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TEXTBOOK OFGENERAL AND ORALSURGERY

Commissioning Editor: Michael ParkinsonProject Development Manager: Hannah KennerProject Manager: Nancy ArnottDesigner: Erik Bigland

TEXTBOOK OFGENERAL AND ORALSURGERY

CHURCHILLLIVINGSTONE

EDINBURGH LONDON NEW YORK PHILADELPHIA ST LOUIS SYDNEY TORONTO 2003

CHURCHILL LIVINGSTONEAn imprint of Elsevier Science Limited

© 2003, Elsevier Science Limited. All rights reserved.

The right of David Wray, David Stenhouse, David Lee andAJ Clark to be identified as editors of this work has been assertedby them in accordance with the Copyright, Designs and PatentsAct 1988

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First published 2003

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NoteMedical knowledge is constantly changing. As new informationbecomes available, changes in treatment, procedures, equipmentand the use of drugs become necessary. The editors and thepublishers have taken care to ensure that the information given inthis text is accurate and up to date. However, readers are stronglyadvised to confirm that the information, especially with regard todrug usage, complies with the latest legislation and standards ofpractice.

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Preface

The scope of dental practice has evolved enormouslysince the era of the barber surgeon. Oral surgery remains,however, not only a traditional skill in dentistry but alsoa core skill for all dental surgeons regardless of their areaof specialism, and therefore it is an important part of theundergraduate curriculum and general professionaltraining.

Over the years, as the medical status of the populationhas become more complex and surgical expertise hasincreased, oral surgery has evolved into identified sub-specialties. These include maxillofacial surgery, which,in the UK, is a specialty of medicine; oral surgery, whichembraces maxillofacial trauma and orthognathic surgery;and dentoalveolar surgery, which is designated surgicaldentistry by the General Dental Council in the UK. Thefirst two - maxillofacial surgery and oral surgery - arethe remit of specialists, whereas all dentists are expectedto be competent in dentoalveolar surgery. A sound know-ledge of basic surgical principles is a prerequisite to thepractice of any of these areas of surgery.

This text includes a consideration of general surgicalprinciples, specialist surgical areas and minor oral surgery.The section on general surgical principles has beenwritten mainly by general surgeons and provides coreknowledge that informs the safe practice of surgery. Itwill be of practical help to those working as senior houseofficers in maxillofacial surgery wards. This section alsoconsiders cross-infection control and provides an over-view of both general anaesthesia and conscious sedation.

The second section includes chapters on individualareas of specialist surgical practice of interest to oral andmaxillofacial operators, written by experts. These arewritten to provide insight into these relevant areas ofsurgical practice so that the dentist can be confident in

the information he or she provides to patients and canalso make appropriate referrals. This section is not intendedto inform practice in these areas and so it is short andreadable.

The third section - oral surgery - is a practical guideto the practice of dentoalveolar surgery or surgical dentistry.It provides core information required to complete theundergraduate curriculum.

The integrated nature of this text, which includesgeneral and oral surgery, is a companion to the Textbookof General and Oral Medicine, and is recommended forstudents studying human disease earlier in the under-graduate curriculum and, subsequently, oral surgery inthe clinical years. Although intended primarily for under-graduate students, the book also provides a compre-hensive range of information for those preparing formembership examinations and will be a useful benchbook in a dental practice environment.

The authors have taken great pleasure and satisfactionin compiling this text, which is unique in bringing togethersuccinct knowledge on the whole scope of surgical prac-tice in dentistry. It is hoped that the reader will also bepleased and satisfied.

Finally, I would sincerely like to thank Dr DeclanMillett, Senior Lecturer in Orthodontics, for providinghis expertise in the areas where there is an interface withorthodontics. I would also like to record my thanks toMrs Grace Dobson and Mrs Betty Bulloch for the manu-script, and to Mrs Kay Shepherd and Mrs Gail Drake ofthe Dental Illustration Department, in addition to thosewho have contributed to this text.

D WrayGlasgow, 2003

VII

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Contributors

Professor Jeremy Bagg, PHD, BDS, FDS RCS(Ed), FDSRCPS(Glasg), FRC Path

Professor of Clinical Microbiology, University ofGlasgowHonorary Consultant Microbiologist, North GlasgowUniversity Hospitals NHS Trust

Mr Philip Barlow, MPhii, BSC, MB ChB, FRCS(Ed)Consultant Neurosurgeon, South Glasgow UniversityHospitals NHS TrustHonorary Senior Lecturer, University of Glasgow

Dr Andrew J E Clark, BSc(Hons), MB ChB MRCS(Ed)Clinical Research Fellow in General SurgeryWestern General Hospital, Edinburgh

Mr Howard A Critchlow, BDS, FDS RCS(Eng), FDSRCPS(Glasg)

Consultant Oral Surgeon, South Glasgow UniversityHospitals NHS TrustHonorary Senior Lecturer, University of Glasgow

Mr Hugh Harvie, BDS, FDS RCS(Ed), FDS RCPS(Glasg), DipFor Med

Head of Dental Division, Medical and Dental DefenceUnion of ScotlandHonorary Senior Lecturer, University of Glasgow

Dr James R I R Dougall, MB ChB, FFA RCSIConsultant in Anaesthesia and Intensive Care, NorthGlasgow University Hospitals NHS TrustHonorary Senior Lecturer, University of Glasgow

Mr W Stuart Hislop, BDS, MB ChB, FDS RCS(Ed), FRCS(Ed),FDS RCPS(Glasg)

Consultant Oral and Maxillofacial Surgeon, Ayrshire

and Arran Acute Hospitals NHS TrustHonorary Senior Lecturer, University of Glasgow

Mr David Lee, BSC, MB ChB, FRCS(Ed)Consultant General and Endocrine Surgeon,Lothian University Hospitals NHS Trust,Royal Infirmary, EdinburghMember of Council, Royal College of Surgeons ofEdinburgh

Mr Jason A Leitch, BDS, FDS RCS(Eng)Lecturer in Oral Surgery, University of GlasgowHonorary Associate Specialist, North GlasgowUniversity Hospitals NHS Trust

Mr Gerald W McGarry, MD, MB ChB, FRCS(Ed),FRCS(Glasg)

Consultant Otolaryngologist, North Glasgow UniversityHospitals NHS TrustHonorary Senior Lecturer, University of Glasgow

Professor Khursheed F Moos, BDS, MB BS, FDS RCS(Eng),FDS RCS(Ed), FDS RCPS(Glasg), FRCS(Ed)

Honorary Professor, University of GlasgowHonorary Consultant in Oral Surgery, North GlasgowUniversity Hospitals NHS Trust

Mr Arup K Ray, MS, MB BS, FRCS(Ed), FRCS(Glasg)Consultant Plastic and Reconstructive Surgeon, NorthGlasgow University Hospitals NHS TrustHonorary Senior Lecturer, University of Glasgow

Mr R J Sanderson, MB ChB, FRCS(Eng), FRCS(Ed)Consultant Otolaryngologist and Head and NeckSurgeon, West Lothian and Lothian UniversityHospitals NHS Trust IX

Mr David Soutar, ChM, MB ChB, FRCS RCPS(Glasg), FRCS(Ed)Consultant Plastic Surgeon, North Glasgow UniversityHospitals NHS TrustHonorary Senior Lecturer, University of Glasgow

Mr David Stenhouse, DDS, BDS, FDS RCPS(Glasg)Senior Lecturer in Oral Surgery, University of GlasgowHonorary Consultant in Oral Surgery, North GlasgowUniversity Hospitals NHS Trust

Mr David Still, BDS, FDS RCPS(Glasg)Lecturer in Oral SurgeryHonorary Consultant in Oral Surgery, North GlasgowUniversity Hospitals NHS Trust

Mr Graham A Wood, BDS, MB ChB, FDS RCPS(Glasg), FDSRCS(Eng)

Consultant Oral and Maxillofacial Surgeon, SouthGlasgow University Hospitals NHS TrustHonorary Senior Lecturer, University of Glasgow

Professor David Wray, MD, FDS Rcs(Ed), FDS RCPS(Glasg), FMed Sci

Dean of the Dental School and Professor of OralMedicine, University of GlasgowHonorary Consultant in Oral Medicine, North GlasgowUniversity Hospitals NHS Trust

X

Contents

List of contributors ix

PART IGENERAL SURGERYSection ABasic principles

1 Introduction 3David Lee and David Wray

2 History taking 5David Lee and David Wray

3 Wound healing and suture materials 7David Lee and Andrew J E Clark

4 Complications of surgery 13David Lee and Andrew J E Clark

5 Fluid balance, metabolism and nutrition 26David Lee and Andrew J E Clark

6 Blood disorders and their management insurgical practice 36David Lee and Andrew J E Clark

7 Cross-infectionJeremy Bagg

46

8 Surgical sepsis 54David Lee and Andrew J E Clark

9 Fractures 59David Lee and Andrew J E Clark

10 General anaesthesia 69James Dougall

11 Conscious sedation techniques 81Jason Leitch

Section BSpecialist surgical principles

12 Fractures of the facial bones 89Khursheed Moos

13 Orthognathic surgery 103Khursheed Moos

14 Salivary gland surgery 110R J Sanderson

15 Plastic surgery 122David Soutar

16 Clefts of the lip and palate 131Arup Ray

17 Management of orofacial malignancy 140William S Hislop and David Soutar

18 Otorhinolaryngology (ENT surgery) 147Gerry McGarry

19 Neurosurgery 161Philip Barlow

20 Temporomandibular joint investigation andsurgery 173Graham Wood

PART IIORAL SURGERY21 Introduction 180

David Stenhouse and David Wray

22 History and examination 181David Wray and Hugh Harvie

XI

23 Basic oral surgical techniques 189David Stenhouse

24 Local anaesthesia 200David Stenhouse

25 Extraction techniques 208Jason Leitch

26 Complications of extractions 212David Still and David Stenhouse

27 Wisdom teeth 219David Still and David Stenhouse

28 Cysts of the jaws 229David Stenhouse

29 Periradicular surgery 238David Stenhouse

30 Preprosthetic surgery 243David Stenhouse

31 Orthodontics and oral surgery 250Harry Critchlow

32 Tissue sampling and soft tissue lesions 257David Stenhouse

33 Pyogenic dental infection and its spread 263David Stenhouse

34 Salivary gland diseases 270David Stenhouse

35 Oral surgery in the medicallycompromised patient 274David Stenhouse and David Wray

36 Diseases of bone 279David Stenhouse and David Wray

37 Dental implants 292Harry Critchlow

38 Cryosurgery and laser surgery 301Harry Critchlow

XII

1

PART IGENERALSURGERY

1

Section ABasic Principles

2

Introduction

If they are to achieve an acceptably high standard ofclinical practice, it is essential that all surgeons -including dentists and oral surgeons - have a backgroundknowledge of surgery in general. A specialised knowledgeof oral and dental disorders and their management is notsufficient. An understanding of the basic principles ofsurgery is essential for all surgeons to be able to applysuch knowledge to their specialty. Once they haveacquired such knowledge, surgeons can use it to form thebasis of their specialty knowledge and utilise it to achievethe standard required and desired.

Such a knowledge of 'surgery in general' is essentialfor dental/oral surgeons to ensure that they will be ableto:

• recognise disease by detecting key abnormalities inthe patient assessment

• recognise important disorders that might impinge ontheir practice

• assess and balance the needs for treatment against therisks of avoiding therapy in the patient withcoincidental illness

• identify illness that needs to be treated• refer patients with specific problems to appropriate

specialists• avoid operating on patients who have specific or

relative contraindications to surgery• understand the need to have the patient in optimal

condition before surgery and how to achieve this• treat and manage basic problems that might arise in

the course of patient care• afford a good level of patient care pre- and

postoperatively• understand the basic principles of surgical techniques• be aware of potential problems, especially life-

threatening complications, which may arise in thecourse of surgery and how to manage these

• understand the role of specialist colleagues in allaspects of patient care.

Part I of this book - 'General surgery' - affords a goodbasis, in simple text, to cover all aspects outlined above.This is subdivided into a section on 'Basic principles',which has been written by general surgeons, followed bya section on 'Specialist surgical principles', which hasbeen written by surgeons who specialise in the field. Thisis followed by Part II - 'Oral surgery' - which is now ableto develop the practice of oral surgery within the contextof, and with the background knowledge of, surgery ingeneral. The text is produced at a level that is suitableboth for undergraduate and postgraduate students.

The chapters in the 'Basic principles' section havebeen selected carefully to cover those topics that are ofimmediate interest to oral and dental surgeons. Thesebasic principles are detailed to allow clear understandingof the topic at undergraduate level. The detail is of morepractical relevance to the postgraduate with patient-careresponsibilities. A chapter on 'History taking' techniqueis followed by chapters highlighting:

• Wound healing, incisions and suturing to achieve thebest surgical and cosmetic results.

• Complications of surgery and how to identify andmanage these.

• Fluid balance, together with the potential problemsand dangers of improper fluid and electrolytebalance, and how to avoid or deal with these.

• Blood disorders, which have a major impact onsurgical practice. Many of the problems are avoidableand this chapter highlights relevant areas.

• Infections related to surgery, either as a presentingproblem or as a consequence of surgery, which play alarge part in patient management. Cross-infection canbe a major problem and the principles of care andhow to avoid the problems are highlighted. The role

1

3

of antibiotics, both prophylactic and therapeutic, isdiscussed.

• The basic principles of fracture management, whichare very important to the oral surgeon; a full chaptercovers this area.

• Anaesthesia and sedation, which form a major sectionof the care of the surgical patient and are discussed indetail.

The 'Specialist surgical principles' section provides asuccinct overview of those specialist areas of surgicalexpertise that lie outside the remit of the dental surgeon,but a sound understanding of these areas is essentialwithin the healthcare team to allow appropriate referral,

provide appropriate information to the patient and toparticipate in the holistic care of the patient.

Part II - 'Oral surgery' - can then be studied based ona robust understanding of basic surgical principles.

As a final comment, it is good practice that allsurgeons should document clearly each step of patient-care in writing, giving the reasoning behind eachdecision made. This is especially the case when makingdecisions that seem to lie outside the scope of normalpractice. It is hoped that this book will afford a supportfor specialist oral or dental surgeons, to help them makeaccurate and calculated decisions that can be justified bythe strength of a good background knowledge of basicsurgical principles applied to good oral surgical practice.

4

History taking

IntroductionHistory taking is a most important process and must berehearsed well. A patient who has not met the surgeonbefore is coming to explain about his or her problem andputting total trust in the surgeon's ability to sort this. Thepatient will be very apprehensive. No matter howefficient and skilled the surgeon is, he or she must makethe patient feel confident. The surgeon's appearance anddemeanor must exude professionalism. A hand-shake, asmile, a pleasant introduction and a caring gesture willmake the remainder of contact with the patient mucheasier and more pleasant.

One's initial approach might have to be modifiedaccording to the patient, for example children, the veryelderly and infirm, patients who are poor of hearing andpatients who are mentally impaired all need differentapproaches. The surgeon must also take account of anyaccompanying relative or friend. It is very important,however, to ensure that the accompanying relative doesnot dominate the consultation.

The history should then be elicited in a rehearsed wayas outlined in Table 2.1.

Part I of this text is concerned with basic principles,and so a detailed section on surgical history is not appro-priate. Details relating to the specifics of history takingare given in Chapter 22. The sections below highlightcertain basic points.

History of the presentingcomplaintThis is the patient's opportunity to tell the surgeon aboutthe problem and it is important to avoid prompting withleading questions. Some patients will give a really goodaccount of their problem but many will need guidance;

Table 2.1 History taking

History of present complaintRelevant medical historyFamily historySocial historyDrug and allergy history

many will also have difficulty in remembering the time-scale of the illness. A good initial beginning with historytaking is to ask the patient to think back to the start of theproblem to ensure that he or she gives an account inchronological order. It is also important, while the patientis giving the history, to ensure that he or she gives a clearaccount of what has happened, and does not discuss whathe or she thinks is the cause of the problem.

Relevant medical historyThis is the surgeon's chance to take a history from thepatient. This part has two aspects: first, the opportunity toelaborate on any points in the history that the surgeon feltwere unclear; second, to enquire from the patient anyaspect of his or her health that might otherwise influencethe treatment plan.

Family historyTwo main items are worth enquiring regarding familyhistory: (1) is there a genetic family problem, especiallyany blood-related problem such as haemophilia? (2)has any member of the family had any problem withanaesthetics, especially muscle relaxants? Prolongedaction of depolarising agents such as suxamethoniumruns in families and should be detected prior to anygeneral anaesthetic.

5

2

Eliciting the significant diseases in family members orthe cause of death of deceased members can give insightinto disease susceptibility such as cancer or cardio-vascular disease.

Drug therapyAs outlined above, it is critical to know about certaindrugs prior to performing any surgery. Dosage of corti-costeroids might need to be increased and anticoagulantsneed to be controlled and monitored carefully. Possibleinteractions between drugs need to be assessed.

Social historyThe patient's occupation might be relevant to thecomplaint or to the opportunity for recovery. The

patient's social circumstances and family support willalso dictate opportunities for convalescence.

Knowledge of tobacco smoking and alcohol con-sumption will not only inform the surgeon of thepotential risks for general anaesthesia and surgery butalso the patient's likelihood of smoking- and alcohol-related diseases.

AllergiesA history of asthma and anaphylaxis is important. Thesurgeon must know about drug allergies and anyidiosyncratic reaction that might have occurred at anytime in the past, no matter how long ago.

Skin allergies, especially reaction to prepping agentssuch as iodine, must be discussed and these agentsavoided.

6

Wound healing and suturematerials

IntroductionThe main goal when trying to get a wound to heal is toachieve anatomical integrity of the injured part and torestore full function. As a secondary consideration, thisshould be combined with an attempt to produce as perfecta cosmetic result as possible.

A sound knowledge of the principles of woundhealing is necessary to achieve these aims and to allowappropriate planning of incisions and their closure. Anunderstanding of the complications that can occur duringwound healing is vital to try to avoid these or to treatthem appropriately if they arise.

To achieve the best result during wound closure, everysurgeon should be aware of the wide selection of suturematerials available so as to be able to choose the mostappropriate for each situation.

Classification of woundhealingA fundamental distinction in wound healing is betweenclean, incised wound edges that are closely apposed toeach other, and wounds where the edges are separated.The former undergo healing by 'primary intention', thelatter by 'secondary intention'.

Primary intention

Where the edges are clean and held together withligatures, there is little gap to bridge. Healing, whenuncomplicated, occurs quickly with rapid ingrowth ofwound healing cells (macrophages, fibroblasts, etc.) andrestoration of the gap by a small amount of scar tissue.Such wounds are soundly united within 2 weeks anddense scar tissue is laid down within 1 month.

Secondary intention

Wound healing by secondary intention occurs when thewound edges are separated and the gap between themcannot be bridged directly. This occurs when there hasbeen extensive loss of epithelium, severe wound con-tamination or significant subepithelial tissue damage.Healing occurs slowly from the bottom of the woundtowards the surface by the process of granulation. Thislarger defect results in a greater mass of scar tissue thanhealing by primary intention. In time, such scarring tendsto shrink, resulting in wound contracture.

Normal sequence of woundhealingDespite the differences in time taken and amount of scartissue produced, the sequence of events in wound healingby primary and secondary intention is similar:

• Skin trauma results in damage to superficial bloodvessels and haemorrhage. Blood clotting results infibrin clot formation, and this is stabilised by anumber of factors, including fibronectin.

• Within 24 h neutrophils have migrated to the area,and epidermal cells have extended out in a singlelayer from the wound edges in an attempt to coverthe defect.

• Between days 1 to 3 the neutrophils are replaced bymacrophages, which clear debris and play a role inproducing the environment that stimulates local andrecruited fibroblasts to produce collagen. This milieu,along with new blood vessel formation(neovascularisation), constitutes 'granulation tissue'.

• Towards the end of the first week neovascularisationis at its peak. In healing by primary intention at thisstage the incised gap is bridged by collagen. The full

>n

7

3

thickness of epithelium is reconstituted, including

epithelial cell migration and proliferation.• During the second week there is increased fibroblast

activity and collagen formation, with decreasingvascularity and cellularity in the wound.

With primary intention by 1 month there is a cellularconnective tissue scar with normal overlying epidermis.By 2 months the wound has regained approximately 80%of its original strength. The redevelopment of strength inthe wound involves remodelling and orientation ofcollagen fibres and continues for a number of months.

In healing by secondary intention there is morenecrotic debris, exudate and fibrin, and a more intenseinflammatory response results. There is a larger defect,therefore, with more granulation tissue and a greatermass of scar tissue. Wound coverage takes longer andwound contraction occurs caused by myofibroblasts.

Regulation of the complex interactions involved inwound healing is achieved by a number of local andsystemic factors. These are produced both at distant sites(e.g. growth factor) and locally by the cells involved inthe healing process. Many factors are involved, importantexamples including cytokines, platelet-derived growthfactor and epidermal growth factor.

Factors affecting healingA number of local and systemic factors affect woundhealing (Table 3.1); these are discussed in turn.

Local factors

Wound sepsis

Removal of hair allows better visualisation of the wound.It also facilitates application of adhesive dressings andsuture removal. However, evidence has shown thatshaving of skin at an early stage preoperatively increasesbacterial counts in the area, and shaving more than 12 hbefore incision can significantly increase the rate ofwound infection. Hair removal should therefore beperformed where necessary just prior to surgery (seeCh. 8).

Preparing the skin with antiseptic wash prior to surgeryis vitally important. Preparation should be thorough.Chlorhexidine and povidone-iodine have been shownto reduce the skin bacterial flora by up to 95%. Mostsurgeons perform a double scrub of the area, preparing

Table 3.1 Factors affecting wound healing

Localwound sepsispoor blood supplywound tensionforeign bodiesprevious irradiationpoor technique

Systemicnutritional deficienciessystemic diseasestherapeutic agentsage

the skin well wide of the area of surgery. Careful handwash by the surgeon using these antiseptics is also veryimportant in reducing wound sepsis.

Poor blood supply

As described above, bleeding and neovascularisationplay fundamental roles in wound healing. Areas withgood vascularity, such as the scalp and face, heal well,whereas those with poor blood supply, such as pretibialskin, heal poorly. Surgical technique can also have asignificant effect on the blood supply to the area. Careshould be taken where possible to maintain the vascularsupply to the incised area. For example, creation of adistally based skin flap is likely to disrupt the vessels tothe skin of the flap, and impair wound healing. Appro-priate planning of incisions minimises vascular damage.

Wound tension

Tension across a healing wound serves to separate thewound edges, impairs the blood supply to the area andpredisposes to complications of wound healing. Careshould be taken, therefore, when planning incisions toavoid creating tension if possible.

Where the gap between the wound edges is large,primary apposition of the edges might not be appropriateor even possible. Bridging of such a gap can be achievedby a number of plastic surgery techniques, including skingrafting or tissue flaps (see Ch. 15).

Better cosmetic results from surgery tend to beachieved if incisions are made along the lines of thecollagen bundles of the skin (Langer's lines). Thesefollow the natural skin creases on the face, transverselyat the joints and longitudinally on the long parts of thelimbs.

8

thickness of epithelium is reconstituted, includingsurface keratinisation, a process that requires both

Foreign bodies

The presence of extraneous material within the woundpredisposes to infection. It also results in a larger andmore prolonged inflammatory reaction, which canpredispose to excess scar tissue formation. Foreignmaterial can enter a traumatic wound at the time of injuryand should be removed at the onset of treatment withadequate debridement.

With surgical wounds, however, complications canresult from endogenous material being inappropriatelypresent within the wound, such as devascularised piecesof fat, necrotic tissue resulting from excess use of thediathermy, or the patient's hair. Thorough wound cleaningbefore closure helps to remove these materials.

Previous irradiation

Areas that have undergone preoperative radiotherapysuffer from a patchy vasculitis, impairing their bloodsupply and hence healing potential. Radiation alsodamages skin stem cells, resulting in poor re-epithelialisation.

Poor technique

Care should be taken when making an incision to createa clean precise cut. The incision should be madevertically through the skin. Gentle handling of tissuesthroughout the operation is important. Rough handlingand damaging of tissues can result in tissue edgenecrosis, predisposing to poor healing and infection.Careful haemostasis not only allows good visualisationduring surgery but also reduces tissue bruising andhaematoma formation.

Choice of appropriate suture material is important.Suture placement should be precise and suture tensionsufficient to result in tissue apposition, but not too tightto cause tissue necrosis. Skin closure should include thestrength-supplying dermis within the bite. Removal ofsutures at the correct time (variable between sites) helpsprevent scarring associated with the sutures themselves.

Nutritional deficiencies

Vitamins important in the process of wound healinginclude A and C. Vitamin A is involved in epithelialisationand collagen production; vitamin C has an important rolein the production and modification of collagen. This hasbeen recognised for centuries by virtue of the diseasescurvy caused by vitamin C deficiency.

Certain minerals are also essential in wound healing.Zinc acts as an enzyme cofactor and has a role in cellproliferation. It accelerates wound healing in experi-mental models. Deficiency may be encountered inpatients on long-term total parenteral nutrition.

Protein is the main building block in wound healing.A malnourished, hypoproteinaemic patient has impairedinflammatory and immune responses, vital for normalwound healing and prevention of wound infection.Protein amino acids are essential for collagen production,which is itself a protein.

Systemic diseases

Several diseases are known to impair wound healing viaa number of mechanisms. Important examples includediabetes, uraemia and jaundice.

Therapeutic agents

Immunosuppressive drugs dampen the inflammatory andimmune responses, hence impairing wound healing.These include chemotherapeutic agents for malignancyand immunosuppressive and antiprostaglandin drugsused for inflammatory conditions such as rheumatoiddisease. Probably the most important and widely usedexample is corticosteroid therapy. Steroids have theadditional effect of increasing the fragility of small bloodvessels.

Age

Prior to puberty, the rate of wound healing is increasedcompared to postpuberty.

Systemic factors

Many systemic factors are necessary for wound healingand deficiency of these impairs the process. Certaindiseases and therapies can also have detrimental effectson the wound.

Complications of woundhealingA number of complications of wound healing can occur;these are listed in Table 3.2.

9

Table 3.2 Complications of wound healing

InfectionDehiscenceIncisional herniaHypertrophic scarringKeloid scarringContractures

Infection

Wound infection is dealt with further in Chapter 8. Asoutlined in Table 8.2 (p. 54), several local and systemicfactors predispose to wound sepsis.

Dehiscence

Total breakdown of all the layers of the surgical repairof a wound is called 'dehiscence'. The mortality ofabdominal wound dehiscence is between 10 and 35%.

Dehiscence can be caused by a number of factors,including those that generally impair wound healing(Table 3.3). Incidence can be minimised by meticuloussurgical technique to negate the technical factors that cancause dehiscence.

Suture breakage can result from poor suture selection.Knot slippage arises as a result of inadequate tying.'Cutting out' of sutures can be due to failure to includelayers with most strength within the bite of the suture.Excess tension on the suture line also impairs woundhealing. Wounds should be sutured with only enoughtension to close the defect.

Incisional hernia

Dehiscence of the deeper layers of a wound in which theskin layer remains intact will result in incisional herniaformation with protrusion of underlying structuresthrough the deeper defect. This is of particularimportance for abdominal wounds, where viscera such assmall intestine can herniate, with the attendant risks of

10

Table 3.3 Factors causing wound dehiscence

Suture breakageKnot slippage'Cutting out' of suturesExcess tension on the suture line

irreducibility, obstruction and strangulation. Incisionalhernias in other areas can be unsightly and cause thepatient discomfort (e.g. herniation of underlying musclethrough a gap in fascia lata following hip replacement).

Hypertrophic scarring

Hypertrophic scarring is essentially excess collagen scartissue formation - almost an overhealing of a wound. Itis non-progressive after 6 months and does not extendbeyond the edges of the wound. It occurs most frequentlyin specific areas, particularly around joints and whereLanger's lines of tension are crossed by the incision.Poor skin suturing technique frequently results in hyper-trophic scar formation, especially where the edges of theskin are overlapping instead of being accurately apposed.

Treatment is difficult and further surgery should notbe attempted for at least 6 months. Excision of the scarand resuturing often has disappointing results, resultingin the same overhealing. Radiotherapy used to be usedbut has now been abandoned. Some improvement can beachieved with local injection of corticosteroids directlyinto the scar, a process that might need repeating severaltimes.

Keloid scarring

Keloid scars are due to abnormal collagen metabolism.The excess scar tissue extends out beyond the woundedges and might continue to enlarge after 6 months.Prevalence is higher in patients with dark skin, especiallythose of African origin, in younger patients and in thosewith burn wounds.

Areas prone to this type of scarring are the face,dorsal surfaces of the body, sternum and deltopectoralregion.

Excision generally results in a larger recurrence,although excision followed by compression bandagingcan have slightly better results. Corticosteroid injectionscan give some improvement.

Contractures

Wound Contractures can occur with any wounds but aremore commonly associated with wounds that experiencedelayed healing (including infection), burns and those inwhich the incision crosses Langer's lines.

Contracture of a scar across a joint can result inmarked limitation of movement. It is therefore essential

to avoid vertical incisions across a joint if possible. At ajoint, Langer's lines tend to run horizontally.

Surgical treatment of a scar contracture might be theonly treatment available and can include skin grafting,local flaps or wound Z-plasty.

Suture materialsClassification

There is a wide variety of suture materials commerciallyavailable. Although the selection for a specific surgicalrepair will vary according to surgeon preference,financial considerations must be borne in mind.

Suture materials are classified as those that areabsorbable and those that are non-absorbable (Table 3.4).Each of these categories is subdivided into sutures madefrom natural fibres, for example, silk, and those that areman made. In addition, sutures can be made from singlestrands (monofilament) or multiple strands (braided).

Most natural materials are now no longer used andcatgut, for example, is no longer commercially available.These materials tended to have a variable suture strength,which was not entirely consistent through the length ofthe thread. Because of this, most surgeons now usesynthetic materials.

Each suture type is available in a variety of widths, thelarger the number, the finer the thread. For example, 1/0suture is very thick whereas 6/0 suture is very fine.

Selection of materials

The first consideration when choosing a suture materialis whether an absorbable or non-absorbable suture isrequired. Closing of the deep layers of a wound is usuallyperformed with an absorbable suture, whereas vascularanastomoses are performed with fine-bore non-absorbablematerials. Where an absorbable suture is required, a

Table 3.4 Classification of suture materials

Absorbablesynthetic, e.g. polydioxanone (PDS) (monofilament),

vicryl (braided)natural, e.g. catgut

Non-absorbablesynthetic, e.g. Prolene (monofilament), nylon

(monofilament)natural, e.g. silk (braided)

knowledge of the time taken for it to dissolve, and hencelose its strength, is necessary.

The strength of the suture also varies with the arrange-ment of fibres, such that braided sutures are stronger thanmonofilament sutures of the same material for the samethickness.

Different materials possess different handlingproperties, for example, Prolene has 'memory' (retainsthe bends in the suture that result from its packaging),and is more difficult to knot. With this in mind, thenumber of throws in a knot should be altered accordingto the suture material to prevent slippage and unravelling.

Tissue reactivity varies between sutures. Materialswith high tissue reactivity, such as silk, cause inflam-mation at the site of the suture and are more likely toproduce suture scarring. The different properties ofvarious suture materials are listed in Table 3.5.

Needles

Sutures are supplied attached to a number of differentneedles and are swaged directly into the end of the needlerather than through the eye of a needle; this avoidshaving to pass a double thickness of suture.

Nowadays, most needles in common use are curvedand are used mounted on a needle-holding forceps.Straight needles are available and used primarily for

Table 3.5 Properties of different suture materials

VicrylCatgutPolydioxanone (PDS)SilkNylonPolypropylene

Absorbable or non-absorbable

AbsorbableAbsorbableAbsorbableNon-absorbableNon-absorbableNon-absorbable

Tissue reactivity

MildHighMildModerateLowLow

Duration of strength

60% at 2 weeksLost in 7-10 days70% at 2 weeks20% at 6 monthsLoses 20% per yearIndefinite 11

subcuticular skin closure, but are associated with a higherrisk of needlestick injury to the surgeon. Other shapes areavailable for specific tasks, such as the J-shaped needlefor femoral hernia repair.

Another variable is the shape of the needle in cross-section. Round-bodied needles are circular in cross-section and do not possess sharp edges. They are used forsuturing delicate structures, such as bowel anastomosis,and are designed to push tissues to either side rather thancut through them.

Blunt needles are also available, and are mostcommonly used for closing the muscle layer of anabdominal wound or for suturing liver. They are intendedto reduce the risk of needlestick injury to the operatingstaff and damaging adjacent structures.

For use on tough tissues, such as skin and fascia, thereis a selection of needles with sharp edges at the tips.These are known as 'cutting' and 'reverse cutting',depending where the cutting edge of the tip is placed.

Nowadays, skin closure is commonly performed withthe use of skin clips. These come in a disposable sterilestapler, are quick to use, cause minimal discomfort to thepatient, and are easily removed.

Qualities of a good incisionAn incision must give good access to the structures beingexplored. It should be positioned such that it can beextended to give greater access if necessary. It should be

easy to perform and should be made with extreme care toavoid skin and tissue damage, which can affect sub-sequent healing. Consideration should be given to thefinal cosmetic result before deciding on the direction ofthe incision, for example, Langer's lines (see Ch. 15).

Surgery should be carried out with care to avoidtissue damage due to bad handling. Excess use ofdiathermy should be avoided, especially at the skin edge.Haemostasis should be meticulous and haematomaformation should be avoided.

For good wound closure, the correct suture materialsand suture needles should be chosen. Where there islikely to be a high degree of tissue tension on the deeperlayers of a wound, a strong suture is required and mustbe placed accurately to grip the strongest layer of theincision. Excess tension on this suture should be avoidedto prevent wound-edge necrosis and wound dehiscence.

Skin closure should be meticulous. This is thesurgeon's signature and poor suturing technique here cancause permanent disfigurement that could have beenavoided. The skin edges should be apposed accuratelywith no overlapping. Where there is tension on the skinedges, for example, following excision of a skin lesionsuch as a mole, fine interrupted sutures or clips are idealto support the skin tension until healing occurs. Wherethere is no skin tension, subcuticular suturing with eithera braided absorbable suture such as Vicryl or a non-absorbable monofilament suture such as Prolene, whichwill be removed in a week, is ideal.

12

Complications of surgery

IntroductionAll surgical procedures carry an innate degree of risk.The benefits of any procedure being performed need tobe weighed against any potential complications so thatthe clinician and the patient can make a balanced andinformed decision about whether the procedure shouldbe performed. It is therefore fundamental to have a soundappreciation of adverse outcomes of surgery and todefine the population of patients that is most likely tosuffer from any such complications.

It is helpful to have a mental framework to categorisecomplications. One such framework that is in commonuse is temporal: early, intermediate and late. In addition,complications can be divided into those that are 'general'and could occur with any operation, and those that are'local' or specific to a particular operation.

General complicationsSurgery is a controlled insult to the patient, whose bodyresponds with a number of well-defined physiologicaland pathophysiological responses that alter the body'shomeostatic mechanisms.

In addition, outside influences are often therapeuticallyimposed, for example anaesthesia, intravenous fluids andimmobility.

Table 4.1 Early-stage complications of surgery

Anaesthesia-related complicationsHypothermiaNerve damageDiathermy-related injuriesHypotensionMetabolic complicationsPain

All of these factors have implications for the patientand for the outcome of surgery.

Early-stage complicationsEarly-stage complications (Table 4.1) will be consideredin turn.

Anaesthesia-related complications

All but a few patients undergoing a surgical procedurerequire some form of anaesthetic, be this local, regionalor general. The principles and adverse effects of generalanaesthesia are described in detail in Chapter 10 andlocal anaesthetics are considered in Chapter 24. How-ever, it is important to give some consideration to thesebecause a significant proportion of complications fromsurgery are related to anaesthesia (Table 4.2). A patient'sability to withstand anaesthesia will often dictate his orher 'fitness' to undergo surgery or will have a bearing onthe surgical approach.

Nausea and vomiting

Temporary nausea is common after general anaesthesiaand might necessitate overnight admission for intendeddaycase patients. Administration of an antiemetic anda delay in restoration of oral intake usually suffice,although pathological causes should be borne in mind.

Table 4.2 Complications related to generalanaesthesia

Nausea and vomitingSore throatMuscle painDamage to teeth 13

4

14

Sore throat

The use of airway adjuncts during anaesthesia, such asan endotracheal tube or laryngeal mask, can causemechanical irritation of the pharynx. The symptomresolves spontaneously and requires reassurance only.

Muscle pain

The use of depolarising muscle relaxants, such assuxamethonium, causes initial muscle contraction andmight result in widespread postoperative muscle ache.

Damage to teeth

Teeth can be damaged during the process of intubationand the anaesthetist must be careful when using alaryngoscope.

Hypothermia

Surgical patients are relatively exposed to any drop intemperature during the course of surgery, especially ifsurgery is over a prolonged time period. Anaesthesia canalter the patient's ability to control body temperature,with many agents causing peripheral vasodilatation withthe consequent danger of hypothermia. It is important,therefore, to maintain a suitable temperature and humiditywithin the operating theatre. The use of warming blanketsand local hot-air circulating jackets can prevent asignificant temperature drop.

Nerve damage

Care must be taken when positioning a patient,particularly when they are under general anaesthesia.Sufficient padding must be used, particularly over bonyprominences. Pressure over peripheral nerves should beavoided where possible. Excessive movement of jointscan also result in nerve damage. For example, thepatient's arm should not be abducted more than 60degrees (particularly in external rotation), to avoidbrachial plexus damage.

Diathermy-related injuries

The high-frequency alternating current of diathermy is aversatile surgical tool used to produce haemostasis. Themain risk from diathermy is of burns because of incorrectusage.

Diathermy can be monopolar or bipolar. The risk ofburn is less with bipolar diathermy, where the tissuegrasped between the forceps completes the circuit, withcurrent flowing from one tip of the forceps through thistissue to the other limb of the forceps.

In monopolar diathermy the current travels in a circuitfrom the diathermy machine, via a cable, to the forcepsthat are holding the bleeding vessel, causing an electro-cautery of the vessel. The current then returns, via thepath of least resistance, through the patient's tissues tothe return plate (which is attached to a remote part of thebody such as the thigh) and then to the diathermymachine. The plate must have a certain surface area suchthat the current is sufficiently dispersed so that the platedoes not burn the skin it is attached to. If the plate isapplied incorrectly, such that only part of it is touchingthe patient, the full power of the current might be toolocalised and a burn can occur in that area. Responsibilityfor diathermy, including the plate, rests ultimately withthe surgeon. Metal objects touching other areas of thepatient provide an alternative route for the current to flowand, again, burns will occur if there is a small surfacearea at the exit site, for example, when there is contactbetween skin and a drip stand.

The diathermy current can ignite flammable gases,including bowel gas, certain anaesthetic agents, andalcohol-based skin preparation solutions.

The presence of a cardiac pacemaker is not acontraindication to the use of diathermy. The return plateshould be remote from the pacemaker and close to theoperative site. Short bursts of current should be used. Theanaesthetist should monitor pacemaker function by pulsemeasurement and cardiac monitoring.

Hypotension

Low blood pressure is a common complication in thepostoperative period. The causes are numerous, of vary-ing severity and can result in shock. Shock can be definedas inadequate tissue perfusion and tissue oxygenation,resulting in organ dysfunction. Postoperative hypotensionis not always pathological. It might not require treatmentand could even be the desired effect of therapy.

Therapeutic hypotension

Patients are often prescribed drugs that lower bloodpressure, such as beta-blockers or ACE inhibitors, toreduce perioperative bleeding. For other medications,

hypotension is a side-effect, an important example beingmorphine, which is often given postoperatively viainfusion. However, it is dangerous to assume that post-operative hypotension is secondary to medication and asearch for other causes should be performed.

Spinal/epidural anaesthesia

Local anaesthetic substances near the spinal nerves blocknot only the fibres carrying pain signals but also thesympathetic fibres that provide vasomotor tone to thelower limbs. Blockade of these fibres results in vaso-dilatation and hence hypotension. A degree of increasedintravascular filling is required to compensate for thisincreased potential intravascular volume. However, it isimportant not to be overaggressive in fluid resuscitationin an attempt to restore a blood pressure. Clinical signsare the key and, if the patient is peripherally well perfusedand there is evidence of normal end-organ function (e.g.good urine output), then the current status might beacceptable.

Again it is essential that hypotension is not attributedto regional anaesthesia until a search for other causes hasproved negative, and it is important to recognise that thesympathetic blockade will decrease the patient's abilityto compensate for fluid loss.

Clinical assessment and close monitoring of bloodpressure should help to define the problem and its extent,and aid in prevention and treatment.

Shock

Shock is classified both in terms of cause and also in termsof severity. The types of shock are listed in Table 4.3.

Obstructive shock

The obstructive form is a rare type of shock, where venousreturn to the heart is impaired resulting in decreased atrialand ventricular filling and therefore decreased cardiacoutput. Important examples are massive pulmonaryembolus, tension pneumothorax and cardiac tamponade.

Pneumothorax is the presence of air within the pleuralspace. Infrequently, the air can be trapped in this spaceby a 'flutter valve' effect from the lung, such that moreair can get into the space but air cannot escape. Thisresults in increased pressure within the pleural spacewith compression of thoracic and mediastinal structuresincluding the lungs, the heart and great vessels.

Table 4.3 Types of shock

Obstructive shockHypovolaemic shockCardiogenic shockSeptic shock

Any pneumothorax has the potential to becomea tension pneumothorax, especially under generalanaesthesia where the patient is being ventilated underpositive pressure. Urgent treatment is required.

Pneumothorax can be caused in the perioperativeperiod as a complication of positive pressure ventilationor insertion of central venous access devices thatinadvertently breach the pleura.

Hypovolaemic shock

The most common cause of postoperative hypotension ishypovolaemia, that is, insufficient intravascular volume.

Hypovolaemic shock is classified with regards toseverity and the clinical signs that accompany it(Table 4.4). This classification is a broad outline andrepresents a spectrum rather than distinct clinical entities.There are also a number of situations where the clinicalfeatures are not reliable:

• Young children and fit young adults have a greatercardiovascular reserve, and might therefore be able tocompensate for blood loss, maintaining their bloodpressure until the blood loss is so large that theydecompensate, resulting in a precipitous fall in bloodpressure.

• Elderly patients have decreased cardiovascularreserve, such that relatively little blood loss can resultin shock.

• Pharmacological agents designed to alter pulse rateand blood pressure naturally have an effect on theclinical signs, a common example being beta-blockerssuch as atenolol, which prevent a compensatory (anddiagnostic) tachycardia. Where confusing variablesare present, further monitoring modalities (e.g. suchas central venous pressure recording) might beindicated to assess the patient's fluid status.

The causes of hypovolaemic shock are primary haemor-rhage, transcellular loss and insensible loss. Primaryhaemorrhage is defined as haemorrhage occurring within24 h of surgery. It is generally due to inadequate

15

Table 4.4 Classification of hypovolaemic shock

Blood loss (mL)Blood loss (%)Pulse (beats per min)Blood pressurePulse pressureRespiratory rate (breaths per min)Urine output(mL/h)ColourMental state

Class /

<750<15< 100NormalNormal12-20>30NormalNormal

Class II

750-150015-30100-120NormalNarrow20-3020-30PaleMildly anxious

Class III

1500-200030-40> 120DecreasedNarrow30-4010-20PaleAnxious, confused

Class IV

>2000>40> 120, threadyDecreasedNarrow>40MinimalWhiteConfused, drowsy

16

haemostasis at the time of operation. It can be clinicallydifficult to decide whether reoperation is required to haltthe bleeding and when. Initial non-operative techniquescan be tried (e.g. local pressure or reversal ofcoagulopathy). However, if there is evidence of ongoingbleeding causing shock, attempts should be made toarrest the bleeding.

A key clinical indicator of whether the blood loss isongoing is the patient's response to fluid resuscitation.Before administering fluid resuscitation, it is importantto consider cardiogenic causes of shock, which might beaggravated by further fluid load (see below). Monitoringof the response can be either by simple clinical meanssuch as pulse and blood pressure recording, or byinvasive monitoring techniques such as central venouspressure measurements. Three categories of response areclassically described:

1. Rapid response: intravenous infusion of a fluid bolus,e.g. 2 L normal saline over 2 h, results in a fast,sustained improvement. This generally indicates aloss of less than 20% of circulating volume, withoutongoing blood loss.

2. Transient response: Fluid bolus initially causes animprovement of clinical measures, although theimprovement is not sustained. This indicates ongoingblood loss or inadequate resuscitation. Blood trans-fusion should be considered, as should measures tocontrol haemorrhage.

3. Minimal response: Fluid bolus results in little or noclinical improvement. Blood loss is ongoing at a ratefaster than the infusion of fluid. Blood transfusion andmeasures to arrest bleeding are urgently indicated.

Certain patients are more prone to haemorrhagiccomplications than others: patients with abnormalities of

blood clotting, such as those on the anticoagulantwarfarin, and also those with fragile blood vessels, suchas the elderly and patients on long-term corticosteroidtherapy.

Transcellular loss can be considerable. An example isloss of fluid into the gastrointestinal tract in cases ofbowel obstruction.

Insensible loss, such as fluid loss by sweating, can begreater than usual for patients in the perioperative period.Exposure of usually covered moist organs at surgery, forexample, intra-abdominal viscera, can greatly increasefluid loss in this way. Postoperative pyrexia also increasesinsensible fluid loss.

These losses must be considered when evaluatingthe amount of fluid required to render the patientnormovolaemic.

Cardiogenic shock

Cardiogenic shock occurs when the heart fails to producesufficient cardiac output to maintain adequate tissueoxygenation, despite normovolaemia and sufficientvenous return (Table 4.5).

Impaired contractile strength can be caused bymyocardial infarction (MI) or left ventricular failure

Table 4.5 Causes of cardiogenic shock

Impaired contractile strengthmyocardial infarctionleft ventricular failure

Disordered contraction, arrhythmiaatrial fibrillationother arrhythmias

(LVF). MI is the death of an area of cardiac muscle. It isdifferentiated from myocardial ischaemia in which thereis a severe reduction in myocardial perfusion but notmuscle death. Such ischaemia occurs, for example, whena patient suffers from angina.

Surgical patients with established ischaemic heartdisease are at increased risk of undergoing perioperativeMI. This is significantly greater in patients who have hadan MI within the 6 months before surgery. As thesepatients have an increased risk of mortality, electivesurgery is not recommended in this period if it can bedelayed without undue risk to the patient. Diagnosis ofperioperative MI can be difficult because pain is notalways a feature, but monitoring during anaesthesia candetect changes in the electrocardiogram (ECG) pattern.Clinical features include the onset of arrhythmias and thesymptoms and signs of heart failure.

Treatment of perioperative MI is a difficult clinicalproblem and specialist cardiology advice should besought. Standard thrombolytic therapy is contraindicatedin the postoperative period because of haemorrhagicproblems.

Acute LVF can result from an acute MI or, morecommonly, simply in patients with ischaemic heartdisease. The diagnosis can be made clinically withbreathlessness, elevated jugular venous pulse in the neck,and peripheral oedema. Simple investigations such aschest radiography should be performed. In severe cases,invasive monitoring techniques such as central venouspressure monitoring might be necessary.

Treatment of heart failure includes reduction of fluidload and administration of diuretics such as furosemide(frusemide) and digoxin.

Cardiology advice should be sought in patients whodo not respond to standard therapy and further specialisedtests might be performed, such as ECHO cardiography orcardiac catheterisation. Such patients probably requirecare in a high dependency unit. Fluid input and outputcharts should be kept, with the amount and rate ofinfusion of intravenous fluids being regulated carefullyto prevent excess infusion and the development ofcardiac failure.

To function as an efficient pump, the myocardiumcontracts in a synchronised order. Disorders of thisrhythm - dysrhythmias - result in ineffective filling andemptying of the chambers of the heart and therefore inreduced cardiac output. A fundamental distinction inassessment of patients with dysrhythmias is whetherthere is associated cardiovascular compromise, such as

hypotension and shock, or whether the patient is able tocompensate and maintain blood pressure.

Atrial fibrillation (AF) is perhaps the most commonperioperative dysrhythmia. The diagnosis of AF is dividedinto those with and without cardiovascular compromise.Most patients know if they have an irregular pulse butare asymptomatic. AF is often detected on admission tothe unit when the pulse is noted to be irregular. Somepatients, however, are symptomatic, possibly withpalpitations, light headedness, syncope or cardiac failure.These patients usually have a rapid, irregular pulse withan uncontrolled ventricular response. As a result, theventricles do not have time to fill adequately beforecontraction, causing decreased stroke volume and hencea drop in cardiac output. An ECG is diagnostic and canalso show signs of myocardial ischaemia.

Urgency of treatment depends on the presence anddegree of complications such as cardiac failure. Insurgical wards, rate control is usually achieved by the useof drugs such as digoxin, which can be administeredeither orally or intravenously. Where digoxin fails tocontrol the heart rate, a number of other antiarrhythmicdrugs can be tried.

Many patients have chronic AF with a controlledventricular rate. Research has demonstrated an outcomebenefit of anticoagulation with warfarin for thesepatients, with a reduction in the incidence of embolicstroke. It is important in such patients to reduce or evenstop the warfarin before surgery (Ch. 6).

Many other types of arrhythmia can occur in thepostoperative period. Although a description of cardiacarrhythmias is beyond the scope of this chapter, it isimportant to note that many arrhythmias can result fromor be exacerbated by electrolyte imbalance, particularlyan abnormal potassium level. Electrolyte levels shouldbe checked regularly and abnormalities corrected (seeCh. 5).

Septic shock

Septic shock is an intermediate-stage complication and isdiscussed below.

Metabolic complications

The insult of surgery causes an alteration in a number ofmetabolic processes (see Ch. 5). In particular, this cancause problems in diabetic patients. Requirements forinsulin can change because patients have to fast. In

17

addition to this, however, the production of endogenousinsulin and its effectiveness (end-organ resistance) arealtered. As a result, blood glucose levels might be erratic.It is vital that this is controlled accurately. In thissituation, for short-term control, diabetes is frequentlyregulated by the intravenous use of glucose, insulin andpotassium.

Classically, the patient presents with symptoms of a deepvein thrombosis (DVT) between postoperative days 5and 7, although it can occur at any stage. A number offactors predispose patients to DVT in the postoperativeperiod (Table 4.7). The degree of risk varies betweendifferent operations, being very low in some but up to40-50% in other operations, such as knee replacements.

Pain

One of the main reasons a patient might be reluctant toconsider surgery is the thought of postoperative pain. Theprinciples of pain control are dealt with in Chapter 23.However, it is worth considering briefly here, as there aresome pathophysiological consequences of ineffectivepain control.

Pain results in increased sympathetic activity, causingincreased heart rate, vasoconstriction and hypertension.This produces an increased demand for cardiac work andthe oxygen supply might not be sufficient to meet thisdemand. Pain can therefore reduce cardiovascular reserveand predispose to cardiovascular complications.

Intermediate-stagecomplicationsIntermediate-stage complications are listed in Table 4.6and are considered in turn.

Deep venous thrombosis (DVT)

Venous thromboembolism is a leading cause of prevent-able postoperative mortality. Clots form in the veins ofthe lower leg or in the pelvic veins during surgery.

18

Table 4.6surgery

Intermediate-stage complications of

Deep venous thrombosis (DVT)Pulmonary embolismSecondary bleedingRespiratory complicationsLine infectionUrinary retention and urinary tract infection (UTI)SepsisSystemic inflammatory response syndrome (SIRS)AnaemiaGastrointestinal ileusPressure sores

Prophylaxis

Surgery predisposes patients to thromboembolism andprophylactic measures are essential. Most units willhave a protocol indicating prophylactic measures to beemployed for different operations. Patients will becategorised into low, intermediate and high risk; depend-ing on the patient, the surgery and other factors as listedin Table 4.7. A suitable combination of measures willthen be employed. Prophylactic measures are eithermechanical or pharmacological.

Mechanical

Thromboembolic deterrent stockings (TEDS) providegraduated calf compression in an attempt to reducevenous stasis in the lower leg. TEDS can be either calf orfull length.

AV boots are pneumatic devices attached to thepatient's feet that intermittently dorsiflex and plantarflex,mimicking the venous pump action of the weight-bearingfoot. These can be used postoperatively in high-riskpatients.

Flotron boots are attached to the patient's calvesintraoperatively. Inflation compresses the calf, producing

Table 4.7 Factors predisposing to deep venousthrombosis (DVT)

ImmobilityBlood viscosityLocal traumaIntraoperative blood stasisMalignancyInfectionOral contraceptive pillPregnancyAir travelThrombophiliaPrevious DVT/pulmonary embolusCardiac failureInflammatory bowel disease

venous flow in the leg, similar to that induced by calfmuscles in the process of walking.

Movement and early mobilisation are also important.All patients should be actively encouraged to movetheir feet and lower legs whilst still confined to bed.Mobilisation is important as soon as the underlyingpathology and operation allow.

of the clot and hence appropriate treatment. Venographyis the gold standard, demonstrating all clots includingthose below the knee. However, this technique is veryinvasive and painful and there is evidence that it mightpotentiate further clotting. Doppler ultrasound scan isnon-invasive and is good for detecting thigh thrombosis,which are arguably the clinically significant ones.

Pharmacological

Heparin is a mixture of polysaccharide substances withvarying molecular weights that inhibits thrombosis bypotentiating the action of antithrombin III. For DVTprophylaxis, low-dose subcutaneous heparin (e.g. 5000international units (IU) twice a day) can be used.Monitoring of levels of anticoagulation is not necessary.

Low molecular weight heparin (LMWH) is thought tobe more effective than standard heparin and is graduallyreplacing this. Standard heparin is enzymaticallydegraded into smaller molecules, which have a differentanticoagulant effect. LMWH results in a reduced risk ofbleeding complications. Also beneficial is the longerhalf-life, such that administration is only necessary oncea day.

Aspirin has an antiplatelet action and therefore anti-thrombotic activity. However, its effects must be balancedagainst the adverse effects of gastrointestinal ulcerationand precipitation of renal failure, particularly in elderlypatients.

Clinical features

The majority of patients with DVT are asymptomatic andtherefore might remain undiagnosed. Symptomatic DVTcauses swelling and pain in the affected leg. This can beassociated with engorged superficial veins and warmthwith a tense and tender calf.

Irrespective of whether symptomatic or asymptomatic,a clot can be cast off from a DVT and float freely in thecirculation until it lodges in the pulmonary vessels. Thisis known as a pulmonary embolus (PE) and can be thecause of sudden collapse and unexpected postoperativedeath.

Investigation

Clinical diagnosis is notoriously unreliable, with accuracyfigures of around 50% even for experienced clinicians.Radiological imaging is essential to determine the extent

Treatment

Treatment is instituted to prevent propagation andembolism of the clot while the body's inherentthrombolytic mechanisms dissolve the clot that hasalready formed. The fact that DVTs situated solely belowthe knee are at low risk of embolisation very muchinfluences the extent of treatment needed for these. Inthis situation, the need for anticoagulation is debatable.

Where anticoagulation is required (especially withthigh or pelvic vein thrombosis) this can be inducedrapidly by intravenous heparin administered by a infusionpump. Longer-term anticoagulation is achieved by theuse of the oral anticoagulant warfarin. How long therapyis continued depends on the patient's circumstances, but3 months is a frequent length of time. Patients with recur-rent DVT/PE might require life long anticoagulation.

Pulmonary embolus (PE)

Aetiology

The majority of PE arise from thrombi in systemic veinsas described above, emboli passing through the rightheart chambers and lodging in the narrow calibrepulmonary arterioles or capillaries. Rarely the emboluscan arise from the right chambers of the heart itself, forexample, resulting from AF.

Pathophysiology

The effects of a PE depend entirely on the size of the clot.A large clot can block the total circulation from the heartcausing cardiac arrest. Smaller emboli block blood flowto the alveoli of the affected part of the lung. This area oflung continues to be ventilated but is no longer perfused,resulting in a block of gas transfer to and from thebloodstream. With a larger embolus, blood pressure inthe pulmonary circulation increases (increased resistance)and venous return to the left side of the heart is reducedwith a consequent drop in cardiac output.

19

20

Clinical features

Clinical features are variable and relate to the amountand size of emboli. Small emboli can be asymptomatic,might cause a shortness of breath, or might induce acardiac arrhythmia such as AF. Death of the affected areaof lung tissue is known as infarction and is generallyprevented in the case of small emboli by collateral supplyfrom the bronchial blood vessels. Clinical signs areusually minimal.

However, moderate-sized emboli can cause lunginfarction with the accompanying symptoms of pain,haemoptysis and more severe shortness of breath. Whereinfarction has occurred a pleural rub may be present onauscultation.

Large and massive PE constitutes a medical emer-gency and resuscitation might be required. Prevention ofblood reaching alveoli results in profound hypoxaemia,and prevention of venous return to the left side of theheart can give a precipitous fall in cardiac output, shockand cardiac arrest. Signs are those suggesting outflowobstruction from the right side of the heart.

Investigation

Electrocardiogram (ECG)

ECG changes are not diagnostic. Most frequently there issinus tachycardia. There might or might not be signs ofright heart strain such as right bundle branch block.

Arterial blood gas analysis

Arterial blood gas analysis demonstrates hypoxaemia,often with hypocapnia, the result of increased respiratorydrive 'blowing off' more carbon dioxide.

Radiology

A chest radiograph is rarely diagnostic. Most changesseen are non-specific with opacification secondary toatelectasis and possibly a pleural effusion. Larger embolican result in a visible cut-off in the pulmonary artery, andlack of vascular pattern distal to this. Wedge-shapedpulmonary infarcts might be visible.

A ventilation/perfusion (V/Q) scan

Labelled isotopes are separately administered at the sametime by inspiration and by intravenous injection. The

perfusion (Q) and ventilation (V) of the lungs can then becompared, a PE producing a mismatch where an area isventilated but not perfused. This picture is frequentlyobscured because, after a period of decreased bloodsupply, alveoli tend to collapse, resulting in reducedventilation as well as perfusion. As a result, the results ofV/Q scans can be indeterminate.

Angiography

Pulmonary artery angiography is the gold standard,directly visualising emboli. It is, however, technicallydifficult and invasive.

Computed tomographic (CT) pulmonary angiogram

The advent of spiral computerised tomography (CT),used in conjunction with intravenous contrast, has ledto a widespread role for this non-invasive, sensitive testfor PE.

Treatment

Prevention of further clot/emboli

The patient requires immediate anticoagulation withintravenous heparin. Low molecular weight heparin isnow licensed for use in PE. However, conventionalheparin infusion has some advantage in perioperativepatients: namely (1) its effect is easily monitored usingactivated partial thromboplastin time (APTT); and (2) itcan be reversed rapidly with protamine, should thepatient develop life-threatening bleeding complicationsof surgery.

Oral anticoagulation with warfarin is indicated for avariable period. Patients who are unable to comply withor tolerate warfarin anticoagulation, or those whocontinue to have 'PEs despite a therapeutic dose ofwarfarin as monitored by the international normalizedratio (INR), might be suitable for a caval filter. This is amechanical filter placed percutaneously through a neckvein into the inferior vena cava, which 'catches' embolifrom the leg veins en route to the right side of the heart.

Removal of clot

Fibrinolytic therapy such as streptokinase (thrombolysis)might be indicated for patients with large PE. This iscontraindicated in the postoperative period because of

haemorrhagic complications. Surgical embolectomy israrely required but is an alternative for life-threateningPE where thrombolysis is contraindicated.

therapy, clear the mucus plugs. It is important to do thisbecause unresolved collapse and mucus clearance pre-dispose to bacterial superinfection.

Secondary bleeding

Secondary bleeding is defined as bleeding occurringmore than 24 h after surgery. It has a number of causes,including dissolution of a clot sealing a blood vessel anderosion or unravelling of a haemostatic ligature.Secondary bleeding is rarely as significant as primaryhaemorrhage, but it can result in hypovolaemic shockand occasionally requires reoperation.

