respond to any test. All other teeth appear vital. Investigations What radiographs would you take? Explain why each view is required. Radiograph Reason taken Bitewing radiographs Primarily to detect approximal surface caries, and in this case also required to detect occlusal caries. Periapical radiograph of the lower right Preoperative assessment for first molar tooth, preferably taken with endodontic treatment or for Fig. 1.1 The lower right first molar. The gutta percha point a paralleling technique extraction should it be necessary. indicates a sinus opening. Panoramic radiograph Might be useful as a general survey view in a new patient and to History determine the presence and position of third molars. Complaint He complains that a filling has fallen out of a tooth on the What problems are inherent in the diagnosis of caries in lower right side and has left a sharp edge that irritates his this patient? tongue. He is otherwise asymptomatic. Occlusal lesions are now the predominant form of caries in adolescents following the reduction in caries incidence over History of complaint the past decades. Occlusal caries may go undetected on The filling was placed about a year ago at a casual visit to visual examination for two reasons. First, it starts on the fissure the dentist precipitated by acute toothache triggered by hot walls and is obscured by sound superficial enamel, and and cold food and drink. He did not return to complete a secondly lesions cavitate late, if at all, probably because course of treatment. He lost contact when he moved house fluoride strengthens the overlying enamel. Superimposition of and is not registered with a dental practitioner. sound enamel also masks small and medium-sized lesions on bitewing radiographs. The small occlusal cavity in the second Medical history molar arouses suspicion that other pits and fissures in the The patient is otherwise fit and well. molars will be carious. Unless lesions are very large, extending  1 CASE 2 A h i g h c a r i e s r at e Fig. 1.2 Periapical and bitewing films. into the middle third of dentine, they may not be detected on bitewing radiographs. The radiographs are shown in Figure 1.2. What do you see? The periapical radiograph shows the carious lesion in the crown of the lower right first molar to be extensive, involving the pulp cavity. The mesial contact has been completely destroyed and the molar has drifted mesially and tilted. There are periapical radiolucencies at the apices of both roots, that on the mesial root being larger. The radiolucencies are in continuity with the periodontal ligament and there is loss of most of the lamina dura in the bifurcation and around the apices. The bitewing radiographs confirm the carious exposure and in addition reveal occlusal caries in all the maxillary and mandibular molars with the exception of the upper right first molar. No approximal caries is present. If two or more teeth were possible causes of the sinus, how might you decide which was the cause? A gutta percha point could be inserted into the sinus prior to taking the radiograph, as shown in Figure 1.1. A medium- or fine-sized point is flexible but resilient enough to pass along Fig. 1.3 Another case, showing gutta percha point tracing the the sinus tract if twisted slightly on insertion. Points are path of a sinus. radiopaque and can be seen on a radiograph extending to the source of the infection, as shown in another case in Figure 1.3. What temporary restoration materials are available? Diagnosis What are their properties and in what situations are they useful? What is your diagnosis? See Table 1.2. The patient has a nonvital lower first molar with a periapical Why is one molar so much more broken down than the abscess. In addition he has a very high caries rate in a others? previously almost caries-free dentition. It is difficult to be certain but the extensive caries is probably, in part, a result of the previous restoration. In view of the Treatment pattern of caries in the other molars, it seems likely that this The patient is horrified to discover that his dentition is in was a large occlusal restoration and the history suggests it such a poor state, having experienced only one episode of was placed in a vital tooth. It probably undermined the toothache in the past. He is keen to do all that can be done mesial cusps or marginal ridge. Three factors could have to save all teeth and a decision is made to try to restore the contributed to the extensive caries present only 1 year later: lower molar. marginal leakage, undermining of the marginal ridge or mesial cusps leading to collapse, or failure to remove all the How will you prioritize treatment for this patient? Why carious tissue from the tooth. Failure to remove all carious should treatment be provided in this sequence? enamel and dentine is a common cause of failure in amalgam See Table 1.1. restorations.  1 3 CASE A h i g h c a r i e s r at e Table 1.1 Sequence of treatment Phase of treatment Items of treatment Reasons Immediate phase Caries removal from the lower right first molar, access cavity Essential if the tooth is to be saved and to remove the source of the apical infection. There is also preparation for endodontics, drainage, irrigation with sodium an urgent need to minimize further destruction of this tooth, which may soon be unrestorable. hypochlorite and placement of a temporary restoration The temporary restoration is necessary to facilitate rubber dam isolation during future endodontic treatment, and it will also stabilize the occlusion and stop mesial drift. Stabilization of caries Removal of caries and placement of temporary restorations in all To prevent further tooth destruction and progression to carious exposure while other phases of carious teeth in visits by quadrants/two quadrants treatment are being carried out. Preventive treatment Dietary analysis, oral hygiene instruction, fluoride advice Should start immediately and extend throughout the treatment plan, to reduce the high caries rate and ensure the long-term future of the dentition. Permanent restoration Will depend on what is found while placing temporary restorations Permanent restorations may be left until last; stabilization takes priority. Table 1.2 Temporary restoration materials Material Examples Properties Situations Zinc oxide and eugenol pastes Kalzinol Bactericidal, easy to mix and place, cheap but not very strong. Suitable for temporary restoration of most cavities provided there is no Easily removed. significant occlusal load. Endodontic access cavities. Self-setting zinc oxide cements Cavit Harden in contact with saliva. Endodontic access cavities. Coltosol Reasonable strength and easily removed. No occlusal load. Polycarboxylate cements Poly-F Adhesive to enamel and dentine, hard and durable. Used when mechanical retention is poor. Strong enough to enable rubber dam placement when used in a badly broken down tooth. Glass ionomer including silver Chem-fil Adhesive to enamel and dentine, hard and durable. Good As polycarboxylate cements and also useful in anterior teeth. reinforced preparations Shofu Hi-Fi appearance. Ketac Silver How would you ensure removal of all carious tissue when a susceptible tooth surface. Denying the plaque flora its restoring the vital molars? substrate sugar is the most effective measure to halt the progression of existing lesions and prevent new ones forming. Removal of all softened carious tissue at the amelodentinal No preventive measure affecting the flora or tooth is as junction is essential and only stained but hard dentine can be effective. A further advantage of emphasis on diet is that it left in place. forces the patient to acknowledge that they must take Removal of carious dentine over the pulp is treated responsibility for preventing their own disease. differently. In a young patient with large pulp chambers there is always a tendency for the operator to be conservative but How would you evaluate a patient’s diet? this might be counterproductive if softened or infected Dietary analysis consists of two elements: enquiry into lifestyle dentine were left below the restoration. Very soft or flaky and into the dietary components themselves. Information dentine must always be removed. Slightly soft dentine can be about the diet itself is of little value unless it is taken in left in situ provided a good well-sealed restoration is placed context with the patient’s lifestyle. Only dietary over it. Deciding whether to leave the last layers of softened recommendations tailored to the patient’s lifestyle are likely dentine can be difficult and the decision rests to a degree on to be adopted. clinical experience. Pain associated with pulpitis indicates a need to remove more dentine or, if severe, a need for elective The diet record should include all the foods and drinks endodontics. Interpreting softened dentine in rapidly consumed, the amount (in readily estimated units) and the advancing lesions is difficult. The deepest layers are soft time of eating or drinking. through demineralization but are not necessarily infected and In this case it should be noted that the patient is a 17-year- may sometimes be left over the pulp. Also, bacterial old student. Lifestyle often changes dramatically between the penetration of the dentine is not reliably indicated by staining ages of 16 and 20. He may no longer be living at home and in rapidly advancing lesions. Removal of the last layers of may be enjoying physical, financial and dietary independence carious dentine may require some courage in deep lesions. from his parents. He may be poor and be eating a cheap More detailed information on caries removal is included in carbohydrate-rich diet of snacks instead of regular meals. problem 9, ‘A large carious lesion’. Long hours of studying may be accompanied by the frequent consumption of sweetened drinks. What is the most important preventive procedure for this Analysis of the diet itself may be performed in a variety of patient? Explain why. ways. The patient can be asked to recall all foods consumed Diet analysis. Caries requires dietary sugars, in particular over the previous 24 hours. This is not very effective, relying sucrose, glucose and fructose, an acidogenic plaque flora and as it does on a good memory and honesty, and is unlikely to  1 CASE 4 A h i g h c a r i e s r at e give a representative account. Relying on memory for more be beneficial to use a weekly fluoride rinse as well. This could than 24 hours is too inaccurate. be continued for as long as the diet is felt to be unsafe. The most effective method is for the patient to keep a written Oral hygiene instruction is also important, but may be record of their diet for 4 consecutive days, including 2 emphasized in a later phase of treatment. It will not stop working and 2 leisure days. The need for the patient to caries progression, which is critical for this patient, and there comply fully and assess their diet honestly must be stressed is only a mild gingivitis. and, of course, the diet should not be changed because it is being recorded. Ideally the analysis should be performed Assuming good compliance and motivation, how will you before any dietary advice is given. Even the patient who does restore the teeth permanently? not keep an honest account has