Respiratory complications

Respiratory complications are perhaps the most commonpostoperative complication. Their severity is a spectrumfrom an asymptomatic pyrexia to life-threatening pul-monary failure. The causes of respiratory complicationsare listed in Table 4.8.

A patient's risk of undergoing a respiratory compli-cation depends on the underlying condition of his or herlungs and the circumstances they are exposed to. Smokinghas a significant impact because smokers are predisposedto bronchitis and emphysema, ischaemic heart diseaseand heart failure. The normal action of the mucociliaryapparatus in the tracheobronchial tree is to clearsecretions and this is significantly affected in smokers.

Atelectasis

Atelectasis describes a degree of alveolar collapse thatoccurs after relative hypoventilation, inability to coughand suppressed ciliary action during general anaesthesia.Small mucus plugs block the alveoli causing them tocollapse. Postoperatively, patients may develop a coughand a mild transient pyrexia. Deep breathing exercises,which might require supplementation with chest physio-

Table 4.8surgery

Causes of respiratory complications of

AtelectasisLower respiratory tract infectionsAspirationAdult respiratory distress syndrome (ARDS)Pulmonary embolusPneumothorax

Lower respiratory tract infection (LRTI)

Microbial colonisation of the lung parenchyma causesinflammation, termed pneumonia or LRTI, where again awide spectrum of severity is encountered.

By far the most common pathogens are bacteria,although other pathogens such as fungi can causeproblems particularly in the severely ill patient requiringmultiple system support. The bacteria implicated arenumerous. Oropharyngeal and particularly trachealinstrumentation for anaesthesia introduce bacteria intothe airways, which are normally relatively sterile.'Community' and hospital acquired (nosocomial)bacteria can also be introduced to the patient's airways,where they colonise retained mucus. A full account ofpneumonias is not in the scope of this chapter, but theprinciples of diagnosis and treatment are essential to anysurgeon's practice. Pneumonia can be classified accord-ing to pathogen or anatomical site affected.

Clinical features

Patients develop a combination of symptoms of varyingseverity, including cough, production of discolouredsputum, pleuritic chest pain, shortness of breath,tachypnoea and pyrexia. Chest examination might reveallocalised areas of decreased chest wall movement, dull-ness to percussion and auscultation reveals a combinationof decreased air entry, crepitations and bronchialbreathing.

Diagnosis

A radiograph can demonstrate areas of consolidationor associated features such as pleural effusion. Radio-graphic changes might take some weeks to clear after thepneumonia has clinically resolved.

Blood tests

The white cell count is usually raised, although there areexceptions, especially in elderly or immunosuppressedpatients. Arterial blood gas analysis reveals abnor-malities, particularly of partial pressure of oxygen, whichwill help direct supportive therapy.

21

22

It is fundamental to try to isolate the infecting organism,so that appropriate antibiotics can be given. This isnot always possible, and repeated cultures and multiplechanges in antibiotic treatment might be required.

Treatment

General supportive treatment should be institutedquickly. Oxygen should be administered at a concen-tration guided by blood gas analysis. Saline nebulisersand aggressive chest physiotherapy help to clear theconsolidation. The patient should be sat up in bed toimprove ventilation/perfusion matching. Bronchodilatorsmay be indicated where there is evidence of somereversible airway narrowing such as a wheeze.

Antibiotic best-guess therapy should be started at thetime of diagnosis. At this stage, culture results are notavailable and therapy should be directed at organismsthat are most likely to be involved. This might involve theuse of more than one antibiotic, and the combinedtherapy has a broader spectrum of activity than a singledrug. Targeted therapy should be tailored accordinglywhen results of sensitivities from sputum culture areavailable. Where severe chest infection occurs, or in casesthat are failing to resolve, the input of chest physicians isinvaluable.

Aspiration

The protective airway reflexes that prevent inhalation ofsubstances from the gastrointestinal tract in the fullyconscious patient are depressed by general anaesthesia.Inhalation of regurgitated gastric contents is known asaspiration and results in a potentially virulent form ofpneumonia. Appropriate antibiotics should be given tocover gastrointestinal bacteria. The acid and digestivejuices from the stomach also contribute in causing asevere chemical pneumonitis.

Adult respiratory distress syndrome (ARDS)

ARDS is a syndrome resulting in lung failure. It ischaracterised by respiratory distress, hypoxaemia that isdifficult to treat, decreased lung compliance and diffusepulmonary infiltrates. Its precise aetiology is not clear,but is probably involved in a systemic inflammatoryresponse syndrome (SIRS). As such, it essentially

constitutes 'lung failure' and frequently precedes or ispart of a multiorgan failure syndrome (MOFS)

There are many known precipitants of ARDS, andeffective treatment of these in an attempt to preventARDS occurring, is the best form of management.Treatment other than that of the underlying cause issupportive, with the administration of oxygen oftenrequiring mechanical ventilation, careful fluid balanceand monitoring of cardiovascular parameters to minimisepulmonary oedema. The prognosis for established ARDSis poor, with figures quoted of around 50% mortality.

Pulmonary embolus and pneumothorax

These conditions have been discussed above.

Line infection

Surgical patients tend to have numerous lines insertedperioperatively. Intravascular lines that are insertedpercutaneously have an inherent risk of becominginfected, predominantly with skin flora. Certain bacteriahave an affinity for sticking to the synthetic material ofthe cannulae. It is important that all lines are insertedwith an aseptic technique and adequately prepared skin.Lines should be inspected regularly for signs of infectionand replaced where necessary. Lines should be removedas soon as they are no longer required. Blood cultures,taken from a line that is suspected as a source of sepsisand also from a peripheral vein, can help elucidate if theline is the cause.

Urinary retention and urinary tract infection(UTI)

Both men and women are at increased risk of UTI post-operatively, predominantly due to urinary tract instru-mentation. Males who have any prostatic symptomspreoperatively are at risk of developing postoperativeurinary retention; preoperative bladder catheterisationshould be considered. Urinary catheters are commonlyinserted before major surgery to ensure accuratemeasurement of postoperative urine output. This aids themonitoring of fluid balance and makes nursing care ofthe patient easier. Catheters should be inserted under anaseptic technique.

Patients with catheters in situ are at risk of urinaryinfections but might be asymptomatic because of the

Sputum culture

catheter. Pyrexia and cloudy urine should alert theclinician. A specimen of urine should be sent for cultureand sensitivity and an appropriate antibiotic started whileawaiting the results. Where metal implants have beenused, as in total hip replacement, prophylactic antibioticsare commonly used while the patient has a urinarycatheter in situ, or, alternatively, individual doses aregiven at insertion and removal of the catheter. This is inan attempt to prevent blood-borne spread of the urinarytract pathogens to the prosthesis, with potential implantfailure.

Sepsis

Sources of postoperative infection are multiple, the mostcommon ones having been dealt with above, and arediscussed in detail in Chapter 8. Other causes are specificto particular operations or types of surgery, such as intra-abdominal sepsis due to a leaking intestinal anastomosis,meningitis after breach of the meninges and deep-seatedprosthetic infection in arthroplasty surgery. Often, theonly overt symptom is pyrexia and a thorough, systematicsearch for the cause is needed, bearing in mind that itmay not be infective (e.g. DVT). Failure to identify acause should be met by starting the process again,reculturing specimens and widening the search to moreobscure causes. Early diagnosis and treatment of infec-tive complications is necessary to prevent progression tosepticaemia and septic shock. Pathogens spread from thesite of initial infection to the bloodstream, where theymultiply, resulting in septicaemia and spread to any partof the body.

adequate intravascular volume and fluid resuscitation isoften necessary before these features are seen.

Septic shock has a high mortality rate (up to 50%) andoften requires the support afforded in an intensive careunit. Septic shock often precedes, and can even be thecause of, multiorgan failure, which in part explains itshigh mortality.

Systemic inflammatory response syndrome(SIRS)

The term SIRS has been coined to describe this commonpathophysiological state and its clinical features. Thecomplex mixture of chemicals produced by the host inresponse to severe sepsis has been implicated as thepathophysiological cause of septic shock and its compli-cations. Similar host responses might occur as a result ofother, non-infective, insults to the patient such as majortrauma, burns and pancreatitis. Multiorgan failure can beprecipitated, with a high mortality.

Anaemia

Blood loss at operation results in a fall in haemoglobinconcentration. Unless the haemoglobin is replaced, theblood has a decreased oxygen carrying capacity withwide-ranging effects including decreased cardiovascularreserve and impaired wound healing. Oral iron therapy isgiven for mild to moderate postoperative anaemia. Lowerlevels of haemoglobin, or cases where oxygen deliverymust be maximised (coexisting disease, or concurrentcomplication), should be restored with blood transfusion.

Septic shock

The presence of bacteria in the bloodstream, particularlythose that possess endotoxin (Gram-negative bacteria),has a profound effect on the cardiovascular system andcan induce septic shock. There is a complex interactionbetween the pathogen and host via multiple mediatorsystems. By a complex process, endotoxin inducesincreased permeability and reduced vascular tone inblood vessels by direct damage to the endothelial lining.This results in a profound decrease in peripheral vascularresistance, and hence hypotension. A greatly increasedcardiac output is required to maintain adequate tissueoxygenation, and might not be achieved, causing shock.

Classically, therefore, the patient has warm peripheriesand a large cardiac output. This, however, assumes

Gastrointestinal ileus

The insult of abdominal surgery can result in temporaryintestinal dysfunction and lack of contraction andperistalsis. Although this is particularly the case for intra-abdominal surgery, it can occur in any severely ill patientespecially those with deranged blood electrolytes. Whenthis occurs, nutrition might need to be given by analternative route, and this is discussed in Chapter 5.

Pressure sores

Breakdown of the skin over an area where pressure hasbeen applied too long is a common postoperative problem.Pressure sores can become infected and cause sepsis, orgrow to involve a significant area of skin. Prevention is

23

the key, as these lesions are notoriously difficult to treatonce established. Expert nursing care is required from anearly stage.

Patients with increased risk of pressure sores are thosewith severe immobility, altered skin sensation, such asthose with spinal cord lesions, and those with poor skinquality such as the elderly and those on corticosteroidtherapy.

Late-stage complicationsThe main aim of surgery is to return the patient to his orher previous good state of health. For numerous reasonsthis might never be achieved. Apart from a failure to'cure' a patient's illness, other patient factors can play arole in the development of long-term disability

Psychological

A minority of patients has difficulty adjusting to illnessand the fact they have had to have an operation.Naturally, this depends on the extent of surgery and thedisease process that has necessitated it. In extreme cases,this attitude can result in adoption of the 'sick role', withabnormal conceptions of health and healthcare-seekingbehaviour. Support groups and psychiatric services canbe beneficial.

Pain

Chronic pain syndromes can occur postoperatively forcomplex reasons. Where simple measures are unsuc-cessful, referral to a pain team might be indicated.

Specific complicationsOperation-specific complications are generally consideredwhen discussing that operation. It is helpful to maintaina framework into which specific complications can fit.These are listed in Table 4.9.

Table 4.9 Specific complications of surgicaloperations

Approach usedSurrounding structures might be damaged accidentally

or sacrificed by necessityHazards of repairs made, including complications of

wound closureRisks associated with materials implantedEffect of removal of diseased tissue

Table 4.10 Local complications of surgery

Earlydamage to surrounding structureshaematoma/bruising

Intermediatewound infectionwound dehiscencewound seromabreakdown of repairfailure of implant

Lateabnormal wound healingloss of functionpsychological

Early complications

Damage to surrounding structures

A detailed knowledge of anatomy is necessary to avoidunnecessary damage to nearby structures and plan suit-able surgical approaches. Patients should be warned ofthe side-effects of damage to structures liable to beaffected such as scrotal paraesthesia following damage tothe ilioinguinal nerve in revision inguinal herniorrhaphy.

Haematoma/bruising

Patients can be alarmed by bruising around the wound.Bruising and haematoma formation cause pain and pre-dispose to wound complications including infection.

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Local complicationsLocal complications related to the wound are listed inTable 4.10 and are discussed in detail in Chapter 3. Thetemporal classification of local complications of surgeryis also listed in Table 4.10.

Intermediate complications

Complications relating to the surgical wound itself arediscussed in Chapter 3. Other complications are discussedbelow.

Surgical repairs made during the operation can failfor a number of reasons, including patient factors (poor

healing), inadequate surgical technique and failure ofmaterials used to carry out the repair. The expectedresults of repair breakdown should be considered and thepatient observed closely for these, followed by appro-priate investigations. The action required once repairfailure has been ascertained varies widely between typesof repair and the extent of failure.

An enormous range of surgical implants is available,all with their own idiosyncrasies. However, they can failfor a number of common reasons, for example, incorrectapplication results in forces being applied that theimplant is unable to cope with. Material defects occuroccasionally and design faults can take up to severalyears to become apparent and be corrected. Syntheticmaterials are prone to infection, which often leads tofailure, and prophylaxis might be required.

Late complications

Abnormal wound healing

Hypertrophic and keloid scarring are discussed inChapter 3.

Loss of function

Where diseased tissue has been removed, the previousfunction of that area is either compensated for by anotherarea, or the patient suffers effects of loss of function.This is an expected side-effect of surgery, rather than acomplication per se, but often requires symptomatictreatment.

Psychological complications

Psychological problems often relate to loss of functionand any disability that arises from this. Obviously, thisvaries enormously between operations and should beborne in mind preoperatively, especially for high-riskoperations such as limb amputations. The patient shouldbe directed to suitable support groups.

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Fluid balance, metabolismand nutrition

26

Fluid and electrolyte balanceThe fluid in the body is separated into different'compartments' - the intracellular compartment (withinthe cells) and the extracellular compartment, which isfurther subdivided into interstitial (between the cells) andintravascular (in the blood vessels) - and in each of theseareas the concentration of salts, or electrolytes, differs.These variations are subject to highly complex controlmechanisms and this degree of tight control is essential tomaintain efficient cell function. Abnormalities of fluid andelectrolyte concentrations can induce life-threateningcellular dysfunction, e.g. cardiac arrhythmias.

The body normally maintains excellent electrolytebalance, better than any doctor could hope to achieve bycareful fluid and electrolyte infusions, and in this regardthe kidneys play a vital role. However, as with any bodysystem, diseases occur that prevent normal homeostasis.In addition, during the perioperative period, patients aresubjected to a number of exogenous influences, forexample, fasting and intravenous fluid administration,which can outstrip the body's normal homeostatic capa-bilities. As a result, great care needs to be taken at thistime with regard to fluid and electrolyte administration,and careful monitoring of electrolyte levels in the body isneeded.

A consideration of the principles of electrolytes balancewill be followed by a discussion of normal homeostaticmechanisms, abnormalities of body water and electro-lytes and finally, a further discussion of fluid replacementand acid-base balance as listed in Table 5.1.

Principles of electrolyte balance

Some common principles apply when consideringhomeostasis of any electrolyte. These are based on anumber of factors:

Table 5.1 Fluid and electrolyte balance

Principles of electrolyte balanceNormal homeostasis

fluid compartmentsbarriers between compartmentshomeostatic mechanisms

Abnormalities of body waterdehydrationfluid overload

Abnormalities of electrolytessodiumpotassium

Fluid replacementAcid-base balance

abnormalitiescompensation

• Distribution and barriers: it is important to know thenormal concentration of an electrolyte in any givenfluid compartment. Fundamental to this is anappreciation of how a concentration gradient betweencompartments is maintained and can be manipulated.

• Output: it is necessary to know the amount of theelectrolyte that is consumed each day through normalcellular and systemic functions, and also how much islost normally by excretion.

• Intake: the amount of the electrolyte that needs to beacquired to maintain normal concentrations of theelectrolyte in the body should be balanced with theamounts actually taken in. Any inefficiency in uptake,either lack or excess from the method ofadministration, needs to be noted and corrected.

Normal homeostasis

Fluid compartments

A patient's body water content depends on the con-stitution of that person's body. This varies according to

5

Table 5.2 Fluid compartments (70-kg man)

Intracellular fluid (ICF)Extracellular fluid (ECF)

interstitial fluidintravascular fluid

28 L14L10.5 L3.5 L

age, sex and percentage of body fat, and can range from50 to 75% of body weight. For simplicity an account ofan average 70 kg man is given.

A 70 kg man is 60% water, and therefore contains70 kg x 0.6 = 42 L water (1 L weighs 1 kg). This is dis-tributed between the two main compartments as shown inTable 5.2.

There are a number of other small extracellular com-partments, which are of less clinical relevance with regardsto salt and water homeostasis, namely transcellular water(e.g. cerebrospinal fluid) and water associated with boneand dense connective tissue.

Barriers between compartments, osmolality andelectrolyte concentrations

Osmolality (measured in milliOsmoles; mOsm) isdefined as the strength of a solution. It is derived from theamount of active ions in that solution. Cations arepositively charged ions and anions are negativelycharged. In each body compartment, there is normally abalance between cations and anions. The main extra-cellular cation is sodium (Na2+) and the main intracellularcation is potassium (K+). The osmolality of plasma isderived from the equation:

2 x sodium (Na) + urea + glucose

The normal range is 280-290 mOsm/L. This value allowsthe clinician to estimate whether the patient has a relativeexcess or lack of water in the body and can be measuredeasily clinically.

The above equation is an approximation only because,although sodium is the main extracellular cation, variousfactors can affect plasma osmolality, causing inaccuraciesthat must be noted clinically. The presence of anexogenous, osmotically active molecule such as alcoholin the blood is a good example, and the body will try tomaintain the correct osmolality of plasma by recruitmentof water from the intracellular compartment.

The intracellular and extracellular fluid are separatedby the cell membrane. This acts as a semipermeable

membrane, allowing free passage of water but notelectrolytes. Because of the difference in concentrationof electrolytes between the two compartments, water willmove from the compartment with lower osmolality tothat with higher osmolality, therefore diluting it. This isknown as an osmolality gradient

To maintain the differences in ions between intra-cellular and extracellular fluids, sodium ions are con-stantly driven from the intracellular compartment by apump mechanism, which actively drives them out inexchange for potassium ions. The enzyme involved inthis active pumping mechanism is ATPase, and thus thisprocess is known as the ATPase exchange pump. As aresult sodium is the major extracellular cation andpotassium is the major intracellular cation. To maintainthe balance of electrical charge, chloride (Cl-) is associ-ated with sodium ions outside the cell and potassium isbalanced mainly by the anion phosphate (PO4

2-) andanionic protein inside the cell.

In the extracellular compartment, intravascular andinterstitial fluid are separated by the endothelium orblood vessel membrane, which, at capillary level, is onecell thick. Fluid balance between these two compart-ments is determined by hydrostatic or blood pressureforcing fluid out from the intravascular area, and oncoticpressure sucking fluid in. The endothelium is freelypermeable to small molecules such as sodium andpotassium ions, and relatively impermeable to the largerprotein molecules in the plasma. As a result, there is aprotein concentration gradient across the endothelium,caused mainly by the plasma protein albumin, which hasan appreciable effect on water movement between thecompartments. Again, fluid moves towards the area ofhighest concentration and this is called oncotic or colloidosmotic pressure.

Homeostatic mechanisms

Sodium regulation

The volume of extracellular fluid (ECF) relates directlyto the total amount of sodium in the body, the vastmajority of which is extracellular. The concentration ofsodium is maintained between narrow limits by freetransfer of water between the ECF and the intracellularfluid (ICF). Hence, a large amount of total sodium,held in the extracellular compartment, recruits waterfrom the ICF, increasing the volume of the ECF anddiluting the sodium such that it is maintained at a normalconcentration.

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Control of total body sodium therefore relates directlyto control of ECF volume. This is subject to homeostaticmechanisms that are both renal and extrarenal in origin,but ultimately alter sodium excretion by the kidney.

Sodium is ultrafiltrated by the glomerulus of thekidney; the rate of this process (the glomerular filtrationrate; GFR) relates directly to renal plasma flow (RPF) orrenal blood flow. Renal blood flow, like the flow of bloodto the brain, is autoregulated such that this is constantwithin a range of systemic blood pressures. The majorityof the filtered sodium is resorbed in the renal tubules,mainly in the proximal tubule with fine tuning occurringin the distal tubule.

Renal mechanisms can involve blood flow or sodiumconcentration. Changes in renal blood flow alter GFRand hence the amount of sodium that is filtered.

Blood flow to the glomeruli of the kidney is monitoredvia receptors in the afferent arterioles. Changes in per-fusion activate messenger systems in the arterioles,which alter the renal vascular tone and correct theabnormality in blood flow. This process is known as'autoregulation' and attempts to maintain the glomerularperfusion as a constant.

One of the factors involved in autoregulation is localproduction of prostaglandins, which alter arteriole walltone. This is an important precipitant of renal failure,particularly in elderly surgical patients with decreasedrenal reserve. The administration of non-steroidal anti-inflammatory drugs (NSAIDs) impairs the patient'sability to produce prostaglandins and hence regulaterenal blood flow.

Changes in renal blood flow also result in modulationof the renin–angiotensin–aldosterone system. Renin isproduced in the juxtaglomerular apparatus in the kidney.A drop in renal perfusion pressure results in release ofrenin into the systemic circulation. This in turn results inconversion of angiotensinogen to angiotensin I and thento angiotensin II, which in turn results in release ofaldosterone by the adrenal glands.

Aldosterone causes increased permeability of thedistal renal tubules to sodium and, as a result, moresodium is reabsorbed, with resultant increased loss ofpotassium. The sodium pulls water with it back into thecirculation, causing salt and water retention and a con-sequent rise in blood pressure.

Extrarenal mechanisms can also occur via themechanisms of autoregulation of blood flow as describedabove; the renal circulation is relatively detached fromthe general vascular tone. However, volume receptors

present in the great vessels in the chest have an effect onrenal perfusion via the sympathetic nervous system.Additionally, activation of stretch receptors in the rightatrium causes release of a hormone called atrial natri-uretic factor. This peptide causes increased sodiumexcretion by reducing sodium resorption in the distaltubule. Hence, sodium and accompanying water isexcreted, resulting in a fall in the ECF volume.

Potassium regulation

Potassium excretion and secretion by the kidney isintimately associated with sodium reabsorption. Nearlyall the potassium that is filtered in the glomerulus isreabsorbed in conjunction with sodium (cotransporter) inthe proximal nephron. In the distal tubule the reabsorp-tion of sodium causes an electrochemical gradient,resulting in secretion of potassium (and hydrogen ions).Therefore, the more sodium that is reabsorbed, under theaction of aldosterone, the more potassium is excreted.

Water regulation

As described above the main determinate of water re-absorption is the osmotic drive associated with sodiumreabsorption. There is capacity for fine-tuning of waterreabsorption, independent of sodium, which occurs in themost distal part of the nephron, called the collecting duct.The hormone antidiuretic hormone (ADH) is producedby the posterior part of the pituitary gland. Its releaseis influenced by numerous factors including plasmaosmolality, stress, surgery and thirst. ADH increases thepermeability of the collecting duct to water, increasing itsreabsorption. This results in water conservation by thebody and is the basis of the ability to concentrate urine.The stress of surgery results in increased ADH release,causing a degree of water retention.

Normal daily water losses in a healthy 70-kg man arelisted in Table 5.3. These losses are balanced by an intake

Table 5.3 Normal daily water losses (70-kg man)

Gastrointestinal (faeces)RespirationInsensible (latent

evaporation from skin)Urine

Total

100mL500 mL700 mL

1700 mL (variable, dependingon fluid status)

3000 mL28

Table 5.4 Normal daily water intake sources

Ingested fluidsFoodMetabolismTotal

1750 mL900 mL350 mL3000 mL

of about 3 L water per day from the sources in Table 5.4.These amounts can be drastically different in the con-ditions described below, where the correct amount offluid to be administered is guided by monitoring fluidoutput and electrolyte concentrations in the blood.

Abnormalities of body water

Dehydration

In the case of water or electrolyte deficiency the kidneyis acted upon by numerous systems (as discussed brieflyabove) to prevent further excess loss while maintainingadequate waste product excretion. However, in extremecircumstances these compensatory mechanisms are out-stripped, causing shrinkage of the body fluid compart-ments. Insufficient fluid in the interstitial space results inloss of skin turgor. Shrinkage of the intravascular volumecauses circulatory changes, which, in extreme cases, canresult in shock. Relative hypovolaemia can occur inconditions affecting vascular tone, such as septic shock(see Ch. 4).

Monitoring of the intravascular fluid is achieved byclinical examination and particularly by measurement ofheart rate and blood pressure. Invasive monitoring of thecentral venous pressure is helpful in severe cases or thosewith confounding variables. The causes of dehydrationare listed in Table 5.5 and are now discussed in turn.

Insufficient intake

Failure to match fluid output with sufficient intake resultsin dehydration. This is a common danger in surgicalpractice, with patients undergoing periods of starvationdue to disease processes, preoperative preparation andpostoperative recovery. Examples are found in allbranches of surgery and include inability to swallow(coma, oral disease) and enforced starvation (prior toanaesthesia, postoperative resting of the gastrointestinaltract). Adequate input is maintained with intravenousfluids, guided by output monitoring and electrolytemeasurement, bearing in mind that a pre-existing deficitmust be compensated for.

Table 5.5 Causes of dehydration

Insufficient fluid intakeExcess loss of fluidHaemorrhageDiarrhoea, bowel obstruction, bowel preparationVomitingFistulaeDiuresisInsensible lossesRespiratory

Excess loss

Common surgical procedures, diseases and complica-tions cause an abnormally high fluid loss. The principlesfor management of these are the same. Treatment shouldbe directed at the underlying cause, in an attempt todecrease future losses. Supportive replacement therapy isdetermined by measuring the amount and type of fluidloss, with special note being made of its electrolyteconcentration so that appropriate loss can be corrected.Direct analysis of the electrolyte concentration of thefluid lost (by laboratory testing) can be helpful.

Haemorrhage

Bleeding can lead to a fluid deficit that requires replace-ment, the principles of which are considered in thesection on shock (see Ch. 4).

Diarrhoea, bowel obstruction and bowel preparation

Gastrointestinal secretions are rich in solutes and theincreased losses occurring in the above conditions canneed aggressive replacement. When the bowel isobstructed, the fluids do not leave the body butaccumulate in the gut lumen, outside the extracellularfluid compartment. This is known as a third-space loss.

Vomiting

Vomitus is also solute rich. In addition, it is highly acidicand the loss of hydrogen ions has an important effect onacid-base balance in the body.

Fistulae

Gastrointestinal fistulae bypass the capability of fluidreabsorption further down the gastrointestinal tract.

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Losses therefore, particularly from high fistulae andparticularly to the skin, can be large and solute rich.

patients, generalised oedema and acute heart failure canbe easily precipitated.

Diuresis: drugs and renal disease

Diuretic drugs used for the treatment of fluid overload(see below) can be overeffective and result in dehydra-tion by losses into the urine. Similarly, a number of renaldiseases, including common disorders such as diabeticnephropathy, result in production of excess amounts ofurine.

Insensible losses

Losses through the skin can be significant. A commonexample is pyrexia, whereby water evaporates from thesurface using latent heat of evaporation.Massive amounts of plasma are lost from the surface ofburns, and one of the mainstays of burns management isfluid resuscitation.

Respiratory losses

The tachypnoea and pyrexia of respiratory complicationsof surgery can result in appreciable fluid loss.

Fluid overload and oedema

Excess body water occurs in several disease processes.The symptoms depend on the cause and the compartmentin which the excess fluid is distributed (Table 5.6).

Excess intake

By far the most common cause of fluid overload insurgical practice is excessive intravenous administration.This is more likely to occur in patients with pre-existingrenal and cardiovascular disease, and such patients there-fore require careful thought about their fluid regime andmay need close monitoring modalities. Maintenanceof accurate fluid balance charts is essential. In such

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Table 5.6 Causes of fluid overload

Excess intakeDecreased lossRenal diseaseLiver disease

Decreased loss

Several medical conditions result in pathophysiologicalsalt and water retention. They are of relevance to surgicalpractice as these patients might require surgical inter-vention, where inappropriate fluid management canexacerbate their condition. The altered cardiovasculardynamics of cardiac failure results in pathophysiologicalalterations in the renin-angiotensin-aldosterone axis,causing salt and water retention and further increases invenous pressure.

A low plasma albumin concentration - hypo-albuminaemia - results in a decreased colloid osmoticpressure of the blood. This results in more fluid shiftinginto the interstitial space, causing peripheral oedema.This fluid is lost from the intravascular space and resultsin activation of mechanisms effecting salt and waterretention.

Renal disease

Diseases that reduce the glomerular filtration rate resultin an impaired ability to excrete sodium. Complex inter-actions are seen in many renal diseases that alter tubularreabsorption of sodium and lead to retention of sodiumand its accompanying water.

Liver disease

Patients with cirrhosis have raised portal venouspressure, causing similar changes to those seen in cardiacfailure and hence salt and water retention. Many of theseconditions require tight fluid restriction. In those patientswho become overloaded with fluid, reduction in bodywater is achieved predominantly with diuretic drugs, ofwhich there are several different classes with differentmechanisms of action.

A commonly used class of drugs is loop diuretics, e.g.furosemide (frusemide), the main effect of which is toblock the sodium-chloride cotransporter in the loop ofHenle. This results in an increased sodium load in thedistal tubules. The tubule attempts to reabsorb this extrasodium, at the expense of excreting potassium andhydrogen ions, but its capacity is not sufficient and moresalt and water is lost to the urine. As a result, the majorside-effects of furosemide (frusemide) therapy are

hypokalaemia, metabolic alkalosis and the effects ofoveraction (i.e. salt and water depletion).

Abnormalities of electrolytes

Sodium

As discussed above, sodium and water homeostasis areintimately related. The classic abnormalities describedbelow relate to plasma sodium concentrations. These canoccur in the presence of low, normal or high levels oftotal body sodium. Daily requirements of sodium in anormal patient are around 120–140 mmol per day (i.e.1 L of 'normal' saline).

Hypernatraem ia

Raised concentration of sodium in the plasma most oftenresults from water deficiency. The raised plasma osmolalityresults in activation of mechanisms to conserve water andincrease intake (e.g. stimulating thirst).

There are many causes of hypernatraemia and onlythose of surgical relevance are given here:

• Insufficient intake of water, e.g. perioperative fasting.• Excessive insensible and respiratory water loss, e.g.

pyrexia, tachypnoea secondary to respiratorycomplications.

• Administration of excess sodium, either withintravenous sodium solutions or medicationscontaining large amounts of sodium.

• Diabetes insipidus (DI), which is either a failure ofproduction (pituitary DI) or lack of response to ADH(nephrogenic DI).

Generally, these causes are easily prevented by con-sideration and monitoring the patient's fluid balance.Correction of the water deficiency is effected withadministration of appropriate intravenous fluids. Sodiumconcentration should be corrected gradually to minimisethe risk of inducing cerebral oedema (as water shiftsfrom the newly hypotonic or isotonic plasma). Treatmentof DI depends on the underlying cause.

Hyponatraemia

Low serum concentrations of sodium can occur in thepresence of high, normal or low total body sodium levels.The clinical picture seen and treatment required dependson which of these is present.

Most commonly seen in surgical practice is combinedsalt and water depletion. The disease processes are thesame as those causing dehydration from excess fluidlosses (see above), particularly where the losses aresolute rich. The decreased extracellular fluid stimulateswater reabsorption under the influence of ADH. Morewater is therefore preserved relative to sodium, dilutingsodium in the ECF, and hence resulting in hypo-natraemia. The clinical signs are as for dehydration.Treatment is by restoration of salt and water byintravenous administration of normal saline.

The processes involved in fluid overload can alsoresult in hyponatraemia, with more water being retainedrelative to sodium. The total body sodium is thereforeincreased, but not as much as the total body water,causing dilution and hyponatraemia. Treatment is asdescribed for fluid overload above.

Potassium

Daily requirements of potassium are between 60 and 140mmol per day. This is dependent on the rate of excretionand also the rate of liberation from the intracellular fluidcompartment (see below).

Hyperkalaemia

A significantly raised serum potassium concentration(>7.0 mmol/L) can cause life-threatening cardiacarrhythmias and urgent treatment is required to preventthese. Symptoms are rare until complications have occurred,so awareness and prevention are essential. Treatment isresuscitative, performing life support manoeuvres whererequired. If complications have not yet occurred, treat-ment is directed at preventing complications and reducingserum potassium levels. Calcium gluconate (10 mL of10%) protects the heart from arrhythmias.

Insulin drives potassium into the intracellular fluid.There is some debate as to whether glucose should begiven simultaneously to prevent a fall in blood glucoseconcentration. Treatment is then directed at the under-lying cause, e.g. renal support may be required. Causesinclude either increased release or administration, ordecreased excretion.

The vast majority of body potassium is intracellular.Cell lysis, or inefficient functioning of the sodium-potassium exchange pump in the cell membrane, resultsin liberation of potassium into the circulation. As aresult, processes that cause cellular damage or cellular

31

dysfunction (e.g. surgery, trauma, acidosis) can increaseserum potassium levels.

Excessive administration of potassium is most fre-quently iatrogenic. Patients receiving supplementationshould receive this slowly, and close monitoring of bloodlevels is required.

Renal insufficiency results in impairment of potassiumexcretion and acute renal failure can result in aprecipitous rise in serum potassium levels. Severe chronicrenal failure can have a similar effect, particularly wheretubular function is affected.

Drugs that affect distal tubular function can causeinefficient potassium excretion. An example is the classof diuretics that antagonises the action of aldosterone(e.g. spironolactone, which prevents the reabsorption ofsodium at the expense of potassium). Similarly, drugsand diseases that affect the rennin-angiotensin-aldosterone axis result in hyperkalaemia (e.g. ACEinhibitors, Addison's disease).

Hypokalaemia

Low serum potassium levels result from insufficientintake or excess loss of potassium. Again, symptoms arerare, but the deficit is rarely life-threatening, unlikehyperkalaemia. An exception is concomitant treatmentwith digoxin, where hypokalaemia causes a dangerouspotentiation of the drug's action and can result in cardiacarrhythmias. Treatment of hypokalaemia is based onreplacing the deficit either orally or in dilute intravenousfluids (never as a potassium salt bolus), and treatment ofthe underlying cause.

There are very many causes of hypokalaemia anddescriptions of all of these are beyond the scope of thischapter. Examples of those most commonly encounteredin surgical practice are given in Table 5.7.

there being some evidence that use of colloids in criticallyill patients actually increases mortality. However, thefundamentals of fluid replacement remain unchangedand a knowledge of the constituents of the infused fluidand its pattern of distribution within fluid compartments,is important. Solutions available for fluid replacementare listed in Table 5.8.

Crystalloid

Crystalloid solutions are those with dissolved solutes.They are cheap, natural and safe when given appropriately.Potassium can be added to bags to maintain plasmapotassium levels.

Dextrose

Glucose solution is isotonic at 5%, and this is thestandard fluid infused. It is transferred freely between allfluid compartments so that only 8% remains in theintravascular space. Its energy content is negligible, theglucose in each 500 mL bag producing only 100 caloriesof energy.

Saline

Isotonic saline is 0.9%, and is called 'normal saline'.Each 500 mL bag contains 75 mmol of sodium, balancedwith 75 mmol of chloride. Following intravenousinfusion, it is distributed freely within the ECF, with 25%remaining intravascular.

Colloid

Colloid solutions contain large-molecular-weight sub-stances that are designed not to cross the vascular

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Fluid replacement

There is a long-standing debate over the relative value offluid replacement with crystalloid and colloid solutions,

Table 5.7 Common causes of hypokalaemia

Insufficient intake: inadequate intravenous replacementExcess gastrointestinal losses: diarrhoea, fistulae, villous

adenomasExcess renal losses: diuretic therapy

Table 5.8 Solutions for fluid replacement

CrystalloiddextrosesalineRinger's lactate

Colloidgelatinesdextransheta starchhuman albumin solution

Blood

endothelium and thus remain within the intravascularspace. They are used to increase the colloid osmoticpressure causing retention of fluid in the circulation.However, some molecules do cross to the interstitialspace, and this proportion can be increased in diseaseprocesses where vascular permeability is affected.

Blood

Where fluid loss is by way of significant haemorrhage,replacement with blood is appropriate. The principles ofblood transfusion are discussed in Chapter 6.

Acid-base balance

For efficient cellular function to occur, the cellular andplasma pH, or hydrogen ion concentration, must bemaintained between narrow limits (pH 7.36-7.44).Values outside these parameters result in cellular andsystem dysfunction, which become profound and canultimately result in cell death and system failure.

Hydrogen ions are generated by several metabolicprocesses, and by equilibration of carbon dioxide (CO2 )in solution. Maintenance of normal pH is achieved througha number of different systems: namely, buffering, respir-ation and renal excretion of hydrogen ions andbicarbonate.

The main determinant of pH is the equilibration ofCO2 in solution. CO2 is generated as a waste product innormal aerobic respiration. It is excreted by the lungsduring respiration. Transport of CO2 from the tissues tothe lungs is performed by the blood, with the CO2 beingdissolved in solution. The enzyme carbonic anhydraseforms carbonic acid according to the Henderson-Hasselbach equation:

This equation has to remain in equilibrium, and is there-fore dependent on CO2 excretion by the lungs and thebicarbonate (HCO3

-) concentration in plasma. Bicar-bonate concentration is controlled by renal excretion.

Other forms of acid are produced by tissues, e.g. lacticacid from anaerobic metabolism. These are buffered inplasma by bicarbonate, phosphate, haemoglobin andother plasma proteins. Renal excretion of hydrogen ionsis important in their elimination.

An important effect of the interaction betweenhydrogen ions and haemoglobin (Hb) is the reduction inthe affinity of Hb for oxygen. As a result, when oxy-

haemoglobin reaches the tissues, where there is a higherconcentration of carbonic and other acids, it more readilyreleases the oxygen it is carrying for use in that tissue.

Abnormalities of acid-base balance

The hydrogen ion concentration can either be increased(acidosis) or decreased (alkalosis). This can be caused byimbalance at any point of the Henderson-Hasselbachequation as a result of either respiratory or renal changesin acid-base management.

Respiratory acidosis

Decreased CO2 excretion by the lungs results inincreased plasma carbonic acid and hence hydrogen ionconcentration. Causes include decreased respiratorydrive (e.g. opiate overdose) and diseases of lungparenchyma that result in inefficient gas transfer.

Respiratory alkalosis

Overventilation increases CO2 excretion, decreasingplasma carbonic acid and hence hydrogen ion concen-tration. Hyperventilation can be psychological, pathological(e.g. tachypnoea of respiratory tract infection) oriatrogenic (e.g. Overventilation of mechanically ventilatedpatients).

Metabolic acidosis

Metabolic acidosis is an increase in plasma hydrogen ionconcentration derived from another source than CO2.Examples include lactic acidosis and diabeticketoacidosis.

Metabolic alkalosis

This is a fall in plasma hydrogen ion concentration notrelated to carbon dioxide. It can result from manyprocesses that cause either increased renal H+ excretionor from excess plasma bicarbonate (e.g. iatrogenicadministration, renal conservation of bicarbonate).

Compensation

The clear-cut abnormalities described above are rarelyseen because the system not affected by the abnormalprocess will act to compensate for the problem. Thus, in

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34

respiratory acidosis the kidney will retain bicarbonateand excrete H+. This in effect causes a partial metabolicalkalosis and combats the fall in pH driven by CO2

retention. Similarly, in metabolic acidosis, respiration isincreased, blowing-off more CO2, causing a compen-satory partial respiratory alkalosis.

Metabolic response tosurgeryThe insult of trauma, including surgery, results in anumber of metabolic changes directed at containing andrepairing the damage. This response is complex andinvolves many metabolic processes and body systems.The effects are mediated by the sympathetic nervoussystem, endocrine, inflammatory and endothelialresponses. Not only has the response been implicated inhealing but, more recently, has been suggested to play animportant pathophysiological role in the complicationsof trauma, such as systemic inflammatory responsesyndrome (SIRS) and multiorgan failure (MOF). A fulldescription of the changes observed is excessive for thepurpose of this chapter, but it is worth highlighting anumber of points that have bearing on everyday clinicalpractice.

Sympathetic activity causes a rise in heart rate andblood pressure, increasing cardiac work. Mobilisation ofenergy stores occurs shortly after injury, causing relativehyperglycaemia and insulin resistance. ADH secretion isincreased resulting in water retention and a fall in urineoutput. Vascular permeability is increased, predisposingto oedema formation. Inflammatory mediators (e.g.prostaglandins and leucotrienes) are produced, causingsystemic effects such as pyrexia; they might also be im-plicated in trauma pathophysiology. The immune systemis impaired, predisposing to infective complications.After the initial brief mobilisation of energy stores(catabolic state) the body enters a more prolongedreparative anabolic state with increased energy andnitrogen demands. Activation of platelets leads to ahypercoagulable state.

Postoperative feedingFor effective healing to occur after trauma or surgery, thebody must be supplied with the correct substrates in

sufficient amounts. Whereas these are normally suppliedvia the gastrointestinal tract by a balanced diet, demandfor, and the ability to attain, the substrates can be dra-matically altered perioperatively.

Patients' ability to ingest, digest, absorb and utilisesubstrates is affected by any number of disease pro-cesses. In cases where the effects of these processes areexpected to be prolonged, or are superimposed on abackground of malnutrition, nutritional support may beindicated. This support can be provided either to the gastro-intestinal tract (enteral) or intravenously (parenteral).

Trauma and major surgery induce metabolic changessuch that energy and nitrogen demands are increased,and this should be taken into account when deciding ona feeding regime. Reasonable figures for normal dailyrequirements of energy and nitrogen are 2000-2500 kcaland 14-16 g, respectively.

Enteral feeding

Where possible, enteral dietary supplementation ispreferable. Stimulation of the gut mucosa with food hasbeen implicated in reducing sepsis in critically illpatients. It is thought that continued mucosal activitymaintains a barrier to bacteria in the gut lumen,preventing them from translocating into the circulation,where they are thought to play an important role in thepathophysiology of multiorgan failure.

Enteral nutritional support can be given as oralsupplements, or where appropriate by intubation of thegastrointestinal tract (e.g. nasogastric, feedingjejunostomy). The feed needs to contain each food group- carbohydrate, fat and protein. These can be given inseveral different proportions and forms, particularlyrelating to protein and its degree of predigestion prior toadministration. Disease-specific diets are also available.Trace elements are also added (e.g. zinc and mag-nesium). Enteral feeding is appropriate in patients whoare comatose, those with oropharyngeal diseases thatprevent ingestion, mastication and swallowing, and somepatients with certain diseases further down the gastro-intestinal tract.

In the presence of a poorly functioning gastro-intestinal tract, enteral feeding can lead to further com-plications, including diarrhoea, vomiting and aspiration.Complications relating to method of administration arenot uncommon, including incorrect positioning of thefeeding tube and bacterial growth in the excellentmedium that the feed provides.

Parenteral feeding

When patients with a non-functioning gastrointestinaltract require nutritional support, and when it is notpractical to gain access for enteral feeding, feeding canbe given intravenously. The feed is designed to meet allthe body's requirements and is termed 'total parenteralnutrition' or TPN.

Constituents

To meet the body's needs, TPN solutions contain fat,amino acids and carbohydrate (mainly glucose). Thecomposition of a feed varies, is prepared for individualpatients and is tailored to their needs. There are a numberof standard feeds with different amounts of nitrogen, andthe majority of energy supplied by carbohydrates or fats.These are further manipulated, for example, with theaddition of potassium, as guided by monitoring of serumlevels and markers of metabolic state.

Complications

The constituents of TPN solutions render them hyper-osmolar, and hence irritant, and when given throughperipheral veins cause thrombophlebitis. They are there-

fore administered via a large-bore central venouscannula. There is, however, an increasing role for peri-pherally sited 'long' feeding lines.

The hyperosmolality of TPN solutions can also causemetabolic complications, most commonly hyper-glycaemia. If this occurs, insulin might be required and,in future feeds, more of the energy should be supplied asfat. Rebound hypoglycaemia can occur on cessation offeeding.

Patients on TPN are more prone to hepatobiliarydisease.

Trace element and vitamin deficiencies can occur,more commonly in prolonged TPN administration, andthese should be replaced accordingly.

However, the majority of complications of TPN relateto the feeding line. The majority of these lines are sitedcentrally, and so are subject to the risks of central lineinsertion (e.g. pneumothorax or arterial puncture). Infec-tion is a common problem, as is secondary linethrombosis and failure. Patients requiring long-term TPNcan benefit from the placement of a buried subcutaneousfeeding line to minimise these risks. All TPN should beadministered through a lumen dedicated solely to it andnot used for other purposes such as intravenous antibioticadministration or blood transfusion.

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Blood disorders andtheir management insurgical practice

IntroductionPoor haemostasis (control of bleeding) is one of the mostcommon surgical complications and can range fromcatastrophic blood loss causing hypovolaemia and shockto small wound haematomas that provide an excellentgrowth medium for microorganisms. By virtue of thecoagulation or clotting cascade, blood and blood vesselsare a self-sealing system, and therefore have an inherentability to provide haemostasis. However, there is nosubstitute for careful technique and meticulous surgicalhaemostasis.

This chapter describes, under the headings shown inTable 6.1 the normal sequence of events involved in bloodclotting and also those mechanisms that prevent clottingin normal, undamaged vessels. Also described are con-ditions where abnormalities in clotting occur, theirrecognition and treatment. The implications of anaemiain surgery are considered, the principles of blood trans-fusion are described and a guideline for the recognitionand care of a patient with potential bleeding problems isprovided. The specific management of a dental post-extraction haemorrhage is considered in Chapter 26.

Normal clotting

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The whole process of blood clotting, limitation of pro-pagation of clot and ultimate dissolution of clot is a com-plex interactive system interdependent on, and subject to,numerous feedback controls. Blood clotting will be con-sidered under the headings listed in Table 6.2.

The immediate response to vessel damage is vasocon-striction, which reduces blood flow in the area therebyreducing blood loss and preventing the fledgling bloodclot from being washed away. This is mediated both as alocal reflex and by a number of mediators that are releasedmainly from activated platelets, such as thromboxane

Table 6.1 Blood disorders and theirmanagement

Normal clottingAbnormal clotting

increased bleeding tendencyincreased clotting tendency

Patients with anaemiaTransfusionSummary and guidelines

Table 6.2 Normal blood clotting

Initiation of clottingplatelet adhesionplatelet activationplatelet aggregation

Stabilisationcoagulationintrinsic pathwayextrinsic pathwaycommon pathway

Limitation of clottingDissolution of clotPrevention of inappropriate clotting

structuralchemical mediators

(TxA2). Thus, although coagulation, as measured byclotting time, takes around 8 min to occur, haemorrhageis reduced and arrested much sooner.

Initiation of clotting

Circulating platelets play a central role in the initiation ofblood clotting by three main mechanisms:

1. Platelet adhesion: platelets possess membrane recep-tors to many proteins not encountered in normal blood

6

or endothelium. Disruption of endothelium exposesplatelets to 'foreign' proteins, for example, differenttypes of collagen, to which they have receptors and towhich they therefore stick.

2. Platelet activation: platelet adherence results in achange in the shape of platelets. Within seconds, byway of complex intracellular messaging, the plateletbecomes 'activated'. This results in synthesis andrelease of mediators such as histamine and TxA2 fromintracellular stores (lysosomes).

3. Platelet aggregation: the conformational changes inthe platelets and the milieu of mediators releasedattract other platelets and allow them to stick to oneanother. This is known as aggregation.

Platelet adhesion, activation and aggregation result in theformation of a platelet plug, which is an attempt to coverthe breach in the endothelium and acts as the starting pointfrom which the rest of the process of coagulation occurs.

Stabilisation

Coagulation

A mature blood clot is a combination of cross-linkedfibrin admixed with blood cells and plasma. Plateletevents described above stimulate a stepwise pathway thatresults in the formation of cross-linked fibrin. This sys-tem is known as the 'coagulation cascade', which consistsof two routes that run in parallel - the intrinsic pathwayand the extrinsic pathway. Current thinking in coagu-lation research is that this might be oversimplified andthere are now thought to be multiple interactions betweenthe pathways, resulting in a more integrated system.However, the sequences described here are accurate andprovide a good framework for understanding the processof coagulation.

Ionised calcium is a crucial cofactor for many of theclotting factors, and deficiency has an important effect oncoagulation.

Intrinsic pathway

This is the more intricate portion of the coagulation cas-cade, and there is debate over the relevance of differentaspects seen in vivo compared to results seen in vitroexperiments. Essentially, contact with injured tissue resultsin activation of factor XII, which in turn activates factorXI, which in turn cascades to the common pathway asshown in Fig. 6.1.

Extrinsic pathway

This is coagulation initiated by tissue factor. Tissue factor(TF) is expressed on the surface of the subendothelialtissue that is exposed when endothelium is damaged.Tissue factor activates factor VII, which, in turn, activatesfactor X, the beginning of the common pathway.

Common pathway

This is the common endpoint of the intrinsic and extrinsicpathways. It begins with activation of factor X and, viathe steps in Fig. 6.1, results in the formation of cross-linked fibrin.

Limitation of clotting

It is vital that clotting is limited to the local area ofdamage to prevent propagation of clot throughout thevascular system. Activated clotting factors are removedfrom the propagating clot by blood flow. There is also aform of negative feedback on clotting by naturallyoccurring substances that inhibit coagulation, some ofwhich are activated by products of the coagulationcascade itself. Examples of these are proteins C and Sand antithrombin III. Abnormalities of these factors cancause disease (antithrombin III deficiency, see below)and knowledge about these can be utilised for therapy(e.g. heparin potentiates antithrombin III).

Dissolution of clot (fibrinolysis)

Ultimately, when the damaged vessel has healed andre-endothelialised, the adherent clot will be removed.This is known as fibrinolysis. In this process, tissueplasminogen activator (TPA), produced by vascularendothelium in the presence of thrombin, acts oncirculating plasminogen to form plasmin; this action isdependent on the presence of fibrin. Plasmin now acts inturn on fibrin, which is degraded to soluble fibrindegradation products (FDPs).

Fibrinolysis maintains vessel patency and helps toprevent overpropagation of clot. Not surprisingly, thereare also inhibitors of plasmin and plasminogen activators.

Levels of fibrinogen and FDPs can be measured andprovide helpful diagnostic clues, for example elevated D-dimer FDP levels are indicative of the presence of bloodclot and can be used in the diagnosis of suspected deepvenous thrombosis (DVT).

This very intricate system of control preventsexcessive bleeding while at the same time preventing

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Fig. 6.1 The coagulation cascade showing the numbered factors (a, activatedform). The factors involved in the intrinsic system, beginning with the activation offactor XII and ending with the activation of factor X are all present in the circulatingplasma: the extrinsic system consists of tissue thomboplastin and includes factor VII,not involved in the intrinsic system. Activated factor X, along with factor V, initiates thefinal steps, culminating in the conversion of fibrinogen to fibrin by thrombin.

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excess intravascular coagulation once clotting has beeninitiated: the body has developed a very finely balancedfeedback system.

Prevention of inappropriate clotting

To prevent inappropriate clotting in normal bloodvessels, physiological systems act to counteract thosethat stimulate blood clotting. Interference with these

systems stimulate the initiation of blood clotting, asdescribed below. The mechanisms that prevent bloodfrom clotting in normal blood vessels can be divided intostructural and chemical:

• Structural prevention mechanisms: the smooth liningof the blood vessel provided by endothelium does notexpress surface proteins that stimulate plateletadhesion as has been described above. Rough or

damaged endothelium (e.g. atherosclerotic plaques)not only allows platelets to come into contact withproteins that they adhere to but also results inturbulent blood flow, which also predisposes to bloodclotting.

• Chemical mediators: normal vascular endotheliumproduces the prostaglandin, prostacyclin (PGI2). Thisopposes the actions of TxA2, causing vasodilatationand opposing platelet activation and aggregation.

Abnormal clotting -increased bleeding tendencyCareful history taking is fundamental in the diagnosis ofbleeding disorders and is essential before surgery. Inpatients who express a past history of bleeding problems,the site and type of bleeding (e.g. spontaneous Vs inducedby trauma) needs to be determined accurately. This cangive clues to the type of bleeding disorder. A history ofexcess bleeding at the time of previous surgery is veryimportant to note. A detailed family history can suggestif such a disorder is inherited or acquired.

Full physical examination can show further evidenceof a bleeding disorder, including bruising, petechiae(subcutaneous red spots that do not blanch on pressureand which represent areas of small capillary bleeding) orprevious bleeding into joints.

However, despite a careful history and examination,excessive bleeding at the time of surgery might be apatient's first presentation of a bleeding disorder, and it istherefore important for a surgeon to be aware of theconcepts and how to control bleeding in this situationshould it occur. Close liaison with a haematologist willbe necessary at this time. The causes of an increasedbleeding tendency are listed in Table 6.3.

Platelets disorders

These can be either quantitative (number) or qualitative(function). Disorders of platelets can result in bleedingfrom small vessels in mucous membranes such as nosebleeds (epistaxis), or in skin causing bruising orpetechiae.

Decreased numbers

This is known as thrombocytopenia. Platelet count ismeasured routinely as part of a full blood count. A normal

Table 6.3 Causes of increased bleeding tendency

Platelet disordersdecreased numbers

idiopathic thrombocytopenic purpura (ITP)hypersplenismdisseminated intravascular coagulation (DIC)

decreased functionVessel disordersCoagulation disorders

inheritedhaemophilia Ahaemophilia B

von Willebrand's diseaseAcquired

liver and biliary diseaseDICmassive blood transfusion

value is 150-400 x 109 per litre. Bleeding is rarely aproblem when the platelet count is above 50. Severe orspontaneous bleeding occurs with values below 20.

There are multiple causes of thrombocytopenia,which can be broadly divided into those with excessiveloss or consumption of platelets and those with impairedproduction. Either form can be congenital or acquired.Important examples are discussed below.

Idiopathic thrombocytopenic purpura (ITP)

This condition is also known as autoimmune thrombo-cytopenic purpura and the platelet count might beundetectable.

Treatment of thrombocytopenia is directed at theunderlying cause (e.g. ITP might respond to steroidtherapy or splenectomy). During surgery, if a patient isactively bleeding with a low platelet count, platelet trans-fusion can provide a temporary solution. However, thesetransfusions are prone to the same fate as the patient'sendogenous platelets (e.g. rapid consumption).

Hypersplenism

This occurs where platelets are sequestered in an enlargedspleen.

Disseminated intravascular coagulation (DIC)

This occurs where platelets and coagulation factors areconsumed in widespread inappropriate coagulationwithin normal blood vessels (see below).

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Decreased function

These disorders can also be congenital or acquired.Assessment of platelet function is difficult and reliance isinitially on the bleeding time, which is the time taken forbleeding to stop under standard test conditions. However.this is a difficult test to standardise and has a wide normalrange between 2 and 10 min.

An important acquired cause of decreased plateletfunction is medication, the most common of which isaspirin. This is now widely used in prophylaxis andtreatment of vascular disease because of its effect onplatelet function and its effects can last up to 10 days.Aspirin should therefore be withheld for 10 days prior tomajor procedures associated with a potential high risk ofbleeding complications.

Vessel disorders

These form a generally rare, heterogeneous group with aclinical presentation similar to that of platelet disorders,but where investigations of platelet number and functionare normal. Essentially, the capillaries are fragile andbleeding occurs more easily. Again, there are congenitaland acquired forms. Corticosteroid therapy is a commonexample of an acquired cause.

One of the interesting congenital causes is hereditaryhaemorrhagic telangiectasia, characterised by recurrentbleeds from mucous membranes. The lesions look likesmall blood blisters and occur particularly on the face,lips, tongue and hands. They bleed freely if traumatised.Control of bleeding is very difficult and this conditionshould be identified before surgery. This is of particularrelevance to dentists.

Coagulation disorders

Disorders of coagulation factors are characterised by amore generalised bleeding tendency than platelet andvascular disorders, including spontaneous bleeding fromlarger vessels and into joints. The vast majority of coagu-lation factor defects encountered in surgical practice areacquired. The most common cause is iatrogenic, relatedto treatment with warfarin. Inherited disorders areuncommon but require special consideration.

A number of laboratory investigations can helpelucidate the type of a coagulation defect. Although someof these are specialised, an appreciation of standardclotting tests is essential for surgeons:

• Prothrombin time (PT): this gives an indication of theextrinsic and common pathways of the coagulationcascade. Abnormalities in these portions of thecascade result in a prolonged time. Times are relatedto an international standardised sample designatedinternational normalised ratio (INR). An INR of 1.0is normal, whereas an INR of 2.0 denotes that thepatient's blood takes twice as long as 'normal' to clotunder test conditions.

• Activated partial thromboplastin time (APTT): thismeasures the efficiency of the intrinsic and commonpathways.

If abnormalities of INR or APTT are discovered thennormal plasma is added to the sample in the laboratory.If this corrects the abnormality, then the problem mustrelate to a factor deficiency or dysfunction (because thefactors present in the normal added plasma corrected theproblem). If the abnormality is not corrected then it islikely to be due to the presence of a substance thatinhibits coagulation. This procedure is known as'correction testing'.

Inherited coagulation disorders:

Inherited defects are specific genetic abnormalities thatgenerally affect only one clotting factor.

Haemophilia A

This is an X-linked recessive disorder that thereforeaffects only males but which is transmitted by females.The prevalence is about 1:10000. Statistically, all thedaughters of haemophiliacs will carry the gene and noneof the sons will inherit the disease or transmit it. How-ever, in the second generation, only 50% of the sons offemale carriers will inherit the disorder and only 50%of their daughters will inherit the gene.

Haemophilia A can be caused by a number of geneticabnormalities, all of which result in decreased or absentfactor VIII:C. Deficiency of factor VIII:vWF results inthe closely related von Willebrand's disease (see below).

Different affected individuals have a different level ofVIII in the blood and there is therefore a spectrum ofdisease. Factor VIII levels can be measured in the patient'splasma and are expressed as a percentage of normal.

Bleeding into joints causing arthritis is common andproduces clinically obvious joint deformities in manycases. Bleeding can also occur into body cavities andintracranially.

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Preoperative transfusion of factor VIII concentrate isaimed at raising factor VIII levels to nearer normal, forexample, 60% for dental extraction, and as near 100% aspossible for major surgery. These levels need to bemaintained postoperatively.

Tragically, many haemophiliacs who received bloodtransfusions prior to HIV blood donor screening intro-duction in the UK contracted HIV, and in these patientshigh-risk precautions are indicated perioperatively.

Haemophilia B

This is also known as Christmas disease. It is similar tohaemophilia A but the disorder is related to deficiencyof factor IX. The incidence is less common, with aprevalence of around 1:100 000 and the defect can becorrected by the transfusion of fresh-frozen plasma(FFP).

von Willebrand's disease

von Willebrand's disease is not sex-linked and can occurvia a number of genetic abnormalities. It is usually due toautosomal dominant inheritance.

Surgery - elective or emergency - on any of the abovepatients should only be performed in close consultationwith a haematologist (preferably the patient's own).

Acquired coagulation disorders

Bile salts are produced by the liver and enter the duo-denum via the common bile duct to aid the absorption offats and fat-soluble vitamins such as vitamin K. Thepresence of vitamin K is essential for the synthesis ofcoagulation factors II, VII, IX and X (and also proteins Cand S). Disorders of bile production and of biliarydrainage will affect coagulation.

It should be noted that the majority of clotting factorsare produced by hepatocytes. Remembering this physiologyis helpful in understanding acquired coagulation defects,of which there are many causes.

Liver and biliary disease

There are many causes of liver dysfunction and a descrip-tion of each of these is beyond the scope of this chapter;one common cause is alcohol-related cirrhosis.

The coagulopathy that results from diffuse liver dys-function is complex. The damaged liver produces too few

clotting factors. Bile salt synthesis, needed for vitamin Kabsorption, is also impaired. Portal hypertension canresult in hypersplenism, and therefore thrombocytopenia.