been made more aware of The mandibular right first molar requires orthograde their diet. If they know what foods to omit from the sheet to endodontic treatment and replacement of the temporary make their dentist happy, at least the first step in an restoration with a core. Retention for the core can be educative process has been made. provided by residual tooth tissue, provided carious How will you analyse this patient’s 4-day diet sheet destruction is not gross. The restorative material may be shown in Figure 1.4? What is the cause of his caries packed into the pulp chamber and the first 2–3 mm of the susceptibility? root canal. If insufficient natural crown remains, it may be supplemented with a preformed post in the distal canals. The Highlight sugar-rich foods and drinks as in Figure 1.4. distal canal is not ideal, being further from the most Note whether they are confined to meal times or whether extensively destroyed area, but it is larger. they are eaten frequently and spaced throughout the day The other molar teeth will need to have their temporary as snacks. The number of sugar attacks should be counted restorations replaced by definitive restorations. Caries and discussed with the patient. Also note the consistency of involved only the occlusal surface but removal of these large the food because dry and sticky foods take longer to be lesions has probably left little more than an enamel shell. cleared from the mouth. Sugared drinks taken immediately Restoration of such teeth with amalgam would require before bed are highly significant because salivary flow is removal of all the unsupported, undermined enamel leaving reduced during sleep and clearance time is greater. Identify little more than a root stump and a few spurs of tooth tissue. foods with a high hidden sugar content because patients Restoration could be better achieved with a radiopaque glass often do not realize that such foods are significant; examples ionomer and composite hybrid restoration. The glass ionomer are baked beans, breakfast cereals, tomato ketchup and ‘plain’ used to replace the missing dentine must be radiopaque so biscuits. that it is not confused with residual or secondary caries on The diet sheet shows that the main problem for this radiographs. A composite linked to dentine with a bonding patient is too many sugar-containing drinks, and frequent agent would be an alternative to the glass ionomer. snacks of cake and biscuits. Most meals or snacks contain a high sugar item and some more than one. The other typical Figure 1.5 shows the restored lower first molar 2 months cause of a high caries rate in this age group is sweets, after endodontic treatment. What do you see and what especially mints. long-term problem is evident? What advice will you give the patient? There is good bone healing around the apices and in the bifurcation. Complete healing would be expected after 6 The principles of a safer diet are shown in Table 1.3 (p. 6). months to 1 year at which time the success of root treatment Dietary advice is almost always provided using the health- can be judged. belief model of health education. However, it is well-known As noted in the initial radiographs, the lower right first molar that education about the risks and consequences of lifestyle, has lost its mesial contact, drifted and tilted. This makes it habits and diet is often ineffective. It is important to judge impossible to restore the normal contour of the mesial the patient’s likely compliance and provide dietary advice surface and contact point. The mesial surface is flat and there that can be used to make small but significant changes is no defined contact point. In the long term there is a risk of rather than attempting to eradicate all sugar from the diet. caries of the distal surface of the second premolar, and the As the diet improves, the advice can be adapted and caries is likely to affect a wider area of tooth and extend extended. further gingivally than caries below a normal contact. The Advice must be acceptable, practical and affordable. In this area will also be difficult to clean and there is a risk of case the patient has already suffered serious consequences localized periodontitis. Tilting of the occlusal surface may also from his poor diet and this may help change behaviour. favour food packing into the contact unless the contour of The patient must be made aware that damage to teeth the restoration includes an artificially enhanced marginal continues for up to 1 hour after a sugar intake. The ridge. explanation given to some patients may be no more than this This tooth may require a crown in the long term. Much of the simple statement. Many other patients can comprehend the enamel is undermined and the tooth is weakened by concept (if not the detail) of a Stephan curve without endodontic treatment. A crown would allow the contact to difficulty. have a better contour but the problem is insoluble while the The patient should be advised to use a fluoride-containing tooth remains in its present position. Orthodontic uprighting toothpaste. During the period of dietary change it would also could be considered.  John Smith 4 day diet analysis sheet for................................. Thursday Friday Saturday Sunday Time Item Time Item Time Item Time Item 7.00 2 cups of tea 7.30 4 chocolate biscuits Before breakfast with 2 sugars tea with 2 sugars sausages 8.30 banana 8.00 chocolate puffed rice pitta bread breakfast cereal Breakfast 8.30 ketchup 1 glass cola drink tea with 2 sugars * 1 glass cola drink 10.30 4 slices toast 9.20 9.30 mug hot chocolate 11.00 1 slice cherry cake hot chocolate packet crisps and peanut butter Morning can of diet cola drink 1 piece cake 11.15 chocolate bar turkey salad 1.00 pm 2 pieces cheese on 1 slice cake 1.00 pm fish pie 12.30 12.30 sandwich toast, garlic sausage tea with 2 sugars 1 glass cola drink Mid-day meal 1 glass cola drink 1 slice cake tea with 2 sugars 1 glass cola drink 4.00 pm fizzy drink 4.30 pm ham 3.00 pm sausages, beans, 2.00 pm tea with 2 sugars chocolate bar 1 piece cake toast. 1 biscuit Afternoon 1 slice cake tea with 2 sugars an orange 4.30 pm 1 piece cake 1 can cola drink tea with 2 sugars 5.00 pm 1 glass cola drink 6.00 pm bar of chocolate salad, garlic burger and chips 8.00 pm spaghetti bolognaise 9.00 pm fish and chips, peas Evening meal 6.00 pm sausage, ham, 7.30 pm 1 can of cola drink ice cream 1 cola drink coleslaw Mil II 1III sausages tea with 2 sugars 9.30 pm Evening 10.30 pm crisps 1 '1 1 1 glass fizzy drink II 1l 1 Fig. 1.4 The patient’s diet sheet. A h i g h c a r i e s r at e 5 1 CASE  1 CASE 6 A h i g h c a r i e s r at e Table 1.3 Dietary advice Aims Methods Reduce the amount of sugar Check manufacturers’ labels and avoid foods with sugars such as sucrose, glucose and fructose listed early in the ingredients. Natural sugars (e.g. honey, brown sugar) are as cariogenic as purified or added sugars. When sweet foods are required, choose those containing sweetening agents such as saccharin, acesulfame-K and aspartame. Diet formulations contain less sugar than their standard counterparts. Reduce the sweetness of drinks and foods. Become accustomed to a less sweet diet overall. Restrict frequency of sugar intakes to meal Try to reduce snacking. When snacks are required select ‘safe snacks’ such as cheese, crisps, fruit or sugar-free sweets, such as mints or chewing gum times as far as possible (which not only has no sugar but also stimulates salivary flow and increases plaque pH). Use artificial sweeteners in drinks taken between meals. Speed clearance of sugars from the mouth Never finish meals with a sugary food or drink. Follow sugary foods with a sugar-free drink, chewing gum or a protective food such as cheese. Why not simply extract the lower molar? Extraction of the lower right first molar may well be the preferred treatment. The caries is extensive, restoration of the tooth will be complex and expensive and problems will probably ensue in the long term. The missing tooth might not be readily visible. To a large degree the decision will depend on the patient’s wishes. If he would be happy with an edentulous space, the extraction appears an attractive proposition. However, if a restoration is required, a bridge will require preparation of two further teeth. A denture-based replacement is probably not indicated but an implant might be considered at a later date. Any hesitancy or uncertainty on the patient’s part might well influence you to propose extraction. Another factor affecting the decision is the condition and Fig. 1.5 Periapical radiograph of the restored lower first molar. long-term prognosis of the other molars. If further molars are likely to be lost in the short or medium term it makes sense to conserve whichever teeth can be successfully restored.  Case 2 have cured the swelling. Although not in pain, he has finally decided to seek treatment. Medical history He is otherwise fit and healthy. Examination A multilocular Extraoral examination He is a fit-looking man with no obvious facial asymmetry radiolucency but a slight fullness of the mandible on the right. Palpation reveals a smooth rounded bony hard enlargement on the buccal and lingual aspects. Deep cervical lymph nodes are palpable on the right side. They are only slightly enlarged, soft, not tender and freely mobile. Intraoral examination SUMMARY What do you see in Figure 2.1? A 45-year-old African man presents in the accident There is a large swelling of the right posterior mandible and emergency department with an enlarged visible in the buccal sulcus, its anterior margin relatively well defined and level with the first premolar. The lingual jaw. You must make a diagnosis and decide on aspect is not visible but the tongue appears displaced treatment. upwards and medially suggesting significant lingual expansion. The mucosa over the swelling is of normal colour, without evidence of inflammation or infection. There are two relatively small amalgams in the lower right molar and second premolar If you could examine the patient you would find that all his upper right posterior teeth are extracted and that the lower molar and premolars are 2–3 mm above the height of the occlusal plane. Both teeth are grade 3 mobile but both are vital. What are the red spots on the patient’s tongue? Fungiform papillae. They appear more prominent when the tongue is furred, as here, for instance when the diet is not very abrasive. On the basis of what you know so far, what types of condition would you consider to be present? Fig. 2.1 The patient on presentation. The history suggests a relatively slow-growing lesion, which is therefore likely to be benign. While this is not a definitive relationship, there are no specific features suggesting History malignancy, such as perforation of the cortex, soft tissue mass, ulceration of the mucosa, numbness of the lip or Complaint devitalization of teeth. The character of the lymph node The patient’s main complaint is that his lower back teeth on enlargement does not suggest malignancy. the right side are loose and that his jaw on the right feels The commonest jaw lesions that cause expansion are the enlarged. odontogenic cysts. The commonest odontogenic cysts are the radicular (apical inflammatory) cyst, dentigerous cyst and History of complaint