Surgical jaundice secondary to obstruction of thecommon bile duct due to gallstones or malignancy of thepancreas prevents bile salts reaching the duodenal lumen.Vitamin K malabsorption results, followed by deficienciesof factors II, VII, IX and X. Other causes of vitamin Kdeficiency, such as dietary deficiency, have the sameresult. However, the effect of 'back pressure' on hepato-cyte function also plays a role in the coagulopathy ofbiliary obstruction.

Vitamin K deficiency can be corrected by parenteralinjection of a water-soluble vitamin K analogue beforeelective surgery, but this will not be immediatelyeffective. It will be several days before the liver cansynthesise sufficient factors to correct the bleedingtendency. Urgent or emergency surgery might thereforerequire infusion with solutions containing the deficientfactors. The INR should be checked immediately beforesurgery, with the aim of reducing it to 1.

Warfarin therapy

Warfarin, a coumarin drug, is a vitamin K antagonist (itprevents conversion of vitamin K to an active form).Warfarin therapy is indicated in a number of commonconditions including atrial fibrillation, pulmonaryembolus and prosthetic heart valve replacement. Normalmedical practice for most conditions dictates thatwarfarin therapy should be administered to achieve anINR of around 3. Excessive bleeding will occur wherethe INR is greater than 2.

The effects of warfarin are slow to reverse because,again, even if vitamin K is administered, the clottingfactors still have to be synthesised. When emergencysurgery is needed, vitamin-K-dependent factor concen-trates can be administered intravenously, reducing theINR quickly, as noted above in obstructive jaundice. Thismust always be done with care. A balance needs to beachieved between maintaining an acceptable level ofanticoagulation (e.g. to prevent thrombosis. of aprosthetic heart valve) and not exposing the patient to therisk of haemorrhage during surgery. It is vital, therefore,that the administration of these concentrates is done inconsultation with a haematologist, and that the INR ismaintained well above 1. It is recommended that patientsundergoing elective surgical should have their warfarinstopped for 2-3 days before surgery and, depending on

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the procedure to be performed, are perhaps switchedperioperatively onto faster and more malleable anti-coagulation therapy with heparin. Coagulation testsshould always be performed on the morning beforeoperation. In most cases, an INR of 2 is acceptable. Indental procedures, an INR of less than 4 is acceptablebecause local haemostatic measures can be used as anadjunct (see Ch. 26).

Disseminated intravascular coagulation (DIC)

DIC is a major complication seen in seriously ill orinjured patients. The triggers to DIC are multiple andinclude infections, malignancy and trauma. Inappropriateextensive coagulation occurs, often in fundamentallynormal blood vessels. This process uses up clotting fac-tors, fibrinogen and platelets, resulting in an increasedbleeding tendency.

Clinical features are paradoxically of both bleedingand organ dysfunction from ischaemic damage caused bymicrothrombi. Investigations show consumption offibrinogen and platelets, an increase in FDPs andderanged clotting studies. Treatment is based on theunderlying cause, along with supportive therapy andtransfusion of clotting factors and platelets that havebeen consumed. As can be appreciated, this is anextremely serious condition.

Massive blood transfusions

Stored blood has relatively low concentrations ofplatelets and clotting factors, particularly factors V andVIII. This is not only because of the short lifespan ofthese substances but also because platelets and clottingfactors are often removed from fresh blood for specificinfusions as described above. In addition to this, storedblood must contain an anticoagulant to prevent it clottingwhile in storage. Citrate, which binds ionised calcium, isused for this purpose. As outlined above, calcium is animportant cofactor in the coagulation cascade. Althoughthis effect of citrate is essential for storage, it means thattransfused blood has poor clotting ability. This is notusually a problem clinically, unless the patient hasreceived a 'massive transfusion' (defined as receiving atransfusion volume greater than the patient's normalblood volume, i.e. 4-5 L). If this happens, the recipient isreliant on transfused factors, of which there are notenough in stored blood. The recipient will thereforerequire simultaneous transfusion with platelets and

clotting factors along with calcium. The management ofsuch patients is again done in close collaboration with ahaematologist.

Abnormal clotting -increased clotting tendencyThis group of diseases is actually more prevalent thandiseases with increased bleeding tendency. Theirrelevance to surgical practice relates to an increased riskof deep venous thrombosis (DVT). Thrombosis can berecurrent or atypical, as in spontaneous axillary veinthrombosis.

Patients with suggestive features require referral tohaematology for further investigation before surgery.Patients already diagnosed with an increased clottingtendency require prophylactic measures against DVT nomatter how minor the procedure (Ch. 4). Patients whohave previously been diagnosed with such a problemmight already be receiving treatment with warfarin,which will alter operative preparation (see above).

Patients with anaemiaThere are many different forms of anaemia, and multiplecauses for each type. A description of these is beyond thescope of this chapter. However, the existence of anaemiain surgical patients has implications that are worth briefconsideration.

Anaemia is defined as a haemoglobin concentrationbelow an arbitrary designated level, which is generallyaccepted as 13 g/dL for men and 12 g/dL for women.Anaemia has a number of pathophysiological con-sequences of surgical relevance (Table 6.4) as a con-sequence of the decreased oxygen-carrying capacity ofthe blood.

Cardiorespiratory problems

The reduced oxygen-carrying capacity of the bloodresults in an impaired ability to cope with the stresses of

Table 6.4 Consequences of anaemia

Cardiorespiratory problemsImpaired wound healingPrecipitation of haemolysis

anaesthesia and surgery. For example, myocardialischaemia is more easily induced and might result in anincreased incidence of myocardial infarction (MI).Postoperative respiratory complications are less welltolerated.

Wound healing

Relative hypoxia impairs tissue healing, and increasesthe risk of infection (Chs 3 and 8).

Precipitation of haemolysis

The hypoxia of anaesthesia can induce haemolytic crisesin certain hereditary haemolytic anaemias such as sickle-cell disease. Preoperative planning, with or withouttransfusion, and careful anaesthesia aim to prevent this.

Operating on a background of anaemia will result inthe patient having fewer reserves to compensate foroperative blood loss. There might be associated depletionof other blood cells, including white blood cells (whichincreases susceptibility to infection) and platelets (whichincreases the bleeding tendency).

As a result, the haemoglobin concentration should bereturned to near normal preoperatively, for example, withiron therapy in elective patients (failure to respond couldindicate an alternative cause of anaemia), or transfusionfor emergency operations.

The oxygen-carrying capacity of transfused blood islowered by the presence of high concentrations of 2,3diphosphoglycerate (DPG) and hydrogen ions, whichshift the oxygen-haemoglobin dissociation curve to theright (this is known as the Bohr effect).

possesses anti-B antibody. AB possesses no antibodiesand is therefore the 'universal recipient'; group Oindividuals possess antibodies to both A and B.

The other major blood grouping is Rhesus factor, andpatients are either positive or negative.

Patients that are group O rhesus negative have no A orB antigens and no rhesus factor, and can therefore betransfused to other groups with minimal risk of reaction('universal donors').

Blood products

The range of blood products available is listed in Table6.5 and are discussed below.

Red cell concentrate (RCC)

Red cells are extracted and suspended in a near optimumsolution containing glucose, adenine, mannitol, sodiumchloride and citrate (the last prevents clotting). Cell lysisduring storage means that each unit contains a highconcentration of extracellular potassium. RCC has ahaematocrit of 65-70% and hence has poor flow charac-teristics. Simultaneous crystalloid infusion reduces thehaematocrit and provides volume repletion.

RCC is used for transfusion in patients with anaemiaand in those suffering acute blood loss, but it has areduced oxygen-carrying capacity (see above). It must beblood group ABO- and Rhesus-factor-compatible (seebelow).

One unit of RCC is derived from one donation. Theshelf-life is 35 days at 4°C. The volume varies by unit,but is approximately 400 mL.

Replacement of blood loss:transfusionWhole blood is rarely given because the scarce resourcesof donated blood are used more efficiently when given inconstituent parts. Blood is commonly fractionated into itsconstituent parts, which are used for specific indications.This ensures more efficient use of each unit of donatedblood.

It is essential that each patient is cross-matchedcorrectly before transfusion. Patients are groupedaccording to antigens expressed on their red blood cellsas A, B, AB and O. Each group contains antibodiesagainst foreign antigen, for example, group A blood

Platelets

Infused platelets are suspended in plasma (and thereforeinfusions contain some clotting factors). Full cross-match is not necessary before transfusion.

Table 6.5 Blood products

Red cell concentratePlateletsFresh-frozen plasmaCryoprecipitateFactor concentratesAlbumin solutionOther 43

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One unit is obtained from 4-6 blood donations. Theshelf-life is 5 days at room temperature and the volumeis 300 mL. No viral inactivation procedures are used inprocessing. Platelets are used perioperatively in patientswith thrombocytopenia.

Fresh-frozen plasma (FFP)

This is pure plasma that is separated and frozen shortlyafter donation. It contains all the plasma-derived clottingfactors, but has relatively low levels of factor VIII andfibrinogen. The shelf-life is 1 year at -30°C and itsvolume is 150-300 mL per unit. FFP is used for cor-recting factor deficiencies.

Cryoprecipitate

Contains high levels of factor VIII and fibrinogen. Again,the shelf-life is 1 year at -30°C. Each unit is approxi-mately 10-20 mL and the standard dose is 10 units.

Factor concentrates

Multiples are available and are either derived fromplasma or are manufactured using recombinant DNAtechnology.

Albumin solution

This is derived from whole blood after removal of cellsand factors. Shelf-life is 3-5 years. It is used to expandintravascular volume, although it has now been largelysuperseded by synthetic gelatin solutions such asgelofusin and haemacel. It is also used for fluid replace-ment after burns and during plasmapheresis

Other

There are multiple other blood products available fortreatment of more unusual conditions, including specificimmunoglobulins.

Complications

The complications of blood transfusion can beimmunological, infective or due to miscellaneous causes(Table "6.6).

Table 6.6 Complications of blood transfusion

Immunologicalimmediate haemolyticnon-haemolyticdelayed haemolytic

InfectiveMiscellaneous

fluid overloadhyperkalaemiacoagulation disorderhaemosiderosishypothermia

Immunological complications

Immediate haemolytic complications

This can result from mismatched blood-cell antigensbetween donor and recipient. The most importantantigens are those of the ABO system. These reactionsare severe and sudden and most often result from humanerror, for example if the wrong unit of blood is given tothe wrong patient because of a labelling, handling orpatient identification error. Activation of the complementsystem occurs when the recipient possesses antibodiesto an antigen on the donated red blood cells, andhaemolysis (breakdown of the red blood cells) ensues.

Clinically, the patient rapidly becomes unwell withfever, hypotension and difficulty breathing. Activation ofcoagulation can occur, leading to DIC. The haemoglobinreleased from the haemolysis, along with hypotension,can cause acute renal failure.

Treatment involves preventing further reaction bystopping the transfusion immediately. The patient mightrequire life-saving resuscitation, including measures tomaintain oxygenation and blood pressure. Intensive caremight be appropriate.

Where a reaction occurs, the unit of blood must bereturned to the laboratory, along with a cross-matchsample from the patient.

Non-haemolytic complications

Febrile, allergic and anaphylactic reactions can occur andwill necessitate immediate cessation of the transfusionand possibly medical resuscitation, depending on theseverity. Allergic and anaphylactic reactions might requireimmediate treatment with adrenaline (epinephrine), anti-histamine or corticosteroids.

Delayed haemolytic complications

These result from incompatibility of blood with regardsto less important antigens. They occur in patients whohave previously been sensitised to the antigens.Examples include Rhesus antibodies and rarer antibodiesto minor antigens such as Kell and Duffy. Haemolysisoccurs several days after the transfusion. The patient isnot generally acutely unwell and might develop jaundiceand anaemia several days after the transfusion.

Infective complications

Blood that is donated in the UK is routinely screened forHIV, syphilis, hepatitis B and hepatitis C. However, anumber of these diseases have a latent period before theirdetection is possible and so transmission of infection canstill occur. Before screening for certain diseases wasintroduced, many blood recipients were infected withhepatitis C and people with haemophilia contracted HIV.

The risk of transmission of infection is related to howmany donors the blood product was derived from and tothe pretransfusion treatment the product has received(see above).

Miscellaneous complications

Fluid overload

The volume load of the transfusion might precipitateheart failure in the elderly or those with a history of heartdisease, particularly as a unit of blood has to betransfused in less than 4 h. Prophylactic diuretic therapyis often given with a transfusion to prevent this. Centralvenous pressure monitoring, in a surgical high depen-dency or intensive care unit, can help to prevent this.

Hyperkalaemia

As mentioned above, stored blood has a high con-centration of potassium and when multiple units aregiven the recipient's serum potassium level can rise todangerous levels. Electrolyte levels must therefore bemonitored.

Coagulation disorder

This was considered under massive transfusion, above.

Haemosiderosis

Patients who receive regular or multiple blood trans-fusions can suffer from iron overload. Excess iron isdeposited in vital organs such as the pancreas, myo-cardium or liver, causing them to dysfunction. This isreduced by using an iron chelator such asdesferrioxamine.

Hypothermia

Blood is stored cooled to 4°C. If large volumes ofunwarmed blood are transfused the patient will sufferhypothermia. The role of blood warmers is particularlyimportant in trauma cases.

Summary and guidelinesBleeding is a potentially serious surgical complicationand a knowledge of the principles of coagulation and ofthe disorders that can precipitate bleeding is essential forall surgeons. Recognition and prevention of a problem isobviously preferable to having to deal with a haemor-rhaging patient, particularly if the problem could havebeen recognised and avoided.

A careful history is essential. This should include ahistory of any previous bleeding problem, especially ifrelated to surgery, a family history of any bleeding problemand a drug history, especially to note if the patient is onanticoagulants, aspirin or corticosteroids.

Examination should look for abnormal bruising orpetechiae, and telangiectasis around the mouth.

If there is any doubt, the advice of a physician orhaematologist should be sought before embarking oneven the most minor surgery.

Where a significant bleeding problem is encounteredat surgery, immediate control by compression should befollowed by urgent admission to hospital for investi-gation and correction of any coagulopathy.

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Cross-infection

IntroductionTo a large extent, the heightened professional and publicawareness of the potential for cross-infection in surgicaland other medical settings has followed the discovery ofhuman immunodeficiency virus (HIV) as the cause ofAIDS. However, although transmission of blood-borneviruses, especially hepatitis B, has been documented insurgical practice, many other microorganisms also pose asignificant threat and most of them are far moreinfectious than HIV. In surgery, bacteria are the majorcause of postoperative sepsis (see Ch. 8). These can beacquired from a number of sources, including the patient'sown bacterial flora and by cross-infection from othercontacts including - importantly - healthcare workerssuch as doctors and nurses.

The extent of the problem and other aspects importantin cross-infection will be considered as described inTable 7.1.

The extent of the problemSurgical-site infections account for 14-16% of allnosocomial infections and are the third most frequentlyreported nosocomial infection. A UK study published in1993 of the excess costs attributable to nosocomialinfection in surgical patients reported a mean extra cost

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Table 7.1 Aspects of infection control

Extent of the problemRoutes of transmissionUniversal infection controlOccupationally acquired infectionHealthcare workers infected with blood-borne virusesAntimicrobial prophylaxis in surgeryCreutzfeldt-Jakob disease

per patient of £1041 and an increased length of hospitalstay of 8.2 days. A more recent study has calculated thathospital-acquired infections (HAI) cost the NHS inEngland £1000 million per annum, and it is believed that5000 patients die of HAI in the UK every year. Similarlylarge figures are available from the USA where, in 1992,the cost of treating nosocomial infections was estimatedat $4.5 billion, of which $1.6 billion was allotted tosurgical-site infections (SSI). These data highlight theenormous problem posed by infection for the healthservices and indicate the importance of measures toimprove infection control.

Routes of transmissionThe possible routes for cross-infection in surgery aresummarised in Fig. 7.1. Direct contact is an importantmechanism of transmission for hospital-acquiredinfections, particularly in surgical units. The bestexample is the fundamental role played by hands asvectors for spread of microorganisms. Many infectionsacquired in hospitals are transmitted on the hands ofhealthcare workers and it is known that regular hand-washing between the examination or treatment ofindividual patients results in a significant reduction in thecarriage of potential pathogens on the hands. Hand-washing has, therefore, been stressed as a simple, cheapand highly effective infection control intervention.Unfortunately, both European and US studies haveshown repeatedly that handwashing compliance rates inhospitals are lower than 50%. The use of alcoholic handrubs, rather than handwashing, is now recommended bysome authorities as a convenient means of improvingcompliance with hand hygiene protocols.

It has been recognised for many years that healthcareworkers can acquire occupational infections, for examplehepatitis B, from patients they are treating. Transmission

w7

Fig. 7.1 Routes of cross-infection in surgery.

of these infections can occur by direct contact with thepatient or indirectly through contact with contaminatedinstruments or surfaces. More recently, there has beenconsiderable professional and media interest in thepossible risk of patients becoming infected from health-care workers who are themselves carriers of blood-borneviruses (see below).

Some microorganisms are transmitted by dropletspread and aerosols are, therefore, another importantpotential mode of spread of infection in surgery. Air-borne spread of infection is a major hazard, for example,in total joint replacement surgery, and use of 'hyper-sterile' (laminar airflow) operating theatres can play animportant role in preventing infection.

Finally, there is a risk that patients might becomeinfected from instruments or other items contaminated

during treatment of a previous patient. Effective sterilis-ation of instruments, which is central to all infectioncontrol policies, will prevent this route of transmission.The importance of thorough decontamination andsterilisation of used surgical instruments cannot be over-stressed. However, the emergence of prion diseases, inparticular variant Creutzfeldt-Jakob disease (vCJD), isnow proving a major challenge, because these agents areresistant to standard sterilisation procedures (see below).

Universal infection controlIn the light of the multiple routes of transmission notedabove, the key principles that underpin modern infectioncontrol procedures are shown in Table 7.2. These applyin all healthcare settings, including dental surgery.

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Table 7.2 Principles of universal infection control

Many different pathogenic microorganisms pose aproblem

There are many sources of infectionAny patient might be a carrier of pathogenic

microorganismsRoutine procedures must be effective in preventing

cross-infectionAll blood, regardless of source, is potentially infectiousThe same cross-infection control procedures must be

used for all patients

First, although there is widespread concern aboutblood-borne viruses such as HIV, a wide range of patho-genic microorganisms is encountered in clinical practice.Thus, attention must be given to preventing the spread ofall infections, both rare and common.

Second, there are many potential sources of infection,most of them unrecognised. For example, carriers ofhepatitis B virus frequently appear clinically well and areunaware of their carrier status. Similarly, patients couldbe colonised by antibiotic resistant bacteria, such asmethicillin resistant Staphylococcus aureus (MRSA),with no outward clinical signs or symptoms. Thus anypatient, regardless of background or medical history,must be considered to pose an infection risk.

The logical conclusion to these concepts is theadoption of universal infection control, whereby everypatient is treated as a potential carrier. The infectioncontrol protocol adopted must be sufficiently stringent toreduce the risk of contamination of patients or staff to alevel that is highly unlikely to cause infection. It alsofollows that patients who are known carriers of pathogens,including blood-borne viruses, will pose no additionalrisk and can be treated safely under the same operatingconditions.

Table 7.3control

Key elements of universal infection

Medical historyCleaning instrumentsSterilising instrumentsUse of disposablesDecontamination of operatory surfacesProtective workwearAvoiding needlestick injuriesImmunising staffSafe waste disposalEffective training of staff

of previous infectious diseases the clinician must beaware that it does not allow for the categorisation ofpatients into 'high risk' and 'low risk' from the point ofview of infectivity to staff and other patients. One currentexception to this concept relates to patients who fall intothe risk groups for CJD (see below).

Cleaning instruments

The cleaning of used surgical instruments to removevisible deposits is an essential step prior to theirsterilisation. In hospitals, both the cleaning and the sub-sequent sterilisation procedures are usually performedin a Central Sterile Supply Unit (CSSU). However,increasing amounts of minor surgery are performed inprimary care and, under these circumstances, thedecontamination of used instruments might be performedin a medical or dental practice. In such cases, instrumentcleaning may be achieved by hand scrubbing in soap ordetergent, but ultrasonic baths and washer disinfectorsare very useful and more effective for many items. Heavy-duty protective gloves should be worn during instrumentcleaning, and care taken to avoid sharps injuries.

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Key elements of universal infection control

The key elements of universal infection control are listedin Table 7.3 and will be discussed in turn.

Medical history

The collection of an accurate medical history is part ofgood clinical practice and is helpful in the identificationof immunocompromised patients. However, although amedical history can provide useful information in respect

Sterilising instruments

After clinical use, all surgical instruments must besterilised before they are used to treat a subsequentpatient. The sterilisation method of choice for heat-stableinstruments is the autoclave. It is critical that the steammakes physical contact with the surfaces of all theinstruments and care must be therefore be taken not tooverload the autoclave and impede steam penetration.Effective monitoring of autoclave efficacy is important.Physical, chemical and biological tests of efficacy areavailable; for example, a chemical indicator strip can

be placed in the centre of the load as a check on theeffectiveness of each cycle of a bench-top autoclave.

Hot air ovens are microbiologically acceptable as asterilisation measure and are used for specific purposes,such as the sterilisation of greases. However, the highertemperature and longer cycle time (160°C for 60 min)make them more damaging to instruments and they arenot ideal for routine sterilisation procedures.

Chemical agents such as aldehydes are notappropriate for routine sterilisation of surgical items andequipment. They are unreliable and some are toxic orcorrosive. However, for certain expensive, heat-sensitiveitems such as endoscopes, high level disinfection withchemicals, under strictly controlled conditions, isemployed.

In the light of concerns over the resitance of prions tosterilisation procedures, there are now calls for the'tagging' (e.g. by bar coding) of all individual surgicalinstruments. This would permit the recording, in apatient's notes, of exactly which instruments were usedand so introduce 'traceability' of instruments into therecycling process. It would, however, be a massivelogistical exercise with major cost implications.

Use of disposables

Disposable items are generally recommended, althoughthere is a cost implication. Disposable items must alwaysbe used once only and then discarded. The routine use ofdisposable instruments for surgery involving tissues thatpose a risk from vCJD, for example tonsillectomies, hasbeen recommended in the UK.

As needles cannot be reliably cleaned and sterilised,they must always be discarded into a sharps bin after useon a single patient. Similarly, a local anaestheticcartridge must never be used for the treatment of morethan one patient.

Decontamination of operatory surfaces

Good hygiene in healthcare facilities is an important andunderrated element of infection control, with particularrelevance to surgical sepsis. In addition to generalenvironmental contamination, surfaces in clinical areascan become contaminated with microorganisms follow-ing contact with tissues and body fluids of patients.Regular cleaning of surfaces with detergent, togetherwith application of disinfectants in appropriate sites, areessential. Other 'surfaces' can also pose a problem, for

example the pens used by healthcare workers, many ofwhich have been shown to be contaminated withpathogens such as MRSA.

In the event of an overt spillage of blood or other bodyfluid, it should be soaked into an absorbent cloth and adisinfectant such as hypochlorite (l0 000 ppm availablechlorine) applied. Alternatively, commercially availablespillage granules could be used.

Protective workwear

All staff should wear protective coats on wards to protecttheir outdoor clothing from contamination. However,white coats themselves become contaminated withmicroorganisms, especially at points of frequent contact,such as the sleeve and pocket. Indeed, the uniforms wornby healthcare workers have been shown to play a role intransmitting bacteria in the hospital setting and theimportance of hygiene, with regular laundering ofuniforms, should again be stressed. Appropriate theatredress, including operating gown, gloves and eyeprotection must be worn routinely when undertakingsurgical procedures, together with a well-fitting surgicalfacemask.

Avoiding needlestick injuries

Sharps injuries are common among staff performingsurgical procedures and many go unreported tooccupational health departments and so are not followedup. However, occupationally acquired infections withhepatitis B and C viruses, and with HIV, have beenrecorded following needlestick injuries and relatedsharps accidents. It is, therefore, essential that healthcareworkers are encouraged to seek appropriate managementfollowing such incidents. The principles of managementof needlestick and related injuries are discussed below.Although some of these injuries are unavoidable, manyare essentially preventable and great care must be takenwhen handling and disposing of all sharps.

Needles should never be resheathed after use, unless asafe resheathing device is used. Care must also be takennot to injure other staff, for example when sharpinstruments are being passed between surgeons andnurses. Unsheathed needles must never be left exposedwhere others might injure themselves. All contaminatedsharp items must be discarded into a sharps box (seebelow) and staff must never put their hands into theopening of the box.

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Immunising staff

Vaccination against hepatitis B virus is now a require-ment in the UK for all healthcare workers undertakingexposure-prone procedures. This vaccine, which containshepatitis B surface antigen (HBsAg), provides protectionfrom one of the most important and serious occupationalinfections of healthcare workers. The course of threedoses of vaccine must be followed by a blood test toensure that the recipient has developed a protective levelof antibody.

For healthcare workers who are non-responders to thevaccine, further serological tests are required to ensurethat they are not high-risk carriers of hepatitis B. High-risk carriers are those who are HBeAg positive or whoare HBeAg negative but with a viral load exceeding 103

genome equivalents per mL. Such individuals pose apotential risk of infection to patients and would not bepermitted to undertake exposure-prone procedures,which clearly include all forms of surgical practice.

Immunisation against other infectious diseases suchas tuberculosis (in the UK), tetanus and poliomyelitis isalso recommended and non-pregnant female personnelof child-bearing age should be protected against rubella.

Safe waste disposal

Hospitals have a responsibility to ensure the safe disposalof all contaminated waste generated during surgery.Arrangements must be made with a local authority orprivate contractor for final collection and disposal.Regulated waste includes contaminated sharps, liquidblood and other body fluids, tissues, and non-sharp solidwaste that is saturated or caked with body fluid.

All sharp items must be consigned to rigid, puncture-resistant containers, which should never be filled to morethan two-thirds of their capacity. The containers shouldbe securely closed and fastened before uplift forincineration. Soft waste contaminated with blood mustbe placed into sturdy, impervious, sealed bags andclearly labelled as infective waste.

Effective training for staff

Good training of all staff engaged in patient care is animportant element of infection control. Good infectioncontrol procedures should become an automatic partof clinical practice for all healthcare workers but,unfortunately, they are often not afforded the priority

they deserve. A written infection control policy must beavailable in all healthcare facilities and proceduresreviewed on a regular basis. The overseeing of all aspectsof infection control in hospitals, including training, is theresponsibility of the Infection Control Committee, whichis usually chaired by a Consultant Medical Microbiologist.This committee will also include one or more speciallytrained Infection Control Nurses, who play an importantrole in dealing with day-to-day cross-infection issues inhospitals.

Occupationally acquiredinfectionsThe main concern of healthcare workers relates to therisk of infection with blood-borne viruses, notably HIV.Hepatitis B remains the major infectious occupationalhazard for surgeons and other healthcare workers who,prior to the availability of a vaccine, were up to ten timesmore likely to become infected than members of thegeneral population. Table 7.4 summarises the relativerisks of infection with HIV and hepatitis B virus.Hepatitis B virus is far more infectious than HIV and it isfortunate that most healthcare workers respond to thehepatitis B vaccine, thereby gaining protection.

According to the most recent figures available, thetotals of 'definite' and 'possible' occupationally acquiredHIV infections have amounted to 319 cases worldwide.These have comprised 102 definite (5 in UK) and 217possible (8 in UK), most of which followed sharpsaccidents with large-bore needles.

The occupational risk of infection with hepatitis Cvirus is not yet clear but several recent studies suggestthat the overall risk is low. However, well-documented

Table 7.4 The relative risks of occupationalinfection with HIV and hepatitis B virus (HBV)

HIV HBV

Minimum volume of blood 0.1 mL 0.00004 mLto transmit infection

Risk of infection following 0.3% 7-30%*needlestick injury from aseropositive patient

*The risk of infection with hepatitis B virus depends onwhether the source patient is a high-risk carrier

seroconversions following needlestick accidents havebeen reported and emphasise the importance of avoidingsuch injuries.

Other infections can be occupationally acquired bysurgeons: there is a documented occupational risk forhealthcare workers of infection with Mycobacteriumtuberculosis. There is no evidence of an occupational riskfor healthcare workers from prion diseases such as CJD.

Management of sharps injuries

Prevention of sharps injuries is extremely important butit is recognised that, within healthcare facilities, andparticularly during surgical procedures, such incidentsare still fairly common. A significant proportion areessentially preventable if staff follow guidelines onhandling sharps and, in addition, many commercialcompanies are now developing new 'needle-less'devices. However, it is impossible to eliminate the riskscompletely. The effective management of sharps injuriesis, therefore, an important issue in the prevention ofoccupationally acquired infections with blood-borneviruses; it also has medicolegal implications.

Every hospital should have a policy and procedurefor managing sharps injuries, and this should be wellpublicised and readily available to all staff. Theprinciples of management are summarised in Fig. 7.2. Allsuch events should be officially recorded in an accidentbook. Immediate first aid involves cleaning the woundunder running water, without scrubbing or manipulation,and the application of a waterproof dressing. Expertmedical advice should then be sought.

Ideally, blood should be taken at the time of theaccident from the healthcare worker and the titre of anti-HBs antibody measured. Residual serum is stored so thatit is available in the future for HIV and hepatitis C virusantibody testing, if necessary.

Although the concept of approaching the sourcepatient is controversial, ideally blood should also becollected from this individual. Appropriate discussionand counselling are obviously essential but, if consent isgiven, the blood can be screened for hepatitis markersand HIV antibody, which in most cases will be negative.Such information can be very reassuring to a healthcareworker who has sustained an injury, but no pressureshould be exerted on the source patient to donate theappropriate sample.

Immediate treatment for the healthcare worker mightinclude passive immunisation for a hepatitis B vaccine

Fig. 7.2 Management of sharps injuries.

non-responder, or a vaccine booster for those whose anti-HBs antibody titre has waned. The administration ofprophylactic azidothymidine (AZT) for those who havesustained an injury from a known HIV-positive patienthas been controversial but recent evidence suggests that,in combination with other antiretroviral drugs, it canfurther reduce the risk of infection. Such prophylaxis isnow officially recommended for significant injuries andshould be administered promptly, ideally within 1 h ofthe injury. However, the treatment is not without side-effects and the risk assessment of the injury should bemade in conjunction with a physician who is experiencedin this area.

Healthcare workers infectedwith blood-borne virusesThere is strong epidemiological evidence that healthcareworkers who are high-risk carriers of hepatitis B virus, asdefined earlier, can transmit hepatitis B to patients if they

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procedures are those in which there is a risk that injury tothe worker could result in the exposure of the patient'sopen tissues to the blood of the healthcare worker. Thosewho are HBsAg positive but not HBeAg positive, andwhose viral load does not exceed 103 genome equivalentsper mL, are permitted to continue with exposure-proneprocedures, providing they have not been associated withspread of infection to patients.

Apart from the case in which a Florida dentist withAIDS apparently transmitted HIV to several patients,there is only one other report of an HIV-infected health-care worker transmitting the virus to a patient. Thisinvolved an HIV-seropositive orthopaedic surgeon inFrance, who apparently transmitted HIV to a patientduring hip surgery in 1992. At the time, the surgeon wasasymptomatic and unaware of his infection. Thus,currently available data suggest that the risk of trans-mission of HIV to patients from HIV-infected healthcareworkers is extremely low. Nevertheless, healthcareworkers who are known to be HIV seropositive are notpermitted to undertake exposure-prone procedures inthe UK.

There is increasing epidemiological evidence thathepatitis C virus can be transmitted from seropositivehealthcare workers to patients during exposure-proneprocedures. UK guidelines published in 2002 placerestrictions on the clinical activities of healthcare workerswho are infected with hepatitis C (HCV RNA positive).

Antimicrobial prophylaxisduring surgeryA number of factors can increase the risk of surgical siteinfection and these are considered in detail in Chapter 8;they can be patient-related or procedure-related (seeTable 8.2). The risk of surgical site infection also dependson whether the surgical procedure is a clean, clean-contaminated, contaminated, or dirty-infected procedure(see Table 8.3).

Improvements in operating room ventilation, sterilis-ation methods, barriers and surgical techniques have allhelped to reduce the incidence of surgical site infections,but the use of topical, oral and intravenous antimicrobialprophylaxis has also played an important role. However,in the current climate of increasing antimicrobialresistance, it is important that prophylaxis is notoverused but is reserved for well-defined indications.

Table 7.5 Goals of surgical prophylaxis

Prevent postoperative infection of the surgical sitePrevent postoperative infectious morbidity and mortalityReduce the duration and cost of health careProduce no adverse effectsHave no adverse effects for the microbial flora of the

patient or hospital

Perioperative antimicrobial surgical prophylaxis isrecommended for operative procedures that have a highrate of postoperative wound infection, when foreignmaterials are to be implanted, or when the woundinfection rate is low but the development of a woundinfection results in a disastrous event. It is beyond thescope of this chapter to provide details of all thosesurgical procedures for which prophylaxis is indicatedbut examples include colorectal surgery and joint replace-ment surgery. The goals of an anti-infective drug usedfor surgical prophylaxis are summarised in Table 7.5. Toachieve these goals, an ideal prophylactic antimicrobialagent should be bactericidal, non-toxic, inexpensive andhave in vitro activity against the common organisms thatcause postoperative wound infection after a specificsurgical procedure.

There is no benefit in commencing intravenousantimicrobial therapy before the perioperative period.Normally, prophylactic antimicrobial agents should beadministered no more than 30-60 min before surgery.A common practice is to administer the intravenousprophylactic agent at the time of induction ofanaesthesia. Therapeutic concentrations of antimicrobialagents in tissues should be present throughout the periodthat the wound is open. For prolonged procedures, orantimicrobial agents with short half-lives, an additionaldose may need to be administered intraoperatively. Theduration of antimicrobial prophylaxis for most proce-dures is controversial, but expert opinion recommends atmost one or two postoperative doses. Prolonged prophy-laxis should be discouraged because of the possibilityof added antimicrobial toxicity, selection of resistantorganisms and unnecessary expense.

Creutzfeldt-Jakob diseaseThe transmissible, spongiform encephalopathies (TSEs)comprise a group of neurodegenerative disorders causedby infection with agents called prions. This group of

undertake exposure-prone procedures. E-prone

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diseases includes sporadic, familial and iatrogenic formsof Creutzfeldt-Jakob disease (CJD). The description ofa new form of CJD, now called variant CJD (vCJD),together with evidence that it is caused by the same agentas bovine spongiform encephalopathy (BSE), hassignificantly raised the profile of the TSEs.

The relevance of TSEs to this chapter is that thesediseases are causing serious concerns in relation to infec-tion control procedures. Prion proteins are remarkablystable and resistant to most conventional sterilisationmeasures. Iatrogenic transmission of human priondiseases via neurosurgical instruments has been reportedand there is some evidence that transmission via othersurgical procedures can also occur. For the sporadic,familial and iatrogenic forms of CJD, the tissues inwhich there is a high level of infectivity are the brain,spinal cord and eye. However, the position is furthercomplicated because vCJD differs from the sporadic,iatrogenic and familial forms in that the lymphoreticulartissues of vCJD cases are also consistently infected withprion proteins.

Current guidelines are that all the instruments used ina surgical procedure on a patient suffering from a TSEmust be disposable and destroyed by incineration. Inaddition, current recommendations from the SpongiformEncephalopathy Advisory Committee suggest using themedical history form to identify patients who may be atrisk of (although not clinically suffering from) iatrogenicor familial forms of CJD. Questions enquire about

previous brain surgery (to identify possible recipients ofdura mater grafts), growth hormone use before the mid-1980s (after which artificially synthesised growthhormone came into use), and close family members whomight have had CJD (to identify those at risk of familialCJD). For patients who are identified as being at risk, anysurgery involving the brain, spinal cord or eye should beundertaken using disposable instruments that are' sub-sequently incinerated. Surgery involving other tissues insuch patients is ideally also undertaken with disposableinstruments and, if non-disposable instruments are used,they must pass through a stringent decontaminationprocess, separately from other instruments. This involvestwo washing cycles and a total of 18 min in a porous load(vacuum) autoclave.

However, no questions in the medical history willidentify those patients at risk of sporadic or vCJD. Thelatter is a major concern because of the infectivity inlymphoreticular tissues. The number of cases of vCJD inthe UK is still low (122 confirmed cases to 3 February2003), and a preliminary screening study of vCJD reactivityin approximately 3000 archived tonsils and appendixspecimens revealed no positive results. However, there isstill concern among many experts that an epidemic,linked to consumption of meat from BSE-infected herds,could develop. The routine use of disposable instrumentsfor all patients undergoing certain surgical proceduresthat involve high-risk tissues is now being given seriousconsideration and, where practicable, implemented.

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Surgical sepsis

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IntroductionThe principles of the control of cross-infection werediscussed in Chapter 7. Sepsis as a specific complicationof surgery is considered in this chapter (Table 8.1).

The body possesses a complex system of mechanismsto protect itself from infection. These include:

• methods to prevent entry of bacteria into the body,such as skin and mucous membranes, which act as abarrier to penetration by organisms

• the mucociliary apparatus in the respiratory tract,which washes bacteria from the respiratory tract

• methods to deal locally with organisms if theymanage to invade the body tissues, for example, thelocal inflammatory reaction resulting in cellulitis andabscess formation

• methods to deal with organisms if they start to invadetissues, including lymph node reaction and systemiclymphocyte response.

Surgery predisposes to infection by affecting the bodydefences at all levels. It also causes a breach in theprotective barrier, allowing organisms a portal of entry.However, tissue damage will also inhibit the inflam-matory response locally by causing tissue ischaemia orby formation of haematoma. Surgery also affects thesystemic response of the body to trauma.

Thus, postoperative sepsis may be local - affectingthe wound itself - or sepsis may occur at a remote site.Chest sepsis is the most common remote site infectionbut other sites may be involved. For example, patientsmay be predisposed to chest sepsis if they have a pre-existing upper respiratory tract infection, if they smokeor if they have chronic lung disease such as asthma orbronchiectasis. An example of sepsis at another site isurinary tract infection resulting from a poor catherisationtechnique. Factors that may increase the risk of wound

Table 8.1 Wound infection following surgery

Classification of woundsInfecting organismsPrevention of wound infectionsClinical features of wound sepsisDiagnosis of wound sepsisTreatment

Table 8.2 Factors that may increase the risk ofsurgical site infection

Patient-relatedagenutritional statusdiabetes mellituscanceruraemiajaundicesmoking statusobesitycoexisting infection at a remote sitecolonisation with microorganismsaltered immune response, e.g. HIVdrugs, e.g. corticosteroids, anti-inflammatories,

chemotherapylength of preoperative stay

Procedure-relatedduration of surgical scrubskin antisepsispreoperative shavingduration of operationoperating room ventilationinadequate sterilisation of instrumentsforeign material at the surgical sitesurgical drainssurgical techniquehaematomapoor blood supply

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sepsis are listed in Table 8.2. These may be patient-related or they may be local, procedure-related factors.This chapter will concentrate primarily on wound sepsis.

Wound infection is defined as a collection of pus in awound. In the initial phase of bacterial penetration of thetissues, the body will host an inflammatory responseagainst the invading organisms to try to contain them inthe area and to destroy them. This inflammation will beapparent clinically as cellulitis, which is a tender rednessof the tissues. However, a similar response may resultfrom inflammation from other causes (e.g. haematoma,excess tissue handling or trauma during surgery). Becauseof this, the presence of cellulitis alone may not alwaysindicate infection.

One can only be sure that a wound is infected whenpus forms, hence the above definition. Studies comparingmethods to control wound infection only discuss woundswhere pus is confirmed to be present.

For a wound infection to occur, there must be asufficient number of organisms inoculated into thewound (>107 viable cocci must be injected into a woundin a normal person to cause an abscess) and conditionswithin the wound area must be suitable for growth of theorganisms. The presence of necrotic tissue, haematoma,seroma and foreign bodies all predispose to sepsis.

Classification of woundsCertain wounds are more prone to infection than others.Surgeons therefore divide wounds into different typesaccording to the level of risk of sepsis (Table 8.3).

Clean wounds

These are wounds in which no viscus has been entered,no septic area has been encountered and there has beenno break in aseptic technique. Such wounds should neverbecome infected; infection rates with such woundsshould be less than 3%.

Clean contaminated wounds

In this situation, the operation enters a non-infected areabut may encounter bacteria. Careful control of the areashould result in minimal spillage of organisms. Examplesof this include surgery on the upper gastrointestinal tract,biliary tree or respiratory tract. Infection rates for thistype of surgery should be less than 10%.

Table 8.3 Classification of wounds

Clean woundsClean contaminated woundsContaminated woundsDirty wounds

Contaminated wounds

This is surgery where there is gross spillage oforganisms, where there is infection already present butwithout pus formation, where there is a major break inaseptic technique or where there is an open wound thathas been exposed for less than 4 h (e.g. following majortrauma). In this type of wound, sepsis frequently exceeds30%.

Dirty wounds

This is an operation through an infected area (e.g.perforated viscus, abscess or traumatic wound) that hasbeen exposed for over 4 h. By definition, all these woundsare infected.

This classification of wounds allows comparative studiesto be conducted between centres and of varyingtechniques to try to control wound sepsis. It also allowssurgeons to monitor their own data to ensure that they areachieving acceptable standards of surgery with regard tosepsis.

Infecting organismsInfecting organisms can be subdivided into two types.

Exogenous organisms

Exogenous organisms are organisms introduced into awound from an external source. The two main exogenousorganisms responsible for wound sepsis are Staphy-lococcus aureus and Streptococcus pyogenes. These areencountered much less frequently than they used to be,with the exception of patients with trauma and/or burns,in whom they are as prevalent as ever. When woundsepsis occurs with these bacteria, it usually indicates abreakdown of sterile surgical technique. The longer anoperative procedure, the more likely the procedure is tobecome infected by an exogenous organism.

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Endogenous organisms

Endogenous organisms are bacteria that are usuallypresent in the body but are non-infective under normalcircumstances. Such organisms are known as commensals.These organisms are encountered in clean-contaminated,contaminated and dirty wounds. Such organisms arecommon in gastrointestinal surgery, for example,Escherichia coli, enteroccocci and Bacteroides species.In clean-contaminated and contaminated wounds, whereit is expected that a significant number of organisms maybe encountered, the use of prophylactic antibiotics givenfrom the time of surgery has been shown in many casesto significantly reduce the risk of wound infection. Suchuse of antibiotics, however, must not be seen to be analternative to meticulous and careful atraumatic surgicaltechnique.

Excessive use of prophylactic antibiotics is notwithout problems, for example, allergic side-effects tothe drug, development of bacterial resistance to specificantibiotics and cross-transfer of these resistant strainswithin the hospital environment (see Ch. 7).

Prevention of woundinfections'Clean wounds' lend themselves to studies of techniquesof control of infection. When the wound sepsis rate ofclean wounds is unacceptably high, it suggests that aproblem within the unit is allowing the introduction oflarge numbers of exogenous organisms into the operationfield.

The infection rate due to exogenous organisms hasreduced dramatically because of aseptic techniques. It isimpossible to sterilise the atmosphere in an operatingtheatre, to sterilise the skin of a patient completely and toavoid the carrying of microorganisms into the operatingarea by theatre personnel. However, equipment anddrapes can be sterilised and much can be done to reduce

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Table 8.4 Prevention of wound infection

EnvironmentTheatre personnelPatient preparationOperating techniqueProphylactic antibiotics

the transport of organisms to the patient's wound. Keyelements of universal infection control were discussed indetail in Chapter 7 but factors relating specifically toprevention of wound infection (Table 8.4) are discussedhere.

Environment

The design of a modern operating theatre with laminarair-flow and air-filtering systems has significantlyreduced the number of organisms in the atmosphere. Inrecent years, however, further advances have made littleeffect on wound sepsis rates because most infections arenow endogenous in nature.

The longer the duration of surgery and the greater thenumber of personnel in theatre, the higher the woundsepsis rate.

Theatre personnel

Contamination of a wound occurs easily from theatrestaff.

The surgeon, theatre assistant(s) and nursing staffshould wash/scrub their hands and forearms with anantimicrobial agent such as chlorhexidine or povidone-iodine to reduce bacterial load on the skin. The initialscrub of the day is the most important and should includea careful nail scrub and a wash lasting at least 5 min.Thereafter, scrubbing for further operations requires onlya 1 min careful wash and nail scrubbing is no longernecessary. This reduces the numbers of skin organismsbut, after 30 min, the bacterial count on the skin starts torise again and may exceed the prescrub levels after 2 h.Staff in intimate contact with an operation shouldtherefore wear suitable sterile protective clothing withsterile gowns and gloves. As there can be a glovepuncture rate of up to 10% by the end of an operation,many surgeons now double-glove. This may also protectthe surgeon from organisms that might be acquired froma patient.

The use of theatre masks is controversial, withevidence to suggest that they are ineffective within arelatively short period of time.

The number of personnel in theatre should be reducedto the minimum, with little movement of staff throughtheatre while surgery is being undertaken.

Staff with a severe upper respiratory infection or sorethroat should be excluded from the theatre area.

Patient preparation Prophylactic antibiotics

Patients who have been inpatients in hospital for asignificant period prior to surgery tend to develop a skincontamination of 'hospital-acquired' organisms. Thesebacteria tend to be highly resistant to commonly usedantibiotics. In such patients, bacterial scrub the nightbefore surgery may be beneficial, although this isunproven.

Any patient harbouring an infection at a site distant tothe operation wound has a significantly increased risk ofwound sepsis, perhaps doubling the incidence. Thereforeany patient with an infected lesion should have thistreated before surgery is contemplated.

Shaving the skin in the area of the operation on thenight before surgery has now been shown to increasewound sepsis rates. Tiny nicks in the skin acquirebacterial contamination, which is at a much higher levelthan in the unshaven skin. Hair removal by clipper isadvised, or it should not be done at all. Certainly, ifshaving is to be performed, this should be done in theanaesthetic area immediately before surgery is about totake place.

Various skin preparation agents for 'sterilising' theskin in the operation field are available, the mostcommonly used being chlorhexidine and povidone-iodine. A double wash is traditionally performed and theoperation area is covered with sterile drapes leaving onlya window for surgery. However, it is not possible tosterilise skin completely by the use of such agents.

Operating technique

Surgical technique is most important in control of woundsepsis. Wound sepsis rates vary between surgeons and arealmost certainly related to individual technique such ascareful handling of tissues, removal of all foreign bodiesor dead tissue, avoiding the use of excess diathermy andsutures, avoiding excessive suture tension, accurateplacement of sutures, and avoiding the formation ofhaematoma. Monofilament sutures are probably asso-ciated with less wound sepsis than braided suturematerials.

A careful audit comparing one surgeon's infectionrates with those of another surgeon usually results in asteady reduction in infection, and this is certainly relatedto increased careful technique. Surgeons should thereforekeep a close audit of their own sepsis rates and, if theyare unacceptably high compared with other surgeons,must address the reasons for this.

As discussed in Chapter 7, antibiotics have been shownto reduce wound sepsis in clean/contaminated andcontaminated wounds only. The use of antibiotics inclean wounds is of no value in reducing wound sepsis butthey should always be given if there is insertion offoreign material or if the patient has cardiac valvulardisease. This is especially important during dentalprocedures.

Clinical features of woundsepsisClassically, wound sepsis produces a tachycardia andpyrexia approximately 2–4 days postsurgery. The patientusually complains of increasing pain in the wound,perhaps exceeding that noted immediately after surgery.

The features of an infected wound usually developvery rapidly. The wound develops a cellulitis, perhapswith some purulent material oozing from the surface ofthe incision or from the suture sites. The wound thenbecomes oedematous and bronzed in appearance withmarked swelling. Attempted palpation reveals a markedlocal increase in temperature and exquisite tenderness.

At this point, removal of some or all of the suturesresults in release of pus and the wound margins will thenbe noted to be lined with slough.

In severe cases, haemorrhagic vesicles may appear,with areas of frank necrosis of tissue.

Especially after bowel surgery, the surgeon shouldalways be aware of the fact that the sepsis may be arisingfrom the peritoneal cavity and not just be superficialunder the skin. Severe wound sepsis may result incomplete breakdown or dehiscence of the wound,necessitating wound resuture.

Diagnosis of wound sepsisThis is usually made on clinical grounds alone.Bacteriology culture swabs may allow confirmation ofthe infecting organism(s) and their antibiotic sensitivity.This is especially useful if the patient does not seem to beresponding satisfactorily to apparently adequate therapyand knowledge of the infecting organisms now obtainedby such swabs will allow a more accurate choice ofantibiotic to be made.

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TreatmentInitial treatment of a suspected wound infection isusually by antibiotics. The choice depends on the type ofwound and the nature of the surgery. In contaminated andclean/contaminated wounds, antibiotic therapy maymerely consist of continuing the prophylactic antibioticoriginally used. Certainly, if there is severe or spreadingcellulitis, antibiotic usage is essential and may be moreeffective if given intravenously.

Where there is obvious pus formation, sutures shouldbe removed from the skin and the wound allowed to gapeor, if necessary, probed. Any pus obtained should beforwarded to the bacteriologist for culture. If there is nosignificant cellulitis, lymphangitis or lymphadenopathy,simple release of pus may be all that is indicated andantibiotics may not be necessary.

After release of pus, the wound should be left open. Itmay be filled with antiseptic packs. There are manydifferent techniques and agents available for dressingsuch wounds and each unit tends to have its ownpreferences. Normally, an infected wound is left to healby granulation from below, with the packs being changedregularly to keep the wound as clean as possible and toallow the granulation to fill the cavity. When the woundis clean and granulating, if it is large, it may besecondarily resutured. In many instances, however, thesewounds reheal rapidly without the need for resuturingand, as soon as the wound has healed by granulation, itwill rapidly re-epithelialise.

Abdominal wounds that have been badly infected andallowed to heal by this method are commonly weakened,with the subsequent formation of incisional hernia.

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Fractures

IntroductionA fracture is a break in the continuity of bone; it can becomplete or incomplete. Fractures are the cause of aconsiderable degree of morbidity and even mortalityacross all age groups. Patients suffer both in the shortterm from pain and in the long term from disability anddeformity. These effects are, in the main, largely prevent-able. A sound appreciation of the principles of fracturesand their management has a profound effect on patients'quality of life, not only in orthopaedics but in many otherspecialties including maxillofacial and oral surgery,neurosurgery and accident and emergency surgery.

A discussion of the aetiology of fractures is followedby their diagnosis and classification. The process offracture healing will also be discussed, followed byconsideration of the management of fractures and thecomplications that can occur (Table 9.1).

This chapter deals with the general principles offracture management and gives specific examples asappropriate. The detailed management of maxillofacialfractures and its variance from general principles isconsidered in Chapter 12.

Aetiology of fracturesFractures can be caused by a number of differentmechanisms (Table 9.2) and this leads to a variation inthe pattern of fractures. The vast majority of fractures arecaused by an excessive force applied to that bone,causing it to break. Biomechanics are the key in relationto bony injury, both in terms of the injury sustained andits appropriate management. A direct force applied to abone will cause a fracture at the site of impact. Indirectforces cause fractures distant to where the force isapplied, such as spiral long-bone fractures.

Table 9.1 Important considerations in themanagement of fractures

Aetiology of fracturesDiagnosis of fracturesClassification of fracturesFracture healingPrinciples of management

treatment of closed fracturestreatment of open fractures

Complications

Table 9.2 Mechanisms of bony fracture

Direct forceIndirect forceStress fracturesPathological fractures

The pattern of fractures also differs with age, relatingto the nature of the patient's skeleton and bone stock.Different types of bone tend to show different types offracture. For example, cancellous bone, when put undersufficient stress, generally undergoes crush fracture,which can be comminuted.

The history will indicate which injuries are likely tobe present and will help to direct investigation. Forexample, in the driver of car involved in a road trafficaccident, the presence of a broken windscreen will alertto the probability of head and facial injuries.

Stress fractures are caused by repeated relativelyminor injury. Their exact aetiology is not known butagain, a detailed history alerts to their possibility as, forexample, in a runner with painful metatarsals.

Pathological fractures occur in abnormal bone. Theforce applied would not normally be enough to cause abreak if the bone was normal. The weakness of the bone

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9

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can be caused by very many disease processes. The mostcommon underlying pathologies for pathological fracturesinclude osteoporosis and malignant infiltration of thebone, either secondaries or rarely primaries. Naturally,the diagnosis of a pathological fracture, and the under-lying pathology, have a bearing on appropriate subsequentmanagement.

Diagnosis of fracturesClinical examination

Injuries to bone are often present in combination withother injuries, and initial consideration should be directedto the patient as a whole and particularly if there is needfor resuscitation.

The fundamentals for diagnosis are based on historyand examination. History has been alluded to above. Adetailed clinical examination, with emphasis directed bythe history not only indicates which investigations arerequired for definitive diagnosis but also alerts to injuryof underlying or surrounding structures.

Look, feel, move is a good way to approach theexamination of bony injury:

• Look: for signs of injury; swelling is often the mostuseful sign. Fractures are associated with a greaterdegree of swelling than soft tissue injuries. Thedistribution of the swelling can also be enlightening.For example, if confined to the joint, swelling canindicate excess fluid or blood in that joint. Deformitygenerally leaves little doubt about the existence ofunderlying bony injury. Bruising might be present ifthere is delay in presentation. It is important to lookfor and document the integrity of the skin overlyingthe injury, as this will allow classification into open(compound) or closed fractures, and will affectmanagement. Colour - particularly distal to the injury- will give clues to vascular status.

• Feel: palpation needs to be done carefully, butsufficiently firmly to give the answers. Often largeareas around the site of injury are tender, but it isimportant to elicit the area or areas of maximumtenderness to direct subsequent investigations, andfocus analysis of those investigations. Temperatureof the injured area should be noted and may indicateinfection, for example, if presentation is delayed.

• Move: initially, patients should be asked to performrelevant movements themselves. If there is significant

injury minimal movement is possible. Often patientsfeel that they are unable to move any of the joints in alarge surrounding area such as a whole limb. Careful'passive' movements can be carried out, alwaysgently and never forcing the movement.

Other tests

The important structures most commonly affected bylimb fractures are either blood vessels or nerves and it isessential to document neurovascular status around, andparticularly distal to, all fractures. Vascular compromisein particular will alter immediate management, in anattempt to restore blood flow.

Vascular

Pulses and capillary refill distal to the site of injuryshould be assessed. Although this is performed at thisstage in a systematic examination, an early assessment ofvascular status should be carried out, for example duringpreliminary history taking.

Neurological

Sensory and motor function should be tested in thedistribution of nerves that may have been affected by theinjury.

Other

Surrounding structures can be affected and are oftenfracture specific. Tendons might be disrupted by thesharp edges of the fracture, for example in the hand. Anystructure lying in proximity to the fracture is at risk andcareful examination should be carried to assess fordamage to underlying structure, such as orbital blow-outfractures (where the inferior rectus can be tethered) orpelvic fractures (where there might be urethral injury);rib fractures can cause lung injury or pneumothorax.

Radiographic examination

There is no place for blanket radiographs. Clinicalsuspicion is of paramount importance. Radiographs aresometimes indicated where bony tenderness cannot beexcluded. For example, unconscious trauma patients musthave cervical spine films.

Radiographs of at least two views at 90° to each otherare essential. A fracture cannot be excluded without theseviews and accurate classification and description of anobvious fracture cannot be complete without them.

Obvious signs of bony injury show as disruption ofthe cortex. However, cortical breaks can be difficult tosee and clinicians should develop a systematic routine forreviewing radiographs that involves tracing around thecortical lines. It is useful to stand back from the radio-graph to assess if its overall appearance is normal, andalso whether the general state of the bone looks normal.

Once a fracture is seen, it is important to look forother fractures associated with it. Rings of bone rarelybreak in only one place and a second fracture should besuspected, for example, in the pelvis or mandible. It mightbe necessary at this stage to obtain further radiographs(e.g. of the joint above and below the fracture).

It is sometimes necessary to rely on more subtleevidence that is visible radiographically. The only clue toa bony injury might be surrounding soft tissue swellingor blood visible within usually empty spaces, such as inmaxillary sinuses.

Further imaging

When used appropriately, plain radiographs have bothhigh sensitivity and specificity. However, they can befallible and, in the presence of a negative radiograph,reliance is on clinical suspicion. If either the mechanismof injury or the clinical examination suggests a particularinjury then further imaging is necessary.

Further plain radiographs might be indicated, eitherdifferent views or films taken with a joint in a particularposition or under stress (for example, flexion/extensionviews).

More sophisticated forms of imaging might benecessary and computerised tomography (CT) scanningis particularly good at showing bony detail. Magneticresonance imaging (MRI) is excellent at showing softtissue detail. Radioisotope-uptake bone scans also have arole in advanced investigation.

Classification of fracturesFractures are classified in many different ways, and oftenthe same fracture is classified simultaneously a numberof different ways. For example, a single fracture can beopen, pathological, displaced, oblique, intra-articular andunstable.

Table 9.3 Classification of fractures

SiteExtentConfigurationOverlying skin integrityPathologicalDisplacementAngulation, rotation, impaction and distractionJoint involvementStability

The following classifications are the most commonand most helpful with regards to treatment and referringthe patient to a surgeon who will undertake treatment(Table 9.3).

Site

The most important consideration is which bone isfractured and which part of that bone is fractured, clearlydocumenting the side, for example, fractured right distalthird of radius.

Extent

This differentiates between a complete disruption ofcortex and a partial disruption of cortex or a crack.Incomplete fractures are more common in children andare known as greenstick fractures.

Configuration

This is essentially the shape or direction of the fractureline. Transverse fractures extend at right-angles to thecortical surface. Oblique fractures are as their namesuggests, as are compression fractures. Spiral fracturestend to occur in long bones and are the result of twistingforces applied distant to the fracture site. 'Comminuted'means that there are a number of bone fragments.

Overlying skin integrity

A breach in the skin over a fracture makes the fractureopen or compound and changes the subsequent manage-ment required, the principles of which are consideredlater in this chapter.

Open fractures can be further classified with regardsto how 'open' they are (the Gustillo and Anderson

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Table 9.4 Classification of open fractures

Grade I : less than 1 cm woundGrade II: greater than 1 cm woundGrade III: extensive skin and soft tissue damage

IIIA: wound can be covered with remainingsoft tissue

IIIB: wound cannot be covered with softtissue, periosteal stripping

IIIC: associated arterial injury

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classification), which has bearing on how likely it is thatthe wound will become infected (Table 9.4).

Pathological fractures

Pathological fractures were considered on page 59, underthe heading 'Aetiology of fractures'.

Displacement (apposition)

A fracture is displaced if the two ends are not in exactanatomical apposition. This is caused by the force of theinjury and/or the action of muscles around the fracturesite. The degree of displacement or shift is often describedsubjectively (e.g. 'moderately' displaced). However,perhaps a more useful description is a measurement ofthe displacement, for example with respect to the widthof the fractured bone. Correcting displacement has animportant impact on fracture healing, deformity andfunction.

Angulation, rotation, impaction and distraction

These are other forms of deformity relating the fractureends to each other. Angulation can be thought of as tiltbetween the ends, and rotation is the degree of twist.Impaction is where the ends are forced into each otherand distraction where there is a gap between the ends inthe axis of the fractured bone. All of these can also resultin healing and functional problems and they mightrequire close clinical and radiological examination todetect them.

Joint involvement

If the fracture line extends into the joint it disrupts thearticular surface and can be regarded as intra-articular.This predisposes to long-term sequelae, mainly osteo-

arthritis. This type of fracture therefore requires anaccurate degree of reduction.

Stability

Unstable fractures are those whose positions are prone tochange. This is often the case even after initial reduction.These injuries therefore require more immobilisation, forexample, with internal fixation. Unstable fractures of themandible are specifically discussed in Chapter 12.

Fracture healingThe process of fracture healing can be convenientlydivided into stages (Table 9.5). It is important to realisethat these stages are not discrete entities, but ratheroverlap and blend into one another. Mediators and factorsaffecting fracture healing are broadly similar to thoseinvolved in wound healing (described above).