odontogenic keratocyst. If this is a radicular cyst it could have The patient has been aware of the teeth slowly becoming arisen from the first molar, though the occlusal amalgam is looser over the previous 6 months. They seem to be ‘moving’ relatively small and there seems no reason to suspect that the and are now at a different height from his front teeth, tooth is nonvital. A residual radicular cyst arising on the making eating difficult. He is also concerned that his jaw is extracted second or third molar would be a possibility. A enlarged and there seems to be reduced space for his tongue. dentigerous cyst could be the cause if the third molar is He has recently had the lower second molar on the right unerupted. The possibility of an odontogenic keratocyst extracted. It was also loose but extraction does not seem to seems unlikely, because these cysts do not normally cause  2 CASE 8 A m u lt i l o c u l a r r a d i o l u c e n c y Radiographic view Reason Panoramic radiograph or an oblique To show the lesion from the lateral aspect. The oblique lateral would provide the better resolution but might not cover the anterior extent lateral of this large lesion. The panoramic radiograph would provide a useful survey of the rest of the jaws but only that part of this expansile lesion in the line of the arch will be in focus. An oblique lateral view was taken. A posterior-anterior (PA) of the jaws To show the extent of mediolateral expansion of the posterior body, angle or ramus. A lower true (90°) occlusal To show the lingual expansion which will not be visible in the PA jaws view because of superimposition of the anterior body of the mandible. A periapical of the lower right second To assess bone support and possible root resorption. premolar and the first molar much expansion. An odontogenic tumour is a possible cause and an ameloblastoma would be the most likely one, because it is the commonest, and arises most frequently at this site and in this age group. There is a higher prevalence in Africans than other racial groups. An ameloblastoma is much more likely than an odontogenic cyst to displace the teeth and make them grossly mobile. A giant cell granuloma and numerous other lesions are possibilities but are all less likely. Investigations Radiographs are obviously indicated. Which views would you choose? Why? Several different views are necessary to show the full extent of the lesion. These are listed in the ‘Radiographic view’ table above. These four different views are shown in Figures 2.2–2.5. Describe the radiographic features of the lesion (shown in ‘Feature of lesion’ table on p. 9). Fig. 2.2 Oblique lateral view. Why do the roots of the first molar and second premolar appear to be so resorbed in the periapical view when the oblique lateral view shows minimal root resorption? The teeth are foreshortened in the periapical view because they lie at an angle to the film. This film has been taken using the bisected angle technique and several factors contribute to the distortion: the teeth have been displaced by the lesion, so their crowns lie more lingually, and the roots more buccally; the lingual expansion of the jaw makes film packet placement difficult, so it has had to be severely tilted away from the root apices; failure to take account of these two factors when positioning and angling the X-ray tubehead. Radiological differential diagnosis What is your principal differential diagnosis? 1. Ameloblastoma 2. Giant cell lesion. Justify this differential diagnosis. Ameloblastoma classically produces an expanding multilocular radiolucency at the angle of the mandible. Fig. 2.3 Posterior-anterior view of the jaws.  2 9 CASE A m u lt i l o c u l a r r a d i o l u c e n c y Feature of lesion Radiographic finding Site Posterior body, angle and ramus of the right mandible. Size Large, about 10 × 8 cm, extending from the second premolar, back to the angle and involving all of the ramus up to the sigmoid notch, and from the expanded upper border of the alveolar bone down to the inferior dental canal. Shape Multilocular, producing the soap bubble appearance. Outline/edge Smooth, well defined and mostly well corticated. Relative radiodensity Radiolucent with distinct radiopaque septa producing the multilocular appearance. There is no evidence of separate areas of calcification within the lesion. Effects on adjacent structures Gross lingual expansion of mandible, expansion buccally is only seen well in the occlusal films. Marked expansion of the superior margin of the alveolar bone and the anterior margin of the ascending ramus. The involved teeth have also been displaced superiorly. The roots of the involved teeth are slightly resorbed, but not as markedly as suggested by the periapical view. The cortex does not appear to be perforated. Fig. 2.5 Periapical view of the lower right first permanent molar. produce this radiographic appearance with prominent expansion. Adjacent teeth are usually displaced but rarely Fig. 2.4 Lower true occlusal view. resorbed. However, aneurysmal bone cyst is much rarer than central giant cell granuloma in the jaws. What types of lesion are less likely and why? As noted above, it most commonly presents at the age of this patient and is commoner in his racial group. The radiographs Several lesions remain possible but are less likely either on the show the typical multilocular radiolucency, containing several basis of their features or relative rarity. large cystic spaces separated by bony septa, and the root Rarer odontogenic tumours including particularly resorption, tooth displacement and marked expansion are all odontogenic fibroma and myxoma. These similar benign consistent with an ameloblastoma of this size. connective tissue odontogenic tumours are often A giant cell lesion. A central giant cell granuloma is indistinguishable from one another radiographically. possible. Lesions can arise at almost any age but the Odontogenic myxoma is commoner than fibroma but both radiological features and site are slightly different, making are relegated to the position of unlikely diagnoses on the ameloblastoma the preferred diagnosis. Central giant cell basis of their relative rarity and the younger age group granuloma produces expansion and a honeycomb or affected. Both usually cause unilocular or apparently multilocular radiolucency, but there would be no root multilocular expansion radiolucency at the angle of the resorption and the lesion would be less radiolucent (because mandible that displace adjacent teeth or sometimes loosen it consists of solid tissue rather than cystic neoplasm), often or resorb them. A characteristic, though inconsistent feature is containing wispy osteoid or fine bone septa subdividing the that the internal dividing septa are usually fine and arranged lesion into a honeycomb-like pattern. However, these typical at right angles to one another, in a pattern sometimes said to features are not always seen. The spectrum of radiological resemble the letters ‘X’ and ‘Y’ or the strings of a tennis racket. apearances ranges from lesions which mimic odontogenic In myxoma, septa can also show the bubbly honeycomb and solitary bone cysts to those which appear identical to pattern described in giant cell granuloma. ameloblastoma or other odontogenic tumours. The Odontogenic keratocyst. This is unlikely to be the cause of aneurysmal bone cyst is another giant cell lesion which could this lesion but in view of its relative frequency it might still be  2 10 CASE A m u lt i l o c u l a r r a d i o l u c e n c y included at the end of the differential diagnosis. It should be included because it can cause a large multilocular radiolucency at the angle of the mandible in adults, usually slightly younger than this patient. However, the growth pattern of an odontogenic keratocyst is quite different from the present lesion. Odontogenic keratocysts usually extend a considerable distance into the body and/or ramus before causing significant expansion. Even when expansion is evident, it is usually a broad-based enlargement rather than a localized expansion. Adjacent teeth are rarely resorbed or displaced. What lesions have you discounted and why? Dentigerous cyst is a common cause of large radiolucent Fig. 2.6 Histological appearance of biopsy at low power. lesions at the angle of the mandible. However, the present lesion is not unilocular and does not contain an unerupted tooth. Similarly, the radicular cyst is unilocular but associated with a nonvital tooth. Malignant neoplasms, either primary or metastatic. As noted above, the clinical features do not suggest malignancy and the radiographs show an apparently benign, slowly enlarging lesion. Further investigations Is a biopsy required? Yes. If the lesion is an ameloblastoma the treatment will be excision, whereas if it is a giant cell granuloma, curettage will Fig. 2.7 Histological appearance of biopsy at high power. be sufficient. A definitive diagnosis based on biopsy is required to plan treatment. Would aspiration biopsy be helpful? prominent outer layer of basal cells, a paler staining zone No. If odontogenic keratocyst were suspected, this diagnosis within that, and sometimes a pink keratinized zone of cells might be confirmed by aspirating keratin. It would also be centrally. One of the islands shows early cyst formation (c helpful in trying to decide whether the lesion were solid or shown in Figure 2.6). At higher power, the outer basal cell cystic. It would not be particularly helpful in the diagnosis of layer is seen to comprise elongate palisaded cells with ameloblastoma. reversed nuclear polarity (nuclei placed away from the basement membrane). Towards the basement membrane What precautions would you take at biopsy? many of the cells have a clear cytoplasmic zone and the An attempt should be made to obtain a sample of solid overall appearance looks like piano keys. Above the basal cell lesion. If this is an ameloblastoma and an expanded area of layer is a zone of very loosely packed stellate cells with large jaw is selected for biopsy it will almost certainly overlie a cyst spaces between them. There is no inflammation. in the neoplasm. A large part of many ameloblastomas is cyst How do you interpret these appearances? space and the stretched cyst lining is not always sufficiently characteristic histologically to make the diagnosis. If the lesion The appearances are typical and diagnostic of proves to be cystic on biopsy, the surgeon should open up ameloblastoma. The elongate basal cells bear a superficial the cavity and explore it to identify solid tumour for sampling. resemblance to preameloblasts and the looser cells to stellate The surgical access must be carefully closed on bone to reticulum. The arrangement of the epithelium in islands with ensure that healing is uneventful and infection does not the stellate reticulum in their centres constitutes the follicular develop in the cyst spaces. The expanded areas may be pattern of ameloblastoma. covered by only a thin layer of eggshell periosteal bone. Once this is opened it may be difficult to replace the margin of a mucoperiosteal flap back onto solid bone. Diagnosis The final diagnosis is ameloblastoma, of the solid/multicys- The histological appearances of the biopsy are shown in tic type. Figures 2.6 and 2.7. What