Inflammatory phase

• Bleeding and clot formation: bleeding occurs fromthe fracture ends, predominantly from periosteal andendosteal vessels. A clot forms between the ends ofthe fracture.

• Acute inflammatory reaction and swelling: aninflammatory infiltrate of white blood cells invadesthe clot and fracture site. Resultant swelling causesloosening of the periosteum.

• Bone necrosis: blood vessel disruption deprivesosteocytes at the fracture end of oxygen and theyundergo necrosis.

• Macrophage infiltration: macrophages and osteoclastsare recruited to the area and remove dead materialincluding bone.

Table 9.5 Stages of fracture healing

Inflammatory phasebleeding and clot formationacute inflammatory reactionbone necrosisgranulation tissue

Reparative phaseprovisional callushealing across fracture gap

Remodelling phase

• Granulation tissue: the blood clot is organised byaround day 3–4 and osteoblasts are generated withinit. Simultaneously, locally released factors stimulateangiogenesis, revascularising the area.

Reparative phase

• Provisional callus: the organised clot containsfibroblasts producing collagen, chondroblasts andosteoblasts laying down matrix. The initial result is amixture of cartilage and connective tissue calledfibrocartilage. This material matures, over the courseof 2-6 weeks, into bone, and is described as callus.

• Healing across fracture gap: ossification begins at thefracture ends, starting subperiosteally. Initiallyrelatively immature and less stable woven bone isproduced. Over 6-12 weeks, ossification occursthroughout the provisional callus, bridging thefracture gap. At the same time, maturation to morestructurally robust lamellar bone occurs and thefracture is united.

Remodelling phase

The healing fracture site continues to adapt to itsenvironment and particularly the forces applied to it forup to 2 years. Different bones have different capacities toremodel and children have a marked ability to remodelcompared to adults, particularly the elderly.

Principles of managementThe patient must be considered as a whole, not asisolated injured parts. As always, the priority is to treatlife-threatening injuries by way of resuscitation. Bonyinjury can indeed be life threatening in itself and hencerequire early treatment, as in the case of maxillofacialfractures such as Le Fort III, which can displace andobstruct the patient's airway, and pelvic fractures, bloodloss from which can cause haemorrhagic shock.

With regards to orthopaedic injuries the priority is totreat limb-threatening injuries such as displaced fracturescausing vascular compromise.

Analgesia is an important early consideration for theobvious reason of patient comfort but also to combat thepathophysiological effects of pain and distress.

Definitive fracture management is determined by thetype of fracture. A fundamental distinction is manage-ment of open compared to closed fractures.

Table 9.6 Treatment of closed fractures

ReductionImmobilisation

plastertractionexternal fixationinternal fixation

Stress and movement

Treatment of closed fractures

The treatment of closed fractures is outlined in Table 9.6.

Reduction

Reduction should be carried out without any delay ifvascular compromise is present, and should takeprecedence over investigation including radiographs.Provided the blood supply is unaffected reduction can becarried out under more considered circumstances.

Reduction is often not required. This is the case withminimally displaced fractures where the process ofremodelling will compensate in the long term.

Where reduction is required, it is ideally effected byclosed manipulation, thereby minimising the risk ofintroducing infection to the fracture site. It is importantto provide adequate analgesia for reduction and thiscan involve regional or general anaesthesia, with theirattendant risks. These risks of reduction might outweighthe benefits where the displacement or deformity willresult in no loss of function.

Different fractures require differing accuracy ofreduction. In general, alignment is more important thanapposition, which the process of fracture healing is goodat compensating.

Intra-articular fractures are a group that requirereduction to as close to the anatomical normal as possible.This is mainly due to the risk of osteoarthritis. Often, thiscan be achieved by closed manipulation. More precisereduction can be achieved by operative open reduction,and this is indicated when closed reduction has notproduced a satisfactory result including if there are softtissues interposed between fracture ends. This is also thecase for extra-articular fractures. Fractures that requireinternal fixation are reduced operatively to the positionthat they are to be held in, during the same operation.

Open reduction requires a form of anaesthesia and -importantly - breaches the protection against infectionthat the skin provides.

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Immobilisation

A degree of movement at the fracture site is beneficialfor fracture healing, by providing a stimulus to callusformation.

Splintage can be thought of as artificial callus put inplace early on. It prevents excessive movement at thefracture site, relieving pain and keeping the fracture endsin close proximity to undergo healing and union, andtherefore also minimising deformity.

There are several methods available for providingimmobilisation; the indications, risks and benefits aredescribed below.

Plaster

Plaster casts are easy, cheap and safe. Modern plastermaterials are light, waterproof and easy for the patient tomanage. They allow patients to mobilise and go homeearly and maintain the fracture in good position. How-ever, they allow little movement, particularly of the jointssurrounding the fracture, and therefore predispose tostiffness.

Plaster casts are most suitable for fractures that areminimally displaced, or those that have been adequatelyreduced and whose new position is stable.

The main dangers of casts are if they are appliedincorrectly. A tight cast can act as a constraint and hencecause a kind of iatrogenic compartment syndrome. Thisis particularly the case shortly after injury, or manipu-lation, and often a 'backslab' (i.e. a plaster that does notgo around the whole circumference of the injured part) isapplied.

Pressure sores can occur within the plaster and skinbreaks can be induced by the patient trying to relievethe itch in the plaster, for example with a knitting needle.These predispose to infection.

Traction

This is used to immobilise some long bone fractures.Force is applied along the long axis of the fractured bone,distracting the fracture ends and keeping them aligned.Traction devices can be attached to bone, skin or band-aging on the injured body part.

External fixation

Pins or screws are inserted proximal and distal to thefracture site, and these 'anchors' are attached to a rigid

external device. This allows unique manipulation and canalso act as a form of localised traction device, or evenprovide a force compressing the fracture ends together,helping to bridge a fracture gap. Wounds can be left opento drain and to be easily inspected with external fixation,and skin reconstruction can be carried out around it.

The types of fractures best treated by external fixationare those that would benefit from the above features,particularly fractures at risk of infection or with signifi-cant soft tissue damage, such as open fractures. Externalfixators are unsightly but, more important, they preventnormal force loading of the fractured bone, slowinghealing. Although the force applied through the devicemight be excessive, for example resulting in overdistraction of the fracture ends, the same device can bemanipulated to compensate this. However, externalfixators are not devoid of the risk of infection and pin-track infection is a considerable problem that can resultin chronic osteomyelitis.

Internal fixation

This form of immobilisation is achieved by open,operative reduction of the fracture, which is then held inplace by any number of devices, most of which are metal,that are left in place and the wound closed over them.The variety of products available is enormous andincludes pins, plates and screws, the particular indi-cations for which are generally fracture specific. Theseare considered further in Chapter 12.

The main advantage of this form of treatment is theaccuracy of reduction that can be achieved and indeedmaintained by the firm immobilisation provided.

This high degree of rigidity at the fracture site is notcompletely beneficial, however, as it does not inducecallus, as previously mentioned. However, the maindisadvantage of internal fixation is the higher risk ofinfection. Not only is the skin's barrier to infectionbreached at operation but microorganisms also tend tostick to prosthetic materials, including metal. Infectionon metal implants is hard to clear, as little systemicantibiotic gets to the site, as do few of the body's naturaldefences. Other complications include fracture of theinternal fixation device, particularly if it takes too great aproportion of the load rather than the healing bone.

Stress and movement

Physiological loading of the fracture site not only allowsearly return of function but also aids healing in the short

term by stimulating callus formation, and in the longterm by providing the basis of remodelling. Early move-ment and physiotherapy of areas and joints around thefracture site help prevent stiffness and deformity in thelonger term.

The caveat is inducing excessive movement at thefracture site, which can also delay healing. This is adelicate balance and the degree and duration ofimmobilisation is fracture specific, and often even patientspecific. Therefore regular clinical review is essential, asis close communication with paramedical specialtiessuch as physiotherapy.

Treatment of open fractures

The main risk of an open fracture per se is that ofinfection. This risk is the result of breach of the barrierprovided by skin, the presence of foreign material anddead tissue in the wound, and impaired blood supplypreventing the body's innate defences getting to the areaas normal.

One of the main principles of treatment is thereforeprevention of infection. This cannot be instituted tooearly and the wound should be covered with a non-adherent sterile dressing as part of first aid management.Ideally, this dressing should be left in place. Antibioticprophylaxis should be given early, as there is inevitablysome delay in definitive management. Intravenous broad-spectrum antibiotics are indicated to cover Gram-negative, Gram-positive and anaerobic organisms.Tetanus immunisation status should be considered earlyand a booster given if indicated. Operative treatment isbased on the principles of debridement and fixation.

Current thinking is to aggressive debridement,removing all foreign material and dead tissue. Thoroughwashing of the wound should be followed by excision ofappropriate tissue. Several visits to theatre might berequired as it becomes apparent postoperatively thatfurther tissue is not viable. Although this can result in asignificant defect, a clean wound is amenable to laterclosure and reconstruction, whereas an infected wound isultimately likely to produce more of a defect. A commondilemma at initial operation is whether to close the wound.In general, only small, clean wounds with minimal softtissue damage should be closed at the initial operation.The fracture ends need to be washed and reduced to anacceptable position. Holding the fracture in the reducedposition is most often achieved with external fixation,which allows best drainage of the wound. Occasionally,

fixation is achieved with plaster or traction. Internalfixation is relatively rare because of the risk of infectionof the implants; however, in experienced hands, and inparticular fractures, it can produce the best results (seeCh. 12).

A postoperative course of antibiotics should becontinued irrespective of the method of fixation.

Complications of fracturesand fracture healingAs discussed in Chapter 4 'Complications of surgery',it is helpful to divide complications into general andspecific (or local), and to subdivide with regards thetimeframe they occur in - early, intermediate and late(see Table 4.10).

General

Early

As alluded to earlier, attention must be paid initially toassociated injuries, most often to other systems, thatmight require life-saving resuscitation treatment.

Injuries to bones, particularly the pelvis and longbones, can result in significant blood loss into the pelviccavity or soft tissues that can cause shock in their ownright, or exacerbate shock of other causes.

Intermediate

Some patients require treatment in hospital and aresubjected to a degree of immobility. This predisposesthem to a number of conditions, perhaps most import-antly deep venous thrombosis (DVT) and pulmonaryembolism (PE). Prophylaxis for DVT is an importantconsideration in inpatients with bony injury, and mostcentres will have a form of protocol for this. Other risksof immobility include pneumonia, constipation andpressure sores, for which careful nursing prevention isthe best form of treatment. Patients requiring operativetreatment are exposed to the general risk of anaesthetic,as discussed in Chapter 10.

Fat embolism syndrome is a phenomenon seen 3 to 10days postinjury, and is most often seen following longbone or pelvic fractures. Clinically, it is characterised byan unwell patient with respiratory distress, who mighthave visible petechial haemorrhages, particularly on the

trunk. Other clinical indicators are tachycardia andpyrexia. Treatment is supportive. Crush syndrome is theconsequence of major trauma whereby muscle crushingcauses significant muscle destruction, with release ofproteins from the damaged muscle. These substancesprevent normal renal tubular function, and acute renalfailure and shock supervene. Treatment is again largelysupportive, with careful fluid and protein balance.Prevention is also important and includes radicalmeasures including removal of severally damagedtissues, e.g. amputation.

Late

Patients might be left with disability, deformity andhandicap. These factors can result in significant social,occupational and psychological sequelae.

Local

Early

The important local early complications have alreadybeen dealt with, being injuries to surrounding structuresincluding blood vessels and nerves.

Intermediate

Local problems occurring at an intermediate stage arelisted in Table 9.7.

Compartment syndrome

This phenomenon generally occurs within hours ofinjury and is associated with injuries in certain areas.Whereas compartment syndrome is most commonlyassociated with fractures, this is not always the case, as itrelates to soft tissue swelling. Swelling within arelatively fixed compartment (e.g. enclosed by bone and

non-compliant fascia) results in compression of the softstructures within that compartment. Both blood vesselsand nerves are squashed, reducing their blood supply andimpairing their function. Tissue ischaemia results in tissuedamage and oedema, and therefore further swelling,causing a vicious circle. This pathophysiology explainsthe symptoms, signs, sequelae and treatment of compart-ment syndrome.

The earliest symptom is of pain in the injured area.This might not seem terribly helpful but the pain ofcompartment syndrome is disproportionately greatcompared to the underlying injury and has a less-than-expected response to analgesics.

The area is exquisitely tender and pain is experiencedon stretching (passively) any muscles that are also beingsquashed within the compartment, or whose bloodsupply is impaired. From these early features there is aspectrum to the late features of compartment syndromethat should not be seen (as treatment will have beeninstituted). The late features are classically described asthe five Ps (Table 9.8).

A high level of suspicion allows monitoring andprevents occurrence. If compartment syndrome isdeveloping, constricting dressings and traction should beremoved and the area elevated to try to reduce oedema. Ifunresolving, it might be necessary to surgically decom-press the compartment, for example by fasciotomy.

Infection

Infection can seriously impair the physiological processof fracture healing described above, and is one of themore common causes of malunion and non-uniondescribed below. Infection is much more common inopen fractures and this is one of the main reasons theyare treated differently.

Another risk factor for the development of infection isthe insertion of foreign bodies. This is particularlyimportant when considering the insertion of metal suchas plates and screws.

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Table 9.7 Local intermediate problemscomplicating fractures

Compartment syndromeInfectionDelayed unionNon-union

Table 9.8 The five Ps of compartment syndrome

PalePulselessParaesthesiaPainfulParalysed

Delayed union Loss of function

In delayed union, fracture healing takes longer thanexpected. This is predominantly a clinical diagnosis withpersistent pain and excessive mobility at the fracture site.Even under normal circumstances, radiological uniontakes longer than clinical union.

There are numerous causes of delayed union and it isless common in cancellous bone than cortical bone.Infection is a common cause and the presence or absenceof infection has an influence on management. Otherimportant causes include poor alignment of the fracture(inadequate reduction), poor blood supply to the fracturesite and excessive mobility at the fracture site.

Non-union

Causes are similar to those of delayed union, with theaddition of interposition of soft tissues. A gap remainsbetween the ends of the fracture, which is radiographicallyvisible, and it might also be possible to see that themedullary cavities have sealed off. Clinically, the patienthas persistent pain and mobility, with or without crepitus,on stressing the fracture site. The diagnosis is thereforeboth clinical and radiological.

Treatment of abnormal fracture union depends onwhether there is infection present. Healing in thepresence of pus and dead bone (sequestrum) is unlikely,and surgical debridement with antibiotic therapy is oftenrequired.

Delayed union is classified into fractures withhypertrophic callus and hypotrophic callus. Where thereis excess callus, normal healing is the rule with a pro-longed period of immobilisation. Where there is minimalor no callus, healing is likely to remain inadequate andoperative treatment, for example with bone grafting maybe indicated.

Late

The late local complications are listed in Table 9.9.

Table 9.9 Late local complications of fractures

Loss of functionOsteoarthritisPost-traumatic ossificationNerve tendon and muscle complicationsAvascular necrosisSuedeck's atrophy

Uncorrected deformity can result in loss of function, asrelationships are no longer anatomical. Similarly, pro-longed immobilisation can result in soft tissue fibrosis,resulting in contractures, for example, fixed flexiondeformity. Other causes of dysfunction include muscleweakness and loose ligament complexes.

Osteoarthritis

Intra-articular fractures that are not correctly alignedresult in abnormal wear of the articular surface,Osteoarthritis. Altered biomechanics from a fracture, forexample, gait, can result in abnormal loads through jointsnot involved in the original injury, also leading topremature wear and tear.

Post-traumatic ossification

This is the laying down of bony elements within softtissues around the site of injury. Its aetiology is notknown. Clinically patients have pain and may have atender palpable mass. Treatment is with rest, and can befollowed up by elective excision of the affected tissues.

Nerve, tendon and muscle complications

Callus or irregularly healed fracture edges can impingeon adjacent tendons or nerves, with either rupture ordysfunction ensuing. These features are often fracturespecific, and seen in classic patterns. Muscles that havebeen involved in compartment syndrome die and contract,producing so-called Volkmann's contractures.

Avascular necrosis

Where the fracture disrupts the blood supply to a piece ofbone, it can undergo necrosis. An example is the femoralhead that derives some of its blood supply through thefemoral neck. The head of femur can undergo late death(avascular necrosis) following a fractured neck of femur,particularly if the fracture is displaced.

Suedeck's atrophy

This is a phenomenon of unknown aetiology, oftenprecipitated by trauma that might be thought to have

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been relatively insignificant. Clinically, it is characterised Treatment is by having an index of clinical suspicion,by persistent, burning pain. Joints are red and swollen, and early institution of physiotherapy and elevation. Ifand later the skin becomes shiny and atrophic. Radio- these measures are unsuccessful then treatments block-graphs show patchy reduction in bone density. ing sympathetic innervation to the area can be of benefit.

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General anaesthesia

IntroductionAnaesthesia means absence of all sensation; analgesiameans absence of pain. General anaesthesia is a statewhere all sensation is lost and the patient is renderedunconscious by drugs. Some anaesthetic agents havelittle analgesic effect whereas some analgesics producelittle sleep. Combinations of drugs are, thus, commonlyused in modern practice although, historically, aninhalational agent, such as ether or chloroform, was allthat was available and was used as a single agent.

The administration of general anaesthesia used tobe performed in a variety of settings, such as dentalpractices. Increased standards have now precluded thispractice and general anaesthesia should be performedonly by qualified anaesthetists in a hospital setting withaccess to appropriate medical support.

Some operations, such as cardiac surgery, areperformed only under general anaesthesia. Otherprocedures, such as dental extraction, can often beperformed under local anaesthesia with or withoutconcurrent sedation, even in small children.

It is important, because of the risks of generalanaesthesia alluded to below, that all methods of

Table 10.1 Aspects of general anaesthesia

Assessment of riskPreoperative assessment and premedicationInduction of anaesthesiaMaintenance of anaesthesiaMaintenance of the airwayInhalational anaesthetic agentsAnaesthetic gasesIntravenous agentsDrugs used to supplement anaesthesiaMonitoring during anaesthesiaPostoperative care

providing pain-free surgery are explained and the patientor guardian allowed to give informed consent to themethods of analgesia or anaesthesia to be employed (seeCh. 22).

The surgeon and the anaesthetist have a sharedresponsibility for the patient's wellbeing, and so anunderstanding of general anaesthesia is important for allsurgeons. General anaesthesia will be considered here, asdescribed in Table 10.1. Local anaesthesia for dentalprocedures is considered in Chapter 24.

Assessment of riskThe patient should first be made as fit as possible foroperation in the time available. Second, the anticipatedbenefits of surgery should outweigh the anaesthetic andsurgical risks involved. The overall mortality rateattributable to anaesthesia itself is approximately 1 in100 000, whereas a broad average of surgical mortality ismore than 1 in 1000. Factors that have been shown tocontribute to this mortality include poor preoperativeassessment, inadequate supervision and monitoring in theintraoperative period and inadequate postoperative care.

Audits of operative mortality commonly use theAmerican Society of Anesthetists' (ASA) physical statusscale (Table 10.2). Fitness for operation is always relativeto the urgency of the proposed procedure.

Preoperative assessmentand premedicationThe anaesthetist must see and assess the patient pre-operatively; failure to do so can be regarded as negligent.Many patients will be seen the night before surgery. Withincreasing economic pressures to admit patients on the

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Table 10.2 The American Society ofAnesthetists' physical status scale

Class IClass IIClass III

Class IV

Class V

Class E

A normally healthy individualA patient with mild systemic diseaseA patient with severe systemic disease that isnot incapacitatingA patient with incapacitating systemic diseasethat is a constant threat to lifeA moribund patient who is not expected tosurvive 24 h with or without operationAdded as a suffix for emergency operation

Table 10.3 Aspects of the preoperative visit

Evaluation of history and physical examinationOrdering of special investigationsInstitution of preoperative managementRisk assessmentDiscussion regarding anaesthetic management which

will involve patient consentPrescription of premedication

day of operation, a screening process must be used toidentify suitable patients. Preassessment clinics with acombination of nursing and medical input are increasinglybeing developed to improve efficiency and streamline'the patient journey'. They must run to carefully designedprotocols.

After a preoperative visit there should be no surprisesfor either patient or anaesthetist. The visit shouldestablish rapport with the patient and should allow timefor the various factors listed in Table 10.3.

History

A comprehensive history is important. It can revealdiseases, particularly of the cardiovascular and respir-atory systems (for which breathlessness and chest painare especially relevant). The identification of pregnancyis important because it is a contraindication to electivesurgery in the first trimester due to the risk ofteratogenicity. Later in pregnancy the patient faces therisks of regurgitation and aspiration of gastric contents.

A past history of HIV infection or other infectiveagents can affect both patients and their carers. A historyof previous anaesthesia can highlight problems of drugallergy, deep venous thrombosis or postoperative nauseaand vomiting. Anaphylaxis is the most serious of these.

Drug history

Many interactions can be potentially dangerous, forexample, anticoagulants might be a contraindication tospinal, epidural or other regional techniques; anti-convulsants might increase the requirements foranaesthetic agents and enflurane, a volatile anaestheticagent, should be avoided as it might precipitate seizures.Beta-blockers have negative inotropic effects and cancause hypotension. They can also mask a compensatorytachycardia, concealing evidence of blood loss. Plasmapotassium concentration should be checked in allpatients taking diuretics because they might havehypokalaemia and careful monitoring of plasma glucosecan be important in patients receiving insulin. Suchmeasures may require a special perioperative regime.Corticosteroids have many well-known complicationsand extra corticosteroid cover to compensate for arelative lack might be needed.

Social history

Ceasing smoking 12 h before surgery can improvethe oxygen-carrying capacity of the blood, althoughabstinence for a longer period is required to reduce theincidence of postoperative respiratory morbidity.Excessive alcohol can result in both hepatic and cardiacdamage. Acute withdrawal in alcoholics can result indelirium tremens, which will require both a sedative suchas a benzodiazepine agent and thiamine (vitamin B1).

Family history

The anaesthetist must be aware of hereditary traits suchas haemophilia and porphyria. Cholinesterase abnor-malities can lead to prolongation of muscle relaxantssuch as suxamethonium.

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Past medical history

This should elicit evidence of asthma, diabetes,tuberculosis, seizures or any chronic major organdysfunction.

Physical examination

A full physical examination is important to complementthe history but the anaesthetist will also pay particularattention to the upper airway with a view to assessing the

ease of tracheal intubation. This will involve assessmentof the teeth and extent of mouth opening and flexibilityof the neck.

Preoperative investigation of elective patients

Healthy patients less than 40 years old do not generallyrequire any preanaesthetic investigation. Only relevanttests should be ordered and these will reflect age,comorbidity and complexity of the surgery. Circum-stances where investigation would be important are listedin Table 10.4.

Other investigations, such as radiography of thecervical spine or lung function tests, will be undertakenfor specific indications.

Table 10.4 Indications of preoperativeinvestigations

Full blood countanaemiafemales post menarchecardiopulmonary diseasepossible haematological pathology, e.g.

haemoglobinopathieslikelihood of significant intraoperative blood losshistory of anticoagulantschronic diseases such as rheumatoid disease

Clotting screenliver diseaseanticoagulant drugs or a history of bleeding or

bruisingkidney diseasemajor surgery

Urea and electrolyte concentrationsmajor surgery >40 yearskidney diseasediabetes mellitisdigoxin, diuretics, corticosteroids, lithiumhistory of diarrhoea and vomiting

Liver function tests: these will be carried out when thereis any suspicion of liver disease

ECG>40 years asymptomatic male or >50 years

asymptomatic femalehistory of myocardial infarction or other heart or

vascular disease<40 years with risk factors e.g. hyperlipidaemia,

diabetes mellitis, smoking, obesity, hypertensionand cardiac medication

Chest radiographybreathlessness on mild exertionsuspected malignancy, tuberculosis or chest infectionthoracic surgery

Preoperative therapy

Patients with respiratory disease can be improved byphysiotherapy or bronchodilator therapy. Prophylacticantibiotics are required in those at risk of subacutebacterial endocarditis. Hypertensive patients can some-times require adjustment of their drug therapy to obtainoptimal control, but it is usually reasonable to proceedwith surgery if their diastolic pressure is below110 mmHg.

Postponement of surgery

If time allows, it is not sensible to anaesthetise a patientwith an acute upper respiratory tract infection andoperation might also have to be delayed for patients withcardiac or endocrine diseases that are not yet underoptimal control. Likewise, resuscitation and restorationof circulating blood volume can require delay inanaesthesia. Elective surgery should not be undertakenunless the patient has fasted for 6 h for solid food, infantformula or other milk, 4 h for breast milk or 2 h for clearnon-particulate and non-carbonated fluids

Premedication

Whereas reassurance and explanation remain the mostimportant components of the preoperative visit, drugscan be used to obtain one or a combination of the effectslisted in Table 10.5.

Anxiolysis is most commonly achieved with the useof benzodiazepines such as diazapem or lorazepam, andthese drugs also cause a degree of anterograde amnesia.Excessive secretions in the airway are less of a problemwith modern anaesthetic agents but can be reduced withanticholinergic drugs either given before or at operation.Three drugs commonly used in this circumstance arethe anticholinergic agents atropine, hyoscine and glyco-pyrronium. Vagal bradycardia, such as occurs with the

Table 10.5 Effect of premedication

Reduction in anxiety and fearAmnesiaReduction in secretionsPotentiation of the effects of general anaestheticsReduction in the volume and acidity of gastric contentsReduction in postoperative nausea and vomitingAttenuation of both the sympathetic and vagal reflexes 71

oculocardiac reflex, can be severe and atropine is protec-tive of all the above. Antiemetics such as metoclopramide,ondansetron or antihistamines are administered pre-operatively from time to time; metoclopramide alsoenhances gastric emptying. If it is desired to reducegastric acidity this can be achieved with sodium citrate,H2 blockers such as ranitidine or proton pump inhibitors.Alleviating the patient's anxiety is most important.

Preparation for anaesthesia

Preparation and communication are vital. Armed withinformation from the previous section and afterdiscussion between surgeon and anaesthetist, a plan ofaction should be formed that will include the assembly ofthe necessary staff, equipment for airway care andmonitoring, intravenous fluids and arrangements forproper postoperative and recovery facilities. The'preflight' check of the anaesthetic machine must becarried out and the nature of the operation to beperformed and consent checked with the patient. Thepatient must be on a tilting bed or trolley. Trained anddedicated anaesthetic assistance is essential.

Induction of anaesthesiaAnaesthesia can be induced by inhalational agents or bydrugs administered intravenously.

concentration (ETCO2) can be monitored; this ismandatory in intubated patients. As consciousness is lost,the airway will require increasing support, which willusually involve pulling up the patient's chin. It can alsorequire insertion of an artificial airway. This might be anoral or nasopharyngeal airway. A laryngeal mask airway(LMA) or an endotracheal tube can be inserted ifrequired. For endotracheal intubation without musclerelaxants the patient must be at a much deeper level ofanaesthesia. Airway obstruction is the most commonlyencountered difficulty. Scavenging systems are usuallyemployed to reduce environmental pollution fromexpired gases.

Intravenous induction

Induction of anaesthesia with an intravenous agent isused for most routine purposes and is the most appro-priate technique for most patients undergoing emergencysurgery. A cannula should be sited in a vein in the backof the hand or forearm to avoid the structures in theantecubital fossa or risk of intra-arterial injection of thebrachial artery. Sterility should be maintained and localanaesthesia used if a large cannula is required forinfusion of fluids. Prior to induction, the patient shouldbreathe 100% oxygen with a tight-fitting mask for 3 minor, alternatively, be asked to take four deep breaths tovital capacity.

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Inhalational induction

Inhalational induction is more commonly proposed foreither young children or those with an obstruction some-where in their airway (e.g. epiglottitis or a foreign body).Rapport and patient confidence are important to ensurethe patient's cooperation, and a gentle and gradualapproach should be used. An anaesthetic mask should beheld gently on or very near the face and the patientshould be talked to calmly and reassuringly while beingencouraged to breathe normally. It is common for nitrousoxide 70% in oxygen to be used; anaesthesia is graduallydeepened as the anaesthetist introduces a volatileanaesthetic agent by increments. Patient monitoring willhave been attached before induction and the patient isobserved carefully for skin colour; the pattern and rateof ventilation and the patient's pulse, blood pressureECG and arterial oxygen saturation by pulse oximetry(SpO2) should all be observed. End tidal carbon dioxide

Emergency/rapid sequence induction

This is most commonly employed for patients with a fullstomach and a risk of regurgitation and aspiration ofgastric contents, provided preoperative evaluationindicates no major difficulty with airway or intubation.With all preparations made, intravenous access securedand suitable assistance, the patient breathes 100%oxygen for 3 min on a tilting trolley. The assistant on theright of the patient applies firm pressure over the cricoidcartilage with thumb and index finger. This posteriorpressure compresses the oesophagus between the cricoidcartilage and the vertebral column. It is applied eitherjust before administration of the intravenous inductionagent or as soon as consciousness is lost. A predeterminedsleep dose of induction agent is followed immediately bya paralysing dose of suxamethonium. As soon as the jawbegins to relax, laryngoscopy is performed and theendotracheal tube placed. Cricoid pressure is maintained

until the cuff of the tube is inflated and correct placementis confirmed. This is intended to prevent regurgitationand aspiration. Further muscle relaxants are not normallygiven until control of the airway is secured, but thistechnique balances the greater risk of aspiration againstthe risk of losing control of the airway. Although thistechnique is commonly used for general surgicalemergencies, it should not be used where there is anyobstruction to the upper airway from trauma or inflam-mation and, in these circumstances, an inhalationaltechnique or awake intubation is more appropriate.

Positioning of the patient for surgery

Patient safety is paramount and the patient should bepositioned carefully, taking into account requirement forboth surgical and anaesthetic access. The anaesthetistmust be aware of the varying effects of differentpositions. Local pressure effects on nerves can result inpostoperative morbidity. Intraoperatively, the head-downor prone positions will make abdominal breathingdifficult. The sitting position requires careful support ofthe head and can result in cardiovascular instability frompooling of blood in the leg veins. The supine position isused for the majority of surgery. Aortocaval compressionin pregnant patients or those with large abdominalmasses can result in hypotension.

Maintenance of anaesthesiaSeveral options are available to maintain anaesthesia.Inhalational agents, intravenous anaesthetic agents orintravenous opioids can be used, either alone or incombination. Muscle relaxants are commonly used tofacilitate tracheal intubation and subsequent ventilationof the lungs. Regional anaesthesia can be used tosupplement any of these techniques.

Inhalational anaesthesia with spontaneous ventilationis appropriate for superficial operations where profoundmuscle relaxation is not required. The patient is allowedto breathe spontaneously and a volatile anaesthetic agentsuch as halothane, enflurane, isoflurane or sevoflurane isused with carrier gases nitrous oxide and oxygen. Mostanaesthetic machines will not deliver less than 30%oxygen and have an interlocking device to ensure this.These volatile agents are delivered from vaporisers,which are specially calibrated containers that will delivera constant percentage of agent irrespective of the gas

flow through them, temperature or pressure. Analgesiaas determined by the patient's response might also berequired.

Minimal alveolar concentration (MAC) is the minimalalveolar concentration of an inhaled anaesthetic agentthat prevents reflex movement in response to surgicalincision in 50% of subjects. This value is commonly usedas an index of relative potency and may be affected bythe patient's age and concomitant use of other drugs.

Signs of anaesthesia

The signs and stages of anaesthesia were originallydescribed by Guedel in patients premedicated withmorphine and atropine and breathing ether and air. Withnewer agents the stages are less clearly differentiated butthey remain a useful general guide.

Stage 1 - analgesia

This can be attained using nitrous oxide 50% in oxygenand provides 'relative analgesia'.

Stage 2 - excitement

This is seen with inhalational induction but withintravenous induction it is commonly bypassed. Theeyelash reflex is often lost at this stage. Breathing isirregular and laryngeal and pharyngeal reflexes are stillactive. Patients might hold their breath and any instru-mentation of the airway can produce laryngeal spasm.

Stage 3 - surgical anaesthesia

The patient develops rhythmic regular breathing and asthey descend through the four plains from light to deep,respiratory reflexes are progressively abolished. Patientscan no longer protect their own airway. The pupilsbecome central and are classically large, although, withthe newer agents, they are often much smaller than withthe older agents.

Stage 4 - stage of impending respiratory andcirculatory failure

In this stage, anaesthesia is too deep and brainstemreflexes are depressed by high anaesthetic concentrations.Anaesthetic agents should be withdrawn and oxygenadministered.

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Maintenance of the airwayMaintenance of the airway and of oxygenation is thecornerstone of safe anaesthesia. Inhalational agents canbe administered with a face mask, a laryngeal maskairway (LMA) or an endotracheal tube.

Face mask

Face masks come in various shapes and sizes and shouldbe chosen for the individual patient to provide anadequate seal. Nasal masks are used during dentalanaesthesia. The mask is held against the patient's faceand the mandible is held forwards because pressure onthe submental soft tissues can exacerbate airwayobstruction by pushing the tongue backwards. Thereservoir bag on the anaesthetic circuit should be seen tobe moving in and out with the respiratory movement ofthe patient. There should be no indrawing of thesuprasternal and supraclavicular areas - this indicatesobstruction. Breathing should be quiet; noisy ventilationor stridor provides further evidence of obstruction. Itshould be always remembered that total obstruction issilent as there is no movement of air. An oropharyngealor Guedel airway can be used to assist in maintenance ofthe airway (Fig. 10.1).

Laryngeal mask airway

Laryngeal mask airways (LMAs) can be considered ahalfway house between a face mask and an endotracheal

tube (Fig. 10.2). They avoid the need for trachealintubation during spontaneous ventilation while at thesame time providing a clear airway without the need tohold on a mask. They can also occasionally be used toassist with difficult intubation.

They should not be used in patients who are at risk ofregurgitation of gastric contents because an endotrachealtube is required to provide secure protection and therewill be occasions when surgical access could beobstructed by the bulk of the cuff on the LMA.

Endotracheal intubation

An endotracheal tube provides the most secure airwayshort of tracheostomy. It is passed via the mouth or noseand between the vocal cords into the larynx. The cuff onthe tube lies below the cords and when it is inflated withair protects the respiratory tract from blood, secretions orinhalation of gastric contents. Likewise, the cuff preventsleakage of air travelling upwards during controlledventilation. The tube also allows access for suction of therespiratory tract. Cuffed tubes are used in adults, whereasuncuffed tubes provide an acceptable seal in children.

There are a multitude of designs for laryngoscopes.The McGill laryngoscope is favoured for childrenbecause their epiglottis is floppy. It has a straight bladeand is designed to lift the epiglottis anteriorly, exposingthe larynx. The Mclntosh laryngoscope, which has acurved blade, is designed so the tip lies anterior to theepiglottis in the vallecula and pulls the epiglottisanteriorly to expose the vocal cords.

Fig. 10.1 Guedel airway in place.Fig. 10.2 Laryngeal mask airway covering the glottis butnot occluding the opening to the oesophagus.

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Laryngoscopy

The position of the patient's head and neck is importantand was classically described as 'scenting the morningair'. The neck is flexed by raising the patient's head ona pillow and the head is extended. The laryngoscope,which is a left-handed instrument, is inserted into theright side of the mouth and pulls the tongue to the left asit is advanced slowly downwards. With the patient on hisor her back, the laryngoscope is thus pulled upwards andaway from the anaesthetist, avoiding levering against theupper teeth. This should reveal the dark, almosttriangular orifice of the glottis. External pressure on thethyroid cartilage can allow better visualisation. The tubeis placed through the glottis and its position withinthe airway should be confirmed by auscultation andmonitoring of expired CO2.

For nasal intubation, slightly smaller tubes are usedafter the introduction of vasoconstrictor into the nostrilsto reduce bleeding.

Tracheal intubation can be undertaken under generalanaesthesia but, where difficulties are anticipated, a tubecan be inserted over a fibreoptic endoscope under localanaesthesia.

Extubation

Patients can be extubated supine if there is no risk ofregurgitation but it is often safer to remove theendotracheal tube with the patient in the lateral recoveryposition. Prior to extubation the patient is given 100%oxygen and suction is performed to remove secretionsfrom the endotracheal tube and from the mouth. Afterextubation the patient's clear airway, ability to breath,cough and clear secretions are carefully assessed whileoxygen is continued by face mask. Laryngeal spasmoccurs if the vocal cords come together as a result ofirritation. A 'crowing' sound is heard and the patient willshow signs of airway obstruction. This is treated byclearing secretions and applying positive airway pressurewith oxygen. Occasionally, reintubation might be required.

Inhalational anaesthetic agents

The range of inhalational anaesthetic agents is listed inTable 10.6.

An ideal inhalational agent should be pleasant andnon-irritant to breathe. It should also be potent and yetproduce minimum depression of cardiovascular andrespiratory systems. It should be safe for repeat

Table 10.6 Inhalational anaesthetic agents

Diethyl etherHalothaneEnfluraneIsofluraneSevofluraneDesflurane

administration and it should be neither flammable norexplosive.

Diethyl ether

Diethyl ether has been abandoned in the West because ofits flammability, but it remains in widespread use in lessdeveloped countries. As it has a higher therapeutic ratiothan more modern agents, it is relatively safe foradministration in the hands of unskilled individuals. Itsuse is limited because it is highly irritant to the respir-atory tract and can cause coughing, breath holding andprofuse secretions. However, at deeper levels it was atone time a recommended treatment for bronchospasm.

Halothane

Halothane is again less commonly used, having been inwidespread use for over 30 years. There has been con-cern because of the rare occurrence of hepatic toxicityafter repeated administrations and it is also a depressantof myocardial contractility. Arrhythmias are also verycommon during halothane anaesthesia. Myocardialexcitability is seen, particularly in the presence ofhypercapnoea, hypoxia and with increased circulatingcatecholamines. Halothane should not be used incombination with local infiltration of adrenaline.

Enflurane

This is a clear, relatively pleasant-smelling agent. Incommon with the other agents it produces a dose-dependent depression in ventilation and tidal volume. Itproduces less depression of the cardiovascular systemand is associated with fewer arrhythmias than halothane.It should be avoided in people with epilepsy.

Isoflurane

Isoflurane produces less myocardial depression thanhalothane or enflurane. It is rather pungent and less

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suitable for inhalational inductions. A large multicentrestudy in North America showed no significant outcomedifferences between these three agents.

Sevoflurane

Sevoflurane, popular for some time in Japan, was onlyintroduced to the west in the 1990s. It is now the mostcommonly used agent for inhalational induction as it ispleasant and non-irritant, and might have a lessdepressant effect on breathing. Solubility characteristicsallow a more rapid induction of anaesthesia. Recovery isalso usually rapid.

Desflurane

Another new agent, desflurane, is the most recent additionto the volatile agents. It has to be given via a heatedvaporiser and allows very rapid alterations in the depth ofanaesthesia with recovery being faster than with any ofthe other agents.

Anaesthetic gasesNitrous oxide

Nitrous oxide delivered via a pipeline or from bluecylinders is used with oxygen as a carrier gas for thesepotent volatile agents. As the MAC value for nitrousoxide is over 100%, it cannot be used with oxygen as ananaesthetic agent without the addition of a potent volatileagent, but it has proved safe over a long period in use. Itis important that a high inspired oxygen concentration isgiven when nitrous oxide administration is discontinued.Nitrous oxide has also been incriminated in alteringvitamin B12 synthesis by inhibiting the enzyme methianinesynthetase, and excessive occupational exposure canresult in myeloneuropathy. This condition is similar tosubacute combined degeneration of the spinal cord andhas been reported in individuals addicted to nitrousoxide.

Oxygen

Although oxygen is life-giving, there are some dangersassociated with its use. It is flammable, it can cause a risein the partial pressure of CO2 (Paco2) in patients withchronic obstructive airways disease and, in high concen-trations, it can lead to loss of pulmonary surfactant. On

occasion, toxicity of the central nervous system can beseen. Hyperbaric pressures result in convulsions.Retrolental fibroplasia is retinal damage with new vesselformation seen in infants exposed to high concentrations.

Intravenous agentsInduction of anaesthesia with intravenous agents isusually more rapid and smoother than with inhalationagents (Table 10.7). The ideal agent should have a rapidonset and recovery time with little hangover effect. Itshould be free of side-effects such as nausea, vomiting,cardiovascular and respiratory depression or toxicity toany major organs and it should also, if possible, beanalgesic in low doses.

After intravenous administration, plasma concen-trations rise rapidly and the drugs diffuse across theblood-brain barrier into the brain producing their effect.Reduced plasma concentrations and drug effects occurpredominantly as they are distributed to other tissues.Metabolism occurs mostly in the liver but contributesrelatively little to the recovery of consciousness.

Thiopentone sodium

Thiopentone sodium is one of a group of barbiturateagents and has proved safe in practice for over 50 years.It is important as a hypnotic but has an antianalgesiceffect that can result in a reduction of pain threshold andrestlessness in the postoperative period. On induction,consciousness is rapidly lost and in the absence of otheragents is not regained for 5 to 10 min. As it does notdepress airway reflexes to the same extent as other agents,laryngeal spasm can be precipitated by stimulation of theairway. There is usually a moderate tachycardia andreduction in blood pressure. It is a relatively long-actingdrug and a hangover effect is common. This length ofaction makes it unsuitable as a drug for use by infusionin total intravenous anaesthesia (TIVA). It is an anti-

Table 10.7

Agent

ThiopentoneEtomidatePropofolKetamine

Intravenous induction agents

Induction dose (mg.kg-1)

3-50.31.5–2.52

convulsant and can be used in the treatment of statusepilepticus but must never be given to patients withporphyria, who might show severe cardiovascular collapseor neurological sequelae.

Etomidate

This is a rapidly acting general anaesthetic agent with aduration of action of 2–3 min. It produces less cardio-vascular depression or vasodilatation than other agentsand is most commonly used in patients with a com-promised cardiovascular system. It causes more excitatoryphenomenon on induction, which, on occasion, can betroublesome. Etomidate depresses the synthesis ofcortisol by the adrenal gland even as a single bolus dose.Its use in intensive care has been abandoned as infusionsresulted in increased infection and mortality probablyrelated to reduced immunological competence.

Propofol

Propofol has become a very popular agent. It has rapidrecovery characteristics and gives rise to a lower instanceof postoperative nausea and vomiting than most otheragents. It is formulated as a white aqueous emulsion,which contains soya bean oil. Loss of consciousness israpid but blood pressure tends to decrease to a greaterdegree than with other agents. Respiratory reflexes aresuppressed quite markedly and there is a low incidenceof coughing and laryngospasm. Many regard propofol asthe agent of choice where a laryngeal mask airway is tobe inserted. Recovery is rapid, with little hangover effect.The drug is redistributed rapidly and probably metabolisednot in the liver but in extrahepatic sites. The eliminationremains constant, even after infusions lasting for severaldays, and it is thus the most suitable current agent fortotal intravenous anaesthesia (TIVA). It is also used byinfusion for sedation in intensive care and is increasinglyused as a form of relative analgesia and sedation duringsurgical procedures. Computer-operated infusion pumpsare available, which aim to deliver a target plasmaconcentration based on patient's weight and age.

Ketamine hydrochloride

This differs from the other agents in producing adissociative state rather than generalised depression ofthe central nervous system. Blood pressure might, in fact,increase with this agent and there is little respiratory

depression. It is used in high-risk shocked patients andhas, therefore, a place in anaesthesia and analgesia intimes of war and at the scene of accidents. It can be givenintramuscularly in low doses to produce analgesia. It hasalso been used in less developed countries, where equip-ment and staff are not readily available. Its use, however,is limited by the occurrence of restlessness, disorientationand often unpleasant nightmares or hallucinations, whichcan recur for up to 24 h.

Drugs used to supplementanaesthesiaAnalgesics

Morphine

Morphine, produced from the poppy Papaver somniferum,and codeine are naturally occurring opium alkaloids.Morphine is the gold standard of analgesics affecting boththe pain threshold and the psychological components ofpain. Although it has little effect on the cardiovascularsystem, depression of ventilation is common; the coughreflex is also depressed. However, administration can belimited by distressing nausea and vomiting and it greatlyreduces gut motility.

Pethidine

Pethidine is a synthetic opioid that, as it tends to relaxthe tone of smooth muscle, can be useful in renal colic;it can also be used to control postoperative shivering.Pethidine, however, should not be given to patients takingmonoamine oxidase inhibitors (MAOI).

Buprenorphine

This can be useful on occasions as it can be administeredsublingually. However, nausea and vomiting may betroublesome and subsequent use of other opioids, forexample, morphine may be compromised as the drugsantagonise at opioid receptors.

Other opioids

Progressively shorter-acting synthetic agents are fentanyl,alfentanil and remifentanil. Remifentanil is sufficientlyshort acting to be useful administered by infusion.

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Opioid antagonists

Naloxone is the drug of choice for reversing opioid-induced ventilatory depression. It should be titratedslowly because convulsions can occur occasionally and itreverses not only respiratory depression but also theanalgesia.

Other analgesics

Non-steroidal anti-inflammatory drugs such as diclofenac,ketorolac and indomethacin can be used as analgesiain a balanced anaesthetic technique. The new alpha2

adrenergic agonist dexmedetomidine is currently provingpromising because it results in profound analgesia withless sedation.

Benzodiazepines

Benzodiazepines such as diazepam and midazolam canalso be used as anaesthetic agents, but they have a longerduration of action than other agents. These drugs canbe reversed with flumazenil, which is a competitiveantagonist and again should be given in small titratedincrements.

Neuromuscular blockade

Muscle relaxation is the third of the triad of anaesthesiathat includes narcosis and analgesia. Neuromuscularblocking agents are classified into depolarising (or non-competitive) and non-depolarising (or competitive)agents.

Depolarising agents

The only depolarising agent now available in clinicalpractice is suxamethonium. After administration it resultsin an initial depolarisation of muscle cells. Muscularcontractions can be seen and are known as fasciculation.Repolarisation does not occur and the muscle becomesflaccid. It produces a profound neuromuscular blockwithin a minute and is useful to achieve rapid trachealintubation in a patient who may have a full stomach.Recovery usually begins to occur within 3 min. It ismetabolised by the enzyme cholinesterase and recoverycan be delayed if this enzyme is either structurallyabnormal or reduced in quantity. This is usually geneti-cally determined and might require the patient to beventilated until muscle function returns. Suxamethoniumcan give rise to muscle pains after operation. A rise in the

plasma potassium can occur, which can be dangerousparticularly in patients with burns or in those withneuromuscular disease.

Non-depolarising neuromuscular blocking agents

These compete with the neurotransmitter acetylcholine atthe postsynaptic junction to prevent the threshold for anaction potential being reached, and so the muscle doesnot contract. Tubocurarine (curare) was used for centuriesby native South Americans as an arrow poison and wasthe first agent to be used in humans. It has, however, beensuperseded. Atracurium degrades spontaneously inplasma and is therefore very safe for patients with liveror renal dysfunction. Such drugs have a longer durationof action of around 30 min. Vercuronium is also usedand, because it releases less histamine, many consider itto be the drug of choice in asthmatics. Pancuronium, andmore recently rocuronium, are aminosteroids. Theadvantage of rocuronium is its very rapid onset, whichprovides good intubating conditions within 90 s.Neuromuscular blockade can be monitored with a nervestimulator intraoperatively and at the end of operationthis block can be reversed by the administration of theanticholinesterase neostigmine in combination with eitheratropine or glycopyrronium. The addition of atropineor glycopurronium reduces respiratory secretions andprevents bradycardia.

Monitoring duringanaesthesiaThe word monitor is derived from the Latin verb monere'to warn'. No device can replace the requirement forthese warnings to be observed, interpreted and actedupon.

Monitoring the circulation

Monitoring of the circulation is necessary to maintainperfusion of vital organs (Table 10.8).

The pulse can be palpated and blood pressuremeasured either indirectly or, if necessary, directly froman arterial cannula. Electrocardiography gives infor-mation regarding heart rate, rhythm and ST changesproduced by left ventricular ischaemia. It should beremembered that it is an index of electrical activity onlyand does not measure the mechanical activity thatsustains life.

Table 10.8 Monitoring of the circulation

Heart rate and pulseBlood pressureArterial oxygen saturationECGPeripheral perfusionUrine production

Pulse oximetry assesses the integrity of the com-ponents of the oxygen-delivery system to the tissues (seeCh. 11). It therefore assesses the oxygen supply to thepatient, the oxygen uptake by the lungs and oxygendelivery to the tissues by the heart and circulation.

Pulse oximeters provide a non-invasive measurementof the arterial oxygen saturation (SpO2). The principleinvolves the proportion of light absorbed by blood. Thisdepends on the wavelength of the light and the ratio ofoxyhaemoglobin to deoxyhaemoglobin. The wavelengthof light known as the isobestic point is where absorptionis the same for oxyhaemoglobin and deoxyhaemoglobin.At other wavelengths the absorption differs. The pro-portion of haemoglobin that is saturated with oxygencan, therefore, be calculated by measuring the absorptionof light at two different wavelengths. As the electronicsare capable of detecting a pulsatile component only thesaturation of arterial blood is recorded. Because of thesigmoid shape of the oxyhaemoglobin dissociation curvearterial oxygen tension falls rapidly with saturationsbelow 90%. The lower alarm limit is usually set at thislevel.

Cyanosis requires 5 grams of reduced haemoglobin.This represents an arterial oxygen saturation of 50%in a patient with a haemoglobin of 10g/d1. Oximetry,therefore, is a much more sensitive indicator of hypoxiathan cyanosis. More intense monitoring of the cardio-vascular system may involve insertion of a central venouspressure line. Pulmonary artery catheterisation will allowboth measurement of filling pressure which reflectsvolume status and measurement of cardiac output. NewerDoppler systems also allow monitoring of these last twovariables. Blood loss should also be monitored.

Monitoring the respiratory system

Clinical monitoring is most important. The patient shouldbe observed for colour, respiratory rate, adequacy ofrespiratory movement and the movement of the reservoirbag or ventilator. Auscultation can detect intubation of a

bronchus, the presence of secretions or the occurrence ofa pneumothorax. It is important to detect respiratoryobstruction, which can be revealed by tracheal tug orparadoxical abdominal movement with the absence ofmovement in the reservoir bag. The inspired oxygenconcentration should always be monitored. When patientsare ventilated there should also be capacity to measureairway pressures, volumes and both the inspiratory andend tidal concentrations of oxygen, carbon dioxide andvolatile anaesthetic agents. Ventilator systems shouldalso be fitted with a disconnection alarm. Capnographymeasures the end tidal carbon dioxide tension (ETCO2)and provides the most reliable evidence of correctplacement of an endotracheal tube. ETCO2 will rise withrebreathing or underventilation and can fall rapidly withpulmonary embolism arising from air, fat or thrombos.

Monitoring the central nervous system

At the present time this is done clinically. The signs ofsympathetic overactivity such as lacrimation, sweating,increasing pupil size or increase in heart rate or arterialpressure indicate that anaesthesia is too light. These signsare, however, not reliable but cerebral function monitors(CFM) are not at present in widespread practice. Thedepth of anaesthesia is often assumed from the measure-ment of end tidal volatile anaesthetic concentrations. It isonly since the advent of neuromuscular blockers and theabolition of patient movement that undetected awarenesshas become a potential complication.

Other monitoring

Peripheral and central temperature measurement, neuro-muscular blockade, together with haematological andbiochemical variables may all be measured. Blood gasand acid-base status can be measured accurately from asample of arterial blood and the patient's coagulationstatus may also require to be assessed.

There is strong evidence that there has been areduction in intraoperative critical incidents and patientmorbidity as a result of the adoption of higher routinestandards of patient monitoring.

Postoperative careThe patient must be supervised and monitored closely atall times and should not be discharged from the recoveryward to the surgical ward until they are fully awake and

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maintaining their own airway, ventilation is adequate, thecardiovascular system is stable and they are not bleedingexcessively.

Central nervous system - conscious level

The patient's airway must be carefully maintained untilthey are awake. If the patient is not awake in a reasonabletime then other factors should be considered. Hypo- orhyperlgycaemia may occur particularly in diabetics andintracranial pathology may occur. The following, mostparticularly, should be excluded: hypoxaemia, hyper-capnoea, hypotension and hypothermia.

Confusion and agitation may occur at this timeparticularly in the elderly. This may be associated withanticholinergic drugs such as atropine or hyoscine butpain may also be a contributory factor. Bladder distensionmay be covert. If neuromuscular blockade has not beenadequately reversed the patient may appear agitated anddistressed with uncoordinated movements.

Oxygen

Particular care should be given to the patient's require-ments for oxygen which should be monitored by oximetry.All patients should be given oxygen postoperatively.

Intravenous fluids

They may also require fluids as a result of either intra-operative blood loss or preoperative fluid depletion.

Analgesia

Good pain control starting in the intraoperative periodshould be established in the recovery ward before returnto the ward. This may be achieved with opioids which ifthe patient is sufficiently awake can be administered by apatient-controlled infusion device. Non-steroidal anti-inflammatory drugs and local and regional techniquesmay also be very valuable.

The recovery ward should have the staff, equipmentand monitoring to deal with the full range of compli-cations. Problems are as liable to arise there as in theanaesthetic room or operating theatre.

Patients should be closely watched for a number ofsurgical complications which may include haemorrhageand blockage of drains or catheters. This high intensityenvironment should allow the patient to return to theappropriate level of ongoing care in the optimumcondition.

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Conscious sedationtechniques

IntroductionThe use of conscious sedation has risen dramatically inrecent years. There are many circumstances responsiblefor this change including reduced general anaestheticnumbers as a result of its potential morbidity (see Ch. 10),regulation by the General Dental Council and increasedpatient education and expectations. The General DentalCouncil's definition of conscious sedation is:

A technique in which the use of a drug or drugsproduces a state of depression of the centralnervous system enabling treatment to be carriedout, but during which communication can bemaintained and the modification of the patient'sstate of mind is such that the patient willrespond throughout the period of sedation.Techniques should carry a margin of safety wideenough to render unintended loss of conscious-ness unlikely.

This definition gives some flexibility regarding drugsused and specific procedures chosen yet it emphasisesthe guiding principle of sedation: the patient is, bydefinition, conscious. Sedation as described here is aninherently safe method of anxiety control.

Sedative agentsSeveral currently available drugs are useful in sedation.In practice, however, conscious sedation usually involvesthe use of inhalational nitrous oxide or the neweranxiolytics, the benzodiazepines.

Nitrous oxide

At room temperature, nitrous oxide is a colourless gaswith, arguably, a sweet smell. It is contained in bluecylinders as a mixture of gas and liquid.

Nitrous oxide is a weak anaesthetic with a minimumalveolar concentration (MAC) of 110% (see Ch. 10).This represents the concentration of gas required toanaesthetise 50% of subjects and is clearly impossibleunless the gas is given in a hyperbaric atmosphere.Nitrous oxide has a blood gas solubility of 0.47, whichmakes it highly soluble in blood. This allows rapid onsetof sedation and equally rapid recovery.

Benzodiazepines

Benzodiazepines were discovered by accident in the1950s in Switzerland by researchers at Hoffman-LaRoche. They were first marketed in 1960 with theintroduction of Librium. Benzodiazepines have a numberof clinical effects: anxiolysis, sedation, amnesia, musclerelaxation and eventually anaesthesia. They produce thisaction by two main routes.

• First, and principally, benzodiazepines act in thecentral nervous system (CNS) via the gamma-aminobutyric acid (GABA) network. GABA is an inhibitoryneurotransmitter found in the brain and spinal cord.Benzodiazepines act by attaching to specific receptorsclose to the GABA receptors, prolonging the time theGABA is attached and producing a sedative effect.

• Second, benzodiazepines can attach directly toreceptors for glycine (another inhibitoryneurotransmitter) in the brainstem and spinal cord,producing anxiolysis and relaxation.

All benzodiazepines produce respiratory depression tosome degree by a combination of CNS depression and

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thoracic muscle relaxation. They also produce mildhypotension as a result of muscle relaxation decreasingvascular resistance. As a result, the heart rate often risesas the body compensates for the reduction in bloodpressure.

AssessmentCase selection is important when considering conscioussedation. An assessment visit prior to sedation isimperative. This visit is used to explain the procedurefully, to assess the patient's level of anxiety and to selectan appropriate sedation method. It should be done in anenvironment that is pleasant and unthreatening. Theassessment includes the history, examination andtreatment planning.

History

An assessment of the patient's anxiety levels anddiscussion of specific phobias will inform the practitionerabout the patient's likely behaviour and cooperationduring the operative procedure.

A comprehensive medical history is required, withspecific enquiry regarding previous general anaestheticsand sedation.

A number of drugs interact with particular intravenoussedation agents and can prolong sedation considerably.These include alcohol, opioids, antidepressants, otherbenzodiazepines and recreation drugs.

All intravenous sedation agents cause some level ofrespiratory depression and therefore patients withchronic obstructive airways disease are at risk. Upperrespiratory tract infections are relative contraindicationsto both inhalational and intravenous sedation and if thetreatment can be put off it should be to allow the patienttime to recover. Asthma is often worsened by stress andanxiety and patients who can be treated without anxietyoften display better control of their asthma throughoutthe procedure.

In general, patients in classes I and II of the AmericanSociety of Anesthetists (ASA) physical status scale (seeTable 10.2) can be treated safely in the primary caresector, but ASA class III patients require management ina hospital environment.

Patients will require an escort to take them home ifthey are having intravenous sedation and will not be ableto drive or to take responsibility for children or relatives

for 12 h; they will not be able to return to work that day.It is therefore important to assess the patient's family andemployment circumstances.

At the assessment visit, it is important to record vitalsigns as baseline readings prior to treatment; these shouldinclude blood pressure and heart rate. Some practitionersadvocate taking the patient's weight, although the dose ofmost intravenous sedation agents does not relate in anyreliable way to weight.

Treatment planning

Conscious sedation offers a spectrum of anxiety controland the appropriate method for each patient can bedecided only after a full history and examination isundertaken. Consent should be obtained from the patientor the patient's guardian. This should be written,witnessed and understandable.

Written instructions telling the patient what he or shecan and cannot do before and after the operation shouldbe given at this visit. These should include the following:

• You must be accompanied by a responsible adultwho must remain in the waiting room throughoutyour appointment, escort you home afterwards andarrange for you to be looked after for the following12 hours.

• You must not eat or drink anything for 2 hours priorto your appointment time; before this you shouldhave a light meal e.g. toast and tea.

• If you are taking any medicines these should be takenat the usual times and should also be brought with you.

• You must not drive any vehicle, operate anymachinery or use any domestic appliance for12 hours after sedation.

• You must not drink alcohol, return to work, make anyimportant decisions or sign any legal documents for12 hours after sedation.

There should also be a discussion of the amnesia thatoften occurs in intravenous sedation.

Table 11.1 Ideal properties of a sedative agent

AnxiolyticEasy to administerCheapNo side effectsQuick onset and recoveryNo respiratory depression

Sedation methodshThe ideal properties of a sedative agent are listed inTable 11.1. No single sedative agent possesses idealproperties and each of the following methods has distinctadvantages and disadvantages.

Oral sedation

Oral sedation is the least specialised of the sedationmethods. It presents a relatively simple way of providingmild preoperative sedation. It is often described aspremedication and can be used alone or in conjunctionwith another sedation method. It is used principally toalleviate fear and anxiety, allowing the patient to tolerateeither deeper sedation or further procedures. Oral sedationis almost universally acceptable because it requires verylittle patient cooperation.

The main disadvantage of oral sedation is theconsiderable individual variation in response. This isdue to different absorption and metabolism of the drugsby individual patients. Benzodiazepines are the mostcommonly used drug for oral sedation. These areconsidered below.