do you see? Does the type of ameloblastoma matter? The specimen is stained with haematoxylin and eosin. At low power the lesion is seen to consist of islands of epithelium Yes, it is important for treatment. There are several different separated by thin pink collagenous bands. Each island has a types of ameloblastoma and not all exhibit spread into the  2 11 CASE A m u lt i l o c u l a r r a d i o l u c e n c y Table 2.1 Types of ameloblastoma Type Features Invades surrounding bone? Solid/multicystic The conventional and commonest type. Yes, in a quarter or less of cases Usually contains multiple cysts and has a multilocular radiographic appearance. Plexiform, follicular and mixed histological variants exist but have no bearing on behaviour or treatment. Unicystic An ameloblastoma with only one cyst cavity and no separate islands of tumour, or just a few limited to the inner part of the No fibrous wall. Presents radiographically as a cyst, sometimes in a dentigerous relationship. Can only be diagnosed definitively as a unicystic ameloblastoma by complete histological examination after treatment. Desmoplastic A rare variant with sparse islands of ameloblastoma dispersed in dense fibrous tissue. Radiographically forms a fine honeycomb Yes, in most cases radiolucency that may resemble a fibro-osseous lesion with a margin that is difficult to define. No large cysts are present. As frequent in the maxilla as in the mandible. Peripheral A solid/multicystic ameloblastoma that develops as a soft tissue nodule outside bone, usually on the gingiva. Usually detected No (the lesion is outside bone) when small and readily excised. This variant is very rare. surrounding medullary cavity. Their characteristics are shown in place to avoid the need for full thickness resection of the in table 2.1. mandible and a bone graft. This causes a low risk of recurrence, but such recurrences are slow growing and may be dealt with conservatively after the main portion Treatment of the mandible has healed. The fact that the ameloblastoma is of the follicular pattern is of no significance What treatment will be required? for treatment. The ameloblastoma is classified as a benign neoplasm. What other imaging investigations would be appropriate However, it is locally infiltrative and in some cases permeates for this patient? the medullary cavity around the main tumour margin. Ameloblastoma should be excised with a 1 cm margin of In order to plan the resection accurately, the extent of the normal bone and around any suspected perforations in the tumour and any cortical perforations must be identified. Cone cortex. If ameloblastoma has escaped from the medullary beam computed tomography (CBCT, computed tomography cavity, it may spread extensively in the soft tissues and (CT) and/or magnetic resonance imaging (MRI) would show requires excision with an even larger margin. The lower the full extent of the lesion in bone and surrounding soft border of the mandible may be intact and is sometimes left tissue respectively. This page intentionally left blank  Case 3 Medical history You checked the medical history before administering the amoxicillin and so you know that the patient is a well- controlled asthmatic taking salbutamol on occasions. She also suffers from eczema, as do her mother and her two children, and uses a topical steroid cream as required. The patient has had antibiotic cover before and refuses treat- ment without. See Case 44 for further discussion. An unpleasant surprise Dental history The patient has been a regular attender for a number of years. She has had previous courses of penicillin from her general medical practitioner for chest infections. What is the likely diagnosis? Anaphylaxis, arising from hypersensitivity to the amoxicillin. SUMMARY A 30-year-old lady develops acute shortness of Examination breath following administration of amoxicillin. The patient’s face is shown in Figure 3.1. What do you see? What would you do? There is patchy erythema. In the most inflamed areas there are well-defined raised oedematous weals, for instance at the corner of the mouth and on the side of the chin. This is a typical urticarial rash and indicates a type 1 hypersensitivity reaction. What would you do immediately? Reassure the patient. Assess the vital signs including blood pressure, pulse and respiratory rate. Lie the patient flat (as there is no difficulty breathing). Call for help. Obtain oxygen and your practice emergency drug box. What are the signs and symptoms of anaphylaxis? The signs and symptoms vary with severity. The classical picture is of: a red urticarial rash oedema that may obstruct the airway hypotension due to reduced peripheral resistance hypovolaemia due to the movement of fluid out of the Fig. 3.1 The patient’s face as she starts to feel unwell. circulation into the tissues small airways obstruction caused by oedema and bronchospasm. Involvement of nasal and ocular tissue may cause rhinitis and History conjunctivitis. There may also be nausea and vomiting. Complaint What does urticarial mean? The patient complains that she feels unwell, hot and The word urticarial comes from the Latin for nettle rash. An breathless. urticarial rash has superficial oedema that may form separate flat raised blister-like patches (as in Fig. 3.1) or be diffuse. In History of complaint the head and neck it is often diffuse because the tissues are The patient has an appointment for routine dental treatment lax. Markedly oedematous areas may become pale by involving scaling and a restoration under local anaesthesia compression of their blood supply but the background is and antibiotic prophylaxis. She took a 3 g oral dose of amox- erythematous. Patients often know an urticarial rash by the icillin 45 minutes ago. lay term hives.  