Diazepam

Diazepam has been the most commonly used oralsedative for many years. The response to the drug varies;a suitable adult regime may be 5 mg the night beforethe treatment, 5 mg on waking and 5 mg 1 h before theprocedure. This will not produce profound sedation butwill allow the patient to approach the procedure withmore confidence and less anxiety. Diazepam does have arelatively long half-life and therefore patients should notdrive or operate machinery for 24 h after the operation,and there is even a risk of some remaining sedation after2-3 days, due to the production of active metabolites.Patients taking diazepam, or other benzodiazepines longterm, become tolerant to the drugs and therefore sedatingthese individuals with further benzodiazepines is verydifficult.

Temazepam

Temazepam has advantages over diazepam because ofits much shorter half-life of approximately 4 h. The dosefor a normal, healthy 70-kg patient should be 20 mgapproximately 30 min before the procedure. This dose

can vary between 10 and 40 mg, according to the patient'sweight, age, medical history and level of anxiety.Temazepam is a class 2 restricted drug.

Midazolam

Midazolam is the principal drug used in the UK forintravenous sedation, however it can be used orally andexperimental results are very encouraging, particularly inchildren and special needs patients. The drug, however, isnot licensed for oral use in the UK. It is used at an oraldose of 0.5 mg/kg.

A number of other drugs besides the benzodiazapinesgive varying degrees of sedation when given orally; how-ever, most are unsuitable for general use. They includeopiates and antihistamines, which are used particularly inchildren.

Inhalational sedation

The use of inhalational sedation has increased in recentyears as a result of the reduced number of generalanaesthetics and its usefulness when treating anxiouschildren. It is often said that inhalational sedation is 50%drug and 50% behaviour management.

History

In 1884 the American Horace Wells attended a local fairand received what was known at the time as 'laughinggas'. He was intrigued by its effects and later had his thirdmolar removed with 100% nitrous oxide anaesthesia.Later in the nineteenth century, this method was used bythe American anaesthetist and inventor Gardner Colton,who gave over 121 000 100% nitrous oxide anaestheticsand reported no deaths. The first anaesthetic machine fornitrous oxide was introduced in 1887 but, by 1945, afterlocal anaesthetic was introduced into dentistry, generalanaesthesia was no longer necessary for dental extraction.A mixture of nitrous oxide and oxygen was first taughtin the undergraduate curriculum in the United States inthe 1960s.

Clinical application

The clinical effects of sedation with nitrous oxide canbe described within the stages of anaesthesia first usedby Guedel (see Ch. 10). The first stage in Guedel's

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classification is called analgesia, and this is split intothree planes, the first two of which can be obtained byconcentrations of 5-25% nitrous oxide and 25-55%nitrous oxide, respectively, and represent the so-calledrelative analgesia phases. It is in these planes that themost useful sedation is found. Going beyond these planesproduces increased dissociation, which most patientsfind unpleasant. There is, however, considerable variationfrom patient to patient and therefore, the dose of the drugis given incrementally.

Inhalational sedation has a number of indications. Aswell as simple anxiolysis it is also useful in patients whohave a hyperactive gagging reflex because it can oftenreduce this sufficiently to allow dental treatment that waspreviously impossible to be carried out. It is also usefulin patients with physical and mental special needs,although there does have to be some level of under-standing and communication because it must be possibleto undertake the behaviour management required toallow the agent to fulfil its potential. It is also usefulin patients with mild medical problems worsened byanxiety, such as well-controlled asthma and epilepsy.

The relative contraindications to the use of inhalationalsedation include upper respiratory tract infections thatmake nasal breathing difficult. The procedure should, ifpossible, be postponed in these circumstances. Particularlyin children, it can be a problem when the tonsils andadenoids are enlarged, again making nasal breathingdifficult. Difficulty communicating or understanding thenasal breathing required makes inhalational sedationvery difficult in children, certainly under the age of threeand in patients with severe special needs.

Inhalational sedation has a number of distinctadvantages over other methods:

• it is non-invasive• it only requires a nasal mask• it has rapid onset and rapid recovery• no fasting is required• it produces anxiolysis and analgesia (it is said that

50% nitrous oxide gives analgesia similar to l0 mg ofintramuscular morphine)

• it requires no electronic monitoring• it is acceptable to most patients• it produces no amnesia of any kind and therefore the

whole procedure is remembered.

The principal disadvantage is pollution. The nitrous oxidethat is expired into the atmosphere and consequentlybreathed in by the staff in the surgery has been related

to a number of medical problems (described in Ch. 10).This has led to a number of safety recommendationsbased around the Health and Safety Executive's 1996decision to set a maximum dose of nitrous oxide of100 parts per million in a time-waited 8-h period. Thesesafety recommendations include active scavenging,which removes the expired gas as opposed to passivescavenging resulting from open windows and fans, theuse of closed circuits so that the expired gas is exhaustedaway from the clinical environment rather than into theroom and the monitoring of pollution levels.

Procedure

The importance of behaviour management to thetechnique cannot be overemphasised. Written consentis mandatory, as is a second appropriate person as achaperone. The Quantiflex MDM machine is the standardmachine used in the UK and it allows a variable mixtureof nitrous oxide and oxygen to be given to the patient viaa nasal mask. The machine is marked in 10% incrementsallowing a minimum of 30% oxygen. The manufacturersreport a 5% error in either direction and therefore theabsolute maximum is 75% nitrous oxide, which is rarelynecessary. This still provides more oxygen than instandard room air.

Gas leaves the two active cylinders at the front of themachine (there are two full reserve cylinders on the backof the machine) and is mixed in the flow control head.The facemask is introduced and the patient is allowed tobreathe 100% oxygen at approximately 5–6L/min for2 or 3 min. The flow rate can be adjusted according to thereservoir bag, which is on the machine. The flow ratewill vary according to the size of the patient and thefrequency of respiration. Nitrous oxide concentration isthen slowly increased in 10% increments, approximatelyevery 60 s, until the patient begins to report signs ofsedation. It is important at this stage to ensure nasalbreathing only, and the patient should be encouraged tospeak only when absolutely necessary.

It requires considerable skill on the part of theoperator to maintain a calm and pleasant environment. Asthe dose increases, the patient will report sensorychanges including paraesthesia in the extremities,tinnitus and a general feeling of warmth. This is a resultof peripheral vasodilation and can be seen in the flushingof the facial features. As the sedation level increases,patients often begin to report visual disturbance and afeeling of remoteness or disassociation. This is the stage

at which maximum useful anxiolysis and analgesia hasbeen obtained; beyond this level patients begin to feellight-headed and then restless and even nauseous. It isimportant to stop before reaching this stage, particularlyin children because they will become uncooperative andit will be very difficult to persuade them that bringing theconcentration down will make them feel better again.

With increased use of the technique, the operatorbecomes very adept at assessing the level of sedationfrom the sensory changes and from the reaction of thepatient. The procedure can then be carried out, includingthe local anaesthetic, which will be significantly easier toadminister because of the analgesia obtained from thenitrous oxide. It is possible to increase and decrease theconcentration according to the procedure that is takingplace, for instance it might be necessary to increase theconcentration for the local anaesthetic injection andreduce it then for the procedure itself. At the end of theprocedure it is important to let the patient breathe 100%oxygen for 2–3 min, to prevent the theoretical risk ofdiffusion hypoxia as nitrous oxide moves in significantquantities from the blood back into the alveoli and isrebreathed, therefore diluting the oxygen available forrespiration producing hypoxia. In reality this is rarely aproblem. The patient should be recovered until they feelfit enough to leave. Approximately 20 min after theprocedure adults can leave unescorted; children requirethe same escort arrangements as they would after localanaesthetic.

Intravenous sedation

Intravenous sedation is, at present, the best method forconscious sedation and is the technique of choice formost adult patients. It requires considerable training andexperience but rewards this with excellent operatingconditions in a calm and relaxed environment even whendealing with severely phobic patients.

History

The first time intravenous drugs were used for sedation,rather than full anaesthesia, was in 1945 when theso-called 'Jorgensen technique' was introduced. Thisconsisted of the intravenous injection of a barbiturate, anopioid and scopolamine. By most standards nowadaysthis would be considered deep sedation at best anddangerous at worst. In the 1960s, however, the discoveryof benzodiazepines revolutionised the practice of

intravenous sedation. Initially in dentistry, intravenousconscious sedation was done using diazepam but this hada number of disadvantages, most importantly itselimination half-life of 43 h and the production of activemetabolites. Patients were therefore sedated to someextent for up to 2 days and there was a risk of reboundsedation. Diazepam is insoluble in water, which means ithas to be either given as a solute dissolved in propyleneglycol, which is painful on injection, or emulsified insoya bean oil, which is the most common formulation.

The next generation benzodiazepine, midazolamsolves many of the problems presented by diazepam. It isa water-soluble imadazobenzodiazepine. Usefully, it iswater-soluble at a pH of less than 4 and lipid-soluble atphysiological pH, making it painless on injection. It isavailable in two preparations: 10 mg in 2 mL of fluid or10 mg in 5 mL of fluid. The latter is used for intravenoussedation because it is easier to control the incrementaldosage. It acts more rapidly than diazepam and has amuch more reliable patient response. It has an eliminationhalf-life of between 90 and 150 min – considerablyshorter than that of diazepam – and is metabolised in theliver.

Clinical application

There are a number of indications for intravenoussedation with midazolam. Psychosocial indications areoften the most common reason for a patient to present forintravenous sedation. This group of patients includesthose with anxieties and phobias related to dentistryincluding needles and drills. There is a specific group ofpatients who have considerable difficulty with vasovagalattacks prior to and during dentistry and intravenoussedation can often help.

There are a number of medical indications forintravenous sedation, particularly if the patient has acondition that is aggravated by stress. This groupincludes those with asthma, epilepsy, hypertension andthose with mild ischaemic heart disease. Intravenoussedation can also be useful in those with mental andphysical special needs.

Other indications for intravenous sedation includedifficult, long or unpleasant procedures and patientpreference.

There are a number of relative contraindications tointravenous sedation. Social contraindications includethose who are unwilling to consider this mode of treat-ment or are extremely uncooperative. It is not possible

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to provide intravenous sedation for an unaccompaniedpatient and it is also difficult with extremes of age. Theuse of intravenous midazolam is controversial in childrenunder 16 years.

Medical contraindications include severe systemicdisease, particularly respiratory disease such as severechronic obstructive airways disease, and severe mental orphysical special needs. A number of drug interactionscontraindicate the use of intravenous benzodiazepines,particularly if a patient has a history of psychiatric treat-ment or has been prescribed benzodiazepines over a longperiod of time, thereby making the patient very tolerantto the drug. Intravenous sedation should be avoidedwherever possible in patients who are either pregnant orbreast-feeding.

The topping-up of midazolam sedation is notrecommended except in very skilled hands and, there-fore, any procedure lasting longer than an hour is reallyunsuitable for this treatment method.

Procedure

An indwelling cannula is mandatory for all forms ofintravenous sedation. It is useful to provide topicalanaesthetic. This can be either Emla® or Ametop®, whichare readily available and allow the painless insertion ofintravenous cannulae.

As with inhalational sedation, it is essential that thereis a second competent person in the room at all timesduring intravenous sedation. This person should be trainedin both monitoring the sedated patient and assisting inthe event of an emergency.

The patient should have blood pressure monitored anda pulse oximeter attached (Fig. 11.1). Midazolam is givenroutinely as a 2 mg bolus and then 1 mg increments every60 s to a standard endpoint. Patients become graduallymore comfortable with their surroundings, their speechbegins to slow and slur, they respond to commands in asluggish fashion and - most importantly - they becomewilling to accept treatment that they previously wouldhave found unacceptable.

Verrill's sign occurs when the upper eyelid covers theupper half of the patient's pupil. This sign is not reliablewith intravenous midazolam and often indicates over-sedation. Eve's sign occurs when the patient is asked totouch his or her nose with the forefinger and is unable todo so, invariably touching the upper lip instead. This isa more reliable sign for the endpoint for midazolamsedation.

Fig. 11.1 Pulse oximeter showing digital display andfinger probe.

It is important not to lose verbal communicationwith the patient at any point and, although response tocommands will be slower than normal, this should stillbe possible. The total dose required varies considerablyas a result of many factors, including anxiety, sleepdeprivation, alcohol consumption in the previous 24 hand other drugs, both prescription and recreational. It isdifficult to be prescriptive about a maximum dose butconsiderable thought should be given before increasingthe dose above 10 mg.

Intravenous midazolam gives approximately 45–60min of useful sedation, during which most procedurescan be carried out. When the procedure is finished thepatient should be given time to recover, either in the sameroom or in a designated recovery area, and should bemonitored continuously. The patient's escort can beinvited to sit with the patient during this period. Thepatient can be discharged approximately 1 h after the lastincrement of drug is given, but this varies from individualto individual and requires assessment of each case. It isimportant to remove the cannula before discharge.Postoperative instructions should be given to the escort,although they should already have been given to thepatient at the assessment visit. The escort should beprovided with a telephone number in case any problemsarise.

MonitoringPatients who are sedated have a reduced perception oftheir surroundings and of their own body. The staff

around them, therefore, assume responsibility for theirvital signs. Monitoring allows early intervention beforeinjury takes place and is used to minimise risk tothe patient. Clinical monitoring is most important andrequires observation of the colour of the patient and theirrespiration. Electronic monitoring via a pulse oximeter ismandatory for intravenous sedation.

In normal, healthy patients the oxygen saturation ofarterial blood will be between 96 and 100%. The oxygensaturation alarm should be set at 90% to allow remedialaction to be taken prior to any injury. The oximeter alsoprovides a constant reading of the patient's heart rate (seeCh. 10).

The principal side-effect of intravenous benzodiaze-pines is respiratory depression. If this occurs, as indicatedby a reducing oxygen saturation, the first step is to talk tothe patient and perhaps to shake him or her gently, askingthem to take deep breaths. This will usually wake thepatient from the light sleep he or she has drifted into andallow them to take a number of deep breaths, thereby,increasing the oxygen saturation to normal. A patientwho is unable to carry this action out unaided is over-sedated and the operator must assist the process ofrespiration by lifting the patient's chin upwards, thrusting

the jaw forwards and tilting the head backwards. Thisallows the airway to be straightened and makes respirationconsiderably easier. The next stage, if necessary, is togive oxygen via a mask, or more commonly via a nasalcannula. Oxygen should be given at approximately 2 to3 L per minute via a nasal cannula or at 5 to 6 L perminute via a mask. If these measures are unsuccessful,the next step is reversal of the sedation agent.

Flumazenil is a benzodiazepine antagonist. It wasdiscovered in 1978 and, although some practitionershave advocated its routine use, it should be used foremergencies only. It belongs to the benzodiazepine groupof drugs but lacks the active benzene ring that makesbenzodiazepines sedatives. Because it has a higher affinityfor receptors than midazolam, flumazenil reverses theaction of midazolam without having any sedative actionof its own. It is available in vials of 500 µg in 5 mlof fluid and the standard dose is 200 µg (2 ml) initiallythen 100 µg increments every 60 s until recovery. It has ashorter half-life (50 min) than midazolam and shouldtherefore be used with care because there is a theoreticalrisk of resedation once the flumazenil wears off and themidazolam reattaches to the receptors.

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Section BSpecialist Surgical Principles

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Fractures of the facial bones

IntroductionFractures of the facial bones are common and present inAccident and Emergency departments and to medical ordental practitioners. Physical violence tends to be themost common aetiology in the UK, followed by roadtraffic accidents and falls; sports and industrial injuriesare relatively uncommon. Most assaults result in low-energy injuries and are associated with excess alcoholconsumption, most frequently in young males. They canbe accompanied by soft tissue injuries. The majority arecaused by fists and boots, glass bottles and knives and, inrecent years, baseball bats. When associated with drugaddiction, gunshot wounds are an increasingly commonfactor.

Most high-energy injuries are traffic related. Despitethe increased use of safety belts and drink drivingregulations, severe injuries are still regularly seen; high-speed accidents often result in fatal or very severeinjuries, although improved car design has lessened therisks to the front-seat passenger and driver. Other lesscommon causes of isolated fractures are industrial andsports injuries, which mostly affect the upper and midface. War injuries tend to be high velocity injuries causedby a mixture of exploding bombs, shells and gunshots,often leading to extensive damage to the soft tissues andfacial skeleton.

Falls commonly cause injury to the nose or the malarcomplex, but less so the mandible. They tend to occurunder 10 years of age and in the elderly infirm patientwith brittle bones.

The general examination

The general examination of the patient should takeaccount of the presence of alcohol and drugs beforeexamination of the facial injuries. Inspection andpalpation of the various parts of the face will pick up

Table 12.1 Fractures of the facial bones

MandibularMiddle third

lateralzygomatic (malar)

centralnasalnasoethmoidalmaxillary

obvious asymmetry, often masked when there is swellingpresent. This examination should be gentle but organisedand precise.

The ears and eyes need to be fully examined and,where an ophthalmic injury is suspected, early ophthalmicconsultation is advisable. At least 12% of all orbitalinjuries are associated with severe ocular injury, which isoften unrecognised. The injuries should be recorded andfurther information sought from accompanying personsat the incident. Other life-threatening injuries must beexcluded. Although conventional radiography is helpfulin identifying fracture sites, obtaining good filmsrequires a cooperative patient, and where this is in doubt,radiography should be postponed.

Fractures of the facial bones affect either the mandibleor the middle third of the face, or both (Table 12.1).These will be discussed in turn.

Mandibular fracturesThe mandible is essentially a bone with three joints, bothcondyles and the dental occlusion, and it is important thatthe condyles remain in their fossae and that the occlusionis correctly maintained. Simple approximation of frac-tures with intermaxillary fixation can lead to respiratoryand masticatory difficulties and is being superseded by

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open reduction and plating. The intraoperative use ofintermaxillary fixation to fix the occlusion is valuablebut, after plating mandibular fractures, this can usuallybe released. Semirigid fixation with miniplates is widelyemployed and although titanium is probably the metal ofchoice, other alloys and stainless steel are also used. Thelast is likely to require removal and they are anoccasional cause of metal allergy.

Clinical features

There is usually swelling and pain at the fracture site.Where there is significant displacement, malocclusionis likely with an inability to bring the teeth correctlytogether. Loosening of teeth commonly occurs at thefracture site, often accompanied by partial avulsion ofteeth and root fractures. Early recognition is essential asdelay can contribute to later infection at the fracture site.Grossly mobile and fractured teeth should be removed.In the younger child where the apices are open, they maybe retained. All fractures where the teeth are involved arecompound into the mouth and there is some risk ofinfection.

There will usually be some asymmetry of the mandiblewith unilateral fractures. With condylar neck fracturesthere is likely to be shortening of the mandibular ramusand an anterior open bite (Fig. 12.1). Where there is grossdisplacement at a fracture site there is often anotherfracture elsewhere (Table 12.2).

Whenever a fracture arises in the tooth bearing area,such as in the mandibular body between the lingula andmental foramen, disruption of the inferior dental nerve islikely, and with wide separation of fragments the nervemay be torn and require repair. The accurate repositioning,stabilisation of fragments and reconstitution of the canal

often results in some recovery of lower lip and chinsensation. Pain and crepitus may be present at thefracture site but should not be elicited, although thereshould be a check for mobility. Trismus is common,irrespective of the site of the fracture, as mouth openingwill increase discomfort. Similarly, dysphagia and lackof control of saliva (which may be blood stained) may bedue to discomfort when approximating the teeth onswallowing.

Bruising in the floor of the mouth is a pathognomonicsign of a mandibular fracture in the edentulous patient.Almost the only other way this can occur is with a pen-etrating injury. More rarely, the fractured or intact condyle,with severe force applied to the chin area, may passbackwards tearing the external auditory meatus. This teartends to occur through the anterior or inferior part of theear canal, often accompanied by leakage of clear synovialfluid or bleeding. If there is a tear on the superior orposterior wall or tympanic membrane it is highly likelythat there is a fracture of the petrous temporal boneaccompanied by hearing loss and a CSF leak.

Fig.12.1 Orthopantomogram showing fractures of themandibular condyles.

Table 12.2 Possible clinical features of common mandibular fractures with displacement

Pain, swelling bruisingSublingual haematomaTrismusMental anaesthesiaOcclusal disharmony'Step' palpableBleeding from earCondyle palpable in fossaIntraoral bleedingCompound

Angle

At angle of jawYesYesYesIf fracture through or adjacent to standing toothYes: at lower borderNoYesPossibleCommonly

Subcondyle

PreauricularNoYesNoPremature contact on affected sideDifficult to palpatePossibleNo: if fracture and dislocationNoVery rarely90

Displacement of the mandibular fracture is very muchrelated to its site. Extensive fractures of the mandibularramus often remain undisplaced because they aresplinted by the masseter and pterygoid muscles.Fractures in the angle region of the mandible, however,are subject to pull from the elevators, pterygoid andsuprahyoid muscles and displacement may well occur,especially when the fracture is bilateral leading toposterior displacement of the distal segment and ananterior open bite with loss of chin prominence. A carefulnote needs to be taken of these in the semiconsciousor unconscious patient, because airway obstruction canoccur. If plating techniques are not available it isimportant to identify the direction of the fracture in theangle region. If, on the orthopantomogram (OPT), it runsobliquely from the external angle to the third molartooth, the proximal fragment tends to displace superiorly.If, on the posteroanterior view, the fracture runs obliquelyfrom the angle region forwards, the proximal fragmentwill again tend to displace but in this case medially as aresult of pterygoid muscle action (Fig. 12.2). The doublyunfavourable fracture will need stabilisation with a wireat the lower border of the mandible or plate or it will tendto torque apart when in intermaxillary fixation. Theseconsiderations tend to disappear with good platingtechniques that encourage accurate fragment inter-digitation to take place (e.g. with a strong upper borderplate placed along the external oblique ridge). Accurate

stable repositioning avoids the necessity for postoperativeintermaxillary fixation.

Radiography

Imaging of the mandible is largely through plainradiographs taken in two planes. The orthopantomogram(OPT) is essentially a lateral view of the whole mandible,which visualises clearly body and ramus fractures butis less effective in the parasymphyseal region (Fig. 12.3).Both condylar heads and necks must be included. Aposteroanterior (PA) view at right angles to this isessential. A reverse Towne's view will often showanteromedial displacement or dislocation of the condylewhen not seen on a standard PA view. Dental andocclusal intraoral views are particularly valuable andshould be taken routinely for suspected dental injuriesand alveolar fractures in the tooth-bearing area. Theydemonstrate the relationship of the teeth to the fracturesand their involvement in the fracture line. Lower occlusalviews are helpful in picking up sagittal fractures in theanterior mandible.

Imaging of the mandibular condyle is sometimesdifficult in young children, especially those under fiveyears where there is comminution of the condylar head inintracapsular fractures, and also where there is suspectedcondylar displacement through the glenoid fossa. Here,computerised tomography (CT) scanning is particularly

Fig. 12.2 Unfavourable fractures at the angle of the mandible and the direction of displacement.91

Fig. 12.3 Orthopantomogram showing a fracture at theangle of the mandible.

Fig. 12.4 Radiograph showing bilateral fractures of themandible fixed with titanium plates.

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helpful in identifying the nature of the injury and theextent of comminution present. This is important in theyoung child where there is always a risk of disturbanceof growth and possibly ankylosis. If the patient is uncon-scious or has sustained injuries such as severe neck orskull fractures or other spinal injuries then CT scanningis essential. Good views of the temporomandibular jointsshould be obtained and are best seen on coronal views.

Treatment

Preliminary treatment includes maintenance of the airwayby clearance of foreign bodies from the area. Localbleeding needs to be stopped by suturing or pressure.Temporary support at the fracture site is given when thereis any delay in treatment using a wire around adjacentteeth at the fracture site to hold the fragments together orby supporting the jaws in occlusion with a head bandage.In the unconscious patient the passage of a suture throughthe tongue to hold this forward with any symphysealbone fragments may also be necessary. All compoundfractures require early antibiotic therapy.

The general principles of fracture treatment arereduction, fixation, immobilisation, prevention ofinfection, and restoration of function. These need to beconsidered in the management of mandibular fractures.

Manual reduction of the fracture by repositioning thefragments can be carried out under either local or generalanaesthesia. For late-presenting fractures the applicationof arch bars to the teeth both upper and lower will allowelastic traction to be applied bringing the fragments intoocclusion.

Fixation, in the dentate patient, can be by a variety ofattachments made to the teeth. These include arch bars oreyelet wiring around individual teeth, cast silver cap

splints and when teeth are missing the use of modifieddentures or Gunning splints.

With the establishment of rigid fixation as the methodof choice for stabilising facial fractures the principle ofintermaxillary fixation for a significant period afterreduction of the fractures has become less important.Whereas in the past fractures were fixed with inter-maxillary fixation and interosseous wiring, or variouscombinations of special wiring techniques, nowadaysthe majority of fractures are fixed with titanium oroccasionally steel alloy plates (Fig. 12.4). Various formsof miniplates are available; usually a 2 mm thicknessplate, with appropriate screws, is required. Most fracturescan be fixed with a single plate provided at least twomonocortical screws are placed on each side of thefracture. In certain areas of the mandible additionalfixation is required, principally in the symphyseal regionwhere two plates are advantageous in preventing torquingof the bone fragments at the lower border. Bone platesare normally inserted through an intraoral approach.Where there is gross comminution of bone or there aremissing bone fragments then the use of a heavier, thickerreconstruction plate should be considered. These heavyplates are more difficult to mould to the bone and areusually inserted through a skin incision just below thelower border of the mandible. Additional corticocancellousiliac crest bone graft is needed when there is bone loss.

The angle region is a common fracture site and here asingle plate along the external oblique ridge is normallyadequate. Teeth in the fracture line can be left if they areundisplaced and intact. If the blood supply at the apexhas been destroyed, if infection is present or if thefracture is treated late, consideration should be given toearly extraction. Teeth not requiring to be retained, suchas an impacted third molar, can be removed at the same

time unless this tends to disrupt the fracture line whenthey should be temporarily retained (see Ch. 27).

The condylar segment in severe trauma may displaceposteriorly, leading to rupture of the external auditorymeatus; only occasionally is it fractured in this situation.

Certain fractures require special treatment: thegrossly infected fracture and the fracture where there issignificant bone loss can be stabilised by the insertion ofpins into the major fragments joined together with a barholding the fragments as far as possible in their correctposition. Following this, the infection will usually settleand any bone loss can be replaced with iliac crest bonegraft.

For the atrophic mandible, especially in the elderlywhere perhaps the main body of the mandible is less than6-8 mm in height, primary bone grafting of the fracturedmandible with split ribs is often the best solution. Theribs are split lengthwise and shaped to the mandible onthe lingual and buccal sides and held in place with atleast two circumferential wires on each side of thefracture line. Additional small screws can be helpful forstabilisation.

The condylar neck is commonly fractured and isdifficult to treat. Low condylar neck fractures, especiallybilateral and displaced or dislocated tend to develop ananterior open bite. Open reduction and fixation with oneor two miniplates is often the treatment of choice. Forsimple single condylar neck fractures, the use of archbars and light elastic traction may be all that is requiredbut, when accompanied by fractures elsewhere (e.g. inthe parasymphyseal region, body or angle), or by mid-face fractures, it is safer to reduce and fix the condyle.

Fractures in young children should be managed con-servatively under the age of 12. No condylar fracturerequires operative treatment as they will all remodel andreform. Comminuted condylar fractures in the youngchild are usually intracapsular and can lead to ankylosis;they require early but gentle mobilisation and generallyshould not be explored. Minor degrees of irregularity inthe occlusion may be acceptable because remodellingoccurs and malocclusions tend to resolve. Simple splintingdevices for pain relief may be required.

Certain general principles need to be mentioned, suchas the provision of adequate analgesia. The semifluid dietgiven should be high in protein and calories. Good oralhygiene should be maintained using chlorhexidine andsaline mouthwashes and a toothbrush.

Good healing requires stabilisation for an adequatelength of time. Indirect reduction of fractures with inter-

maxillary fixation alone, although successful, often takes6 weeks to unite. For most fractures, callus provides anosteoid mass of tissue around the fracture site giving itsome stability. Conventional miniplates allow for excellentrepositioning of the fractures provided they are correctlyadapted to the surface of the mandible and they providethe necessary immobilisation across the fracture.

Care needs to be taken to avoid the insertion ofminiplate screws into the inferior dental canal or theroots of the teeth. With accurate reduction of the fracture,any sensation lost due to separation of the fractureusually recovers, but this may be incomplete when therehas been extensive damage to the inferior dental nerve orconsiderable delay in treating the fracture.

Complications

Complications associated with mandibular fractures arenot uncommon and, although they can be related to thefixation used (e.g. plates), are often due to infection orexposure of the plate into the mouth. It does notnecessarily follow that a plate has to be removedimmediately if there is infection, only if infection persistsand there is a lack of bony union will this be necessary.Minor infections do not necessarily prevent union whenthere is adequate drainage and the fractures are wellfixed. Delayed union may result from infection arisingfrom the teeth, bone or a breakdown of the soft tissues. Itmight also be caused by a poor reduction of the fracture,interposition of soft tissue into the fracture line andmobility of fragments. These problems run a high risk ofdelayed or non-union. Complicating local pathology suchas a cyst or tumour may be present but even then mostfractures unite. Malunion is the result of poor reductionof fragments, rarely seen with modern open techniques.It can occur with late-treated or untreated fractures.Osteotomy of that malunion may be required to achievea normal occlusion and symmetry of the mandible.

There is some argument about the retention of teeth inthe fracture line. If very loose or displaced, they maywell be lost at the time of injury, shortly afterwards orlater if there is extensive exposure of the root surface. Avery mobile tooth in the fracture line is likely to be non-vital and is best removed to prevent delayed union eventhough there is plate fixation at the fracture site.

In fractures around the condyle, angle region andramus there may be late onset trismus after much traumato both muscle and bone or comminution in that area.More rarely, ankylosis will result, or bony hyperplasia of

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either the coronoid or condylar processes, typically inyoung children. Early mobilisation of fractures in youngchildren is essential as union occurs quickly, often within3–4 weeks. It is essential to keep the condyle moving withcomminuted condylar head fractures and haemarthroses.Condylar remodelling occurhs over a period of monthsand symmetry usually returns in childhood fractures.

Persistent mental anaesthesia can occur as a resultof damage to the inferior dental or mental nerves oroccasionally at the site of the lingula. Severe damage orsection of the nerve in the body of the mandible mayrequire nerve repair and consideration should be givento this. Anatomical reduction of the fracture must beobtained so that the inferior dental canal is maintained.

Middle third fracturesThe middle third of the face consists of nasoethmoidalcomplex, the maxillae and smaller bones attached to ittogether with the malar complexes. It lies between the

mandible and the cranial cavity and calvarium, inparticular the frontal and sphenoid bones. Fractures,when of some severity, are likely to involve the cranialcavity especially following high-velocity or high-energyinjuries associated with road traffic trauma or gunshotwounds. Cranial involvement should be excluded at anearly stage as this may require neurosurgical interventionor a combined approach.

Classically, middle third fractures are divided intocentral and lateral middle third fractures, the lateralmiddle third being essentially the malar or zygomatico-maxillary complex. Central middle third fracturesinclude nasal, nasoethmoidal and maxillary fractures.The original descriptions of Le Fort in 1901 dividedmaxillary fractures into the Le Fort I fracture, which isa subzygomatic fracture separating the dentoalveolarcomplex from the nasal and antral cavities passingthrough the pterygoid plates (Fig. 12.5).

The Le Fort II fracture is a pyramidal fracture, againsubzygomatic, which may involve the cranial cavity inthe cribriform plate area. There may be significant

b)

94 Fig. 12.5 (a) Lateral view of skull showing middle third fractures; (b) Oblique view of skull showing middle third fractures.position of Le Fort I fractures. position of Le Fort II fractures. - position of Le Fort III fractures.

damage to the orbit involving the infraorbital nerves,nasolacrimal apparatus and medial canthal ligamentsoften associated with blowout fractures of the orbits. TheLe Fort II fracture passes across the bridge of the nose,not always at the frontonasal junction but through thenasoethmoid and lacrimal bones, then usually betweenthe nasolacrimal duct and infraorbital nerves and aroundthe zygomatic buttress to the pterygoid plate area, wherethere may also be fractures (Fig. 12.5). The nasal septumwill be separated.

The Le Fort III fracture is a craniofacial dysjunctionseparating the whole of the midface structures from thecranial bones. This extends from the frontozygomaticsutures across the sphenoid bone into the inferior orbitalfissure and through the ethmoid, lacrimal bones, nasalseptum and frontonasal junction and then across to theother side often with some comminution. The zygomaticarches will be fractured and there will be separation orfractures of the pterygoid plates (Fig. 12.5).

Displacement of all midface fractures tends to bedownwards and backwards, thus creating an anterioropen bite appearance, with lengthening of the midface asthe solid structure of the basisphenoid prevents upwarddisplacement.

Zygomatic (malar) bone fracture

The malar complex or zygomatic bone constitutes thelateral middle third of the face and it is commonlyfractured in isolation. Fractures occur close to the suturelines often with comminution of the anterolateral wall ofthe maxilla and sometimes at the zygomatic arch orinfraorbital margin. The masseter muscle exerts somepull on the malar and there is a tendency for it to displaceif not adequately fixed.

Clinical features

These include swelling, circumorbital ecchymosis andsometimes surgical emphysema, as a result of blowingthe nose often after an epistaxis (Table 12.3). Infectionmay spread from the nasal cavity into the sinus and softtissues. Unilateral epistaxis commonly occurs except inzygomatic arch fractures.

Subconjunctival haemorrhages are common and tendto be in the inferior and lateral aspect in malar fractures.

Diplopia is not uncommon. In the initial phase itmay be due to swelling or bleeding around the inferiorextra ocular muscles causing restriction of upward gaze.

Table 12.3 Possible clinical features ofzygomatic (malar) fracture

Swelling: periorbital and over prominence of cheekHaematoma

periorbital (black eye)in buccal sulcussubconjunctivalepistaxis (via blood in air sinus)

Anaesthesiainfraorbital + anterior and middle superiordentalzygomaticofacial, zygomaticotemporal - these are rare

Eye problemsloss of acuity/blindness (rarely)diplopiaenophthalmosdrop in interpupillary line levelexophthalmos (proptosios) – rare after injury but

possible on reductionTrismus: obstruction of coronoid processStep palpable: possible at: frontozygomatic suture,

infraorbital margin, zygomatic arch

Occasionally, the inferior rectus or inferior obliquemuscles are damaged by bone fragments and, morerarely, their nerve supply is damaged. True trapping ofthe muscle can sometimes occur between bone fragments.Much more commonly there is displacement of the orbitalcontents with prolapse of orbital fat into the antrum. Thisis known as a blowout fracture. Within the orbital fatthere are fine fibrous tissue bands attached to the musclesheaths which catch on bone fragments and restrictnormal eye movements. Where there is a very largedefect, gross displacement of the orbital contents canoccur into the antral cavity. This may be accompanied bya medial wall blowout, which must be identified andtreated.

Whenever there is a floor blowout enophthalmos(retraction of the eyeball within the orbital cavity) islikely to be present usually with a drop in pupillary level.This must be identified because it might not beimmediately evident because of intraorbital bleeding andoedema. It is crucial that the bony orbit is fully restoredand the walls rendered intact, otherwise enophthalmoswill persist.

Occasionally, the malar is grossly displaced mediallywith severe proptosis of the eye, which can need earlyrelease, there being a risk of damage to the cornea fromexposure and of a retrobulbar haemorrhage with -ultimately - loss of vision. Careful examination of the

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eye itself, and appropriate referral for an ophthalmicopinion, is mandatory when eye injury itself is suspected.

Rarely, with severe lateral middle third injuries thereis crushing of the superior orbital fissure resulting in asuperior orbital fissure syndrome with ophthalmoplegia,a dilated pupil, ptosis, supraorbital anaesthesia andproptosis; when there is associated blindness fromdamage to the optic nerve or optic foramen this is calledthe orbital apex syndrome. Vision is rarely recoverablewhen the optic nerve is damaged but pressure can berelieved where there is gross proptosis by drainage of anyretrobulbar haemorrhage reducing the risk of visual loss.A strict protocol should be adopted for the managementof orbital injuries, with frequent reassessment of the atrisk patient. In most cases the superior orbital fissuresyndrome recovers spontaneously. Structures in thenarrowest upper part of the fissure recover most slowly,the abducent and the lower branch of the oculomotornerve recover more quickly; surgical intervention is notnormally required.

Asymmetry from displacement of the malar complexmay not be apparent immediately because of theswelling. An examination of the patient from above andbelow, palpating the cheek prominences and orbitalmargins, will usually show any flattening or asymmetry.If there is any doubt about this, waiting up to 10 days willclarify the position and any aesthetic need for treatment.Separation of the frontozygomatic suture can lead toinferior displacement of the malar complex and globe butan intact periosteum will prevent this. Infraorbital margindisplacement is usually posterior and inferior or acombination of both, when the arch is displaced. Thepupillary and canthal position should be noted and thezygomatic arch checked for any step deformity.

Infraorbital anaesthesia is common with malar frac-tures, because the fracture line passes close to or throughthe infraorbital foramen or canal. The anterior superiordental nerve branch may also be damaged, causingnumbness of the incisor and canine teeth. If the nerve iscrushed or severely damaged, full recovery is unlikely. Insevere injuries damage to the zygomaticofrontal andzygomaticotemporal nerves will result in numbness overthe cheek prominence and temporal region. Accuratereduction of the malar assists recovery of infraorbitalsensation.

Trismus is common with malar fractures often due tothe impingement of the malar complex on the coronoidprocess or its fracture with bleeding into the masseter,temporal and pterygoid muscles. This should recover

with reduction of the fractures and haematoma absorption.Ecchymosis in the buccal sulcus due to bleeding at thefracture site is frequently seen.

Radiography

Imaging of the malar has become contentious in recentyears. The 10° and 30° occipitomental views show dis-placement of the malar complex and the submentovertexview, the zygomatic arch and malar prominence (Fig.12.6). Other views have been abandoned as a result of CTscanning. It also provides clear information on soft tissuechanges in suspected blowout fractures. For simpledisplaced fractures of the malar with no obvious orbitalfloor damage, a single 15° occipitomental radiograph isacceptable. MRI scanning has a small place in thediagnosis of blowout fractures. B scan ultrasonographycan be used for detecting the medial wall blowout whenCT scanning or MRI are not available.

Treatment

If there is gross swelling it is usually worth waiting up to10 days for it to reduce for a better assessment of theorbit, its contents and its position. If, however, there arecompelling reasons for early treatment then often theearlier the treatment the simpler the fixation can be.

In the UK, the Gillies temporal approach is widelyused for reduction. A Rowe's or Bristow elevator ispassed under the temporal fascia from a hairline incisionand is used to lift the malar forward and slightly laterally.Occasionally, the malar remains stable but morecommonly additional fixation is required.

Fig. 12.6 30° occipitomental view showing displacementof the malar complex (fracture lines arrowed).

It is possible - under local anaesthesia - to elevate asimple malar fracture with a hook through a small cheekincision, lifting it anterolaterally into a stable position.However, for most unstable fractures additional fixationis required. Usually, fixation with one or two miniplatesfor low-energy injuries at the zygomatic buttress orfrontozygomatic suture where there is separation, isrequired. At the infraorbital margin a microplate providesthe most aesthetic fixation.

Following malar repositioning, the orbital floor needsto be checked and any significant defect needs to berepaired. Calvarial bone graft is best for large defects butfor small defects silicone sheeting with dacron mesh hasbeen widely used. It works well, but there is a compli-cation rate and around 12% are eventually lost or requireremoval; a medial wall defect can be similarly repaired.Microplate fixation is used for simple orbital rim frac-tures. For comminuted complex fractures, fixation at thefrontozygomatic suture and – intraorally - the buttress,are the minimum requirements. Additional plates may berequired at the infraorbital margin, across a main bodyfracture and along the zygomatic arch (Fig. 12.7).

Nasal and nasoethmoidal fractures

Nasal bone fractures are the most common facial bonefracture caused by direct violence. They may be laterallydisplaced or anteriorly depressed. Many are simple

Fig. 12.7 Radiograph showing a reduced malar fracturefixed using microplate (A) and miniplate (B).

requiring minimal treatment but where there is bonydisplacement then reduction is required with straighten-ing of the septum.

Clinical features

The clinical features depend on the extent of violenceand displacement of the nasoethmoid and adjacentstructures. Typically, there will be bilateral periorbitalhaematomata, oedema and nasal obstruction with atendency to mouth breathe accompanied by epistaxis.Nasal obstruction can be caused by septal displacement,which needs to be identified. Lateral displacement iscommon and may be associated with damage or separ-ation of the cartilages and fractures of the nasal bridge.With more severe trauma, the nose becomes saddleshaped, shortened and broadened. With upwards forcethere may be telescoping of the nasoethmoidal complexinto the frontal sinus and then intracranially through thecribriform plate. There is likely to be telecanthus andseparation of the medial canthal attachments. Damage tothe nasolacrimal apparatus can occur and penetratinginjuries can tear the nasolacrimal duct. Obstruction of thecanaliculae and duct stenosis at the lacrimal sac can leadlater to drainage problems. Damage to the cribriformplate area may result in persistent cerebrospinal fluid(CSF) rhinorrhoea. This needs to be recognised early andmanaged appropriately. It is sometimes difficult toascertain whether the clear discharge from the nose isCSF or mucus. Once bleeding has stopped it is possibleto identify this by testing the fluid for glucose ortransferrin, which will not be present in mucus. Othertests, such as radioisotope studies, can be used to identifydifficult and intermittent CSF leaks.

Radiographs

Radiographs of the nasal bones or nasoethmoidalcomplex are usually unsatisfactory, with around 50% ofthe fractures not adequately shown. Markeddisplacements can be seen on 10° and 30° occipitomentalviews where there is displacement of the septum, but thisis usually clinically obvious. Nasal bone fractures canoften be seen on a soft tissue lateral view. The detail of anasoethmoidal injury can only be ascertained from goodCT scans. MRI can also be helpful where there is a CSFleak, as this is likely to show rather better than on CTscans. Medial wall blowout fractures, comminution ofthe nasoethmoidal complex and involvement of the

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frontal sinus will be well demonstrated on CT scanstaken in the coronal and axial planes.

Treatment

Simple nasal bone fractures can be repositioned withWalsham's forceps. In addition, the nasal septum needsto be straightened with Asche's forceps and the lowerportion of the septum relocated in its groove on the nasalfloor. Where there is doubt about the support for the nasalbones and the septal position, gentle packing withVaseline® gauze is usually all that is required. The use ofan external splint is controversial; some feel it helps tohold the complex in place, others use Steri-strips® tosupport and maintain the position.

In the past, when there has been a degree oftelecanthus present, various forms of external fixationusing transnasal wires with lead plates or acrylic buttonshave been used to bring the canthal attachments intoposition. This has sometimes proved successful but itdepends on the size of the bone fragments. In most caseswhere there is significant telecanthus, exploration andopen reduction is necessary. Any damage to thenasolacrimal system needs to be repaired before closureof the soft tissues. Additional support of the soft tissuesin the medial canthal area is valuable. A nasal plastermay be applied and sometimes a small nasal pack. Earlytreatment is essential for severe nasoethmoidal injuries,ideally within 10 days of the injury.

Maxillary fractures

The Le Fort I, or Guerin's, fracture is the simplest low-level fracture; Le Fort II and III fractures frequently caninvolve the cranial cavity. Some symptoms of eachfracture are common but others are individual. It is notunusual to see combinations of Le Fort fractures, withperhaps a Le Fort I or Le Fort II on one side and a Le FortIII on the other, depending on the force applied to themidface. There may be a midline split of the palate,which, if wide, will require repair.

Clinical features

Bilateral periorbital ecchymosis and oedema are typicallyseen with Le Fort II and III fractures, and sometimeswith Le Fort I fractures. Subconjunctival haemorrhagesare usually seen with Le Fort II and III fractures butwhere there is good drainage of blood into the antrum

they may be absent; they are limited by the cornealattachment and extend into the fornix and tend to besegmental rather than complete. There is a flattened dishface appearance to the face and often an increase in themidface height with extensively mobile fractures.

The midface may be foreshortened and impacted up-wards and posteriorly with an accompanying telecanthusbut in general there is an anterior open bite with gaggingof the bite posteriorly and trismus. A check should bemade for a split of the palate by gently springing themolar teeth apart on their palatal surface. Sometimes thissplit is obvious but there may be just bruising in the mid-line. A check on the mobility of the teeth and fragmentsshould be undertaken.

In the Le Fort II fracture, typically, there is densebilateral infraorbital anaesthesia. A mild degree ofanaesthesia may be present in the Le Fort I and also inthe Le Fort III fractures, with numbness in the cheeks,upper lip and lower half of the nose.

The orbits are involved in Le Fort II and III fracturesand diplopia and restriction of eye movements may beevident. There may be marked proptosis of the eyes dueto intraorbital bleeding and oedema. The eyes must beexamined carefully to exclude any serious globe damage;the incidence of which varies in different case seriesbut around 20% is a likely figure, with around 10%permanent visual loss. In craniofacial injuries there maybe visual field changes. Retinal detachments and otherintraocular injuries must be excluded to avoid theirdeterioration during mobilisation of the midface orintraorbital surgical intervention. Usually, if 7-10 daysare allowed to elapse it becomes safe to operate on theorbit. Careful examination of the lids and surface of theeye will identify lacerations and other injuries; an earlyophthalmic assessment is advisable.

CSF rhinorrhoea and bleeding from the nose arecommonplace in Le Fort II and III fractures. Patientsshould be questioned for any discharge or a salty taste atthe back of the throat. They should be sat up and leantforwards, placing a filter paper strip under the externalnares. If after 15 min there is no staining then it is unlikelythat leakage is present. The CSF leak usually stops afterfixation of the midface. In the absence of any intracranialinjury, early reduction of the facial bone fractures isadvised. A persistent CSF leak beyond 10 days after jawfixation is an indication for dural repair. Neurosurgicalviews are mixed on the repair of dural leaks: some insiston repair of all, others feel that only persistent leaksbeyond 10 days need repair. Small defects will be plugged

by brain tissue and fibrosis and the defect seals off in thecribriform plate area, however CSF leaks elsewhere maypersist, especially in the frontal sinus area.

Where there is insignificant displacement of themidface then the dental occlusion can be maintained. Acheck on the mobility of the midface by supporting thehead and feeling with a finger in the palate will indicateany movement there. Tapping of the teeth of a fracturedmaxilla will give a hollow percussion note. With signifi-cant displacements and an anterior open bite usually themidface is easily repositioned but in late fractures theremay be a degree of impaction and mobility may bedifficult to ascertain.

With major midface injuries the rest of the cranio-facial skeleton should be examined fully to excludemandibular condylar and skull fractures. Intracranialinvolvement in major Le Fort II and III fractures oftengives rise to anosmia. Early anosmia may be due tooedematous thick nasal mucosa, which settles over a fewweeks. Disruption of the olfactory nerves can lead topermanent anosmia.

Radiography

Imaging in the midface has radically changed in recentyears with the availability of excellent CT imaging,however certain basic radiographs may be taken inAccident and Emergency departments (i.e. 10° and 30°occipitomental views and a true lateral facial bone view,including the anterior skull). If the lateral radiograph istaken with the patient horizontal, any intracranial air willbecome obvious. Posterior maxillary displacement willbe seen, as will damage to the pterygoid plates. In majorinjuries, mandibular and skull imaging should be under-taken with appropriate intraoral views. Neck injuriesmust be excluded and the cervical spine should be appro-priately imaged. Coronal and axial CT scans are takenfor nasoethmoidal injuries. MRI has only a limited placein midface injuries. However some blowout fractures arerather better seen on MRI and for all forms of braininjury this form of imaging is superior. To avoid repeatscans, patients with cranial injuries should if possiblehave their midface imaged at the same time.

Treatment

Emergency treatment of severe injuries is primarily thatof troublesome bleeding and respiratory problems. Shock,which can result from blood loss or related cranial or

other injuries, needs to be identified (see Ch. 4). Carefulexamination will ascertain the reason for this. Relief ofpain is not usually a major issue with midface injuries.Narcotics should be avoided as they can confuse neuro-logical examinations and interfere with the consciouslevel.

It is usual to give antibiotic prophylaxis for potentialcraniofacial communications, aerocoeles and CSF leaks,although recent guidelines suggest this is unnecessary(see Ch. 19). In the past, penicillin and sulphonamideswere given; more recently, cephalosporins have replacedthem. If antibiotics are given they should cross theblood-brain barrier, but in the presence of injury thispresents no problem. Extensively compound dirty fracturesmay require additional antistaphylococcal antibiotics.

Reduction and fixation of fractures is normally carriedout under general anaesthesia. Care should be taken toensure an intact airway in the pre-, peri- and postoperativeperiods.

High-energy injuries should be differentiated fromlow-energy injuries. The latter usually have a simplerfracture pattern with less displacement and often minorsoft tissue injuries. The essence of reconstruction is toensure that the facial projection is correct, that the facialwidth is not increased and that the facial height iscorrectly maintained.

With low-energy injuries, relatively simple forms offixation for Le Fort I and Le Fort II fractures are ofteneffective. When there is minimal displacement, sand-wiching techniques can be used with external pins intothe supraorbital ridge, attached by bars to the dentition ofthe maxilla or mandible with intermaxillary fixation.Additional malar complex fractures can be individuallyexplored and fixed after the central midface.

A greater degree of surgical intervention is requiredfor high-energy midface injuries. In recent years theconcepts of treatment and protocols have radicallychanged. Vertical strutting may be identified in theanatomy of the midface with three principal buttresseson each side – nasomaxillary, zygomaticomaxillary andpterygomaxillary (at the junction of the maxillarytuberosities and pterygoid plates) - extending up to theskull base. Comminution in those areas is uncommonand it is usually possible to plate those sites.

Access to the upper midface is obtained through thecoronal scalp flap and to the inferior orbit through alower eyelid or transconjunctival incision. The subciliaryapproach tends to yield more complications than a mid-lower lid incision made through a skin crease. The

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transconjunctival approach is also widely used, with acrow's foot extension at the lateral canthus. This givesgood access to the inferior orbit but is limited for themedial and lateral orbit the latter being better approachedbicoronally. A buccal vestibular incision is used to givegood access to the buttress areas. Reconstitution of thezygomatic arch requires a bicoronal incision, taken welldown and extended around the tragus or in a preauricularskin crease.

The general principles for management are to exposeall fracture sites or at least have good access to them andto apply fixation with miniplates. Where there are smallfragments (e.g. at the infraorbital margin), the use ofmicroplates is advantageous. Where there are sizeablemissing fragments, primary bone grafting with calvarialbone graft is the best solution. All bone fragments shouldbe preserved and used. Projection of the midface isobtained by reconstruction and fixation of the zygomaticarches, frontozygomatic sutures and by nasoethmoidreconstruction to complete the orbit. The maxillarydentoalveolar segment is realigned at an occlusal leveland plated at the malar buttress. The junction of thegreater wing of sphenoid and malar complex intra-orbitally needs no fixation but should be checked for anymalpositioning. The dental occlusion, intact mandibulardental arch and rest of mandible are critical for accuratethree-dimensional fixation of the middle third.

The principles are to obtain first projection of theface, then the width followed by the vertical dimension.Care needs to be taken to avoid overclosure of the jaws;hence the necessity for the mandible to be renderedintact. Facial width is corrected by plating the zygomaticarches and frontozygomatic sutures and by reconstructionof the nasoethmoidal complex and infraorbital margin.Finally the height of the face is settled with buttressplating.

There is always some conflict over management ofthe soft tissues. If they are completely stripped off thebone they tend to sag, not only as a result of their ownweight but because of oedema and haematoma present. Itmay be possible to leave portions attached to large bonyfragments. This should be done if it is without detrimentto repositioning bone fragments, otherwise reattachmentof the soft tissue by suturing periosteum at various sitesis essential to avoid displacement of, for example, themalar fat pads. Finally, orbital wall defects especially inthe floor and medial wall are repaired and when necessarythe superior and lateral walls. After medial canthai recon-struction the lateral canthi are checked and if necessary

stabilised with light wires to the supraorbital ridges.Incision lines should be closed in layers with appropriateattention to suturing the galea prior to skin closure withclips or sutures. Large scalp areas should have suctiondrainage for at least 24 h. Small facial incisions areclosed in layers with subcuticular or small interruptedsutures. The intraoral vestibular incision is sutured with aresorbable material.

Blowout fractures

Certain classic signs present notably diplopia, a loweringof pupillary level and enophthalmos, which are pathog-nomonic of this injury. There is often accompanyinginfraorbital anaesthesia. The diagnosis is confirmed byCT scanning. Treatment is based on persistence ofdiplopia and enophthalmos greater than 3 mm or a markedloss of orbital contents out of the orbit. Surgery shouldideally be done within 10 days to achieve a good result.

Access for the pure blowout with no significant orbitalrim fracture is best through a transconjunctival approach.If there are other fractures, a lower lid blepharoplastyincision is effective but in the elderly an infraorbital skincrease incision is safer. For reconstruction, cranial boneor cartilage grafts or an alloplastic material such as asilicone rubber with dacron mesh are widely used.

Craniofacial fractures

Serious craniofacial injuries require early recognitionand joint management with a neurosurgeon. The headinjury takes precedence in the management of the patientand with a deteriorating conscious level early evacuationof a blood clot can be lifesaving. Facial injuries and theirinvestigation take second place. Major high-energyinjuries should be treated relatively early, preferably7–10 days from time of injury to obtain a good result. CTscanning and an ophthalmic assessment of cranio-orbitalinjuries will be needed.

With injuries of this severity, cervical spine injuriesand their management must be considered. Fractures ofthe odontoid peg may be seen in association with cranio-facial injuries. When presenting to the maxillofacialsurgeon, regular checks on eye opening, best verbalresponse and best motor response (Glasgow Coma Scale)are necessary; any deterioration requires neurosurgicalassessment. A careful visual check on acuity, eye move-ments and visual fields is needed. Sensory changes needto be identified and the cranial nerves should be fully

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tested. The external auditory meati should be inspected forany sign of a petrous temporal fracture, noting any CSFotorrhoea or haemotympanum. CSF rhinorrhoea needs tobe identified. Isolated cranial nerve injuries (e.g. to theabducent nerve) are not uncommon. Fractures passingthrough the frontal sinus area may involve the trochlea andlead to a superior oblique paresis (Brown's syndrome).Gross periorbital swelling can make the assessment oftelecanthus or traumatic hypertelorism difficult and CTscanning is essential to distinguish these.

Whenever there is displacement of the cranial com-ponents in craniofacial injuries a combined neurosurgicalapproach is required, and frequently when a CSF leakpersists (see Ch. 19).

Complications

Cranial

The most common cranial complication is a persistentCSF leak. Failure to recognise this can lead to late onsetmeningitis. This should be searched for pre- and post-operatively.

Frontal aerocoeles are not uncommon and arise as aresult of air being forced into the extradural or subduralspaces at the time of injury, often when there are airwaydifficulties. They can usually be managed expectantlyprovided the airway is well maintained with oralendotracheal intubation or a tracheostomy. Intracerebralaerocoeles are an acute emergency and require imme-diate neurosurgical intervention.

Occasionally, there is infection postsurgically, withloss of the frontal bone flap necessitating late aestheticreconstruction with a titanium plate.

Postconcussional headaches are common followingcraniofacial injuries and may be persistent. Post-traumaticepilepsy from local brain injury or surgical repair requiresanticonvulsant therapy.

Ophthalmic

Blindness can occur with severe pressure on the opticnerve or from its avulsion in major trauma. Fundalexamination is essential, to detect this and injuries suchas retinal detachments, choroidal tears and lens dis-locations. Persistent diplopia can result from damage tomuscles or persistent trapping and failure to repositionprolapsed orbital contents. Enophthalmos persists follow-ing loss of orbital contents or an increase in orbital sizefollowing poor surgery.

Proptosis is much less common; it can be due to aninward repositioning of one of the orbital walls. Cornealexposure is a risk when there is marked proptosis. It canoccur following operative treatment of orbital injuries.The eye should be lubricated with chloramphenicol dropsand ointment.

Nasolacrimal

Nasolacrimal damage occurs with severe midfaceinjuries, often from penetrating objects or gross commi-nution. Early assessment after the injury is worthwhileand immediate reconstruction of the ducts and sac shouldbe carried out if at all possible. The nasolacrimal ductand sac is kept patent with a drainage tube. Initialepiphora occurs but usually settles with adequatedrainage. Poor drainage will lead to infection anddacryocystitis and recurrent infections will requiretreatment and dacryocystorhinostomy. Careful evaluationwith appropriate imaging can be helpful in identifyingthe site of the obstruction.

Neurological

Neurological deficit is not uncommon with midfaceinjuries. In the orbit, damage can occur to the optic nerve.Total or partial loss of sight is not so uncommon (around10-12%). Persistent ophthalmoplegia occurs most oftenin relation to the abducent nerve with a lateral rectuspalsy, less commonly from oculomotor or trochlear nervedamage. There may be sensory loss from supraorbital,supratrochlear or infraorbital nerve damage. Mostcommonly there is numbness of the upper lip, cheekand side of nose. Damage to the zygomaticofrontal andzygomaticotemporal nerves may lead to persistent painin their distribution but this is uncommon.

Nasal

Oroantral and oronasal fistulae occasionally occur andthese are easily treated by appropriate flap closure.Persistent antral infection when there is an obstruction tothe orifice in the lateral nasal wall may necessitate someform of antrostomy, but modern endoscopic surgery isoften effective.

Dental

Malocclusions may result from failure to reduce themaxillae they usually present with an anterior open bite

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or retropositioned maxilla. Only osteotomy cansatisfactorily correct this (e.g. a Le Fort I osteotomy).Occasionally, there is trismus and ankylosis from fusionof malar to the coronoid process. This requires operativeintervention with separation of the fragments, bestcarried out via a bicoronal and intraoral approach.

by onlaying cold-curing acrylic. A major displacement ofa segment requires osteotomy surgery with or withoutbone grafting; minor degrees of deformity requireonlaying or masking procedures using cranial bone graftor alloplastic materials. High quality early correctivesurgery almost always produces a better result.

Late deformity

Severe craniofacial injuries in children can lead to a lackof development of the midface, especially the frontonasalarea with a resulting saddle nose. Reconstruction with acantilever bone graft may be helpful but it is difficultto achieve adequate nasal lengthening. There may be apseudohyperteloric appearance with canthal drifting.Late correction is difficult but if there is adequate nasalprojection a slight increase in width of the nasal bridgemay be acceptable. Much scarring around the medialcanthus makes later surgery difficult. A failure to reducethe midface at the Le Fort II and III levels will result inmajor dishing of the face. At the Le Fort III level there isan increased breadth of the face and vertical shorteningonly correctable with a major osteotomy. Hollowing in thetemporal regions, usually following repeated bicoronalflaps being taken down, can be corrected by inserting analloplastic material in the temporal fossa. Irregularities ofthe frontal bone and supraorbital ridges can be corrected

Current developmentsThe development of resorbable bone plates may wellresult in their replacing metal plates. This would avoid thedoubtful necessity for metal plate removal, consideredessential in some countries. Polylactide and other similarmaterials are being used for this purpose.

Where there has been non-union the use of substancessuch as bone morphogenic protein with its insertion atthat site might well prove valuable and where there hasbeen extensive bone loss again it may be possible to usebone morphogenic protein at the site of interpositionalfibrous tissue or muscle.

There is also the possibility of using distraction osteo-genesis in the mandible to create missing bone followinggun shot wounds. These techniques are now availableand should be considered for more complex fracturesituations.

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13Orthognathic surgery

IntroductionOrthognathic surgery is widely carried out for thecorrection of dentofacial deformities. Until the early1970s there were relatively few techniques available forthis correction but since that time great advances havebeen made, with regard to assessment, preparation forsurgery (which is often accompanied by orthodontictreatment) and surgical technique.

A proper assessment of the patient must be carried outin the first instance. The reason for the request forelective surgery needs to be ascertained. In most casesthere is a concern about appearance. However, otherfactors, such as mastication, speech, temporomandibularjoint symptoms and occasionally other features (e.g.ocular problems) in relation to craniofacial deformitymay need to be considered. Proper patient selection ismandatory for a successful outcome.

Preoperative assessmentAs part of the preparation for Orthognathic surgery, thepatient must undergo assessment and treatment planning(Table 13.1).

Assessment

Psychological

A psychological and social assessment is required forpatients with unreal expectations and dysmorphophobia.The patient's personality may be affected by the facialdeformity and they sometimes present in an aggressiveway, or they may be withdrawn. However, the majorityare able to give a clear indication of their concerns.Patients with significant deformity may be improved byrelatively simple surgery that allows them to be accepted

Table 13.1 Preoperative assessment, treatmentplanning and preparation in Orthognathic surgery

Assessmentpsychologicalaestheticorthodonticclinicalradiographic

Treatment planningcephalometricdental castsphotographic

Preparationphotocephalometricorthodonticsplint construction

in society. The type of job that the patient has, and his orher home background and social position may have aneffect on the type and extent of surgery; the expectationsfrom surgery for those in the public eye, who oftendemand a perfect dentition and occlusion, is often greaterthan for others, for whom the simple correction of majorjaw deformity and a minor discrepancy in the occlusionwill be acceptable.

It is important to have an assessment of the familysituation during the planning process and time shouldbe taken for identifying and prioritising a problem list,discussing the issues not only with the patient but alsothe family. With treatment being essentially elective,risk-benefit needs to be taken into account.

Aesthetic

An understanding of facial aesthetics is essential.Measurements are only a guide to a pleasing and accept-able profile, they do not necessarily make one.

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13

The balance of the facial parts needs to be considered,particularly identifying that part which is out of balance.There may be an apparent proclination of the upperincisors in association with gross mandibular retrusion.The latter needs to be corrected and the former does notneed to be changed.

Orthodontic

It is essential to have a good orthodontic assessment andpreparation prior to surgery to obtain a sound interlock-ing postoperative occlusion. To prevent relapse, pre-surgical orthodontic treatment is, in most cases, requiredand a refusal to participate in this needs to be taken veryseriously when deciding upon surgery. It is important torecognise that orthodontic treatment alone can rarelycorrect a significant discrepancy in jaw size. Pressures tocorrect discrepancy in jaw size early in childhood need tobe resisted. Although severe retrusion of the mandibleand maxilla may be an indication for this, when extremeprotrusion is corrected early in adolescence, growth islikely to continue and further surgery will be required atthe end of the growth period.

In the next decade it is likely that many severedeficiencies in jaw size will be corrected by distractiontechniques, with osteotomy surgery being largely reservedfor the end of the growth period (see p. 102).

Clinical

The first step in treatment planning must be the correctdiagnosis of the deformities present and the associateddental problems. Measurements of the face need to betaken from both full face and profile views followed byan oral examination and assessment of nasal and temporo-mandibular joint function. This will need to be evaluatedradiographically, photographically and with dental casts.Additional investigations such as computerised tomo-graphy (CT) scanning, full speech assessment and in somecases a full ophthalmic and neurological assessment willbe needed where changes to the jaws also involve theupper midface.

Radiographic

There are two basic aspects of appropriate imagingfor orthognathic surgery. Conventional radiographs arerequired for the diagnosis of pathology and to showdetail of the jaws and teeth. These will include panoramic

104 radiographs, intra-oral views, occipitomental views to

exclude infection in the midface and views of thetemporomandibular joints where there is a likelihood ofchanges occurring there. Radiographs are also requiredwhich are used essentially for planning purposes. Theseinclude the lateral and posteroanterior (PA) cephalogramand sometimes the submentovertex view to showasymmetry.

The lateral and PA cephalograms need to be taken ina standard position with the head in the natural positionand the Frankfort plane horizontal. The soft tissues needto be imaged and it is therefore necessary to use appro-priate intensifying screens for the lateral cephalogram.

Treatment planning

The basis of planning for the correction of jaw deformityis through cephalometry. The skeletal, soft tissue anddentoalveolar relationships are taken into considerationin the three dimensions of anteroposterior, vertical andtransverse, and various analyses can be used for theidentification of the discrepancy in jaw size.

Cephalometric

To assess the projection of the maxilla and the mandiblein the anteroposterior dimension, SNA, SNB and Pogonionpoints and angles are measured on a cephalogram. Thevertical dimension is assessed, not only in relation to themaxilla but also the mandible. The occlusal plane and theupper and lower incisal angulations and the relationshipof the lips and soft tissues to the dentition and to the jawbones are measured.

Dental casts

A clinical study of the patient's occlusion is helpful but aproper analysis of the dental occlusion can only beobtained by assessment of the study casts and theseshould normally be placed on an anatomical articulator.

Photographic

Although it is customary to take photographs for recordpurposes, a lateral profile photograph may also beproduced life size on an acetate sheet and superimposedon the cephalogram. If they are matched carefully to thesoft tissues on the cephalogram, 'surgery' can be carriedout on the photograph. This form of photocephalometricplanning has provided a reliable way of demonstrating tothe patient the changes that can occur following surgery

and predictions using this method are helpful whenmaking a decision as to precisely what changes should bemade and whether these are acceptable to the patient. Itis essential that the photographs are taken in the naturalhead position and that there is no posturing. Colourtransparencies of the head and neck, both lateral profilepositions, full face and with close-ups of the dentalocclusion and in a smiling position are desirable. Varioustracing methods are used for the photocephalometricplanning and the exact method chosen and thecephalometric points used will depend on the orthodontistand surgeon.

Preoperative preparation

Photocephalometric

In the process of photocephalometric planning theosteotomies are carried out on the lateral profile as theywould be at the time of surgery. That is, the lines drawnshould be as for the osteotomy cuts. For bimaxillarysurgery, especially when height changes are involved, itis usual to move the maxilla first so that the upperanterior teeth are placed in their optimal position. Themandible can then be rotated appropriately to achieve asatisfactory interincisal relationship. The posterior partof the maxilla can then be adjusted to complete theocclusion.

It is essential to remember that the soft tissues donot move the same amount as the hard tissues. When themaxilla is advanced using a Le Fort I osteotomy theupper lip is likely to move forwards only half of thatdistance and the tip of the nose by one third. For Le FortII osteotomies, this changes to two-thirds movement, andfor the middle third at the Le Fort III level the movementis approximately 1:1, whereas an advancement genioplastywill move the soft tissues approximately 85-90% of thebony advancement. Vertical changes of the chin as theyaffect the soft tissues are close to 1:1. These changes areestimated and recorded photocephalometrically.

Orthodontic

Orthodontic treatment can take 18 months or more toobtain the optimal position for surgery. It is generallybetter to complete orthodontic treatment prior to surgery;only minor realignment should be left until after surgeryas any need to open the occlusion postoperatively maylead to a degree of relapse.

Splint construction

Following completion of photocephalometric planning,the precise movements need to be transferred to theappropriately articulated casts so that a good occlusion isobtained. The precise jaw movements need to be definedwhen an ideal occlusion has been found.

Once the casts are set up on an articulator, andfollowing the measurements from photocephalometricplanning, each jaw movement is carried out. From thisoptimal position, thin acrylic occlusal splints can bemade to record each movement. Each splint needs to bechecked individually in the mouth with the upper teethand lower teeth after any occlusal equilibration has beencarried out. They should be made within 1-2 days ofsurgery because minor changes in the occlusion in thepostorthodontic period are not uncommon. The positionalchanges of the casts are transferred to the jaws at the timeof surgery and appropriate markings made on the upperand lower portions of the maxilla.

Mandibular surgeryMandibular surgery can be divided into several sections:

1. surgery in which the jaw is moved in an antero-posterior direction by an osteotomy either in theramus or body of the mandible

2. surgery to the dentoalveolar area, such as segmentalsurgery to shift teeth and alveolus but maintaining theintegrity of the lower part of the mandible

3. surgery to the chin, moving it in a superior, inferior,posterior or anterior direction sometimes accompaniedby levelling and reshaping.

The best operation should be chosen for the patient by asurgeon proficient in all forms of jaw surgery.

Mandibular prognathism

Mandibular prognathism is probably the most commondeformity that requires surgical treatment. It may becorrected in several ways.

Vertical subsigmoid

The vertical subsigmoid osteotomy, (vertical ramusosteotomy) is currently done through an intraoralapproach sectioning the ramus from sigmoid notch tomandibular lower border. The coronoid processes may

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Fig. 13.1 Vertical subsigmoid osteotomy. The ramus issectioned from the sigmoid notch to the lower border of themandible and the fragments are overlapped.

Fig. 13.3 Diagram showing a sagittal split osteotomy.

Fig. 13.2 Diagram showing body osteotomy of themandible with the segment of bone to be removed alongwith the first premolar (hatched).

also be sectioned (Fig. 13.1). This is followed by over-lapping the proximal fragment and shaping it to lie flatagainst the posteriorly repositioned ramus and mandibularbody in its optimal position. Usually this particularoperation is stabilised by keeping the teeth in occlusionwith intermaxillary fixation for at least 4-6 weeks.

If intermaxillary fixation has to be avoided then it ispossible to use the sagittal split osteotomy (see below),taking the distal fragment posteriorly with removal ofbone followed by screw or plate fixation.

Body osteotomy

It is also possible to carry out a body osteotomy when106

there is spacing in the lower jaw or a single tooth can

be removed (e.g. in the premolar region; Fig. 13.2). Thisis often helpful in correcting vertical changes in themandible and can produce a very good occlusion. Surgerytends to be carried out in front of the mental nerve, if atall possible, by removing the first premolar and adjacentbone, although it is acceptable to take the inferior dentaland mental nerves out of the canal and foramen andreposition them if this produces a better occlusion. Thisallows both height changes and some tipping of thedistal segment. It does, however, require careful planningand some expertise. Fixation will be with bone platesaccompanied by light intermaxillary fixation with elasticsin the first instance.

Mandibular retrusion

Sagittal split osteotomy

Mandibular retrusion is most commonly corrected withan Obwegeser sagittal split osteotomy. The Obwegeserdal Pont osteotomy splits the ramus and angle region ofthe mandible sagittally and then slides the segments apartmaintaining the integrity of the inferior dental bundle(Fig. 13.3). Fixation is usually by means of three screwsor a plate sometimes accompanied in the early stage bylight intermaxillary fixation. The sagittal split osteotomyhas been modified to produce better contact with less riskof fragmentation and an improved blood supply reducingthe risk of aseptic necrosis at the angle of the mandible.

Most surgeons now fix the mandible with semirigidfixation. This reduces the relapse rate, ensures bonecontact and a correctly aligned occlusion.

Fig. 13.4grafted).

Inverted L osteotomy (hatched area bone

Inverted L osteotomy

The inverted L osteotomy is used for lengthening theramus of the mandible and is particularly helpful insyndrome and congenital deformity patients (Fig. 13.4).This can be done either through an intraoral or extraoralapproach but if a considerable amount of bone graft isrequired then it is usually easier to do this through anextraoral submandibular approach. Rigid fixation withplates can be used to stabilise the segments.

Segmental osteotomy

Segmental procedures are largely carried out in theanterior mandible. It is essential that the blood supply ismaintained through the genial muscles on the lingualside and these must not be detached from the bone ornecrosis of the whole segment will occur. The approachto the lower anterior segment is with a mucosal lipincision (Fig. 13.5). If the segment has to be significantlyraised then some form of interpositional material such asbone or hydroxyapatite may need to be placed in thespace accompanied by good plate fixation.

Chin deformities

The chin deformities of retrogenia and progenia arecorrected by advancing or retruding the lower bordersegment of the mandible at the chin. Fixation is normallyby means of wires or screws or occasionally plates.Changes in the chin for vertical reduction, require a pieceof mandible to be removed 5 mm below the level of theteeth. Fixation is applied to the upper and lower segments

Fig. 13.5 Segmental osteotomy. The first premolar and awedge of bone have been removed (red arrow) to allow thesegment to be repositioned back (black arrow).

usually with wires or alternatively screws and plates.Vertical augmentation of the anterior mandible requires abone graft into the space created and care needs to betaken to avoid retropositioning the chin point when thisprocedure is carried out.

Maxillary surgeryMaxillary osteotomies can be divided up into threeprincipal types. The first involves the dentoalveolarcomponent of the maxilla at a low level, the Le Fort Iosteotomy. This parallels the low level fracture of themaxilla that occurs in association with trauma. The LeFort II and III osteotomies involved are at a higher leveland involve the nasoethmoidal complex and, for the LeFort III, the whole midface. Essentially, this becomes acraniofacial dysjunction (see Ch. 12).

Le Fort I osteotomy

By far the commonest procedure carried out in themidface is the Le Fort I osteotomy, which correctsdiscrepancies in jaw size involving the lower half of themaxilla and the dentoalveolar component. Thus the LeFort I osteotomy is used for advancement of the lowermidface and for inferior and superior repositioning. Anyform of setback of the maxilla involves removal of aportion of the dentoalveolar segment because it is not

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possible simply to set back the maxilla in its entiretybecause it impinges on the pterygoid plates. It is oftendifficult to obtain a satisfactory occlusion, usually due tonarrowness of the maxilla, especially in secondary cleftdeformities where there is scarring and collapse and inthis situation the maxilla should be expanded prior tosurgery. Small degrees of expansion can be carried outorthodontically and in children rapid expansion is oftena way of separating the two halves of the maxilla throughthe midline palatal suture. In the older age groupsegmental surgery or alternatively surgical expansion ofthe maxilla is required. Presurgical planning is essentialto detect any discrepancy in the arch size and anyproblems with the occlusion following repositioning ofthe maxilla.

Any verticomaxillary excess in the lower face heightcan be corrected by raising the maxilla through removalof a segment of bone on both sides, which includes thelateral nasal walls and nasal septum. In the reverse sit-uation where there is shortness of lower face height, thiscan be corrected by an inferior repositioning Le Fort Iosteotomy, with bone grafting of the space created.Superior repositioning tends to be a stable procedure,whereas inferior repositioning has a reputation for somedegree of relapse and therefore appropriate compensationsmight be needed. The tooth position must be relatedaccurately to the upper lip at rest. Any shortness of theupper lip will not allow for major inferior repositioningnd likewise raising the maxilla excessively with a shortupper lip can similarly give an ugly appearance.

Complications

Complications with this surgery include haemorrhage, afailure to reposition the segments, damage to the teeth(especially the roots) and loss or damage to the bloodsupply of the segments; all of these are avoidable. Thepatient needs to be warned of the potential risks of thistype of surgery. Residual oronasal or antral fistulae canoccur but these are uncommon. Fortunately, completenecrosis of the segment occurs only rarely, usually whenthe soft tissue flaps have been damaged extensively.Hyperbaric oxygen therapy is sometimes helpful in thissituation.

Le Fort II osteotomy

The Le Fort II osteotomy has a unique place for patientswith central midface hypoplasia extending into the

nasoethmoidal area. It allows a certain amount oflengthening of the midface, especially of the nose with acomplete advancement of the central midface.

Various modifications of the Le Fort II osteotomyhave been carried out in the past, simply advancingthe infraorbital margins, leaving the nose behind oradvancing the malars and infraorbital margin leaving thenose behind (Kufner osteotomy). These have a small butuseful place in the armamentarium of osteotomies. Withrigid plate fixation intermaxillary fixation postoperativelyis not required.

Complications

The complications associated with Le Fort II osteotomyare similar to those associated with a Le Fort I; occasionalorbital complications or damage to the infraorbital nerveor nasolacrimal duct can occur, but this is unusual. Thereis a slight tendency to vertical relapse anteriorly and thisis important when maxillary inferior repositioning isbeing carried out and account needs to be taken of thiswhen planning. If onlaying of the maxilla especially overthe malar prominence is required then cranial outer platebone graft is best, fixing this to the anterior maxilla andmalar bones with small screws.

Le Fort III osteotomy

The subcranial Le Fort III osteotomy and its variants areused primarily for correction of total midface hypoplasia,usually of craniosynostotic origin, typically in the Apertand Crouzon's syndromes. In this situation there isusually significant proptosis of the eyes, severe malar andmaxillary hypoplasia and a class III malocclusion with ashort midface height. This can be accompanied by otherproblems such as sleep apnoea, postnasal choanal atresiaand sometimes a cleft deformity. There is often a skulldeformity that may require correction either at the sametime or at a later date. It may be necessary to carry outbimaxillary surgery in this situation, with the advance-ment of the midface as well as its vertical repositioning.A Le Fort I osteotomy may be needed at the same timefor vertical repositioning and to achieve a goodocclusion.

Careful preoperative assessment is essential,particularly with CT scanning to exclude any prolapse ofcranial contents into the naso-orbital areas. Preoperativeophthalmic assessment is also important because changeswill occur within the orbits themselves and it is not

uncommon to see some diplopia following surgery, whichusually settles spontaneously but sometimes requiresextraocular muscle surgery. The approach to the uppermidface is through a coronal flap, which is extendeddown into the preauricular areas on both sides, togetherwith an intraoral approach through vestibular incisions.The latter allows for a Le Fort I osteotomy to be carriedout at the same time. Sometimes it is possible to do all thesurgery through these two incisions, but in other cases itis preferable to use the transconjunctival approach to theorbital floors, which allows accurate cutting andrepositioning in that area. Fixation with multipleminiplates is required and orbital floor repair.

The Le Fort III osteotomy is occasionally used forpost-traumatic cases and rarely for secondary clefts. Itcan also be used in Treacher-Collins syndrome and otherconditions. There is an increasing tendency to think thatthis type of osteotomy surgery is becoming outmodedand advancement through distraction may well be theanswer because this avoids the extensive bone grafting.

Complications

A number of complications can arise from this complexsurgery. Immediate complications associated with thesurgery are a cerebrospinal fluid leak if an inadvertentcommunication with the cranial cavity has occurred.Troublesome bleeding can occur probably from damageto the maxillary vessels or from the pterygoid veins.There can be airway problems and iatrogenic damage tothe endotracheal tube; rarely, blindness has been reportedand occasionally postoperative infections associatedwith the bone grafting procedure. Later problems aremeningitis and postinfective epilepsy. In addition toblindness, diplopia, residual exophthalmos or the

development of enophthalmos, ptosis of the lids orcorneal ulceration can complicate the orbital surgery.There may be an inferior and lateral medial canthal drift.Nasolacrimal damage has been reported, includingdacryocystitis and epiphora, the latter normally recoversspontaneously. Nasal obstruction and paranasal sinusinfections rarely occur. There may be damage to the supraand infraorbital nerves and rarely to the oculomotornerves and muscles, or facial nerve and occasionallyanosmia. Dental malocclusion with an anterior open bitedeformity is occasionally seen, as well as trismus.Residual deformity can result from relapse orasymmetric correction and temporal hollowing. Speechis occasionally affected, with the development ofhypernasality.

Distraction osteogenesisDistraction osteogenesis is now being widely practised asan alternative approach to osteotomy surgery. Whereasmost mandibular and midface osteotomies are carried outtowards the end of the growth period, distraction therapyis possible from infancy. An osteotomy is carried out,gently mobilised and then gradually separated with adistraction apparatus at a rate of 1 mm a day. This can becarried out in the mandible for vertical repositioning, forhorizontal advancement and for transverse changes. It isused in the maxilla, principally for advancement andinferior repositioning and this can be at Le Fort I, II andIII levels. It avoids the necessity for bone grafting andseems to be a stable process. There are a significantnumber of reports on the various osteotomies and theirdistraction but there have been no long-term comparisonsbetween conventional osteotomy surgery and distractionosteogenesis.

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Salivary gland surgery

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Saliva is produced by the three pairs of major salivaryglands - the parotid, submandibular and sublingual glands- as well as the many hundreds of small salivary glandsscattered throughout the buccal and pharyngeal mucosa.The majority of surgical pathology affects the parotid orsubmandibular gland, with the sublingual and minorsalivary glands being less frequently affected. Both theanatomy and physiology of salivary gland function isimportant in surgical pathology and these will bediscussed first.

AnatomyParotid gland

The parotid gland is the largest of the salivary glands. Itlies just in front of the ear extending from the zygomaticarch downwards to between the angle of the mandibleand the mastoid process. This inferior portion is alsoknown as the tail of the parotid gland. The anterior bordercorresponds approximately to the ascending ramus of themandible (Fig. 14.1). It is important to appreciate thatthe tail of the parotid gland extends into the neck andthat lesions in this area can affect the parotid gland andare sometimes mistaken for lymph nodes in the neck.Swellings in this area should be assumed to be arisingfrom the parotid until proven otherwise (see below).

The facial nerve is intimately associated with theparotid gland and runs through the gland, dividing it intoa superficial lobe, which arises lateral to the facial nerve,and a deep lobe, which arises deep to the facial nerve.This is an artificial division and no true anatomical planeexists between the superficial and the deep lobe. Anormal parotid gland consists of 80% superficial lobeand 20% deep lobe. The facial nerve enters the parotid

Fig. 14.1 Anatomy of the parotid gland.

gland from the stylomastoid foramen and, shortly afterentry, divides into an upper and lower division. Theupper division gives off a temporal branch that suppliesthe muscles of the forehead and eye, a zygomatic branchthat supplies the muscles of the eye, and occasionally abuccal branch that supplies the muscles of the nostril andupper lip. The lower division gives off a mandibularbranch that supplies the muscles of the lower lip and acervical branch that supplies platysma in the neck. Thelower division often also gives off the buccal branch.(Fig. 14.2). The facial nerve controls the muscles offacial expression.

The parotid gland is drained by the parotid duct,which opens into the mouth opposite the second uppermolar tooth.

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Fig. 14.2 Branches of the facial nerve.

Submandibular gland

The submandibular gland lies in the submandibulartriangle bordered anteriorly by the digastric muscle,posteriorly by the stylomandibular ligament andsuperiorly by the mandible. This gland also has a

superficial and deep part, the superficial being the largest.The superficial lobe lies superficial to the mylohyoidmuscle, whereas the deep lobe lies deep to the mylohyoidmuscle and is drained by a duct that drains forwards andupwards to open close to the frenulum in the floor of themouth (Fig. 14.3). Three nerves are closely linked to thesubmandibular gland - the marginal mandibular branchof the facial nerve, the lingual nerve and the hypoglossalnerve. As mentioned above, the marginal mandibularnerve supplies the muscles of the lower lip and damageto this nerve will leave the patient with deformity. Thelingual nerve supplies sensation to the anterior two-thirdsof the tongue whereas the hypoglossal nerve suppliesmotor function to the tongue muscles.

Sublingual gland

The sublingual gland is the smallest of the major glandsand lies beneath the mucosa of the floor of the mouthnear the midline. It drains into the mouth by small ducts,as well as by ducts that open directly into the sub-mandibular gland duct. It is closely associated with thelingual nerve.

PhysiologyBetween 1 and 1.5 L saliva are produced a day. In theresting state, the submandibular gland produces most

Fig. 14.3 Anatomy of the submandibular gland.111

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saliva but on stimulation most saliva is produced by theparotid gland. The parotid gland produces a seroussecretion whereas the sublingual and submandibulargland produce two-thirds mucous and one-third seroussecretion. Serous secretion contains amylase for digestion,whereas the mucous secretion contains mucin forlubricating purposes. Removing a major salivary glandhas a negligible clinical effect upon saliva production.

Investigation of salivarygland diseaseRadiological investigations

Plain radiography

Plain radiographs are usually only of use in diagnosingthe presence of stones in the submandibular gland asthe majority in this gland are radiopaque (Fig. 14.4).Plain radiography is of little value if parotid duct stonesare thought to be present because the vast majority areradiolucent; sialography is of more use.

Sialography

Sialography consists of injecting radio-opaque contrastmedium into the submandibular duct orifice or theparotid duct orifice, depending upon which gland isbeing investigated, and radiographs being taken. It isuseful in the diagnosis of radiolucent stones and ductstrictures. Sialography is of some value in sialadenitiswhere a 'tree in leaf' or 'snowstorm' appearance is oftenseen (Fig. 14.5). Sialography can also show tumours ofthe parotid gland indirectly by showing duct displace-ment but computerised tomography (CT) and magneticresonance imaging (MRI) are much more useful for this.It should be noted that sialography is contraindicated inthe presence of an acute infection as it may worsen thecondition.

Ultrasound

Ultrasound is a relatively quick and easy way ofidentifying localised swellings of the salivary glands:usually tumours but also abscesses. It has the advantageof no radiation and can be easily combined with fine-needle aspiration cytology. Its disadvantage is that it isnot always easy to define deep lobe involvement of theparotid gland and is also operator dependent.

Fig. 14.4 A lower occlusal radiograph showing a sialolithin the submandibular duct.

Fig. 14.5 A parotid sialogram showing the 'snowstorm'appearance of punctate sialectasis in a patient withSjogren's syndrome.

CT scanning

CT scanning is useful in defining tumours of the salivaryglands as it usually locates the tumour well and definesextension outside the gland. It also shows lymph-

adenopathy in the neck, which is useful in assessingmalignant tumours as well as possible bone invasion(Fig. 14.6). Its disadvantage is that it involves a sub-stantial dose of radiation to the patient and it does notalways detect tumours in the deep lobe of the gland ifthey have the same radiological density as the gland.

MRI scanning

MRI scanning is probably the best investigation ofsalivary gland tumours as it gives excellent detail of sizeand position and there is no radiation (Fig. 14.7). Itsdisadvantages include availability, and some patientscan't tolerate it because of claustrophobia especially as ittakes a lot longer to perform than CT, and bony detail isnot as well seen.

Radioisotope scanning

At one time, radioisotope scans were used to helpdifferentiate different types of tumours in, especially, theparotid gland. The procedure was unreliable and nowwith the advent of fine-needle aspiration is no longerperformed to investigate salivary gland tumours, althoughit is still occasionally used in assessing function of thesalivary glands.

Fine-needle aspiration

Fine-needle aspiration is a very valuable tool in thediagnosis of salivary gland tumours. It is an easyprocedure and can be performed in the outpatient clinic.With the aid of an experienced cytologist its yield isgood. However, it is sometimes not always possible todifferentiate one type of tumour from another. Thediagnostic success rate for malignant tumours is about70% whereas for benign tumours it is about 90%. Therisk of tumour seeding following fine-needle aspirationis more hypothetical than real and, if it does occur, isexceedingly rare. Its use in non-neoplastic swellings isless well defined as interpretation of these specimensis difficult even for experienced cytologists.

Fig. 14.6 Computerised tomography (CT) scan of aparotid Warthin's tumour.

Fig. 14.7 Magnetic resonance imaging (MRI) scan of aparotid pleomorphic adenoma.

Salivary gland biopsy

Open biopsy of a parotid swelling should be performedonly if it is certain that the lesion being biopsied is not

a tumour, as biopsy of a tumour risks seeding it andmaking subsequent management more difficult. It issometimes useful when the cause of a diffuse salivarygland enlargement remains obscure, or if the diagnosis of

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Fig. 14.8 Incision for a biopsy of the parotid gland. Thebiopsy incision should be placed in part of the standardparotidectomy incision as shown above, depending on thepart of the gland to be biopsied.

lymphoma is suspected. Very occasionally, an open biopsyis necessary to make the diagnosis of a tumour involvinga salivary gland. If this is the case, the specimen shouldbe sent for frozen section to confirm or deny the presenceof a tumour and, if tumour is confirmed, then thedefinitive surgical procedure should be performed at thetime of the frozen section. The site of skin incision isimportant when performing a biopsy of the parotid glandand its correct position is shown in Fig. 14.8. It is alsovery important to be aware of the position of the facialnerve when performing a biopsy of the parotid gland soas not to damage it. Biopsy of minor salivary glands isdiscussed in Chapter 34.

Salivary gland swellingsMost surgical pathology of the salivary gland presents asa swelling in the associated gland and it is helpfulclinically to characterise the swelling as one that affectsthe whole of the gland or as a discrete swelling thataffects only part of the gland. Most discrete swellings arecaused by a tumour, whereas swellings affecting thewhole of the gland are usually caused by sialolithiasis,sialadenitis or sialadenosis (Table 14.1). There isobviously some overlap in this classification but it ishelpful in the clinical context.

Table 14.1 Salivary gland swellings

Discretetumours

Diffusesialolithiasissialadenitissialadenosis

Sialolithiasis

Sialolithiasis, or salivary gland stone disease, is causedby the presence of stones either within the gland itself orin the duct that is draining the gland, symptoms beingmore common when the stones are found in the ducts.The presentation and diagnosis of these are considered indetail in Chapter 34.

Stones in the anterior part of the submandibular ductcan be removed via the mouth by opening (andmarsupialising) the duct (see Ch. 34) but if the stone isfurther back in the duct, or in the submandibular glanditself, then it is safer to remove the gland externally by aneck incision to avoid damage to the lingual nerve.Recurrent parotid duct stones are rare and if they cannotbe removed through the mouth and are considered verytroublesome then they require a parotidectomy, but this isvery unusual. Dilatation of the parotid duct has been triedfor parotid duct stones, especially when they areassociated with a stricture in the parotid duct, and this isworth trying as it is a lot less invasive and has lowermorbidity than a parotidectomy, but its effectiveness isdoubtful.

Sialadenosis

Sialadenosis is defined as a non-inflammatory salivarygland disease due to metabolic and secretory disordersof the gland parenchyma, accompanied by recurrent,usually painless, bilateral swelling of the glands due toacinar enlargement.

Sialadenosis has an equal incidence in the two sexesand occurs most commonly in the fourth to seventhdecades. The disease is suspected when there is recurrentenlargement of both pairs of the major salivary glands,usually the parotids (Fig. 14.9). The gland enlargementcan persist from weeks to months. It is usually associatedwith an underlying condition. Sialadenosis has threemajor causes:

Fig. 14.9 Sialosis occurring in a patient with a history ofalcohol abuse.

• Endocrine: gland enlargement has been described inmost endocrine diseases but it is particularly linked todiabetes mellitis. It can also occur during pregnancyand lactation where its cause is thought to beendocrine in origin.

• Dystrophic/metabolic: this is most commonly seen inchronic starvation and is thought to be linked to thedeficiency of proteins and vitamins. This is also thereason it is sometimes seen in alcoholics.

• Neurogenic: dysfunction of the autonomic nervoussystem can give rise to sialadenosis and this is mostcommonly seen in people taking drugs that affect theautonomic nervous system, such as some antihyper-tensive drugs, It may also be the reason it is seen inpatients who are anorexic but there is probably also anutritional element in this as well.

The diagnosis is made upon the history and clinicalappearance associated with an underlying cause. A parotidbiopsy is needed occasionally, and histology will thenshow acinar enlargement.

The underlying disease is treated but it is very rarethat a parotidectomy will be needed for cosmetic reasons.Even with treatment of the underlying disease, it iscommon for the parotid enlargement to persist.

Table 14.2 Sialadenitis

Acutebacterialviral

Chronicchronic recurrent parotitistuberculosisradiationSjögren'ssarcoidosis

Sialadenitis

Sialadenitis is inflammation of the salivary glands, mostcommonly the parotid, and can be categorised into acuteand chronic types (Table 14.2).

Acute Sialadenitis

Acute sialadenitis may be bacterial or viral in nature.Viral sialadenitis is self-limiting and only bacterialsialadenitis will be considered here.

Bacterial infection usually presents with a suddensense of swelling of the affected gland and there may beredness of the overlying skin. Pus is often seen exudingfrom the salivary gland duct into the mouth and thepatient is unwell. Most acute bacterial infection is relatedto a reduction in the flow of saliva and this is commonlysecondary to an underlying disease such as poorlycontrolled diabetes mellitis or renal failure and occurs inolder patients. There is often an association with poororal hygiene. It used to be a common postoperativefinding but now, with the use of antibiotics and betterfluid management and postoperative oral toilet, it hasbecome an uncommon disease.

Treatment is usually with antibiotics and correction ofthe underlying disease processes if present. Sialogogues(e.g. citrus-flavoured sweets) are often given to encouragethe flow of saliva. If an abscess develops it may needdraining externally. Care must be taken not to damage thefacial nerve when the parotid gland is affected.

Chronic sialadenitis

Chronic sialadenitis has several causes (see Table 14.2)and usually presents with persistent inflammation andenlargement of the affected gland.

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Chronic recurrent parotitis

This presents mainly as a unilateral or alternatingswelling of the parotid gland, which can be painful. It ismainly a disease of children and the saliva can be verymilky or purulent. Attacks occur at variable intervals andin between attacks the child is totally symptom free. Theunderlying cause is not known but it is thought that ductectasia may be a predisposing factor.

Diagnosis is again made from the history andsialography can be considered. Duct ectasia supports thediagnosis when seen on sialography.

Treatment is symptomatic as the underlying cause isnot fully understood. It often involves antibiotics andanalgesia and sialogogues are often given. Most cases inchildhood disappear after puberty. If the attacks continue,ligation of the parotid duct or a tympanic neuroectomycan be recommended. It is very occasionally necessary toperform a parotidectomy.

Tuberculosis

Tuberculosis can present as a chronic sialadenitis,affecting mainly the parotid or submandibular gland. Itsdiagnosis may not be suspected if the patient is notknown to have tuberculosis and is often diagnosed bybiopsy when the cause of a unilateral parotid glandenlargement remains obscure. Occasionally the diseasecan cause a fistula to develop into the skin above theparotid and this is strongly suggestive of tuberculosis.

Radiation sialadenitis

The salivary glands are very sensitive to the effects ofradiation and this is especially a common problem inpatients who have been irradiated for head and neckcancer, as the major and minor salivary glands are oftenincluded within the field. They present with a dry mouthand the presence of thick tenacious saliva, which can bevery distressing. Unfortunately the symptoms tend not toimprove with time.

Treatment is symptomatic and although many typesof artificial saliva are available on the market, theirclinical effectiveness is not high.

Sjogren's syndrome

A consideration of Sjögren's syndrome is beyond thescope of this chapter. The significance of Sjögren's

syndrome to surgical practice is that there is an increasedincidence of malignancy associated with this condition,especially non-Hodgkin's lymphoma. If there is an asso-ciated parotid swelling with Sjögren's syndrome thenthere is a 70-fold increase in the development of a non-Hodgkin's lymphoma. In patients with no salivary glandswelling this decreases to a 10-fold increase in incidenceof non-Hodgkin's lymphoma and these patients shouldtherefore be followed-up to watch for this.

There is no specific treatment for Sjögren's syndromeapart from symptomatic treatment and treatment of theunderlying connective tissue disease present. A rapidlyenlarging salivary gland should be biopsied to rule-out alymphoma.

Sarcoidosis

Sarcoidosis can effect the salivary glands, especially theparotid glands, causing them to enlarge. Treatment isusually with corticosteroids.

Tumours of the majorsalivary glandsSalivary gland tumours usually present as a discreteswelling or nodule in the associated gland. Over 90% ofsalivary gland tumours are epithelial in origin and mostsalivary gland tumours are benign. A classification ofsalivary gland tumours is given in Table 14.3. Eighty percent of tumours arise in the parotid gland, 10% in thesubmandibular and 10% in the minor and sublingualglands.

Most tumours present as a slow growing swelling inthe associated salivary gland and the patient may havenoticed it for some time. It is important, especially in theparotid gland, not to confuse a swelling in the tail of theparotid with a swelling in the lymph node. Indeed, in thisregion it can be difficult to differentiate a salivary glandtumour from a lymph node on clinical grounds alone.This is where fine-needle aspiration and imaging areuseful. When a patient presents with a lump in the parotidgland, it is important not only to examine the lump itselfbut also to document the function of the facial nerve. Theoropharynx should also be examined, as in deep lobetumours of the parotid gland they can often be seenprojecting into the oropharynx and pushing the tonsilinwards. It is also important to examine the neck for anyother associated lymphadenopathy.

Table 14.3 Salivary gland tumours

Benignpleomorphic adenomamonomorphic adenomas

Warthin's tumour (adenolymphoma)duct adenomabasal cell adenomaoncocytomaother adenomas

Malignantintermediate

mucoepidermoidacinic cell

carcinomasadenoid cysticcarcinoma expleomorphicadenocarcinomasquamous cell

non-epithelial tumoursmetastases

The majority of salivary gland tumours are benign butmalignancy should be suspected if there has been a rapidgrowth in the lump associated with pain or if there is anassociated facial nerve paralysis, which is almost alwaysindicative of malignancy. Malignancy should also besuspected if there is ulceration of the overlying skin orthere is associated lymphadenopathy present in the neck.

Investigation of the salivary gland lesion shouldinclude fine-needle aspiration, which will help to differ-entiate a lymph node in the tail of the parotid from a truesalivary gland tumour. It will also be able to give an indi-cation of the type of salivary tumour present, although itis not 100% sensitive or specific, and indeed interpretationof parotid tumours by fine-needle aspiration can bedifficult. CT scanning of a parotid swelling is also usefulbecause it will indicate if there is any deep lobe involve-ment of the parotid gland and also show if there is anyother associated lymphadenopathy in the neck. It mayalso help to differentiate a lymph node from a trueparotid swelling.

Benign salivary gland tumours

Pleomorphic adenoma

The most common benign tumour is the pleomorphicadenoma (Fig. 14.10). This is a benign tumour that ismost commonly seen in the parotid gland. Histologicalexamination shows that there are two elements, an

Fig. 14.10 Pleomorphic adenoma of the parotid gland.

epithelial element and a stromal element. There is anincidence of malignant degeneration in pleomorphicadenomas of the order of 3%. This is usually in thosetumours that are of longstanding and have been presentfor over 20 years. Also, on histological grounds, the greaterthe epithelial component of the pleomorphic adenoma,the greater the chance of malignant degeneration.

The treatment of pleomorphic adenomas is removal,providing the patient is fit enough. As most arise in thesuperficial lobe of the parotid gland this requires a super-ficial parotidectomy. The operation consists of removingthe superficial lobe of the parotid gland (i.e. that part thatlies lateral to the facial nerve), but leaving the deep lobein situ. However, tumours that arise in the deep loberequire removal by a subtotal or total parotidectomy. Thisfirst involves performing a superficial parotidectomy andthen carefully mobilising the facial nerve, to allow thedeep lobe to be removed. The pleomorphic adenomashould not be enucleated as there is an increased chanceof recurrence of the tumour with this. Although, macro-scopically, the tumour appears to have a reasonably well-defined capsule, histological studies show that the capsuleis incomplete and there is often breach of the capsule by

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tumour cells. The tumour should therefore be removedwith a margin of normal parotid tissue. This is sometimesdifficult if the tumour is itself lying against the facialnerve. As the surgical practice of lumpectomy has greatlyreduced over recent years, the incidence of recurrence ofpleomorphic adenoma has also equally reduced.

Adenolymphoma or Warthin's tumour(monomorphic adenoma)

This benign tumour often occurs in the tail of the parotidgland. It has a male predominance and usually occursin the sixth and seventh decades. Ten per cent of thesetumours are bilateral and present characteristically as asoft, fluctuant, mobile mass. The tumour is thought toarise histologically from duct epithelium. Again, providingthe patient is fit and well, a superficial parotidectomy isthe treatment of choice but if it is absolutely sure thetumour is an adenolymphoma (confirmed by fine-needleaspiration) then a lumpectomy will suffice becauserecurrence is unusual. Equally, malignant degenerationdoes not occur. In elderly patients, in whom this tumouris common, follow-up is wise to make sure there is nosudden change in the parotid swelling (which may indicateanother pathology), rather then subject the patient to aparotidectomy.

Malignant salivary gland tumours

As indicated, malignant salivary gland tumours areuncommon. Interestingly, of all tumours occurring in theparotid gland, just 13% are malignant. The incidenceincreases in the submandibular gland, where of alltumours presenting, 32% are malignant. Malignancy ismuch more common in the sublingual and minor salivaryglands, with the majority of salivary gland tumours beingmalignant (56%). The vast majority of malignant salivarygland tumours occur in adulthood and are very rarebefore puberty. The most common malignant tumourbelow puberty is the mucoepidermoid carcinoma. Theaetiology of malignant salivary gland tumours is notknown but malignant degeneration can occur in apleomorphic adenoma.

The six most common types of malignant salivaryglands tumour are acinic cell, mucoepidermoid, adenoidcystic, adenocarcinoma, squamous cell and carcinomaexpleomorphic. The first two – acinic cell andmucoepidermoid – are often known as intermediate

tumours because, depending on their histology, they canbehave in a relatively benign or aggressive fashion.

The treatment of malignant salivary gland tumours isexcision, if possible. Depending upon the size of thetumour, its position and its histology, this may requireremoval of the facial nerve and other surroundingstructures, including the ear and petrous part of thetemporal bone, and part of the mandible.

Postoperative radiotherapy may be necessary. Radio-therapy can be offered in tumours that are thought to beinoperable, but this is usually in a palliative role only.

Acinic cell tumour

This tumour is more common in males and tends topresent as a well-localised lesion. Histologically, it isthought to arise from the boundary zone between theacinar and intercalated ducts. Overall, with resection,about 20% may recur. Pathology is very important aslow-grade acinic cell tumours behave relatively benignly,whereas high-grade acinic tumours behave in a malignantfashion.

Treatment is excision and, in tumours that are histo-logically high-grade, postoperative radiotherapy is oftengiven. If neck nodes are present at presentation then aneck dissection will also be included in the resection.Prognosis is generally good, with a 5-year survival ofover 85%.

Mucoepidermoid tumour

The mucoepidermoid tumour is again similar to theacinic cell tumour in that it that it can be classified intohistologically low-grade and high-grade types; the low-grade type is relatively benign whereas the high-gradetype is a truly malignant tumour. The tumour is thoughtto arise from the ductal epithelium. Tumours with a highmucous content tend to have a low malignant potentialwhereas the highly cellular tumours tend to have a highmalignant potential. Treatment is similar to that of theacinic cell tumour.

Prognosis is dependent on histological type, withwell-differentiated tumours having a 5-year survival ofover 90% but poorly differentiated tumours having a5-year survival of only 20%.

Adenoid cystic tumour

Adenoid cystic tumours of the salivary gland areinteresting in that they often present with a long history

of a swelling of the affected salivary gland. They arecharacterised histologically by perineural spread and areoften associated with pain. Seventy per cent of adenoidcystic tumours actually arise from the minor salivaryglands. There are three histological types: one with atubular pattern, one with a cribriform pattern and onewith a solid pattern. The tubular has the best prognosis,whereas the solid pattern has the poorest prognosis.Cribriform has an intermediate prognosis. Interestingly,although it is sometimes very difficult to cure adenoidcystic tumours, they tend to be very slow growing and thepatient can live a long time with this disease. Indeed,many patients have lung and liver metastasis but can livefor many years even with these present.

Treatment is by excision and postoperative radio-therapy is often given as this is thought to increase localcontrol of the disease. Whether the facial nerve should besacrificed, because of its propensity for perineural spreadin this disease, is controversial. Most surgeons would tryto save the nerve because of the propensity of this tumourfor distant metastases and also due to the difficulty inobtaining local control despite apparent adequate localexcision. If neck nodes are present then a neck dissectionwill also be required.

Prognosis is again dependent upon histological typeand also on length of follow-up. The tubular variety ofadenoid cystic has a 5-year survival of over 95%, withthe 10-year survival being only slightly less than this.The cribriform and solid types have a 5-year survival of65% but at 10-year follow-up this drops to 15%, thusillustrating its propensity for late recurrence.

Adenocarcinoma of the salivary gland

This is a very aggressive tumour and has a poorprognosis. It is important to exclude metastasis of adeno-carcinoma from elsewhere to the parotid gland beforesubscribing the tumour to the gland itself e.g. lung andbreast. Treatment is by surgical excision, often combinedwith postoperative radiotherapy. Prognosis is poor, witha 5-year survival of 40%.

Squamous carcinoma

Again, this is usually a disease of elderly males, often intheir eighties. It has a poor prognosis and it is important,as in adenocarcinoma, to exclude metastasis to theparotid gland often from the skin before subscribing it asa primary tumour of this area.

Treatment is usually by surgical excision if possibleand, again, postoperative radiotherapy is usually given,especially if the tumour is large, the resection wasincomplete or the margins were involved. Prognosis ispoor, with a 5-year survival of 35%.

Carcinoma expleomorphic

This tumour arises from a pre-existing pleomorphicadenoma and presents as a sudden growth of a knownpleomorphic adenoma. It has a poor prognosis and it isoften associated with facial nerve palsy. Treatment is asfor squamous carcinoma. Prognosis is poor, with a 5-yearsurvival of 15%.

Complications of salivarygland surgeryFacial nerve function

The patient should be warned preoperatively about therisk of damage to the facial nerve. Permanent paralysis ofthe facial nerve should be less than 1% in experiencedhands. Some degree of temporary paralysis is not toounusual after a parotidectomy, and is more common whenthe deep lobe has also to be removed, as this requiresmuch more manipulation of the facial nerve. Thisrepresents a degree of neuropraxia of the facial nerve,which should recover fully over a period of 2-3 months.

Various devices are used to help locate the facialnerve and thus prevent injury, the most useful being thefacial nerve monitor and stimulator, which warns thesurgeon when he or she is working close to the nerve, andalso allows the nerve to be stimulated for confirmation. Itis important when using such devices that the patient isnot paralysed, and the anaesthetist should be aware ofthis. Unfortunately, technology is not infallible andexperience of parotid gland surgery is the best methodof avoiding damage to the facial nerve. Stimulating thenerve and seeing the face twitch can confirm that thefacial nerve is working after a parotidectomy.

In submandibular gland surgery it is important toavoid the marginal mandibular branch of the facial nervethat runs in the tissue superficial to the submandibulargland. If this is damaged it leaves the patient with anunsightly droop to the corner of the mouth. Other nervesat risk in submandibular gland surgery include the

lingual nerve (supplies taste and touch to the tongue) andthe hypoglossal nerve (supplies motor function to thetongue).

Greater auricular nerve

The greater auricular nerve is usually divided in parotidgland surgery and this leaves the patient with a numbfeeling of the lower half of the ear lobe. This is of nogreat consequence to the patient as it will often recover,but the patient should be warned of it preoperatively. It isoften possible to save a branch of the nerve, which some-times prevents this from happening.

Frey's syndrome

Following a parotidectomy, the patient may complain ofsweating of the skin over the area of the parotidectomy,especially on eating. The problem is quite commonfollowing a parotidectomy but is only troublesome inabout 10% of patients. This is thought to occur becauseof the inappropriate regeneration of injured autonomicnerve fibres, which are misdirected and supply the sweatglands of the overlying skin. Elevating a thick skin flapwhen performing the parotidectomy can reduce itsincidence. Most cases are not too troublesome and can becontrolled by the use of an antiperspirant. More trouble-some cases may require other procedures such as atympanic neurectomy or the interposition of a tissue flapbetween the skin and the parotid bed, procedures thathave a variable rate of success.

Salivary fistula

This occurs very occasionally after performing asuperficial parotidectomy, and usually presents as salivaappearing from the wound several days after surgery. Themost surprising thing is that it does not occur morefrequently as functioning parotid tissue is left behind (thedeep lobe). The vast majority settle with conservativetreatment, which usually includes a pressure bandage andoften the prescribing of an anticholinergic drug tosuppress saliva production. It is sometimes confused witha seroma that can also occur, occasionally, after surgery.To distinguish a seroma from a salivary fistula, the fluidshould be aspirated and its amylase content measured,this being very high in a fistula.

Other conditions of thesalivary glandsDrooling

Drooling is a normal phenonomen when it is associatedwith teething in childhood, but at most other times it isabnormal. It is often seen in patients with cerebral palsybut it also may be seen in adults with neurologicaldiseases such as Parkinson's disease. It can be caused bythe overproduction of saliva or the presence of anabnormal swallowing reflex. Various surgical treatmentshave been described for the treatment of drooling,including rerouting of the submandibular ducts to draininto the tonsil fossae and also excision of thesubmandibular glands with rerouting of the parotid ducts,with varying degrees of success. Tympanic neurectomyalso has been shown to be of benefit in the short term but,like all autonomic nerve surgery, its long-term results aredisappointing.

Branchial cleft anomalies

First branchial cleft anomalies can present as a sinus,fistula or a cyst, usually in childhood or in the youngadult. The sinus tract often has an external opening in ornear the external auditory meatus. If a true fistula ispresent this has an internal opening into the pharynx nearto the posterior tonsillar pillar. It is often seen in asso-ciation with abnormalities of the ear. One-third of firstbranchial clefts are bilateral. They usually present as acystic swelling in the region of the parotid gland and theyhave a variable relationship to the facial nerve Treatmentis by surgical excision and this usually requires a super-ficial parotidectomy and exposure of the facial nerve fortheir complete removal.

Salivary duct cysts

These usually occur in the parotid gland and are morecommon in men often in their seventh or eighth decades.They present as a swelling in the affected gland, whichon aspiration reveals a clear coloured fluid, and they oftencompletely disappear on aspiration. Often the diagnosisis only made when the cyst is removed, as it is not alwayseasy preoperatively to distinguish this from cysticdegeneration in a Warthin's tumour.

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Ranulaget so large that it interferes with speech or eating.

A ranula is a sublingual swelling. Most consist of a mucus Treatment consists of uncapping and marsupialising it.filled cyst that lies under the mucosa, just lateral to the Very occasionally, the ranula can penetrate through thefrenulum. It is thought to be a retention cyst that arises mylohyoid muscle and into the neck, when it is known asfrom the obstruction of one of the several ducts draining a plunging ranula. This requires excision, as does athe sublingual gland. It presents as an asymptomatic simple ranula if it recurs after uncapping.swelling of the floor of the mouth, but occasionally can

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Plastic surgery

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IntroductionPlastic surgery techniques are widely used to treat avariety of diseases and deformities in an effort toreconstruct both form and function. The basic principlesare fundamental to all surgical practice involving thehead and neck. Advances in plastic surgery techniqueshave opened up new possibilities for reconstruction inthe head and neck. Many of these advances have arisenfrom an increasing understanding of the structure oftissues, their anatomy and their vascularity.

This chapter will concentrate on plastic surgerytechniques that are applicable in the face and head andneck region. This area of the body is one of the mostimportant in determining body image where deformitiesor disfigurement are clearly identifiable. It is also the areaessential for communication with the outside world,allowing us to express emotions such as happiness oranger, which are transferred into visible changes in theface.

A description of the tissues, the skin and facialmuscles will be followed by a consideration of incisions,lacerations, skin grafts and flaps (Table 15.1).

The skinThe skin of the head and neck has several unique featuresthat differentiate it from other areas in the body. Itcommunicates with the respiratory tract via the nostrils,the digestive tract via the oral cavity and the conjunctivallining of the eyelids. The skin of the head and neck has arich blood supply via a complex network of intercom-municating vessels. These can dilate under physical oremotional stress, changing skin colour and appearance(e.g. blushing). This high intensity blood supply opensup plastic surgery techniques that are not routinelyavailable elsewhere in the body.

Table 15.1 Plastic surgery techniques

Incisionslines of electionsurgical access

Treatment of lacerationsManagement of scarsWound closure

skin graftssplit thicknessfull thicknesscomposite

skin flapslocaldistantfree

Novel methodsprefabricationtissue engineering

The skin is also not a single entity. There arevariations in skin thickness and in the distribution of hairgrowth, the latter being a sexual characteristic. There aredifferences in fixity and laxity of the skin with the eyelidsbeing very thin and elastic to allow free mobility.Elasticity and mobility is seen in facial expression and inthe development of creases and wrinkles associated withincreasing age. There are also variations in skin colour,particularly in the face, partly as the result of exposure tothe elements or related to skin diseases such as rosacea.In addition, the face has key landmarks such as the ears,the eyes, the nose and the lips. There are clear boundariesthat separate cheek skin from eyelid skin or nasal skin.These separations have allowed the face to be dividedinto cosmetic units and have changed the thinking infacial reconstructive plastic surgery. Understanding thespecial characteristics of the skin of the face is anessential component of all surgery in this area.

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Facial musclesMuscles of the face can be divided into two broadgroups. The first group concerns functioning of the jawsand is sometimes termed muscles of mastication. Theseinclude the temporalis muscle, and masseter. Thesemuscles are innervated by the trigeminal nerve. Thesecond group of muscles is known as the muscles offacial expression and forms an extensive network ofinterconnecting and interweaving fibres, joined togetherto produce a powerful composite muscle complex. Themuscles of facial expression are innervated by the facialnerve. The muscles are separated from the skin andsubcutaneous tissue by an extension of the superficialcervical fascia. This specialised layer is known as thesuperficial muscular and aponeurotic system (SMAS),which is continuous with the platysma of the neckinferiorly and the galia of the scalp superiorly. It is alsoattached to the periosteum of the zygomatic arch. Thisplane has become increasingly important in face-liftingprocedures. Within this SMAS there are connectionsto the overlying skin, which aid the muscles of facialexpression in creating creases and wrinkles and con-tributing to facial expression. The other importance ofthe SMAS is that the facial nerve lies deep to it, thereforethe superficial surface provides an excellent plane forsurgical dissection, without risk of damage to the facialnerve. The special characteristics of facial skin and thecomplexity of the underlying facial musculature, play animportant part in all facial surgery.

IncisionsIncisions are used either for excision or for access toareas in the head and neck. Such incisions therefore haveto be capable of extension should this be required, butshould also give a good cosmetic result. Wherever possible,incisions should be placed in the line of election.

Lines of election

Wrinkle lines (lines of facial expression)

Wrinkling of the skin occurs in response to underlyingmuscular contraction, and therefore is noticeable ingrimacing, showing the teeth, pursing the lips, closingthe eyes tightly or in facial expressions of anger or joy.Such wrinkle lines are clearly identified in older peopleas permanent crease lines. Where the lines are not visible,

Fig. 15.1 Lines of election on the face.

as in young patients, the direction of the skin creases canbe determined by considering the direction of the under-lying muscle. The wrinkle line lies perpendicular to thelong axis of muscle activity. An example is the frontalis,which works vertically to elevate the eyebrow but createshorizontal furrows in the forehead. The orbicularis oris,which runs horizontally along the upper and lower lips,produces vertical wrinkles in the skin (Fig. 15.1).

Contour lines

Contour lines occur at the junction of cosmetic units.Examples include the nasolabial crease, which separatescheek skin from nasal skin and cheek skin from the lips,and the mental crease, which separates the lower lip fromthe chin. Incisions should not cross cosmetic units andcontour lines.

Surgical access

The head and neck has many hidden areas that aredifficult to visualise and thus add to the problems ofsurgery. Advances in endoscopy equipment have certainly

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improved matters but in many tumour situations directvisualisation requires better access both for tumourexcision and for reconstruction. Such access incisionsshould have minimal morbidity, in terms of function andcosmesis.

Maxillary sinus tumours may be effectively dealt withby endoscopic surgery, as in functional endoscopic sinussurgery (FESS) (see Ch. 18). Another approach is via theupper labial sulcus, which exposes the anterior part of themaxilla. When more exposure is required, a modifiedWeber Fergusson incision can be used. This essentiallysplits the lip in the line of the philtrum and extends alongthe nasal base and superiorly as a lateral rhinotomy at thejunction between cheek skin and nasal skin. It can befurther extended in a vertical direction to the gabellafrown lines, or in a horizontal direction in a pretarsal line.This allows the soft tissue to be hinged laterally to exposethe maxilla. This approach can also be used as a midlinefacial split by incorporating bone separation of the facialskeleton and palate which, like the upper face, isessentially split into two halves.

For the oral cavity, access can be improved by a lowerlip incision placed in the midline in a vertical plane. Thisincision can also be extended to curve round the mentalcrease, keeping in the contour line and extending downinto the neck, extending laterally in the crease line in theneck. This, combined with an access osteotomy of themandible, allows the mandible to swing out, givingexcellent exposure and access to the oropharynx.

Such incisions used for access stay within the lines ofelection, and give excellent functional and aestheticresults (Fig. 15.2).

Facial lacerationsThe integrity of the skin can be broken as a result ofsharp or blunt trauma or following abrasion. The extentof facial lacerations or wounding is often difficult todetermine, partly because of profuse bleeding but alsobecause of oedema, which distorts the anatomy. Thehistory and mechanism of the injury are essential, andfurther investigations are often required (see Ch.12).

Wounds often require exploration under generalanaesthetic to determine their extent and damage tounderlying structures, notably nerves, vessels andmuscles. There are some differences in the managementof facial lacerations compared with wounds outside thehead and neck area. Wound debridement is usually not asradical as elsewhere. This is because of the exceptional

Fig. 15.2 Incisions for surgical access: bicoronal, upperlip and lateral rhinotomy, lower lip and chin.

blood supply to facial structures and because of theimportance of maintaining specialised tissues (e.g. eyelidand lips). What is vital in debridement is to remove allforeign material such as gravel. Foreign bodies maycause problems subsequently and gravel appears astattooing of the scar. It is essential that meticulous woundclosure in layers matches anatomical structures (e.g.eyelids, lips, nostrils, ear), to avoid notching deformitiesand irregularities subsequently. It is important to repairall structures at the time of primary wound closure. Ifbranches of the facial nerve are divided they should berepaired using an operating microscope. If the parotidduct is divided it should similarly be repaired or a stentinserted, with an approximation of the divided ends. Allmuscles should be repaired meticulously, paying particularattention to orientation of the fibres. The process ofwound healing is covered in Chapter 3.

Management of scarsScars in the head and neck are not only disfiguring andnoticeable but often have a social stigma attached. Initial

wounds can look quite satisfactory but, as healingprogresses, scar formation develops. This appears asreddening and increasing size of the scar as it tends tobecome wider and raised from the skin surface. The scarbecomes hard and can be associated with itch and pain.As the scar matures it should become softer paler andflatter. The final scar should look paler than the surround-ing skin, flat and soft and have an atrophic appearance(i.e. look thinner than the surrounding skin), with no skinappendages such as hair or sweat glands.

This cycle of scar maturation can take 1–2 years, andpatients often require support throughout this phase.Occasionally, intralesional injection of corticosteroidscan accelerate the process of maturation; it can also be auseful treatment for itchy and painful scars. Cosmeticallyunsightly scars are usually those that cross the lines ofelection. The pull of the muscle tends to widen the scarwith the passage of time and, as these scars do not lie inthe relaxed tension lines, scar maturation tends to bepoor. Cosmetically unsightly scars can require thedirection of the scar to be altered, or the length of the scarto be broken up. A Z-plasty is a useful way of changingthe direction of facial scars so that at least one limb of thescar lies in the line of election (Fig. 15.3) and alsobreaks-up the length of the scar. Sometimes, facial scarsbecome soft and flat but retain a red colour; lasers cansometimes help in this situation.

Fig. 15.3 A Z-plasty in lower eyelid reconstruction.

Wound closureThe details of wound closure and wound healing havebeen discussed previously (Ch. 3). As far as plasticsurgery techniques are concerned,wounds may be closeddirectly by edge-to-edge apposition or by techniques thatinvolve the import of tissues. Tissue can be importedeither as a graft, which is a non-vascularised piece of skin,or as a flap, which brings with it, its own blood supply.

Skin grafts

Skin grafts have no blood supply and rely on survival byrevascularisation from the surrounding tissue. A graftwill therefore not survive in areas of poor vascularity,such as bare bone (without periosteum) bare cartilage(without perichondrium) or overexposed joints. Graftsare also not applicable where protection is required overmajor vessels and nerves.

Split thickness skin grafts

These grafts comprise the epidermis and some dermalelements but leave sufficient dermis to allow rapidhealing with re-epithelialisation of the donor site. Largeamounts of skin can be harvested and such grafts areuseful for resurfacing large areas of skin loss, such asoccurs following burn injuries. The thicker the graft, themore dermal skin appendages it contains, leading to lesslikelihood of subsequent contracture and a more normalappearance of the skin. Hypopigmentation and poorcolour match in the skin of the head and neck is likelyparticularly with thinner grafts. Common donor sites forsplit thickness grafts include the thigh the upper arm andbuttock. Due to the raw surface that remains prior to re-epithelialisation, donor sites can be painful in the earlypostoperative period.