3 CASE 14 An unpleasant surprise What is the pathogenesis of anaphylaxis? Allow the patient to adopt the most comfortable position for breathing and give oxygen (5 litres per minute) by facemask. Anaphylaxis is an acute type 1 hypersensitivity reaction triggered in a sensitized individual by an allergen. The Because there is bronchospasm, give the following drugs in allergen enters the tissues and binds to immunoglobulin E order: (IgE) that is already bound to the surface of mast cells, Adrenaline (epinephrine) 1 : 1000, 500 micrograms present in almost all tissues. Binding of allergen to IgE induces intramuscularly. The easiest form to administer is a preloaded degranulation and the release of large amounts of ‘EpiPen’ or ‘Anapen’, which are available for both adults (300 inflammatory mediators, particularly histamine. This causes micrograms/dose) and children (150 micrograms/dose). the vasodilatation, increased capillary permeability and Alternatively, a Min-I-Jet prepacked syringe and needle bronchospasm. assembly or a standard vial of adrenaline solution, both containing 1 milligram in 1 millilitre (1 : 1000), may be used. Type 1 hypersensitivity is also known as immediate However, both of these latter methods require a delay in hypersensitivity but onset was delayed for 45 minutes. administration to prepare the injection. You need to be Why? familiar with whichever form is held in your practice as delay Acute anaphylactic reactions may occur within seconds or in calculating doses and volumes is clearly undesirable. may be delayed for up to an hour depending on the nature Adrenaline (epinephrine) may also be given subcutaneously of the allergen and the route of exposure. It takes time for an but the absorption is slower and this route is no longer oral dose of antibiotic to be absorbed and pass through the recommended. Note that autoinjectors are designed for circulation to the tissues, in this case 45 minutes. The reaction self-administration and so provide a slightly lower dose than would be expected about 30 minutes after intramuscular is recommended. The recommended site for the administration of an allergen but almost instantaneously after intramuscular injection is the anterolateral aspect of the intravascular administration. The time of onset is middle of the thigh, where there is most muscle bulk. If unpredictable. Some allergens such as peanuts and latex can clothing prevents access, the upper lateral arm, into the cause rapid reactions despite being applied topically. The deltoid muscle, is an alternative site. In an emergency it may variability in onset of reactions explains why patients should be necessary to inject through clothing but this is not be observed for an hour after administration of antibiotic recommended. In the past the tongue has been proposed a cover. potential site because it is familiar to dentists, but it is highly On examining for the signs noted above you discover that vascular allowing rapid uptake of drug and unlikely to be the patient is breathless and a wheeze can be heard during acceptable to the conscious patient. both inspiration and expiration indicating small airways Chlorphenamine (chlorpheniramine) 10 mg intravenously obstruction. She feels hot and has a pulse rate of 120 beats will counteract the effects of histamine. per minute and blood pressure of 120/80 mmHg. She is Hydrocortisone 100–200 mg intravenously or conscious but the effects are becoming more severe and the intramuscularly. rash now affects all the face and neck region and has spread onto the upper aspect of the thorax. The appearance of one Intravenous fluid. Only required if hypotension develops. A arm is shown in Figure 3.2. suitable regime would be 1 litre of normal saline infused over 5 minutes with continuous monitoring of the vital signs. Treatment The last three actions require intravenous access and this may be difficult to achieve in an individual with reduced What treatment would you perform? circulatory volume and hypotension. Finding and entering a collapsed vein is difficult even for the experienced and is Before the breathing problems were noted you correctly laid best attempted as soon as adrenaline has taken effect. If the patient flat. However, their lungs must now be raised necessary massage the arm towards the hand to try to above the rest of their body to prevent oedema fluid inflate the vein. The importance of gaining venous access collecting in the lungs. depends on circumstances. If medical or paramedical help is likely to arrive quickly, no more than adrenaline may be required. If not, these extra drugs may be important. Though the circulation may be maintained effectively by adrenaline, its action is short lived and you will only have a limited number of doses available. It is probably worthwhile insert- ing a Venflon-type intravenous cannula or at least a but- terfly needle for any patient that develops difficulty breathing. If the reaction becomes more severe, it may be more difficult to insert later. The presentation of drugs useful for anaphylaxis is shown in Figure 3.3. Why must the drugs be given in this order? Adrenaline is the life-saving drug and must be given straight Fig. 3.2 The patient’s arm 5 minutes later. away, before circulatory collapse. It is rapidly acting.  3 15 CASE An unpleasant surprise A F B C E D Fig. 3.3 Typical presentations of drugs used to treat anaphylaxis. A. Oxygen mask. B. Hydrocortisone. Vials of lyophilised powder for reconstitution in water for injection, NOT saline. Administer wit