Full thickness skin grafts

These include the full thickness of the skin and dermisdown to the subcutaneous fat, therefore the donor siterequires to be closed. Skin retains the characteristics ofits donor site. To obtain a good colour and texture match,grafts have to be harvested from the head and neckregion. Common donor sites include the postauricularskin, the preauricular skin and the supraclavicular skin,with direct closure of the donor site. Full thicknessgrafts, because they contain the dermis, are not prone to

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Fig. 15.4 (a) Extensive basal cell carcinoma eyelids-(b) planned excision and cervical facial flap; (c) compositechondromucosal graft (arrowed) from nasal septum-(d) postoperative appearance.

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contracture and give good quality pliable skin, with abetter colour match, when harvested from the head andneck region.

Composite grafts

Composite grafts are peculiar to facial reconstruction andare used in specific areas. Defects of the nostril, whichinvolve the skin, cartilage, nostril rim and nasal mucosallining, can be reconstructed using a composite graft fromthe ear. Excising a wedge from the ear provides two skinsurfaces with a portion of cartilage in between. This canbe inserted to reconstruct the nostril providing skin forlining for the nasal mucosa, cartilage to give supportand shape of the nostril and skin for external nasalreconstruction. A similar wedge can be used for recon-struction of the columella and septal lining.

In lower eyelid reconstruction, lining and support canbe provided using a composite graft from the nasalseptum, comprising mucosa and underlying cartilage.

Table 15.2 Advantages and disadvantages of skin graft types

Graft Advantages Disadvantages

Thin split-thickness graft

Thick split-thickness graft

Full thickness grafts

Composite grafts

Size - large grafts. Good graft take.Rapid re-epithelialisation and healingof donor site

Size - large grafts. Less contractionthan thin grafts. Stable

Good colour and texture match ifharvested from head and neck.Not prone to contracture. Stable

Good tissue match. Composite tissue

Shrink and contract. Poor colour andtexture match. Often unstable. Painfuldonor site

Slow healing of donor site. Donor sitehypopigmentation. Possible scarring atdonor site. Poor colour match for face

Size limited by necessity to close donorsite primarily

Unpredictable graft take. Limited size

Graft success is unpredictable. In nasal reconstructionrevascularisation has to occur from the edges of graftinsertion, since there is no graft bed. Survival can beimproved by enlarging the skin reconstruction elementas a full thickness skin graft, to carry the compositetissue at its distal end. In eyelid reconstruction, a wellvascularised flap is required to cover the graft and ensurerevascularisation (Fig. 15.4). The advantages of thedifferent types of grafts are listed in Table 15.2.

Skin flaps

Skin flaps carry with them their own blood supply andcomprise both skin and subcutaneous tissue. Flapsadjacent to the defect requiring reconstruction are termedlocal flaps. Those from further away and not contiguouswith the defect are known as distant flaps. Distant flaps,which remain attached to the body, are further termedpedicled flaps, whereas those that are detached from thebody and revascularised by anastomosing the arteries andveins, are called free flaps.

The success of flaps is totally dependant on theirvascularity. Where the blood vessels supplying anddraining the tissue is known, flaps are given names,either based on the geographical area (e.g. delto-pectoralflap), on the vascular pedicle (e.g. deep circumflex iliacartery flap) or on the tissue types that the flaps contain(e.g. pectoralis major, myocutaneous flap). Flaps maytherefore be skin flaps (which incorporate skin and fat),myocutaneous flaps (incorporating muscle and skin),muscle-only flaps or composite flaps, involving a widevariety of tissues that can include skin, fat, muscle,nerve, tendon and bone in any combination. Where the

blood supply is not named or known, vascularity of theflap assumes an indeterminate pattern. These flaps arecalled random pattern flaps and are restricted to localskin flaps. They are particularly useful in the face becauseof the intense vascularity of this region.

Local flaps

By definition, these flaps are continuous with the defectto be reconstructed. Many in the face are random patternflaps and are named according to their geometrical design(e.g. transposition flaps, rotation flaps, rhomboid flaps).Essentially, local flaps transfer tissue from an area whereit is available into the defect that requires reconstruction.In the face, common areas of tissue availability are theglabellar region, the preauricular region and the neck.When designing local flaps, it is important to pay attentionto the lines of election. Local flaps generally provide agood colour and texture match in the face but are limitedby tissue availability (Fig. 15.4).

Tissue expansion

One method of increasing the role of local flaps is to usetissue expansion. An inflatable prosthesis is inserted -subcutaneously - and the tissue is gradually distended byinflating the prosthesis over a period of weeks. Thisincreases the tissue availability for local flap transfer. Itis most useful in tissues that can be readily expanded(e.g. forehead and scalp) because of the firm base of thecranium. In scalp reconstruction, in particular, it allowsreconstruction of hair-bearing skin, thus replacing liketissue with like.

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Distant flaps

These flaps have the disadvantage of often being outsidethe head and neck area, therefore they do not providegood skin colour and texture match. However, thedeltopectoral flap, taken from the upper chest, can beused effectively to resurface the neck and will extend upto the zygomatic arch. It is certainly adjacent to the neckskin area and probably provides one of the best colourmatches. This flap has to be taken up in two stages, withthe pedicle divided at 3 weeks and subsequently returnedto its original site (Fig. 15.5). This essentially means thatthe blood supply, which enabled the transfer of the flap,is divided, and the tissue has to survive from ingrowth ofvessels from the original defect.

More useful flaps are those in which the vascularpedicle can be transferred to the head and neck in a singlestage and maintained permanently in this transferred

position. This retains the blood supply to the transferredtissue, promoting wound healing. One of the major flapsof this type is the pectoralis major myocutaneous flap(Fig. 15.6).

Free flaps

The advent of the operating microscope has opened upnew possibilities in reconstructive surgery. The ability torevascularise tissue by anastomosing small vessels of1-3 mm in diameter has enabled the transfer of specifictissue types. The golden rule of plastic surgery is toreconstruct like tissue with like. For example, the abilityto reconstruct the jaw with vascularised bone hasrevolutionised head and neck cancer surgery (see Ch. 17)(Fig. 15.7). Similarly, facial paralysis can be improvedby transferring a functioning muscle flap, reconstitutingits vascular and neural supply. Large volumes of skin canbe transferred to resurface defects for the head and neck,but here the problems of tissue type and colour matchbecome apparent (Fig. 15.8). A notable feature of thesewell-vascularised distant flaps is that they maintain thecharacteristics of their original donor sites. A free skinflap placed for intraoral reconstruction remains as a freeskin flap, with keratinising squamous epithelium, anddoes not change its character to mucosa.

Improved understanding of the anatomy of the bodyhas provided an increasing number of donor sites forfree tissue transfer and surgeons are no longer restrictedby the need to raise flaps in close proximity to the headand neck. A variety of specialised tissues can now betransferred in an attempt to replace like with like.

128 Fig. 15.5 A deltopectoral flap: (a) incision lines;(b) transposed flap in place.

Fig 15.6flap.

A pectoralis major flap isolated on its vascular

Fig. 15.7 (a) Fibula osteocutaneous flap; (b) radiographshowing flap restoring mandibular contour.

Fig. 15.8 A scapula flap: (a) flap elevation; (b) showingpoor colour match.

Free flaps are designed on particular vessels and theytend to have a very good vascularity, which is dependenton a successful microvascular anastomosis of both arteryand veins. There is significant evidence of the vascularityof free flaps, in their ability to heal wounds in the headand neck, and their ability to tolerate postoperativeradiotherapy in cases of malignancy. Free flaps continue

to have a major impact on the cosmetic and functionaloutcomes following major head and neck surgery.

Novel methods

Plastic surgery is concerned with excision and the creationof surgical defects and their subsequent reconstruction.

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A wide variety of methods are now available but somespecialised tissues in the head and neck are virtuallyirreplaceable and it is often difficult to replace like tissuewith like. In an attempt to solve some of these problems,there has been a move towards prefabrication and tissueengineering.

Prefabrication

Prefabrication involves multistage surgery to create apurpose-designed flap to reconstruct a particular defect.A simple example of prefabrication is to harvest buccalmucosal grafts and insert these grafts under the skin andonto the fascia of the forearm. These grafts will take on

the fascia and form a mucosal surface. The flap com-prising the fascia and this new mucosa can be transferredsubsequently as a radial forearm free flap, to providemucosal reconstruction of the oral cavity.

Tissue engineering

Tissue engineering is in its infancy. Specific tissue typescan be grown (e.g. epithelium or bone) under a variety ofgrowth stimulators. Tissue engineering in essence createsnew tissue, which can be of a specialised nature. Thesetechniques are being developed in the laboratory andlook promising in the reconstruction of the specialisedtissues of the face and head and neck in the future.

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Clefts of the lip and palate

IntroductionClefts of the lip and palate are one of the most commoncongenital facial malformations described in humans.They remain, however, poorly understood and present asignificant challenge for reconstruction.

Early records of successful repairs of clefts of the lipexist in Eastern texts and the earliest recorded case ofa successful repair of a cleft lip appears to be aroundAD 390 in China. Over the centuries, many techniques havebeen reported to disguise the visible deformities of cleftlip or the occlusion with cleft lip and palate, as well assurgical techniques for their repair.

Surgeons dealing with clefts of the lip and palate todaymust recognise that although significant advances havebeen made in surgical and anaesthetic technology, the tech-niques of repair are far from perfect and remain an areaof immense controversy and intense debate.

An understanding of the management of cleftdeformities requires a knowledge of the embryologyof the face and the classification of cleft deformity. Thestructural abnormalities that comprise the cleft deformitydictate the patient management and, in particular, thesurgical procedures employed. These will be discussed inturn (Table 16.1).

Table 16.1 Management of cleft deformities

EmbryologyClassification of cleft deformityStructural abnormalities of cleft deformityPatient managementSurgical treatmentSurgical proceduresPhilosophy

EmbryologyThe embryological development of the face is a complexprocess but occurs very early in fetal life. The face de-velops from a central or frontonasal process, which growsforwards and over the developing brain. Two maxillaryprocesses advance anteriorly between the optic vesiclesand the primitive stomodeum and two mandibular pro-cesses advance beneath the stomodeum. The distal end ofthe frontonasal process is defined into medial and lateralnasal processes by the olfactory placodes (Fig. 16.1).

Fusion of the maxillary processes with the frontonasalprocess results in the formation of the premaxilla, whichbears the incisor teeth. Facial features become recognis-able by the fifth to sixth week of intrauterine life. Fusionof the maxillary palatine processes with each other andthe premaxilla (between the lateral incisor and canineteeth) commences at around the eighth week of intra-uterine life at the area defined by the incisive foramen andprogresses posteriorly to the uvula by the twelfth week.

It was initially believed that facial clefts occurred as aresult of failure of fusion of the ectodermal processes

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Fig. 16.1 Development of the face at 5 weeks.

16

described above. However, patterns of presentation ofclefts of the lip and palate have resulted in increasingsupport for theories suggesting that clefts of this regionare likely to be due to a failure of migration of theectomesenchymal cells responsible for the formation ofthe deeper tissues, such as the muscles and nerves,resulting in inadequate tissue support between the twoepithelial layers and consequent breakdown.

The presentation of clefts of the secondary palate isconsistent with failure of fusion of the margins of thepalatal processes.

Clefting may arise as part of a syndrome. Non-syndromic clefting arises as a result of a genetic linkcombined with environmental insults in utero, althoughthe mechanisms remain unclear.

Classification of the cleftdeformityThe deformity in clefts of the lip and palate can rangewidely in severity and extent, rendering attempts toclassify them into a limited set of patterns somewhatimpractical. The various terms used to describe palatalclefts are defined in Table 16.2.

Clefts of the lip may be barely noticeable, withminimal surface abnormalities or asymmetry of verticalheight indicating an underlying abnormality of muscleanatomy, a 'forme fruste' or microform cleft lip. The

deformity can range from this to a complete cleft of thelip, alveolus, primary palate and secondary palate.

Clefts of the palate alone may similarly manifest awide range of severity. There may be no surface or visibleevidence of clefting, but abnormalities of soft palatalfunction only displayed by features suggestive of velo-pharyngeal incompetence. This occult submucous cleftmay occur in an otherwise intact palate with minimalsurface evidence of an underlying abnormality of muscleanatomy. The clinical features of submucous cleftdeformity are listed in Table 16.3.

Although clefts of the lip and primary palateassociated with clefts of the soft palate and/or theposterior hard palate with an intervening bridge of intacthard palate are rare, they have been described. Similarly,clefts of the palate alone involving the bony palate maybe unilateral with partial or complete attachment of thevomer to one side.

Structural abnormalities ofcleft deformityTo fully understand the rationale for treatment of clefts ofthe lip and palate, it is essential to comprehend the com-plex nature of the underlying functional and structuralabnormalities associated with this deformity. Thecomponents of the anatomical deformity are listed inTable 16.4 and these will be discussed in turn.

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Table 16.2 Terms used to describe palatal clefts

Primary palate

Secondary palate

Complete cleft palate

Incomplete cleft palate

Submucous cleft

Unilateral palatal cleft

Bilateral palatal cleft

Palate anterior to the incisiveforamen

Palate derived from the palatalshelves of the embryo.(posterior to the incisiveforamen)

Cleft extending to the incisiveforamen

Cleft not extending to theincisive foramen

Cleft of the muscle layer only inthe soft palate (usually withnotch on the posteriorborder of the hard palate)

Vomer attached to one of thepalatal shelves

Vomer totally separated fromthe palatal shelves

Table 16.3deformity

Clinical features of submucous cleft

Bifid uvulaNotching of the posterior edge of the hard palateMidline translucency of the soft palateAbsence of musculus uvulae

Table 16.4deformity

Anatomical components of a cleft

LipNoseAlveolusPrimary palateSecondary palateMaxillaMandibleOther

The lip

There is soft tissue discontinuity of the lip involving thevermilion and skin. Disruption of the orbicularis oriswith abnormal attachments of the muscle to the skin, thelateral crus of the alar cartilage and the underlying boneoccurs. Some authorities have proposed that the extent ofmuscular abnormality is far more extensive on the affectedside and includes the muscles of facial expression andnasal sphincters, thus requiring a meticulous restorationof functional muscular anatomy.

The nose

The deformity of the nose is minimal or absent in cleftsof the lip that are incomplete with a largely intactanatomy of the orbicularis oris. 'Forme fruste' nasaldeformities may occur occasionally with otherwise intactlips, suggesting that components of the nasal deformityare related to abnormal insertions of the disrupted fibresof the facial muscles.

There is nasal deformity in more complete clefts ofthe lip. The alar cartilage is caudally displaced and themedial crura and alar domes are separated. This results inapparent shortening of the columella on the cleft side anddeviation of the nasal tip towards the cleft side. The bodyof the cartilage may be elongated and rotated. The caudaledge of the septal cartilage may be dislocated. The nasalfloor may be stretched and lower in incomplete clefts andabsent in complete clefts. In addition, the nasal liningmay be webbed with a band of skin across the upperlateral wall.

The alveolus

The premaxillary portion of the alveolus carries theincisor teeth and forms the primary palate, which is thepart of the palate anterior to the incisive foramen. Thegap in the alveolus usually occurs between the lateralincisor and canine teeth and extends obliquely towardsthe incisive foramen. The extent of alveolar clefting mayrange from barely visible notching of the gingiva to acomplete cleft, but the visible manifestations may notcorrelate directly with the extent of underlying bonydisruption.

The primary palate

Clefts of the primary palate extend posteriorly to theincisive foramen, resulting in a deficiency of the nasal

floor. The alveolar arch component on the cleft side(referred to as the lesser segment) tends to be rotatedmesiopalatally and the primary palatal component on thenon-cleft side (referred to as the greater segment) isrotated outwards by the action of the abnormally attachedfacial muscles. The combination of these deformities canresult in a virtual appearance of a significant tissue deficitat the site of the cleft. The septal cartilage is also deviatedas the premaxilla is rotated out.

The secondary palate

The secondary palate extends posteriorly from theincisive foramen to the uvula and is composed of thebony hard palate and the soft palate. Unilateral clefts ofthe bony hard palate result in the separation of the palatalshelf on the affected side from the contralateral palatalshelf at the midline. The affected shelf is often smaller inlength and width and may also be retrodisplaced. Thetransverse deficiency (in width) can be exaggerated bythe cranial tilt of the shelf. The attachment of the vomerto the contralateral shelf may be variable in extent. Theposterior palatal arch width is greater than normalbecause of lateral displacement of the maxillarytuberosities.

The soft palatal component of a cleft palate results ina midline deficiency that can be overt (e.g. in a completecleft) or submucous, with continuity of the lining but adeficiency of the muscles in the midline. The muscles ofthe soft palate are attached abnormally to the posterioredge of the hard palate and the edges of the cleft. Theanteroposterior length of the soft palate is reduced.

The maxilla

The maxilla on the affected side is deficient in verticaland anteroposterior dimensions.

The mandible

The dimensions of the mandible may be smaller inpatients with clefts of the palate, especially as part of thePierre Robin sequence and the potential for growth mightbe compounded by the existing maxillary deformity.

Other anomalies

The abnormal anatomy of the muscles of the soft palate,especially the tensor veli palatini, is believed to be

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responsible for interference with aeration of the middleear due to failure of adequate eustachian tube openingduring swallowing, yawning and other pharyngealmovements.

Patient managementThe management of clefts of the lip and palate ismultidisciplinary and requires the involvement of severalspecialities, which constitute a cleft team. In most cen-tres, the minimum complement of a cleft team involvedin the primary management would consist of a surgeon,orthodontist, speech and language therapist, ENT surgeonand audiologist. The participation of several other disci-plines is also crucial in the management of the child witha cleft deformity, including paediatricians, geneticists,paediatric dentists, hygienists, prosthodontists, psy-chologists and specialist nurses and dieticians.

The initial management of the child born with a cleftdeformity is essentially supportive. The birth of a babywith a facial deformity is often a traumatic experience forthe parents and other members of the family. The staffinvolved in immediate perinatal care (the obstetricians,midwives and paediatric perinatologists) must be able torecognise and deal with the shock and distress of theparents, as well as with any medical problems that mayarise. It is vital that the parents are visited as soon aspossible by a member of the cleft team to discuss thelong-term management of the condition. A considerableeffort must be made to allay the fears and anxieties of theparents and relatives with detailed discussions to explainthe nature of the problem and the long-term prognosis oftreatment.

Parents of babies born with clefts are often overcomeby feelings of guilt and self-accusations of punishmentfor past sins, as well as with a significant loss of self-esteem generated by feelings that the appearance offacial deformity in the baby is a manifestation of theirown imperfection. The absence of perceptible emotionaldistress should not be considered as evidence of coping.It is essential to explore the parents' feelings, ideallywith the support of a clinical psychologist, as rejection ofthe baby will have significant long-term consequencesfor both the parents and the child. Non-syndromic cleftsof the lip and palate are unlikely to present any seriousmedical problems and the only immediate concernsare mainly related to potential airway problems and

134 feeding.

Airways

Newborn babies are obligate nasal breathers and anyevidence of airway obstruction should be assessedimmediately by careful suction of secretions occludingthe oropharynx, and by measures to prevent the tonguefrom blocking the airway.

The Pierre Robin sequence is associated withmicrognathia (a small mandible with obvious lack ofchin prominence), relative macroglossia (a tongue thatappears disproportionately large) with a tendency todevelop glossoptosis (falling backward of the tongue intothe oropharynx) resulting in intermittent airway obstruc-tion, and a cleft palate. Although originally labelled as asyndrome, it is now recognised that this combination offeatures may be associated with a variety of conditions.Feeding difficulties associated with the respiratoryobstruction are also very common.

Various manoeuvres have been utilised to prevent theglossoptosis, which is the fundamental cause of theintermittent airway obstruction. These include nursing inthe prone position in special harnesses, suturing the tongueto prevent retraction, nasopharyngeal or oropharyngealairways, endotracheal intubation and tracheostomies.The problems of airway obstruction tend to be morepronounced when the baby is more relaxed or asleep andare unusual when awake, crying or in the uprightposition. Fortunately, severe problems of airway obstruc-tion warranting a tracheostomy or other surgical pro-cedures are relatively rare. However, it is essential torecognise the condition and institute early appropriatetreatment. Failure to recognise the problem is potentiallyfatal because of the possibility of acute obstruction,progressive exhaustion or brain damage associated withchronic hypoxia. Pulmonary hypertension and cardiacfailure may result from the chronic hypercapnia andhypoxia.

In mild cases, simple postural measures are oftenadequate and careful supervision with the judicious useof devices such as pulse oximeters and sleep apnoeamonitors to detect episodes of airway obstruction aresufficient. The immense emotional and physical stressimposed on the parents or carers of the child must not beunderestimated. It is essential to ensure that the child iskept in a suitable high-dependency or intensive carefacility until it has been established that the risk ofapnoea or cyanotic spells is minimal and the parents feelcomfortable about the prospect of managing the problemat home.

It may be necessary to arrange readmission to hospitalto 'wean' the infant from the apnoea monitor and demon-strate to the parents that the airway problems are unlikelyto constitute a serious risk. A combination of establishingbreathing patterns and the progressive growth of themandible often results in fairly rapid improvement in thesituation. In severe cases requiring surgical interventionsuch as tracheostomies, it may take a long time todecannulate the child.

Feeding

Feeding problems associated with clefts of the lip aloneare unusual. Mothers should be encouraged to attemptbreast-feeding as an adequate lip seal over the nipple canbe achieved. Clefts of the palate, and especially the sec-ondary palate, result in an inability to generate sufficientoropharyngeal negative pressure and tongue compressionagainst the palate. Milk reflux into the nasal cavity andassociated problems such as respiratory difficulties andfatigue, as well as frustration on the part of the mother,compound the problems. Historically, feeding with spoonsand cups have been advocated to allow gravity-assistedpresentation of the feed into the oropharynx, as the abilityto swallow is not affected by palatal clefts.

A wide variety of proprietary teats with compressiblereservoirs and feeding devices have also been designed tofacilitate feeding by minimising the need to suck or byattempting to obturate the palatal cleft. Feeding platescomprising an acrylic palatal coverage constructed on adental cast and secured with ribbon attached to extraoralflanges improve sucking ability, but there is less need forthese nowadays with improvements in other feeding tech-niques, and they are now not generally recommended. Inmany instances, a normal teat with an enlarged holeto permit a steady, gravity-assisted delivery of milk intothe oropharynx is adequate and the mother should beencouraged to identify, by a process of trial and error, thebest method suited to mother and baby. However, it iscrucial that this process is undertaken under the super-vision of a cleft nurse specialist or other member of thecleft team with a specific interest and knowledge offeeding problems in babies with clefts.

Feeding may be seriously compromised by associatedrespiratory or other problems and it may be necessary toresort to nasogastric tube feeding if adequate nutritioncannot be delivered by oral feeds. However, residentnasogastric tubes are associated with significant mor-bidity, such as increased risk of respiratory infections,

pulmonary aspiration and gastro-oesophageal reflux. Inextreme cases, percutaneous gastrostomy might haveto be considered. Careful and regular monitoring ofweight gain and development is essential to ensure thatnutritional requirements are being met.

Surgical treatmentThe fundamental objectives of surgical treatment forclefts of the lip and palate are listed in Table 16.5. A widerange of procedures and protocols for surgical manage-ment of this deformity has been described and contro-versies exist regarding the optimum modalities oftreatment. Rather than becoming immersed in thisdebate, it is advisable to grasp the underlying rationale oftreatment (Table 16.6).

Surgical proceduresThe evolution of surgical procedures for the treatmentof cleft deformities has only been possible because ofadvances in the field of anaesthesia, and especiallypaediatric anaesthesia. The earliest repairs of clefts of thelip consisted of hastily paring the edges of the cleftdeformity without the benefit of anaesthesia andattempting to suture or appose the edges in an effort toseal the gap. Palatal clefts were treated with simpleobturators or crude surgical attempts to repair the cleft

Table 16.5 Objectives of surgical treatment ofclefts

The restoration of normal facial appearance and facialsymmetry

Normal speechNormal occlusionNormal hearing

Table 16.6 Treatment of the cleft deformitycomponents

Correction of the surface geometry of the affectedtissues

Restitution of the underlying structural and functionalanatomy

Modulation of growth and development of the jaws anddentition

Development of normal speech and hearing135

Table 16.7 Rule of 10s

Age: 10 weeksWeight: 10 lbHaemoglobin: 10 g/dL

Table 16.8 Stages of cleft repair

Primary surgerySecondary surgeryRevision surgery

defect. As repair of palatal clefts under such conditionswas associated with risks of considerable blood loss orother complications, they were often undertaken in adultsand, until the 1970s, repair of palatal clefts was notrecommended before the age of 18 months. Repair of lipclefts was advocated by the rule of 10s (Table 16.7).These classic recommendations for the timing of surgeryare still widely applied today in several leading cleftcentres in the world.

Repair of the cleft deformity can be divided into threecategories (Table 16.8).

Primary surgery

The objective of primary repair is to close the cleft gap,restore the symmetry or dimensions of the lip by

addressing the geometric deformity and restore theunderlying structural and functional anatomy of theaffected tissues.

The lip

The timing of cleft lip repair ranges from neonatal repairto delaying surgery to between 6 and 9 months of age.The advantages and disadvantages of neonatal repair arelisted in Table 16.9.

Lip adhesion

Lip adhesion involves merely approximating the skinwithout muscle repair. Although it is routine practice insome leading centres to employ lip adhesion as a primaryprocedure at varying times, there is no evidence tosuggest that the procedure confers any long-term benefitand it has the disadvantage of increasing the total numberof operative procedures if palatal repair is not undertakenat the time of the definitive lip repair.

Proponents of primary lip adhesion argue that itserves the same function as preoperative orthopaedics tomould the component tissues into a more favourableposition without the considerable inconvenience andcumbersome nature of the process. Lip adhesion mayhave a role in wide bilateral clefts or in wide unilateralclefts if preoperative orthopaedics have failed to narrowthe cleft gap or the risks of breakdown of a definitiverepair are likely to be high.

Table 16.9 Advantages and disadvantages of neonatal repair of cleft lip

Advantages Disadvantages

Theoretical advantage of scarless fetal wound healingReduction of psychological trauma period for parents

and possibly better maternal bonding because ofrestoration of facial aesthetics

Higher levels of circulating maternal immunoglobulinsconferring improved resistance to infection

Higher haemoglobin level with possibly better woundhealing

Dimensions of lip and nose are only slightly smaller thanat 3 months. Surgical planning is not compromised

Parents take home a baby with a repaired lip cleft

Underlying alveolus is more malleable and moulded afterrepair

Tissues are more friable and delicateNeed for postoperative intensive care, which may adversely

affect maternal bonding and compound psychologicalstress factors

Underlying cardiac or other abnormalities may not bemanifest at this age. Risk of producing a patent ductus

Neonatal jaundice and risks associated with neonatalanaesthesia

Primary rhinoplasty with alar cartilage dissection is difficult.Functional restoration of muscle anatomy is difficult.Anatomical landmarks are not clearly defined

The period of psychological adaptation to an unrepairedcleft may reduce long-term unrealistic expectations

Repair is more difficult in wide or bilateral clefts with noopportunity to utilise preoperative orthopaedics136

Lip repair at 3 months

This is the traditional recommended timing for lip repair.The anatomical landmarks are well developed at thisstage permitting accurate planning and restoration of thegeometric anatomy of the soft tissues. The nasal tissuesand alar cartilages are also sufficiently developed topermit dissection for a primary rhinoplasty.

Lip repair at 6 months or later

It is easier to repair the palate and undertake a morecomprehensive palatal repair, especially of the primarypalate and the nasal floor, using the 'working forwardfrom the back' approach. Some proponents advocate aone-stage repair of the entire deformity at this age.'Functional' repair of the muscles of the lip, nose andpalate are believed by advocates of the Delaire functionalrepair philosophy to be possible at this stage, when thecomponent muscles of the orbicularis oris and perinasalmuscle ring can be more readily recognised.

The correction of the vertical dimensions of thevermilion itself is equally important and the value ofidentifying the 'dry' vermilion and restoring the verticalheight of the dry vermilion - and avoiding any use of'wet' vermilion as a substitute - is being increasinglyrecognised.

The importance of the restoration of the muscularanatomy of the orbicularis oris in maintaining theproportions of the lip, and especially the symmetry of theface during dynamic movements, is crucial. Meticulousattention needs to be directed to the careful detachmentof the abnormal insertions of the muscles into the softtissues and bony structures adjacent to the cleft as well asreconstruction of the superficial and deep components ofthe muscle. Some authorities propose that the accuratereconstruction of the superficial part of the orbicularisoris, which arises from the muscles of facial expression,requires radical subperiosteal mobilisation of the facialsoft tissue mask to adequately reposition the muscles offacial expression and reconstitute the anatomy of the lip.

Reconstruction of the anterior nasal floor and anyassociated cleft of the primary palate is desirable at thetime of the primary lip repair as the access to these areasis considerably facilitated at this time.

The nose

Primary correction of the cleft nasal deformity is nowwidely accepted as an essential procedure for the resto-

ration of the symmetry of the nose. Several techniqueshave been described. Those utilising extensive incisionsof the nasal lining should be avoided as the risk ofstenosis of the nasal airways is high.

The restoration of the nasal architecture, form andsymmetry can be properly achieved only by utilising thetissues of the nose. The alar cartilage on the cleft side, orboth alar cartilages in a bilateral cleft, may be mobilisedquite radically through the cleft lip incisions, avoidingthe need for any incisions in the nasal lining. The growthand development of the nose is very dependent on thenormal flow dynamics of the nasal airways and the temp-tation to use the lining of the inferior turbinates or similarstructures, which result in gross distortion of the airwayarchitecture, should be avoided.

The alveolus

Primary repair of the alveolus has been attempted bymany authorities in an attempt to stimulate normal dev-elopment of the alveolar arch form. Primary bonegrafting, with cancellous bone at the time of lip repair,has been largely abandoned because of long-term facialgrowth problems that result. There is at present somerenewed interest in gingivoperiosteoplasty, which con-sists of initial orthodontic manipulation to produceabutment of the gingival cleft edges prior to the lip repairand a simple restoration of the gingival continuity withminimal dissection at the time of the lip repair.

Alveolar closure undertaken in the mixed dentition,just prior to the descent of the canine, is often referred toas a secondary alveolar bone grafting procedure to dis-tinguish it from alveolar closure undertaken at the time oflip repair. This is a planned procedure in terms of thetiming of surgery and is undertaken at the age whensufficient permanent teeth have erupted to allowpreoperative orthodontics with expansion of any collapseat the site of the cleft and alignment of the alveolarsegments.

Resorption of the alveolar bone graft is likely to occurif canine descent does not follow soon after theprocedure, and the bone grafting is therefore timed tocoincide as closely as possible with the time of expectedcanine eruption at the site of the cleft. At the time ofalveolar bone grafting, it is common practice to augmentthe bony foundation of the alar base on the cleft side withcancellous bone chips or corticocancellous bone block toimprove the projection and symmetry of the nose.Revision surgery might be indicated also for the lip and

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138

the nose to minimise the total number of surgicalinterventions.

The primary palate

Closure of the primary palate at the time of the lip repairis recommended as access to this area is extremelydifficult after lip closure. The repair may be a single layerrepair using the mucoperiosteal lining of the vomer. Two-layer closures have been described if the gap is narrow orusing buccal mucosal flaps for the oral lining.

The secondary hard palate

The cleft of the bony secondary palate is often quite wideand attempts to achieve closure may require extensivelateral releasing incisions. Studies evaluating facialgrowth in patients with unrepaired clefts of the palate ordelayed repairs clearly suggest that surgery of the palatemay be directly implicated in the subsequent restrictionof facial growth.

Some authorities undertake repair of the palate in twostages by initially repairing the soft palate, whichencourages descent of the hard palatal shelves andnarrowing of the cleft gap, allowing closure at a secondstage with minimal dissection.

The soft palate

Early observations that the anteroposterior length of thepalate was deficient led to the design of passive pushback techniques aimed at lengthening the palate to allowvelopharyngeal contact. Detachment of the abnormalinsertions of the muscle elements into the soft tissues andposterior edge of the bony hard palate and restoration ofthe muscular anatomy of the soft palate is essential toachieve effective velopharyngeal closure.

Secondary surgery

Secondary procedures in the management of cleft lip andpalate may be grouped chronologically, as listed in Table16.10.

Fistula closure

Fistula closure following palatal cleft repairs is oftenundertaken early if it is felt that the fistula may causefunctional problems with speech, swallowing or nasalregurgitation of ingested foodstuffs. The presence of a

Table 16.10 Secondary surgical procedures

Fistula closureSurgery for speech - pharyngoplastyRhinoplastyOrthognathic surgery

fistula does not warrant closure if there is no demon-strable or predicted functional problems likely to beassociated with the fistula.

Surgery for speech

As speech develops, the regular and expert assessment ofa cleft speech therapist is essential to detect and rectifyproblems of articulation or other speech problems. Velo-pharyngeal incompetence resulting from ineffectiveclosure of the velopharyngeal aperture is often notcorrectable by conservative treatment and early surgicalintervention may be warranted.

Pharyngoplasties are designed to reduce the dimen-sions of the velopharyngeal aperture to facilitate closureor simply increase the resistance of the airway tominimise nasal air escape. They are broadly classified asdynamic - procedures (e.g. orticochea pharyngoplasty),which are designed to mobilise the palatopharyngeusmuscle bundles in the posterior tonsillar pillars andattach them to the posterior pharyngeal wall - or passive- procedures that simply narrow the velopharyngealaperture or augment the posterior pharyngeal wall usingimplanted materials.

Rhinoplasty

The preschool age is also a common time for parents torequest secondary corrective procedures for theasymmetry of the nose by a rhinoplasty procedure. If anadequate primary rhinoplasty was undertaken and thedegree of asymmetry is within expected limits, everyadditional procedure undoubtedly confers additionalscars within the nasal tissues, which may compromisethe final result. Secondary rhinoplasty at this age, or inthe preteen age group, should be undertaken only forgross or obvious deformities causing problems of sig-nificant psychological or functional distress.

Secondary rhinoplasty at or nearing the end of thegrowth phase is common. If orthognathic surgery isplanned, it is often preferable to undertake the surgeryfollowing the orthognathic procedures to restore the sym-metry and aesthetic balance of the face, and especially

the bony foundations of the nose. The procedure can becombined with the orthognathic operation, if preferred,to minimise the number of operative interventions.

Orthognathic surgery

With improvements in primary surgical techniques andthe recognition of the potentially harmful effects ofsurgery on facial growth and symmetry, it is anticipatedthat a smaller proportion of patients will eventuallyrequire orthognathic procedures.

In those patients with gross occlusal problems causedby restriction of midfacial growth or other facial skeletalproblems, Le Fort osteotomies, bimaxillary surgery, dis-traction osteogenesis, on-lay bone grafts or other pro-cedures may be indicated. Fixed orthodontic appliancesare required to achieve the optimal occlusal outcome inconjunction with surgery. The use of osseointegratedimplants and facial reconstruction is becoming morecommon in the management of patients with clefts.

PhilosophyThe management of the patient with a facial cleftdeformity is a lifelong project. The long-term con-sequences of each procedure undertaken must beanalysed carefully to weigh-up the potential advantagesand disadvantages with the full involvement of, initially,the parents or carers and subsequently the patient. Allmembers of the cleft team should share equal responsi-bility in the decision-making process. It is essential thatthe care of cleft patients is undertaken by dedicated cleftteams with adequate centralisation of resources andpatient referrals. Continuous and intercentre audit of theoutcome of established protocols of care, which arestrictly enforced, is essential to monitor outcome andrefine techniques. It will also help to identify factors forpoor outcome. The search for the optimum protocol ofcare is currently a subject of considerable interest andspeculation.

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Management of orofacialmalignancy

IntroductionOral cancer is the eighth most common malignancyworldwide, although the prevalence varies from countryto country. In countries such as India, oral malignancyaccounts for 40% of the total, whereas in the UK around4000 new cases present every year, accounting foraround 3% of all new malignancies. Around 50% ofthese patients will die from their disease and overallsurvival rates have not improved over the last threedecades, despite advances in surgical and oncologicaltechniques.

The incidence of oral cancer has been rising steadilyover recent years; the reasons for which are unclear. Oralcancer generally appears from the sixth decade andincreases in incidence in subsequent decades. It shouldbe appreciated, however, that oral cancer can occur at anyage and the recent rise in incidence has been moreapparent in the younger age groups.

Oral cancer is almost exclusively squamous cellcarcinoma, which accounts for 90% of the total; theremaining 10% is made up by salivary gland tumours(8%) (see Ch. 14) and oral lymphoma (2%).

Over the past 30 years, social deprivation has becomestrongly linked with oral cancer. In the early 1970s, oralcancer was spread relatively evenly over all socialclasses. When the detrimental effects of smoking becameclear, the better educated tended to reduce their cigaretteconsumption, but those living in deprived areas have con-tinued to smoke to a much greater degree. The aetiologyof oral cancer is, however, complex. The high-risk popu-lation is that least likely to attend the dentist and there-fore most likely to present with advanced disease.

In the UK, the majority of patients tend to presentwith advanced disease and, by definition, a poor prog-nosis. In many European countries, more than 70% ofpatients present with early disease, increasing the chanceof cure and reducing the need for radical treatment.Despite the fact that treatment for oral cancer hasadvanced considerably over the last 30 years, survivalhas not improved. This is due to the lack of under-standing of tumour biology. Research into tumourbiology is coming to the fore, hopefully allowing thedevelopment of new treatments.

Various aspects of the diagnosis and treatment of oralcancer are discussed here (Table 17.1).

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Table 17.1 The diagnosis and management oforal malignancy

AetiologyMorbidityPremalignancySigns and symptomsStaging of diseaseClinical investigationMultidisciplinary treatmentTreatment planningTreatment of the neckReconstructionQuality of life issues

Aetiology of oral cancerThe aetiology of oral squamous cancer is complex. Themain factors associated with this disease are tobacco andalcohol consumption. Each of these factors increases thelikelihood of oral cancer and both show a strong dose-related increase in incidence. It would seem that heavysmoking and heavy drinking have a synergistic effect,leading to an exponential rise in relative risk (Fig. 17.1).

Tobacco is the main aetiological agent associated withoral cancer. The risk of oral cancer is related to thenumber of cigarettes per day and the length of time the

17

patient has smoked, giving rise to the concept of packyears, where a pack is equivalent to 20 cigarettes:

This formulation allows a calculation of the relative riskof each patient. The relative risk returns to that of a non-smoker 10 years after the cessation of smoking. Topicaltobacco, particularly, when mixed with areca nut, slakedlime, and betel and placed as a quid in the buccal sulcus,is a potent carcinogen. On the Indian subcontinent, wherethe practice of chewing tobacco is common, oral cancermakes up 40% of the total incidence of all carcinomas; itis also prevalent in Asian communities in the UK.

Alcohol per se does not appear to be a potentcarcinogen but seems to potentiate the effects of tobacco.Someone who smokes 30 or more cigarettes per weekhas a relative risk of seven-fold that of a non-smoker. Aperson who drinks 40 or more units of alcohol per weekhas a relative risk of six-fold; if these factors arecombined then the relative risk of oral cancer increasesby a factor of 38.

Recent research suggests that genetic factors play asignificant part in the promotion of oral cancer. Cancer is

prevalent in some families and this can include oralcancer. There is a cohort of patients who develop oralcancer in the third or fourth decade. This group, mainlywomen, develop aggressive cancers with a poorprognosis.

Cellular biology investigations show that disturbancesin the regulators of cell growth and cell death (apoptosis)lead to the development of oral cancer. This is a rapidlyexpanding field and it is likely that new prognosticindicators and cancer treatments will come from thisresearch.

Other agents that may be implicated in oral cancerpathogenesis include malnutrition, poor dental hygiene,infective agents and sunlight in lip cancer.

Oral cancer morbidityThe number of deaths from oral cancer has been risingover the last 30 years. The death to registration ratio is0.4, which is higher than many other cancers and similarto cancer of the uterine cervix and breast. The site inthe mouth is an important prognostic indicator, with thetongue having the poorest prognosis and highest mortality(Table 17.2).

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Fig. 17.1 The risk of oral cancer by alcohol/tobacco consumption.

Table 17.2 Registration and deaths by site inScotland 1991-1996

Site Registrations (%)

Tongue 25.0Unspecified mouth 19.2Floor of mouth 17.6Lip 14.5Oropharynx 12.5Ill-defined sites 6.3Gum 4.7

Deaths (%)

29.919.512.92.4

14.516.54.2

Cancer surveillance group 1998

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Survival rates have not improved over the past50 years, mainly due to late presentation of patients withthe disease. It has been shown that the delay in presen-tation correlates well with social deprivation. Educationprogrammes are required to target the at-risk groups, andonly when lifestyle begins to change is there a likelihoodof an improvement in survival.

Premalignant lesionsThe vast majority of oral malignancies arise frompreviously normal epithelium. A small number of newmalignancies may develop from abnormal mucosa.

White or red patches may precede the development ofcancer and allow the opportunity of early biopsy. Thiswill determine whether a lesion is premalignant. The siteand colour of these lesions can give some idea of theirmalignant potential. A speckled or red lesion is morelikely to be premalignant than a homogeneous whitelesion. A lesion situated in the floor of mouth or lateralborder of the tongue, irrespective of colour, has a higherchance of being premalignant. Biopsy is helpful indetermining the malignant potential of any lesion. Alesion that persists for more that 2 weeks followingremoval of chronic trauma should be referred for biopsy.Many of these lesions are likely to be asymptomatic.

Signs and symptoms of oralcancerTumours can be very advanced before patients developsymptoms that cause them to present to their doctor ordentist. Early warning signs include soreness in themouth, a lump or thickening, a red or white patch or a

non-healing ulcer. Later symptoms include interferencewith speech or swallowing, weight loss, trismus, aninfected ulcer, pain referred to the ear, sensory dis-turbances and the appearance of a neck lump. Tumoursmay be of considerable size before the latter symptomsbecome apparent.

On examination, oral tumours have a variableappearance. They may present as a white or red patch,with or without an ulcer or erosion or as a lump orthickening with intact mucosa. Classically, the squamouscell carcinoma presents as an ulcer with a rolled marginwith induration around it. There may be fixation tosurrounding tissue and the ulcer may bleed readily afterminor trauma. Tumours of the oropharynx and tonguebase may first present as a neck lump. To make a diag-nosis a biopsy is mandatory.

Staging of the diseaseCancer is staged using the TNM classification, where Tmeasures the primary tumour size, N the draining lymphnodes, and M distant metastasis (Table 17.3). Using thisclassification, these can be further stratified to stages(Table 17.4). Using this universal language to identifythe extent of disease helps provide a prognosis, which isdependent on stage. It also helps in defining treatmentprotocols and in the analysis of management and survivaldata. Knowing the extent of the disease is of primeimportance for clinicians working in multidisciplinaryteams so that the true extent of the disease is known.

Table 17.3 TNM staging

Tx Tumour cannot be assessedTO No evidence of primary tumourT1 Tumour <2 cm in greatest dimensionT2 Tumour >2 cm but <4 cmT3 Tumour >4 cmT4 Tumour invading adjacent structures (e.g. skin,

cortical bone, deep muscles of tongue)NX Regional lymph nodes cannot be assessedNO No regional lymph nodes palpableN1 Single ipsilateral lymph node <3 cmN2a Single ipsilateral node >3 cm but <6 cmN2b Multiple ipsilateral nodes <6 cmN2c Bilateral or contralateral <6 cmN3 Any node >6 cmMX Distant metastases cannot be assessedMO No evidence of distant metastasesM1 Distant metastases present

Table 17.4 American Joint Committee onCancer Staging guidelines on clinical staging

Stage 0Stage 1Stage 2Stage 3

Stage 4aStage 4bStage 4c

Tis NO MOT1 NO MOT2 NO MOT3 NO MOT1-3 N1 MOT4 NO–1 MOT1–4 N2–3 MOT1-4 N1-3 M1

The extent of the disease will determine the prog-nosis. The prognosis for stage 1 and 2 disease is good,with reported 5-year survivals rates of 85% and 70%,respectively. The outlook for stage 3 and 4 disease ismuch poorer, with survival rates of around 45% and25%, respectively. The presence of lymph node meta-stases can reduce survival by 50% and lymph nodes dis-playing extra capsular spread reduces the 5-year survivalto as low as 17%.

Initially, disease is staged clinically. However, clinicalexamination is a poor indicator of the actual extent ofdisease. Palpation of the neck is only sensitive andspecific in around 66% of cases and detection of lymphnodes smaller than 2 cm is difficult, even under generalanaesthetic.

Clinical investigationClinical examination

When a patient presents with oral cancer, the suspicionneeds to be proven histologically. This is straightforwardif the lesion is in the anterior part of the oral cavity and abiopsy can be harvested under a local anaesthetic. If thisis not possible then it is performed during an examinationunder general anaesthetic. The examination underanaesthetic allows the surgeon to examine the oral cavity,oropharynx, nasopharynx, hypopharynx and larynx forsecond primary tumours and, as previously mentioned,the neck is also examined while the patient is relaxed.Fine-needle aspiration of any neck lumps can be carriedout at this stage.

With oral cancer, almost 70% of second primariesoccur elsewhere in the oral cavity or oropharynx. Themajor causes of tobacco and alcohol affect the whole ofthe aerodigestive tract. This suggests that the whole tractis at risk from cancer and more than one area can be

affected at any one time. The term 'field change' wascoined to describe situations where large areas of theupper aerodigestive tract are affected with malignant orpremalignant change. For this reason, some units carryout bronchoscopy and oesophagoscopy at this time.However, these procedures show low pick-up rates forsecond primaries and tend to be used only when thepatient has symptoms.

A tumour found initially is known as the indexprimary. If a second distinct primary tumour is found atthe same time this is known as a simultaneous primarywhereas a second tumour found within 6 months of theindex tumour is known as a synchronous primary. Anysecond primary found after the initial 6-month period isdescribed as a metachronous primary.

Most patients with oral cancer are likely to be heavysmokers and drinkers. It is important that all investi-gations necessary for deciding whether the patient isphysically and mentally fit for treatment are carried out.Particular attention should be paid to the cardiovascularand respiratory systems, the nutritional status of thepatient, and his or her social circumstances. A psycho-logical assessment can also be of value. This is to allowan informed decision to be made on any furthertreatment.

Imaging

A plain chest radiograph provides useful informationbecause many patients suffer from chronic obstructiveairways disease and some even have a second tumour. Anorthopantomogram with other views of the mandible(e.g. occlusal views) provides information on thecondition and thickness of the mandible and the state ofdentition, and is an essential part in planning treatmentfor oral cancer. Sophisticated techniques such as com-puterised tomography (CT) scans or magnetic resonanceimaging (MRI) are used for assessment of both theprimary and metastatic disease. Many centres favour aCT scan from the diaphragm to the base of the skull toidentify evidence of second primaries in the aero-digestive tract, the state of the lungs, and the extent of theprimary disease and metastasis in the neck. An MRI scanis slightly more sensitive and specific than a CT scan forsoft tissue imaging, with sensitivity up to 83% andspecificity of around 85%. Positron emission tomo-graphy (PET) scanning is emerging as a useful methodfor detecting tumours, and also recurrence in previouslytreated areas, with sensitivities and specificities reported

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as slightly more than 90%. It is poor at anatomicallydefining tumours but images can be combined and super-imposed on CT or MRI scans to help determine resectionmargins.

The use of lymphoscintigraphy techniques in deter-mining nodal involvement and directing sentinel nodebiopsy (see below) is showing significant promise indetermining malignant lymph nodes.

The multidisciplinaryapproach to treatmentThe multidisciplinary approach to the treatment of oraland oropharyngeal cancer is now fundamental and allunits treating this disease should have a team ofspecialists. The surgical disciplines of otolaryngology,plastic surgery and maxillofacial surgery should all beinvolved. A clinical or radiation oncologist with aspecialist interest in head and neck malignancy is alsomandatory. A specialist nurse, speech and languagetherapist and nutritionist should also be present and acytopathologist should be on hand to give the result of anyfine-needle aspirates while the patient waits in the clinic.A psychologist and social worker are also helpful in pre-treatment assessment and post-treatment rehabilitation.

This multidisciplinary clinic is where all new patientsare assessed. In this environment, the patient's diseasecan be discussed and a treatment plan formed and put tothe patient, based on all the information gleaned from theexamination and special investigations. Family and socialproblems that might impact on treatment or quality of lifefollowing treatment should also be discussed. Patientswho have been treated are also followed-up at this clinicand problems with ongoing care can be identified andtreated.

Treatment planningAlthough there have been advances in treatment, thesurvival rates have not really improved. However,techniques have helped to improve the quality of life formany cancer patients even if survival has not beenprolonged.

Treatment comprises surgery, radiotherapy or com-bined treatment (particularly for larger or more aggressivetumours). These treatments have been the mainstay oforal cancer treatment for the last 50 years. Radiotherapyis given in divided doses, usually over a period of 6 weeks.

One local regime is to give 66 Gy in 33 fractions over aperiod of 61/2 weeks. Other forms of hyperfractionationcan be given to reduce the length of treatment and increasethe concentration of the radiotherapy effects.

Chemotherapy has a small role to play but, as newdrugs are developed and the biology of the diseasebecomes more understood, its role may increase. Chemo-therapy seems to be most effective when it is combinedwith radiotherapy concomitantly. Currently, the mosteffective drugs are platinum-based in combination with5-fluorouracil. Synchronous chemoradiotherapy seemsto show some survival advantages as well as improvedfunction in large posterior tumours.

Brachytherapy, or implanted radiotherapy elements,to the local site may be used to deliver a high dose ofradiotherapy to the index primary tumour while sparingthe surrounding tissues (e.g. the salivary glands). Plastictubes are looped through the tumour from the neck and,after volumetric planning has been carried out, can beloaded with radioactive wires. If the wires are too farapart then insufficient radiotherapy levels will bedelivered to the tumour. Conversely, if the wires are tooclose then tissue necrosis will ensue. Brachytherapy is animportant option for treating the tongue, particularly theposterior tongue, because it allows function to bepreserved. The most common side-effect from brachy-therapy treatment is pain at the tumour site.

The positive neck is usually treated surgically with theaddition of postoperative radiotherapy dependent on theextent of neck disease.

In the UK, if combined therapy is required then thesurgery is carried out first in most cases.

When dealing with oral and oropharyngeal tumours, itis critical that surgical margins should be clear of tumourby more that 5 mm on the pathological specimen, becausethis will have a considerable bearing on the outcome. Ithas been shown that survival rates are reduced by 10% onsimilar tumours, despite all other remedial treatment, ifthe tumour is not completely excised. Many factors seenon the pathological specimen will affect the outcome anda specialist pathology service is therefore mandatory.Tumour thickness, perineural invasion, vascular invasion,lymphatic invasion, differentiation of the tumour cellsand whether the invasive front is cohesive are importantin deciding further treatment. Tumour thickness has abearing on the prognosis, with tumours less than 2 mmthick having a much better prognosis than those with atumour thickness greater than 4 mm. If the invasive frontis cohesive then the prognosis is better than that with a

non-cohesive front, while perineural invasion has beenassociated with local recurrence. Not surprisingly,lymphatic invasion is associated with spread to the lymphnodes whereas vascular invasion increases the likelihoodof distant metastases. When surgery is performed thenthe decision to give postoperative radiotherapy may notbe made until the final pathology is reviewed.

Treatment of the neckTreatment of the neck in oral and oropharyngealmalignancy has raised a lot of debate in recent years. Theneck is divided into seven levels to describe the positionof the regional lymph node basin (Fig. 17.2). Only levelsI to V need to be considered when discussing oralmalignancy; levels VI and VII tend to be associated withthyroid and parathyroid tumours.

Some definitions need to be discussed when referringto neck dissections. A therapeutic neck dissection takesplace when disease is obviously present in the neck andthe dissection is undertaken to ablate the disease. Anelective neck dissection is used to describe a neck dis-section that is undertaken when there is no obvious diseasein the neck but there is a high chance of occult diseasebeing present or where the neck is opened for access. Thistype of neck dissection has become more common sincethe advent of free tissue transfer, during which the neckneeds to be opened to facilitate microvascular reconstruc-tion of the oropharyngeal defect. Many terms have been

Fig. 17.2 The seven levels of the neck. Showing theposition of the regional lymph node basin (level VI is deepand level VII is lower midline; not shown).

used to describe neck dissections, such as 'functional','supraomohyoid', 'lateral', 'radical', 'extended radical'and 'modified radical'. These terms are confusing andcan mean different things to different people. It is nowproposed that two terms are used to describe neckdissections:

• If five levels have been removed then this should bedescribed as a comprehensive neck dissection.

• Anything less than five levels should be termed aselective dissection.

As with all neck dissections, the preserved structuresshould be described and the dissected levels should benamed in selective dissections. This system tends toremove any ambiguity when describing the dissectioncarried out. In comprehensive neck dissections, theaccessory nerve should be saved if possible, but not at theexpense of good oncological resection, as sacrifice of thisnerve leads to poor shoulder function and pain. Otherstructures, such as the internal jugular vein andsternocleidomastoid, should also be spared if possible.

Surgery is usually the initial treatment for the overtlypositive neck with the possible exception of advancedneck disease (N3) where preoperative radiotherapy orchemotherapy can be used to shrink the mass prior tosurgical intervention. For positive disease, most surgeonsfavour some form of comprehensive neck dissection,attempting to save vital structures wherever possible,without compromising the oncological resection.Management of the N0 neck and the role of elective neckdissection has been subject to considerable debate. Thereis some evidence that elective neck dissection confers asurvival advantage over monitoring the patient andcarrying out a subsequent therapeutic neck dissectionwhen overt disease develops. Many centres adopt theprotocol where, if the likelihood of metastatic disease ishigher than 20%, elective neck dissection should beconsidered.

In the clinically N0 neck, it is perfectly acceptable tocarry out some form of selective neck dissection and, fororal cancer, most surgeons dissect only levels I to IVbecause metastasis in level V in a clinically negative neckis exceptionally rare. All vital structures should be sparedto maintain as near normal function as possible but it isimportant to realise that neck dissection is likely to incursome morbidity no matter how carefully the dissection isearried out.

Sentinel node biopsy is currently under investigationbut offers a promising way forward for dealing with the

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clinically N0 neck. The basis of sentinel node biopsy isthat tumour will migrate to the regional nodes and willfirst collect in a node called the sentinel node. Thesentinel node can be identified by using a triple diag-nostic approach of lymphoscintigraphy, injection of bluedye and a hand-held gamma probe for localisation at thetime of surgery. This offers a relatively easy way of har-vesting the sentinel node for histological analysis. If thenode turns out to be positive for metastatic tumour, thepatient goes on to have a neck dissection.

wound healing by a mixture of contacture and re-epithelialisation. One problem with laser excision is thatany resection specimen will have thermal damage andpathological examination of margins will be impossible.In theory, scarring is less and, if selection of the tumouris correct, then function will be minimally affected. Re-epithelialisation is most effective where there is nopossibility of contracture. Raw surfaces can be left in thehard palate, for example, which will re-epithelialise overa period of time.

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Reconstruction in the headand neck regionThe main aim of reconstruction around the head and neckis to maintain form and function. Many techniques haveevolved over the years, resulting in improvements infunction and cosmesis and allowing larger and morecomplex defects to be reconstructed. Despite this,survival rates have not improved, although quality of lifeis much better. Depending on the defect, a reconstructionladder can be used, starting with the simplest and leadingto the most complex techniques.

A basic principle of reconstruction is to replace liketissue with like. Unfortunately, this is rarely possible inreplacing oral mucosal lining, which is very specific. Theoral mucosa is moist, sensate, and has specialisedreceptors for taste. It is sometimes fixed to bone, as in thegingiva and hard palate, or is elastic and freely mobile, asin the buccal area, ventral surface of tongue and floor ofmouth. As there is no ideal replacement for oral mucosa,most techniques rely on importing skin. The dis-advantage of this is that skin is dry, often insensate, andhas no specialised receptors for taste. Often, the best thatcan be achieved is to restore the anatomy of the oralcavity in an effort to maintain form and function.

Primary closure

Primary closure is the simplest form of reconstructionand is particularly helpful in lip reconstruction. It ispossible to resect up to one-third to one-half of the lipwithout using any flap reconstruction. Primary closure isalso used after resection of small tumours of the mobiletongue, floor of mouth and buccal mucosa. Superficialtumours can be excised using a carbon dioxide or KTPlaser (see Ch. 38). The use of a laser allows the excisionor ablation of tumours without reconstruction, the

Skin grafts

It is perhaps surprising that skin grafts can take success-fully within the contaminated and wet environment of theoral cavity. They are best used as split thickness graftsand in situations where there is a well-vascularised graftbed such as the muscle of the tongue. The grafts are fixedby sutures, using a quilting technique to avoid shearingduring movement of the oral cavity. Grafts are also usefulfor increasing the height of the labial sulci as investibuloplasty where they can be held in position byfixed splints.

Other methods of reconstruction, including local anddistant flaps, are discussed in Chapter 15.

Quality of life issuesAs mentioned previously, survival has not improvedsignificantly over the past 20 years and one of the maintreatment goals is to improve the quality of life for oralcancer patients. The problem is how to measure qualityof life. This is now being resolved with questionnaires totry to assess this aspect of treatment. These question-naires look at psychological and social aspects ofpatients' lives as well as functional performance. The twoquestionnaires usually used are The European Organis-ation for Recognition and Treatment of Cancer (EORTC)and The University of Washington Quality of LifeQuestionnaire (UW-QOL). The EORTC contains generalquestionnaires for all cancers and a head and neckmodule specifically for cancer in that region, whereas theUW-QOL is a head-and-neck-specific questionnaire.With the use of these questionnaires it is becoming easierto recognise which treatments help or adversely affectquality of life. This area of cancer management is still inits infancy, but will generate a lot of interest and will helpdefine the best treatments in the future.

Otorhinolaryngology(ENT) surgery

IntroductionOtorhinolaryngology, more commonly known as ear,nose and throat (ENT) surgery, deals with conditionsaffecting the head and neck, upper aerodigestive tract andorgans of special sense. The range of conditions managedby ENT surgeons is vast and includes conditions asdiverse as neonatal airway obstruction, cerebellopontineangle tumours and cosmetic rhinoplasty. The scope ofENT reviewed in this chapter has been limited to thatwhich may be encountered in dental and oral surgicalpractice. Relevant conditions include those affecting thepharynx, nose, paranasal sinuses and neck. Specialattention is given to management of airway obstructionand aspects of head and neck malignancy (Table 18.1).

Techniques of examinationin ENTLike dental surgeons, ENT practitioners can see mostof the organs and areas of interest. Even areas that arenot easily or directly visualised, such as the larynx andparanasal sinuses, can be examined indirectly usingspecialised instrumentation such as mirrors and endo-

Tabte 18.1 ENT conditions encountered indental practice

Airway obstructionDiseases of:

phaarynxnoaseparanasal sinuses

NeackEpistaxisHead and neck malignancy

Fig. 18.1 Examination of the larynx and pharynx usingtraditional headlight indirect laryngoscopy.

scopes. The special techniques of physical examinationin ENT are difficult to master and trainees in thespecialty spend many months acquiring the basic skillsneeded to view the larynx, nasopharynx and posteriornasal cavity. Traditionally, the pharynx and larynx havebeen examined using mirrors and headlight illumination(Fig. 18.1), but recently fibreoptic and rigid endoscopeshave superseded these techniques (Fig. 18.2).

After an initial review of emergency airway manage-ment we will consider some of the more common andrelevant ENT conditions. For reasons of relevance andbrevity, otology has been excluded.

Emergency management ofupper airway obstructionPerhaps the most challenging clinical situation is apatient with sudden, severe airway obstruction. Although

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Fig. 18.2 Modern flexible fibreopticnasopharyngolaryngoscopy.

this scenario is fortunately rare, it is important thatclinicians operating in the oral cavity and pharynx havean awareness of the possible causes of acute airwaycompromise and have the necessary equipment and skillto deal with it. The laryngeal airway is a narrow andfunctionally complex system whose most important roleis to separate and protect the airway from the digestivetract. The diameter of the space between the vocal cords(glottis) is such that even small foreign bodies can causesevere and life-threatening airway obstruction. This riskof airway obstruction is greater in children due to therelatively small dimensions of the juvenile larynx and thenatural tendency for children to put toys, beads, pen-lids,etc. into their mouths. Other causes of acute airwayobstruction are shown in Table 18.2.

Table 18.2 Causes of airway obstruction

Foreign bodiesfood boluspart of a toy, pen toptooth

Infectionacute epiglottitis

Traumalaryngotracheal traumaorofacial trauma

Caustic inhalation/ingestionLaryngeal tumour

carcinoma148 papilloma

Acute airway obstruction

Sudden complete laryngeal obstruction is easily diag-nosed, as severe respiratory distress is rapidly followedby cyanosis and collapse. More often, however, laryngealobstruction is incomplete and is signified by a lessdramatic increase in respiratory effort, difficultyspeaking and stridor. Stridor is a coarse inspiratory noiseproduced as the patient attempts to inhale forciblythrough a narrowing at the level of the larynx. Stridor iseasily distinguished from stertor, which is a rattlinggurgling noise produced by soft tissue obstruction orretained secretions at the level of the oropharynx.

Immediate management of laryngealobstruction

Emergency management depends on the degree ofobstruction and the level of expertise and equipmentavailable to deal with it. Mild stridor requires urgentmanagement but allows time for specialist help to besummoned, whereas acute severe respiratory collapsedemands immediate on-the-spot treatment. It is importantthat all practitioners have a rehearsed plan and thenecessary instrumentation available for dealing withcatastrophic airway obstruction, even though most willnever encounter such a case.

The options for treating are shown in Table 18.3. Ofthese techniques, only the Heimlich manoeuvre andlaryngotomy are appropriate to non-specialist settings.Endotracheal intubation and tracheostomy requireadvanced skills and instrumentation.

Heimlich manoeuvre

The Heimlich manoeuvre is a technique for relievingairway obstruction caused by an impacted foreign body.If the patient can cough or speak, then the airwayobstruction is incomplete and the Heimlich manoeuvre isnot appropriate. Stand behind the patient with the armsencircling the patient's abdomen and crossed at the levelof the patient's umbilicus. A forceable thrust upwards

Table 18.3 Treatment of laryngeal obstruction

Heimlich manoeuvreAspiration and endotracheal intubationLaryngotomy (cricothyrotomy)Tracheostomy148

Fig. 18.3 The Heimlich manoeuvre.

and backwards is used to compress the patient'sabdomen in an attempt to push the diaphragm upwardsand expel the lodged foreign body (Fig. 18.3).

Laryngotomy

If all else fails and the patient is in extremis, an emergencysurgical opening into the airway below the level of thevocal cords (most likely level of obstructing lesion) hasto be created. The cricothyroid membrane provides ananatomical window for gaining access to the airway.Anaesthesia may not be appropriate as, by the time adecision is made to perform a laryngotomy, the patient isusually semiconscious.

For laryngotomy, full extension of the neck isessential. If the subject is a child, lay the patient acrossthe knee of an assistant with the neck hyperextended andfirmly palpate the midline structures of the neck. Startingfrom the prominence of the thyroid cartilage, run a fingerdown the midline until the prominent ring of the cricoidcartilage is palpated. Above the cricoid ring and below thelower border of the thyroid cartilage lies the cricothyroidmembrane. With the neck sufficiently extended, thereare no intervening structures between the cricothyroidmembrane and the skin. As a first step, a wide-bore

needle or cannula can be inserted through the membraneinto the airway and this may be sufficient to temporarilyrelieve the obstruction. A horizontal stab incision is thenmade using a knife or scalpel and, without withdrawing,the blade is turned through 90° to open the incision. Oncethe cricothyrotomy has been performed it can be heldopen using a small tube and, in some extreme situations,the outer cylinder of a pen has been used with success!

Specialised cricothyrotomy sets, which include asmall-bore endotracheal tube and a specially designedscalpel, are commercially available. General dentalpractitioners and others carrying out procedures in theoropharynx in non-hospital settings would be welladvised to purchase a cricothyrotomy kit and keep asmall emergency tray set up in their surgery to deal withsuch an unlikely emergency.

The pharynxAnatomy and physiology of the pharynx

The pharynx is a fibromuscular tube that constitutesthe upper aerodigestive tract. It is formed by thebuccopharyngeal fascia and the overlapping pharyngealconstrictor muscles, which extend from the level of thebase of the skull to a lower limit at the sixth cervicalvertebra (C6). At C6 the cricopharyngeus fibres of theinferior constrictor form the upper oesophageal sphincter.The pharynx is usually divided into three regions: thenasopharynx, oropharynx and hypopharynx.

The nasopharynx extends from the skull base to thelevel of the hard palate. It is lined by transitional respir-atory epithelium and contains abundant lymphoid tissue.The main structures of clinical note in the nasopharynxare the nasopharyngeal tonsil, or adenoid, and theeustachian (pharyngotympanic) tubes, which communi-cate between the middle ear and the nasopharynx.

The oropharynx extends from the level of the hardpalate to the hyoid bone and is lined by stratifiedsquamous epithelium. Anteriorly, the oropharynxcommunicates with the oral cavity at the palatoglossalfolds. Lymphoid tissue is abundant and, in the oro-pharynx, the most prominent aggregations of lymphoidtissue are the palatine tonsils and the lingual tonsils.

The hypopharynx extends from the level of the hyoidbone to the upper oesophageal sphincter (cricopharyngeusfibres of the inferior constrictor). It is lined by stratifiedsquamous epithelium and communicates anteriorly withthe larynx.

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Benign conditions of the pharynx

Nasopharynx

The nasopharynx is often involved in upper respiratorytract infections, and the common cold is usually associatedwith nasopharyngitis. Symptoms of nasopharyngitis consistof discomfort and pain associated with swelling of thelymphoid tissue, which leads to nasal obstruction andseromucinous secretion more commonly referred to ascatarrh. Nasopharyngitis is usually a self-limiting conditionbut, in some patients, chronic low-grade inflammation canoccur, leading to nasal obstruction and chronic catarrh.

In children, the nasopharyngeal tonsil, or adenoid, canoccupy almost all of the nasopharyngeal space. Acuterespiratory infections can cause acute adenoiditis withmucopurulent postnasal discharge, nasal obstruction andfever. Such episodes of acute infective adenoiditis arecommon in childhood and may lead to chronic adenoidalhypertrophy, mouth breathing, nasal obstruction andchronic mucopurulent postnasal discharge. The juxta-position of the eustachian tubes to hypertrophied andinflamed adenoids is thought to be important in thecausation of middle-ear effusions. The adenoid maytherefore be important in the most common cause ofhearing impairment in childhood – otitis media witheffusion, more frequently known as 'glue ear'. Childrenwith enlarged and inflamed adenoids often have difficultyeating because they are obligate mouth breathers.Symptoms include disturbed sleep, nocturnal cough andmiddle-ear effusions. Adenoidectomy offers an effectivetreatment in such children.

The adenoid gradually atrophies with age and becomesrelatively less important as the nasopharynx grows, thusadenoid problems in adults are rare. Symptoms suggestiveof adenoidal hypertrophy in the adult should raise thesuspicion of a nasopharyngeal tumour (see below).

Oropharynx

Acute infective oropharyngitis presents as a sore throat,pain on swallowing and fever. The cause is usually viraland the condition is self-limiting, responding to sympto-matic measures such as paracetamol, saline gargles anda high fluid intake. Throat swabs seldom yield anysignificant growth. Severe, non-resolving pharyngitisshould raise the possibility of glandular fever.

Chronic pharyngitis presents as persistent, dry, sorethroat and irritation and discomfort on swallowing. Often

the cause cannot be ascertained, but there appears to bean association with nasal disease. The treatment ofchronic pharyngitis involves identification of the cause,treatment of any nasal disease, increased fluid intake andavoidance of antibiotics, as these can sometimes lead tosecondary candidiasis. In some cases, topical nasalsteroid sprays can help reduce the inflammation.

Tonsillitis

Acute tonsillitis is a common cause of a sore throat.Although the initial organism may be viral, super-infection with a beta-haemolytic Streptococcus usuallyensues. Acute tonsillitis can also be a complication ofglandular fever. The symptoms are sore throat, pain onswallowing (odynophagia), systemic malaise, headacheand fever. Because of pain on swallowing, patients tendto avoid eating and drinking and, therefore, can becomesignificantly dehydrated and debilitated. Diagnosis isusually obvious with trismus, tonsillar hypertrophy, andpus visible in the tonsillar crypts; there will be associatedcervical adenitis. Treatment involves high fluid intake,analgesics and penicillin. In severe cases the patient maybe unable to swallow oral antibiotics, thus, a short courseof intravenous benzyl penicillin may be indicated (Fig.18.4). Complications of tonsillitis include a peritonsillarabscess (quinsy).

Tonsillectomy

Tonsillectomy used to be an extremely common operationand was often used incorrectly as a treatment for non-specific sore throat (pharyngitis).

Fig. 18.4 Acute tonsillitis.

Tonsillectomy is carried out by dissecting the tonsilsfrom their fossae and ligating any bleeding pointsencountered. The most frequent major complication ispostoperative haemorrhage, which occurs in approxi-mately 2% of cases. Minor secondary tonsillar haemor-rhage can also occur up to 2 weeks after the operationand is usually managed conservatively using antibioticsand saline gargles.

Indicatons for tonsillectomy

Current indications for tonsillectomy include: a clearhistory suggesting that the sore throats are due totonsillitis on five or more occasions per year over aperiod of at least 1 year, or evidence that these episodesof sore throat are disabling and preventing normalfunction at school or work.

Patients often complain of white or yellow lesions ontheir tonsils. These are foul tasting and may be associatedwith halitosis. Examination shows numerous whitegranules occupying the tonsillar crypts; these are oftendiagnosed incorrectly as food debris. In fact, the mostfrequent cause of this is actinomycotic colonies withinthe tonsillar crypts. Actinomycetes are normal oralcommensals but in some patients they 'overgrow' andform so-called 'sulphur' granules within the tonsillarcrypts. Patients often use antiseptic mouthwashes totry and cure the problem, but this may well be the causerather than the cure! Treatment includes reassuranceand the avoidance of antiseptic mouthwashes. Somepatients, however, are significantly debilitated by thisproblem and this may be seen as a rare indication fortonsillectomy.

Tonsillectomy can also be used in the surgical treat-ment of snoring. Significant debilitating snoring, whichcan lead to extreme social distress, is related to obesityand, in some cases, tonsillar hypertrophy. Most surgicalprocedures for snoring involve modification andstiffening of the soft palate. The uvulopalatopharyn-goplasty (UPPP) operation involves palatal shorteningand tonsillectomy. However, there is no good evidencethat snoring surgery is beneficial, as results are oftenpoor and snoring recurs within 2 years of successfulsurgery in 60% of patients. Snoring alone is not anindication for tonsillectomy.

Prions have been demonstrated in tonsillar tissuefrom patients with new variant Creutzfeldt–Jakob disease(vCJD; see Ch. 7). Because of the potential risk of

transmission of prion disease, disposable instruments arenow recommended for all tonsillectomies.

Hypopharynx

Benign hypopharyngeal disease often presents as afeeling of something in the throat with or withoutdysphagia. An accurate history needs to be taken from allpatients complaining of pharyngeal discomfort anddysphagia. Warning signs and symptoms are, weightloss, pain referred to the ear and dysphonia (hoarseness).

A common benign cause of 'a feeling of something inthe throat' is the globus pharyngeus syndrome, whichused to be referred to as globus hystericus. This conditionis thought to be due to neurological incoordination of thecricopharyngeus muscle. It is more common in femalesand is not associated with pain, referred otalgia or weightloss. It is important to note that globus pharyngeus is adiagnosis of exclusion that is made only after normalendoscopy and/or normal barium swallow investigations.

A pharyngeal pouch is a diverticulum at the lowerpart of the pharynx. Cricopharyngeal spasm is implicatedin its causation. Patients present with intermittentdysphagia and regurgitation of partially digested food-stuffs. A characteristic appearance is seen on a bariumswallow (Fig. 18.5) and the diagnosis is confirmed atrigid endoscopy. Treatment of pharyngeal pouch can becarried out by open (excision) or endoscopic means(drainage of pouch into oesophagus).

Tumours of the pharynx

Tumours of the pharynx will be considered under benignand malignant lesions affecting the nasopharynx, theoropharynx and the hypopharynx in turn.

Nasopharynx

Benign tumours of the nasopharynx

Tumours of the nasopharynx present with symptomsthat can be confused with adenoid enlargement or nasalobstruction. Thus, a high index of suspicion is requiredand all cases should undergo pernasal endoscopicexamination.

Juvenile nasopharyngeal angiofibroma (JNA) is abenign vascular tumour that occurs in adolescent males.It presents with unilateral nasal obstruction and epistaxis.

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Fig. 18.5 Contrast radiograph of a pharyngeal pouch.

JNA is of unknown aetiology but hormonal influencesassociated with puberty are thought to be implicated. If atumour is identified in a young male it is important toconsider the possibility of a JNA because biopsy couldprove catastrophic! MRI and angiography confirm the

diagnosis and treatment involves embolisation prior toresection.

Malignant tumours of the nasopharynx

Malignant tumours of the nasopharynx are, fortunately,uncommon. Symptoms include nasal obstruction,epistaxis and, in some patients, deafness due to a middle-ear effusion secondary to eustachian tube obstruction. Inadvanced cases, nasopharyngeal malignancy will invadethe skull base and give rise to cranial nerve palsies.Nasopharyngeal cancer is usually squamous but poorlydifferentiated or anaplastic variants are not uncommon.Salivary gland tumours (adenoid cystic carcinoma) andnon-Hodgkin's lymphoma also occur.

Nasopharygeal carcinoma is much more commonin parts of Asia than in the UK. In Hong Kong,nasopharyngeal carcinoma is one of the most commonhead and neck malignancies, and its aetiology is thoughtto involve an interaction between infection with theEpstein–Barr virus and racial/genetic predisposition.Malignancy in the nasopharynx often metastasises earlyto upper deep cervical lymph nodes. Presentation isusually late and curative surgical treatment is seldompossible. Radical radiotherapy (with or without chemo-therapy) can give good results in those patients who arediagnosed in the early stages.

Oropharynx

Benign tumours of the oropharynx

Benign tumours of the oropharynx are relativelyuncommon. Tonsillar inclusion cysts, which present assmooth, rounded swellings associated with the upperpole of the tonsil are commonly mistaken for tumours.

Viral papillomata can be found on the faucial pillars,tonsil and posterior pharyngeal wall. Their presenceraises the possibility of coexisting laryngeal and genitalpapillomatosis. Treatment includes excision or laserablation.

A lingual thyroid presents as a smooth swelling in themidline of the posterior one-third of the tongue. It is dueto a thyroid developmental abnormality that results inpersistence of thyroid tissue in the region of the foramencaecum.

Tumours of the minor salivary glands may also presentin the oropharynx. Numerically they are most likely tobe pleomorphic salivary adenomas, but low-grade

mucoepidermoid tumours should also be considered (seeCh. 14).

Malignant tumours of the oropharynx

Malignant oropharyngeal tumours most commonlyinvolve the tonsils. Squamous cell carcinoma is the mostfrequent histology and aetiological factors includealcohol and smoking. Tonsillar carcinoma often presentslate with spread into the adjacent structures of the softpalate, tongue base and mandible. There is a high inci-dence of nodal spread to the deep cervical chain at thetime of diagnosis. Early tonsillar carcinomas can betreated by radical radiotherapy. More advanced casesneed major surgical resection, which involvesmandibular splitting for surgical access. Excision of thetumour and adjacent involved structures (mandible,pharyngeal wall, tongue) and comprehensive neckdissection (Ch.17) is followed by reconstruction usingradial artery free grafts or pectoralis majormyocutaneous flaps (Ch. 15).

The oropharynx may also be the site of non-Hodgkin'sand Hodgkin's lymphomas arising in the lingual andpalatine tonsils. Treatment of lymphoma includes radio-therapy and chemotherapy.

Hypopharynx

Benign tumours of the hypopharynx

The hypopharynx consists of the piriform fossae, theposterior wall and the postcricoid region. Benign tumoursof the hypopharynx are extremely unusual and presentwith symptoms similar to the globus sensation. Fibromas,schwannomas, papillomata and benign salivary tumourscan all occur.

Malignant tumours of the hypopharynx

Although any hypopharyngeal site can be involved,the most common lesions affect the piriform fossa andpostcricoid regions.

Piriform fossa tumours are predominantly squamouscell carcinomas. They present with vague symptoms of afeeling of 'something in the throat' and intermittent,variable dysphagia. As the tumour enlarges and invadesadjacent structures the patient will present with otalgiadue to referred pain. Dysphagia increases and weight lossand aspiration of secretions ensues. In a high proportion,

the presenting feature is cervical lymphadenopathy dueto nodal metastases. The symptoms of piriform fossatumours are often relatively minor and it is thereforeessential that a high index of suspicion is maintained. Inparticular, patients should not be diagnosed as sufferingfrom globus pharyngeus unless a full endoscopicexamination has been carried out. Piriform fossa tumourscan be treated using radiotherapy (if diagnosed earlyenough), but advanced disease requires laryngectomy,partial pharyngectomy and reconstruction. Adjuvantradiotherapy is usually required and comprehensive neckdissection is used to treat nodal disease.

Postcricoid carcinoma has a presentation similar toother hypopharyngeal conditions. Dysphagia is severeand progressive, with weight loss in advanced cases.Clinical examination reveals pooling of secretions in thehypopharynx and patients will often have cervicaladenopathy. Examination under anaesthesia and biopsythrough rigid hypopharyngoscopes establishes thediagnosis. Staging relies on the findings at examinationunder anaesthesia and computerised tomography (CT) ormagnetic resonance imaging (MRI) results (see Ch. 17).Early-stage disease can be treated using radical externalbeam radiotherapy but more advanced cases requiresurgery. Due to a high incidence of synchronous oeso-phageal malignancy (skip lesions) concomitant resectionof the oesophagus and gastric or free jejunal interpositionis the surgical treatment of choice.

LarynxBenign and malignant disease of the larynx will beconsidered after a review of its anatomy and functions.

Anatomy and physiology of the larynx

The larynx occupies the junction between the commonaerodigestive and respiratory tracts. The basic frameworkof the larynx consists of the thyroid cartilage articulatingsuperiorly with the hyoid bone and inferiorly with thecricoid bone. Superiorly, the epiglottis and aryepiglotticfolds form the laryngeal inlet region, which leads downto the middle section of the larynx consisting of the falseand true vocal cords. The false vocal cords, or vestibularfolds, lie above and parallel to the true vocal cords andare separated from them by the shallow gutter of thelaryngeal ventricle. The principal nerve supply to thelarynx comes from the recurrent laryngeal branch ofthe vagus nerve, which reaches the larynx after looping

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round the arch of the aorta on the left, and round thesubclavian artery on the right. The blood supply is derivedfrom branches of the superior and inferior thyroidarteries, lymphatic drainage is to the upper deep cervicalnodes superiorly, lower deep cervical nodes inferiorly,and pre-thyroid nodes anteriorly.

The functions of the larynx are phonation andprotection of the lower airway.

Disorders of the larynx may impair the ability of thevocal cords to adduct, resulting in aspiration andweakness of the voice. Inability to abduct the vocal cordsto produce a satisfactory laryngeal airway may result inairway compromise which will present as stridor andshortness of breath. Lesions of or on the vocal cords willalter vocal cord tension and resonance leading to hoarse-ness (dysphonia) as the presenting symptom.

Examination of the larynx

Traditional indirect laryngoscopy used headlight illumi-nation and an angled mirror. The technique is difficultand some patients are unable to tolerate the examination.It is more common today to examine the larynx using afibreoptic laryngoscope passed via the nasal cavity (seeFig. 18.2). This produces an excellent view of the vocalcords and allows function to be assessed under directvision.

Chronic laryngitis

Chronic, painless dysphonia is more common in peoplewho smoke and in those who use their voice to excesssuch as, amateur singers, teachers and lecturers. In itssimplest form, chronic laryngitis is associated with non-specific, low-grade inflammatory thickening of the vocalcords. This produces an alteration in voice quality thatresponds slowly to conservative measures. Severe casescan progress to Reinke's oedema of the subepithelialspace of the vocal cord. This leads to severe dysphoniaand, on examination, swollen oedematous vocal cords areevident. In extreme cases Reinke's oedema can producesevere polypoid swelling of the vocal cords.

Vocal nodules are another feature of chronic laryngitisand appear as small fibrotic thickenings of the centralportion of the vocal cord. Excision can be carried outusing endoscopic microsurgical techniques, or withendoscopic laser therapy.

Vocal cord papilloma

Viral papillomata of the larynx due to the humanpapilloma virus can affect all ages but are more commonin children and young adults than in older people. Theusual presentation is dysphonia but papillomatosis canalso cause respiratory distress.

Benign laryngeal disease

Acute laryngitis

Acute laryngitis is common and often accompaniesupper respiratory tract infections, especially if associatedwith simultaneous voice abuse and ingestion of irritants.Alcohol, cigarettes and voice abuse (shouting or singing)can cause acute inflammation of the vocal cords, as canmechanical and chemical irritation. The patient com-plains of hoarseness and a mild sore throat, sometimeswith pain on swallowing. In the absence of bacterialsuperinfection, acute irritant laryngitis usually settleswith voice rest, a high fluid intake and simple analgesics.If associated with an upper respiratory tract infection,acute laryngitis may progress to bacterial infection,which will present with more severe symptoms and fever.Diagnosis is made on fibreoptic endoscopy. Treatmentinvolves broad-spectrum antibiotics. Failure to respondwithin 2 weeks is an indication for referral to an ENT

154department.

Vocal cord palsy

Vocal cord palsy presents as painless dysphonia and acharacteristic 'bovine' cough. It is caused by damage toeither recurrent laryngeal nerve. Left recurrent laryngealnerve damage is more common due to its longer coursein the thorax. The most common cause of a left vocalcord palsy is a bronchial cancer and, in all patientspresenting with a palsy, a chest radiograph is mandatory.Other causes of vocal cord palsy include inadvertentdamage to the recurrent laryngeal nerve during thyroid orcardiothoracic surgery.

Malignant tumours of the larynx

Cancer of the larynx is the most common head and neckmalignancy encountered by ENT surgeons. Any of thelaryngeal subsites (supraglottis, glottis or subglottis) canbe involved but in the UK the glottis is the most commonsite. Even very small tumours involving the vocal cordsproduce significant dysphonia. The dysphonia produced

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by a laryngeal cancer is indistinguishable from thatproduced by a vocal nodule or chronic laryngitis and,therefore, all patients with hoarseness should be treatedseriously and early referral in those who do not resolveshould be routine. Laryngeal cancer is more common inheavy smokers than in non-smokers, and alcohol intakeappears to be synergistic in supraglottic disease. Patientspresent with dysphonia and, in advanced cases, withrespiratory compromise. Squamous cell carcinoma is theusual histology.

Investigation includes indirect or endoscopiclaryngoscopy.

The treatment of laryngeal carcinoma depends onthe site and stage of the disease. Early tumours can beeffectively treated using courses of radical radiotherapy.More advanced cases of laryngeal carcinoma almostinvariably require total laryngectomy followed byadjuvant radical radiotherapy and comprehensive neckdissection to eradicate disease.

Following total laryngectomy, speech rehabilitation isrequired. The most common technique employs a one-way tracheopharyngeal speaking valve, which is placedbetween the back wall of the trachea and the reconstructedpharynx. This allows the patient to exhale air from thetrachea into the pharynx. The shunted air moves thepharyngeal walls and produces vibrations, which canthen be modulated into a form of speech. Most patientsfollowing total laryngectomy manage to achieve goodvoice rehabilitation using these valves.

wall. The nasal cavities communicate with the naso-pharynx behind and with the nostrils anteriorly. Thelateral nasal walls are formed by the inferior middle andsuperior turbinates with their associated meatuses. Thenasal floor is the hard palate and the roof of the nasalcavity lies in the region of the cribriform plate. The nasalcavity has a particularly rich blood supply that is derivedfrom both the external and internal carotid circulations, afeature that is in part responsible for the frequency ofspontaneous nasal bleeding (epistaxis).

The nose has five principal physiological functions(Table 18.4).

Nasal malfunction leads to dry, cold, unfiltered airreaching the nasopharynx with resultant risks ofinflammation and secondary infection. Nasal conditionscan therefore manifest as rhinorrhoea, nasal airwayobstruction, pharyngitis and mouth breathing, andabnormalities of olfaction (hyposmia).

Causes of nasal obstruction

Rhinitis

Rhinitis is defined as inflammation of the lining of thenose characterised by one or more of the followingsymptoms: nasal congestion, rhinorrhoea or sneezingand itching. There are many different causes of rhinitisbut the most prevalent is the common cold (Table 18.5).

NoseAnatomy and physiology of the nose

The nose is divided by the piriform aperture into ananterior (facial) component and a posterior nasal cavity.Both components are subdivided into right and left by thenasal septum. The nasal septum is predominantly bonyin the posterior cavity and cartilaginous anteriorly. Theexternal nose is covered by skin, subcutaneous tissue anda musculoaponeurotic layer. The upper 40% of theexternal nose consists of paired nasal bones, whicharticulate with each other and with the frontal processesof the maxillae and the maxillary processes of the frontalbones. The lower 60% of the external nose is cartilaginousconsisting of the paired upper lateral cartilages and lowerlateral cartilages.

Posteriorly, the right and left nasal cavities areseparated by the nasal septum, which forms their medial

Table 18.4 Functions of the nose

AirwayFilterHumidificationHeat exchange (warming inspired air)Olfaction

Table 18.5 A simplified classification of rhinitis

Allergicseasonal and perennial

Infectiousacute and chronic

Otheridiopathicoccupationalmedicamentosahormonalvasomotor 155

The treatment of rhinitis depends on the cause. Thecommon cold is usually self-limiting and responds tothe short-term use of topically applied decongestants(ephedrine or xylometazoline), which most patients selfprescribe. Most other forms of chronic rhinitis respondto potent topical steroids such as beclomethasone ormometasone, but these drugs should not be used withoutmedical supervision. Persistent nasal obstruction, rhinor-rhoea and nasal congestion, especially if unilateral, shouldbe seen as a reason for referral to a specialist.

Septal deviation following nasal trauma

The quadrilateral cartilage of the septum may befractured, resulting in a septal deviation that can giverise to nasal obstruction. Characteristically, this producesunilateral nasal obstruction and examination reveals aconvexity of the septum touching the lateral nasal wall.The unilateral nature of the symptoms helps distinguishthis from rhinitis. Treatment consists of the operation ofseptoplasty, which resects and straightens the quadri-lateral cartilage, perpendicular plate of ethmoid andvomer, and thus recentralises the septum. Fig. 18.6 The paranasal sinuses.

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Nasal polyps

Nasal polyps are inflammatory masses that originatepredominantly from the lining of the ethmoid sinuses.Polyps are more common in patients with asthma and, ina proportion of patients, there is an association withaspirin allergy. Symptoms are similar to severe rhinitis,with total nasal obstruction, hyponasal speech, hyposmiaand nasal discharge. Diagnosis is usually easy on nasalexamination. Polyps should be referred for specialistassessment to exclude tumour. Topical or systemiccorticosteroid medication can shrink polyps but surgicalremoval is often required, followed by topical medicationto prevent recurrence.

Foreign bodies

Children often put foreign bodies into their nose. Theclassic presentation is of unilateral, foul-smelling rhinor-rhoea (oezena). Common foreign bodies include piecesof foam rubber mattress or pillow, organic matter such aspeas, and parts of toys, beads, etc. Often, by the time ofpresentation there is a secondary vestibular infection,which makes the nose very tender to touch and makes

instrumental removal difficult. A suspected foreign bodyis a reason for specialist referral and children willoccasionally require general anaesthesia for its removal.

Paranasal sinusesThe nose and paranasal sinuses can be considered to be asingle functional unit. There are eight main paranasalsinuses, all of which drain into the nasal cavity. Six majorsinuses drain into the narrow middle nasal meatus, whichis, therefore, a key area in the causation and treatment ofsinus disease. Figure 18.6 shows the general positioningand relationship of the maxillary, ethmoid, frontal andsphenoid sinuses.

Sinusitis

Sinusitis may be acute or chronic, inflammatory orinfective.

Acute inflammatory sinusitis is seen in patients withacute seasonal allergic rhinitis, commonly known as hayfever. As such, this condition is seldom diagnosed andthe treatment relies on treating the inflammatory rhinitis

with topical antihistamines and decongestants. It is onlyonce inflammatory rhinitis becomes chronic and sinusoutflow tracts become blocked with oedematous, swollenmucosa that chronic inflammatory sinusitis sets in.

Chronic inflammatory sinusitis occurs in people withallergic nasal conditions (asthma, allergic rhinitis, aspirinsensitivity). It is usually associated with an allergic orinflammatory rhinitis, which is characterised by boggyswelling of the nasal mucosa. Patients present with nasalobstruction, a feeling of congestion, pressure betweenthe eyes and over the nasal bridge and postnasal dischargeof mucus. Treatment includes long-term low-dose topicalnasal corticosteroids. Antihistamines may be of value inacute flare-ups.

Acute infective sinusitis is an almost universal occur-rence during the common cold. This is due to rhinovirusinfection and is usually a self-limiting condition needingonly general supportive measures in the form of analgesicsand nasal decongestants. Topical nasal decongestants(e.g. ephedrine) are preferred over systemic versions.Secondary bacterial infection of ethmoid, maxillary,frontal or, less frequently, sphenoid sinuses can occurfollowing viral infection. Bacterial sinusitis is charac-terised by pain, which may be severe, and poorly localised(either to the forehead or malar region). There will be aswinging pyrexia with purulent rhinorrhea. Patients oftencomplain of upper dental pain due to involvement of themaxillary sinus. Acute infective sinusitis is a commonsequel to an upper respiratory tract infection and shouldbe seen as a potentially serious condition. Treatment withlocal topical decongestants and systemic antibiotics isrequired and failure to improve within 3 weeks necessi-tates specialist referral. Although most cases of infectivesinusitis respond to the above measures, some go on todevelop complications such as orbital cellulitis, orbitalabscess, frontal lobe abscess, meningitis or cavernoussinus thrombosis.

Plain sinus radiographs have little or no role in theinvestigation of sinusitis, which is mainly a clinical andendoscopic diagnosis. Nasal endoscopy will often revealoedema and pus in the region of the middle meatus.Failure to respond to conservative measures is an indi-cation for surgical drainage of the infected sinus eithervia an external or endoscopic intranasal route.

Chronic infective sinusitis may occur in some patientsas a result of an anatomical abnormality or an unresolvedor inadequately treated infection. Chronic sepsis is mostcommon in ethmoid and maxillary sinuses and lessfrequently observed in the frontal or sphenoid sinuses.

Bacterial infection results in oedema and secondarydevelopment of polypoid mucosa, which ensures that thesinus ostia remain blocked, impeding sinus drainage,which in turn prevents resolution of the infection.Symptoms include nasal obstruction, chronic foulsmelling rhinorrhea or postnasal discharge. Specialistreferral is required and evaluation will include nasalendoscopy and CT scanning of the sinuses. Surgicaltreatment of chronic infective sinusitis aims to secureunobstructed mucociliary drainage from the majorsinuses. Modern surgical approaches are referred to asfunctional endoscopic sinus surgery (FESS). FESS aimsto remove obstructing hyperplastic tissue from the regionof the natural sinus ostia in the middle nasal meatus toenable drainage of purulent secretions.

Paranasal sinus tumours

Fortunately, tumours of the paranasal sinuses areuncommon. The most frequently involved sinus is themaxillary, with the ethmoid being the second mostcommon site.

Maxillary sinus carcinoma

Carcinoma of the maxillary antrum usually presents lateas the volume of the sinus allows the tumour to enlargewithout causing symptoms. Presentation, therefore,usually occurs only when the tumour invades beyond themargins of the maxillary sinus. Symptoms are due toinvasion medially into the nasal cavity, superiorly intothe floor of the orbit and laterally into the cheek, andinferiorly, into the upper alveolus. Thus, the patient maypresent with swelling of the cheek, unilateral epistaxis,unilateral nasal obstruction or diplopia. Histology istypically squamous cell carcinoma, but poorly differen-tiated or anaplastic variants are common. Diagnosis ismade on nasal examination, nasal endoscopy and CTscanning. Treatment includes radical surgical excision inthe form of total maxillectomy with or without orbitalclearance, followed by radical radiotherapy and treat-ment of nodal disease.

Ethmoid carcinoma

Ethmoid carcinoma is less common than maxillary sinuscarcinoma but, similarly, presents late. Invasion of themedial orbital wall, nasal cavity and anterior skull baseleads to the presenting symptoms. Nasal obstruction

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Section B Specialist Surgical Principles

and epistaxis is universal. There is thought to be anaetiological association with exposure to lignins, whichare contained within certain hardwoods. Thus, ethmoidalcarcinoma has features of an occupational disease incarpenters. Diagnosis and treatment is similar to maxillarysinus carcinoma.

The prognosis in sinus carcinoma is poor.

Epistaxis

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Epistaxis is defined as spontaneous bleeding from thenasal cavity. It is an extremely common condition andmost people will at some point in their life suffer from anosebleed. The range of severity is vast, from the mildself-limiting nosebleed experienced by most people, tosevere torrential arterial haemorrhage that carries asignificant mortality and morbidity. Epistaxis can beclassified into two main groups: childhood and adult.

Childhood epistaxis

Childhood epistaxis is common from age four. It ischaracteristically minor but none the less alarming.Nosebleeds occur sporadically, with a predilection fornocturnal bleeding. The source of the bleeding is usuallyon the anterior nasal septum at a rich vascular plexusknown as Little's area. This location has led some tobelieve that nose-picking is the main cause, althoughthere is evidence to suggest other causes may beimportant. The management of childhood epistaxisincludes pinching the nostrils over the soft, lower lateralcartilages, which produces direct pressure over Little'sarea (the Hippocratic method). Once bleeding has stopped,some antibiotic ointment can be applied to the anteriornares to reduce any associated vestibulitis. Cutting thechild's fingernails can also help. Persistent or recurrentnosebleeds in children should be referred for specialistopinion, which will usually lead to the offending bloodvessel being identified and cauterised.

Adult epistaxis

Adult epistaxis can be a potentially life-threateningcondition, which has a peak age of onset of 60 years.This type of epistaxis is characterised by suddenunilateral severe arterial bleeding. Bleeding in adultsoften comes from arterial branches of the sphenopalatineartery in the posterior reaches of the nasal cavity. Thishas led to the term 'posterior epistaxis' being used. Not

surprisingly, this condition does not respond to directdigital pressure over the ala-nasi (Hippocratic method).The management of a severe epistaxis relies on resusci-tation of the patient followed by attempts to identify thesource of the bleeding. The nose is examined using aheadlight, nasal speculum and suction. It is often difficultto identify the bleeding point because of its posteriorposition. If the source cannot be found, otolaryngologistsuse endoscopes to examine the posterior nasal cavity andidentify the bleeding vessel, which can then be cauterisedunder direct endoscopic vision. In the absence ofspecialised equipment, posterior epistaxis is usuallymanaged by some form of tamponade, using eitherspecially designed balloon catheters or nasal packing.Admission to hospital is required and a search foraetiological factors should be undertaken (aspirin use,alcohol excess, thrombocytopenia). Unlike childhoodepistaxis, which is recurrent, adult epistaxis tends to becharacterised by a single severe episode of bleeding.

The neckAnatomy

The neck is divided into three zones: an anterior trianglewith its apex inferiorly and two posterior triangles withtheir apices superiorly. The anterior triangle is boundedlaterally by the anterior border of the sternomastoidmuscles. Superiorly, its base is formed by the mandibleand, inferiorly, the apex lies in the region of the sternalnotch. The posterior triangles are bounded anteriorly bythe posterior border of the sternomastoid muscle,posteriorly by the anterior border of trapezius, inferiorlyby the clavicle, and the apices lie posterosuperiorly in theregion of the occiput and mastoid processes. Figure 18.7shows the triangles of the neck with the associated lymphnode groups that they contain. Neck swellings arecommon clinical problems and it is important that adiagnostic strategy is used when dealing with suchswellings. The majority of neck swellings are to be foundin the anterior triangle and a simple strategy can be usedto subclassify into midline: upper or lower, and lateral:upper or lower swellings.

Metastatic nodal disease in the neck

It is important to realise that the lymph node chains of theneck are frequently involved in metastatic spread from

Fig. 18.7 Triangles of the neck and associated lymphnodes. 1, submental nodes; 2, submandibular nodes;3, jugulodiagastric nodes; 4, parotid/facial nodes;5, mastoid nodes; 6, occipital nodes; 7, upper deepcervical nodes; 8, mid deep cervical nodes; 9, lower deepcervical nodes; 10, supraclavicular nodes; 11, posteriortriangle nodes.

cancers of the upper aerodigestive tract and head andneck. It is, therefore, essential that any patient with anunexplained swelling in the neck is investigated carefullyto exclude a carcinoma of the head and neck. Examinationof the oral cavity, oropharynx and nasopharynx, andfibreoptic examination of the larynx and hypopharynxare essential when assessing lymph node swellings.Indeed, an isolated lymph node is a common presentationfor tumours of the piriform fossa and nasopharynx.

It used to be common practice to biopsy or exciselymph nodes to obtain a diagnosis. The practice ofdiagnostic excision biopsy of lymph nodes in the headand neck is generally considered obsolete now thathighly reliable fine-needle aspiration cytology is avail-able. The procedure of fine-needle aspiration cytologycan distinguish between malignant and non-malignantadenopathy in over 90% of cases. If a malignant cytologyaspirate is obtained, an examination under anaesthesia isrequired in combination with detailed imaging of theupper aerodigestive tract, head and neck, and chest. Oncea primary has been identified, planned curative treatmentcan be carried out with nodal disease being treated byradical radiotherapy or neck dissection. Excision of anundiagnosed lymph node, only to later discover that it

contains squamous carcinoma, is highly undesirable asthe risks of skin implantation with tumour are signifi-cantly increased and further curative resection will becompromised.

Lymphoma involving nodes of the neck is an exceptionto the above. Once lymphoma has been diagnosed (usingfine needle aspiration cytology), node sampling is usuallyrequested in order to histologically type the lymphoma.However, sampling a known lymphomatous node afterpositive cytology is different from exploratory biopsy ofan undiagnosed, possibly carcinomatous, node.

Midline swellings

A midline swelling in the upper neck can represent asubmental lymphadenopamy secondary to oral or dentalsepsis. However, the possibility of metatastatic nodalspread has to be borne in mind in all patients presentingwith a neck lump and, in the upper neck, a thoroughexamination of the oral cavity is essential.

In children, dermoid cysts can present in the uppermidline neck, and these developmental cysts may containsquamous debris, hair and even teeth! A midline swellingin the region of the hyoid bone may represent a thyro-glossal cyst. This is a developmental abnormality withcystic thyroid tissue persisting along the thyroglossalduct. A thyroglossal cyst characteristically movesupwards on tongue protrusion due to a continuity of thecyst with the thyroglossal tract leading to the foramencaecum of the tongue. In the lower neck, midlineswellings are most frequently related to the thyroidgland. Clinically, it is usually easy to distinguish betweenswelling of the thyroid gland and a swelling in thethyroid gland. Swellings of the thyroid gland may be dueto simple goitre but thyroid cancer must be excluded.Diagnosis is made by fine-needle aspiration cytology andappropriate use of magnetic resonance imaging and radio-isotope scanning. Occasionally, an early laryngeal cancerpresents with metastatic spread to the midline pretrachealor Delphian node.

Lateral neck swellings

Lateral swellings in the upper neck may represent diseaseof the submandibular salivary gland or inflammatory ormetastatic adenopathy of the submandibular, tonsillar andupper deep cervical nodes. Inflammatory or neoplasticdisease of the parotid gland can also present as an upperneck lump. In all of these conditions clinical examination

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of the upper aerodigestive tract and judicious use of fine-needle cytology will elucidate the diagnosis.

A smooth, firm swelling at the anterior border ofthe sternomastoid near the junction of its upper andmiddle third is characteristic of a branchial cyst. Theseare thought to be developmental abnormalities and are,therefore, more common in children and young adultsthan in older people. Diagnosis is confirmed by fine-needle aspiration, which produces turbid, straw-colouredfluid, the cytology of which reveals cholesterol crystals.Treatment of a branchial cyst is by surgical excision.

In elderly patients, atheromatous or even aneurysmalcarotid arteries can present as a pulsatile lateral neckswelling. Auscultation will often reveal a bruit, andultrasound or MRI can confirm the diagnosis. If a carotidaneurysm is suspected, then fine-needle cytology shouldnot be performed!

The lower lateral neck is a very common site formetastatic adenopathy. Hypopharyngeal tumours often

spread to the lower cervical chain first. However, spreadfrom below the clavicles is not uncommon and theVirchow node of gastric cancer and supraclavicular massof Pancoast's tumour should be borne in mind. Again,clinical examination and cytology will often lead to thediagnosis.

Tuberculous lymphadenopathy seems to show apredilection for the lower lateral (posterior triangle)nodes.

Occasional rarities such as cervical ribs and subclavianartery aneurysms may present as masses in the lowerlateral neck.

With almost all of the swellings encountered in theneck, a diagnosis can be made on clinical examinationcoupled to judicious use of imaging and cytology. Ashas been stressed, all neck lumps should be consideredmalignant until proved otherwise, and incisional orexcisional biopsy should be avoided.

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Neurosurgery

IntroductionNeurosurgeons (previously called neurological surgeons)are concerned principally with conditions affecting thecentral nervous system (CNS), the brain and spinal cord,in which the management of the patient may be aidedby surgical means. The boundaries of what constitutes aneurosurgical problem are not clear cut and there areinteresting areas of overlap with several other specialties.There is an increasing trend for major operations in suchboundary areas to be undertaken by a team of surgeonsfrom two or three specialties, particularly if skin andtissue cover or surgical reconstruction is required, or ifthe surgical approach to the intracranial lesion is via themaxilla, oral cavity or petrous bone.

Surgery to the spinal column is undertaken by bothneurosurgeons and orthopaedic surgeons. Some neuro-surgeons distinguish between vertebral surgery, that issurgery to the bones, joints and intervertebral discs of thespine, and spinal surgery, which involves treatment ofintradural spinal tumours, arteriovenous malformationsof the spinal cord and syringomyelia. Most neurosurgeonsand some orthopaedic surgeons handle vertebral surgery,the most common surgical procedures being for prolapsedintervertebral discs and associated spondylitic changes.Generally speaking, only neurosurgeons would tacklespinal surgery.

Neurosurgeons have traditionally had close links withneurologists. The ready availability of sophisticatedimaging techniques has rendered much detailed neuro-logical examination redundant. Nevertheless, there arestill areas where close cooperation is required betweenneurosurgeons and their physician colleagues, such asthe surgical treatment of epilepsy, movement disordersand trigeminal neuralgia.

This chapter will describe the general neurosurgicalapproach to problems and outline the common neuro-

Table 19.1 Aspects of neurosurgery

History and examinationConscious levelsInvestigationsNeurosurgical conditions

traumaintracranial haemorrhageintracranial neoplasmsintracranial infectioncongenital lesionshydrocephalusvascular compression syndromes

surgical conditions (Table 19.1). Spinal and vertebralsurgery, although forming a large part of the modernneurosurgical workload, will not be discussed other thanfor the sake of completeness.

Neurosurgical history takingand examinationIn neurosurgical patients the history is of major diag-nostic value. A patient who is fully conscious will oftenbe able to describe clearly any neurological signs andexamination simply confirms the patient's account. Thespeed of onset of symptoms is usually important. In apatient with a reduced conscious level who is unableto give a history, every attempt must be made to obtaina reliable history from relatives or other witnesses. Incases of trauma, the exact mechanism of injury is oftenuseful.

The details of how to carry out a full neurologicalexamination will be found in any general medicinetextbook and will not be repeated here. Unfortunately,students are often taught as if there is such a thing as a 161

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routine neurosurgical examination in which all neuro-logical signs and symptoms are tested for. Time con-straints alone would preclude such an approach. Inpractice, neurosurgical history taking and examination isnot routine or list based, but more heuristic, that is, goaldirected, testing one hypothesis after another. Forexample, in a patient with a purulent middle ear infectionand symptoms of intracranial infection (headaches, neckstiffness, disturbance of conscious level), history takingand examination should be directed initially at detectingsigns of a lesion, such as cerebritis or abscess, in the areaof brain most likely to be affected. Thus, a middle earinfection can spread superiorly to the temporal lobe,giving rise to a contralateral hemiparesis, visual fielddefect and, in the dominant hemisphere, dysphasia; orinfection can spread posteriorly into the posterior fossa,producing cerebellar signs such as ataxia, nystagmus andipsilateral incoordination. Therefore these symptoms andsigns would be specifically asked and tested for. Such agoal-directed approach does, of course, presume a reason-able basic knowledge of neuroanatomy.

It will be clear in the above example that if such apatient has a limb weakness, detailed testing of individuallimb muscle groups and reflexes will add very little to theclinical picture and is therefore unnecessary. By contrast,in a patient with a suspected spinal cord lesion, testing ofindividual muscle groups and of reflexes may be of greatvalue in determining the level of the lesion and whichspecific nerve roots may be involved. The examinationperformed therefore depends on the clinical question tobe answered.

Neurosurgical history taking and examination is goaldirected, and the goal is in three stages. The first stage isanatomical localisation, the second is to determinegeneral pathology and the third is to determine detailedor special pathology. It is the hallmark of inexperience totry and make a diagnosis of special pathology in the earlystages of a patient's presentation. The danger of this isthat a patient is labelled with a condition and otherpossibilities are ignored.

Anatomical localisation

It is usually possible to locate a lesion to one of the threemain compartments of the CNS, supratentorial (cerebralhemispheres), infratentorial (brainstem and cerebellum)and spinal.

Certain features always indicate supratentorial path-ology. These features are anosmia (inferior frontal lobes),

dysphasia (dominant hemisphere) and seizures (alwaysarise in the cerebral cortex).

Infratentorial (posterior fossa) lesions are charac-terised by brainstem or cerebellar signs such as ataxia,incoordination, nystagmus, dysarthria and dysphagia.Cranial nerve palsies may often be associated with infra-tentorial lesions and the presence of a cranial nerve palsyand a contralateral hemiparesis is virtually diagnostic ofa brainstem lesion. Mass lesions in the posterior fossacommonly present with signs of raised intracranialpressure from hydrocephalus secondary to obstruction ofcerebrospinal fluid (CSF) flow through the aqueduct orthe fourth ventricle.

Spinal lesions are characterised first by an absence ofthe symptoms and signs characteristic of an intracraniallesion, and no disturbance of consciousness. Second,there will often be pain or tenderness at the site of avertebral lesion. Third, spinal lesions commonly presentwith bilateral limb symptoms or signs, which is lessusual with brain lesions. Fourth, due to the arrangementof the sensory and motor tracts within the spinal cord,there are characteristic syndromes associated with lesionsof the spinal cord.

When localising spinal lesions it is important to dis-tinguish between upper motor neuron and lower motorneuron lesions. The lower motor neuron starts at theanterior horn cell of the spinal cord. A lesion involvingthe anterior horn cell, the nerve root, or the peripheralmotor nerve will tend to cause lower motor neuron signs,that is hypotonic weakness, muscle wasting, and reducedor absent reflexes. Lesions of the spinal cord itself willtend to produce upper motor neuron signs - weaknesswith increased tone, increased reflexes and clonus. Aspinal lesion will commonly produce a mixture of uppermotor neuron signs (below the level of lesion) and lowermotor neuron signs (at the level of the lesion) and thusprecise anatomical localisation is often possible.

General pathology

The second stage of the goal of history taking is todetermine, as far as possible, which general pathologicalcategory the patient's complaints suggest. The generalcategories are congenital, degenerative, traumatic,infective/inflammatory, vascular and neoplastic. A historyof trauma in the recent past will be important. A suddenonset (over a few seconds) of neurological symptoms orsigns suggests a vascular origin (if trauma is excluded);an onset over hours or days suggests infection, particularly

if there is pyrexia and meningism or evidence ofinfection elsewhere; and a more gradual onset (weeks ormonths) would point to a neoplastic process or a chronicsubdural haematoma. In younger patients, congenitallesions will be more likely, although congenital lesionscan present at any age.

The purpose of anatomical localisation and attempt-ing to define general pathology is to help decide which isthe next best investigation to determine special pathol-ogy. Modern neuroradiological investigation is sophisti-cated and accurate but may also be time consuming andexpensive. Therefore it is important to be thoughtfulabout the sequence of investigations most likely to yielduseful information.

Special pathology

To make a specific neurosurgical diagnosis usuallyrequires further investigations. For example, a patientwith sudden onset of dysphasia and a right hemiparesishas most likely sustained a vascular lesion (generalpathology) affecting the left hemisphere. A computerisedtomography (CT) scan is required to distinguish thespecial pathology of an infarct, a haemorrhagic infarct, oran arterial haemorrhage. If a haemorrhage is detected, acerebral angiogram will usually be needed to display anunderlying vascular abnormality such as an aneurysm orarteriovenous malformation.

The range of neurosurgical investigations that may berequired to make a precise diagnosis are described later.It is frequently the case, particularly with CNS tumoursor infection, that a biopsy will be required to make adefinitive diagnosis.

Conscious level andnon-localising symptomsSeveral common presenting neurosurgical syndromesallow only the vaguest anatomical localisation.

Symptoms and signs of raised intracranialpressure (ICP)

The classic presentation of acute raised ICP is headache,vomiting and papilloedema; with a more chronic build-up of pressure, headache and vomiting may be lessmarked, even absent. In babies whose skull sutures havenot formed raised ICP may simply cause the headcircumference to enlarge beyond normal.

Any intracranial lesion can produce raised ICP if it islarge enough, or situated in such a position as to obstructthe flow of CSF and cause hydrocephalus.

If unrelieved, raised ICP can lead to herniation of thebrain through the tentorial hiatus or foramen magnum(coning). Raised ICP can lead to decreased cerebralperfusion; if ICP rises to equal blood pressure, cerebralperfusion ceases.

Meningism

This refers to the syndrome associated with meningitis,namely headache and neck stiffness, usually accompaniedby vomiting. Meningitis means simply inflammation ofthe meninges. The most common cause in the com-munity is probably viral meningitis, normally a benign,self-limiting condition. Bacterial meningitis is lesscommon but is life threatening. Bleeding (from anycause) into the subarachnoid space also producesmeningism. Chemical (non-infective) meningitis issometimes seen following neurosurgical operationswhen, for example, cyst contents have escaped into theCSF. All types of meningitis and most cases of CSF orintracranial infection (cerebritis or brain abscess) willgive rise to meningism.

Reduced conscious level:the Glasgow Coma ScaleA pathological reduced conscious level can be caused bybilateral cerebral hemisphere lesions, brainstem com-pression or ischaemia, reduced cerebral perfusion,metabolic disturbance or seizure activity. Most intra-cranial neurosurgical pathologies can give rise to areduced conscious level by reason of pressure, direct orindirect, on the brainstem, or by causing raised ICP andreduced cerebral perfusion. Many non-CNS systemicpathologies will also produce a reduced conscious level,for example hypoglycaemia, liver failure, hypoxia (cardiacor respiratory abnormalities) and sepsis. Therefore areduced conscious level in itself is not an indication ofprimary intracranial pathology.

Conscious level is universally assessed using theGlasgow Coma Scale (Table 19.2). The three com-ponents of consciousness - eye opening, verbal responseand motor response - are assessed individually. Whenassessing each of these components it is important thatthe examiner starts 'at the top' and works down. Thus,when assessing eye opening, spontaneous eye opening or

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Table 19.2 The Glasgow

Feature

Eye opening

Verbal response

Best motor response

Total Coma score

Coma Scale and score

Scale responses

SpontaneousTo speechTo painNoneOrientatedConfused conversationWords (inappropriate)Sounds (incomprehensible)NoneObeys commandsLocalises painFlexion - normalFlexion - abnormalExtendNone

Score notation

4321543216543213/15 to

15/15

164

eye opening to speech should be looked for before testingeye opening to pain.

The correct way to test for a motor response oftencauses some difficulty. If a patient does not obey simplecommands, a localising (purposeful) response is testedfor. By convention, painful pressure is applied to thesupraorbital margin and if the patient brings a hand up tothe site of the pain, then the patient is localising. Botharms are tested by holding one arm down at a time.

If the patient does not localise, the other responses aretested by applying pressure to the fingernail bed. Aflexion or extension response refers to movement at theelbow. The intermediate response, abnormal (or spastic)flexion is charted if there is either preceding extensionmovement in arm, or extension in a leg, or two of thefollowing: stereotyped flexion posture, extreme wristflexion, adduction of arm or fingers flexed over thumb.Because of the difficulty of describing this response,spastic flexion can be omitted from the Coma Scale, butis important to record, if present, as a focal sign (Fig.19.1). If in doubt, record normal flexion.

When recording conscious level, the 'best' motorresponse is taken. This means the arm with the bestresponse, not the best response over time. So if a patientis localising pain with the right arm but flexing to painwith the left arm, the conscious level is judged aslocalising. However, the flexion response in the left armis an important focal sign, indicating a lesion probablyaffecting the right hemisphere.

It is common, especially in trauma patients, to beunable to record one or more aspects of the Coma Scale.The patient's eyes might be closed by swelling, or directlyinjured, making eye opening not possible. The patientmay be dysphasic, or have an endotracheal tube ortracheostomy, making verbal response unrecordable.There may be a high spinal injury, brachial plexus lesion,or limb fracture, making motor response unreliable. In allthese situations it is important simply to give the reasonfor not recording the response, rather than to guess atwhat it might be (see Fig. 19.1).

Coma is defined as not obeying commands, not eyeopening even to pain, and not uttering recognisablewords. A severe head injury is one where coma, asdefined, is present for 6 h or more.

Each component of the Glasgow Coma Scale can beallocated a numerical value, the sum of which can givethe Glasgow Coma (GC) Score (see Table 19.2). The GCScore was devised in the 1970s to allow information onlarge numbers of head-injured patients to be stored andanalysed by computer. The GC Score is useful forgrouping head-injured patients by severity, for displayingrisk factors, and as a form of shorthand used in producingguidelines. Despite widespread practice to the contrary,the GC Score should never be used to describe anindividual patient's conscious level in a clinical situation.To do so often results in confusion and significant loss ofinformation. In clinical practice, always use the verbaldescription of the three components of the GC Scale.

Fig. 19.1 Stylised neurosurgical observation chart of a patient deteriorating with a left-sideextradural haematoma who improves following surgical evacuation. The Glasgow Coma Scale (GCS)uses the best motor response but limb asymmetry is also charted; if a response is inaccessible, thereason is given (e.g. C, eyes closed by swelling; DYS, dysphasic). The GC Score is not used forindividual patients in a clinical situation.

Neurosurgical investigationsand proceduresThe purpose of neurosurgical history taking and exam-ination is to determine anatomical localisation and, ifpossible, general pathology. This in turn guides theinvestigations that are most likely to assist in furtherdiagnosis (of special pathology) and management.

Lumbar puncture

This is used to diagnose infection of the CSF, in whichcase the white cell count will be raised. Bleeding into theCSF (from, for example, a ruptured intracranial aneurysm)is diagnosed by frank blood-staining of the CSF and/orxanthochromia in the supernatant. Lumbar puncture (LP)

is contraindicated in the presence of an intracranial masslesion; an LP in this circumstance may lead to a pressuredifferential and subsequent downward herniation of thebrain (coning). This can result in rapid death.

Nerve conduction studies andelectromyography

These are tests performed by neurophysiologists andmay be very useful in distinguishing nerve root abnor-malities from peripheral nerve entrapment or peripheralneuropathy.

Plain radiography

Plain radiographs of the head or spine can be particularlyuseful in cases of trauma. Radiographs of the skull can

165

166

show a fracture, a depressed fracture, air in the head orforeign bodies following a penetrating wound. Manyhead injuries are associated with spinal injury, particu-larly of the cervical spine, and cervical spine radiographis almost routine following any significant head injury.Some brain tumours contain calcification or cause boneerosion, which is visible on a skull radiograph. Manypituitary tumours show erosion or expansion of thepituitary fossa on a lateral skull radiograph. In babies orchildren a skull radiograph can show premature fusion ofthe sutures (craniosynostosis), and chronic raised ICPgives patchy thinning of the skull vault - the copper-beaten appearance. Some spinal cord tumours or cystsmay cause expansion and erosion of adjacent vertebra.

CT scan

This investigation has revolutionalised neurosurgery. Nolonger do neurosurgeons need to rely on careful, detailedneurological examination to identify the exact site of, forexample, a brain tumour.

MRI scan

This gives exquisite anatomical images. The two mainadvantages of the MRI scan over the CT scan are, first,that it is not affected by thick bone and is therefore usefulfor imaging the posterior fossa and spine. Second, it canimage in any plane, and this is particularly informative insagittal images of the spine.

The disadvantages of the MRI scan is that it is expen-sive and time consuming. It is contraindicated in patientswith pacemakers, implanted stimulators or ferromagneticimplants or foreign bodies. Some claustrophobic patientscannot tolerate lying in the scanner.

Angiography

Carotid and vertebral angiograms are used to visualiseintracranial aneurysms, arteriovenous malformations(AVMs), and the vascular supply of tumours. Access isusually via the femoral artery, threading the trackercatheter along the aorta under X-ray control.

Craniotomy

This refers to a flap of bone that is removed with a sawand replaced at the end of the procedure. The craniotomyflap may be of any size but is usually greater than 3 cmdiameter. A craniotomy may be an osteoplastic flap,

where the temporalis muscle is left attached to the bone,or a free flap. A craniotomy is the standard neurosurgicalprocedure to gain access to the intracranial contents.

Neurosurgicai conditionsTrauma

No head injury is so trivial that it can be ignored,or so serious that it should be despaired of.

These words are as true today as when written byHippocrates. Head injuries are common and the majorityare minor and do not require investigation or hospitaladmission. Nevertheless, the potential for complicationsis always present.

Head injuries can be classified anatomically accord-ing to the structure(s) affected (scalp, skull, dura, brain),pathologically, depending on the type of brain damage(primary, secondary, focal, diffuse), or aetiologically,according to the mechanism of injury (blunt, penetrating,acceleration/deceleration, missile).

Isolated scalp injuries are common but not usuallyserious. Blood loss may look frightening but is rarelyenough to cause shock, with the exception sometimes inbabies. The history is always important and may alert theexaminer to the possibility of a penetrating wound or adepressed fracture, both of which will normally requireneurosurgical exploration. First aid treatment of a scalplaceration is to stop the bleeding by direct pressure.Thereafter direct primary suture is usually possible.

A skull fracture may be of the vault or the skull base.A closed (or simple) skull fracture has no overlying scalplaceration. A compound (or open) fracture impliescommunication of the fracture with the atmosphere. Acompound depressed fracture of the skull vault usuallyrequires an operation to debride the wound, elevate thefracture and inspect the underlying dura and brain forlacerations. The main aim of this procedure is to reducethe risk of intracranial infection by removing all foreignmaterial and repairing the dural defect. Penetratingwounds are dealt with in the same way. Simple depressedfractures do not require surgery.

Fractures of the skull base are difficult to see withradiographs but can be diagnosed clinically by thepresence of well-defined periorbital haematomas (racooneyes) and subconjunctival haemorrhage with no posterior

Table 19.3 Risk of an operable intracranial

GCS (/15)

15

9-14

3-8

GCS, Glasgow Coma scaleAdapted from Teasdale et al

Risk

1 in 3615

1 in 51

1 in 7

haematoma in head injured patients

Other features

NonePost-traumatic amnesia (PTA)Skull fractureSkull fracture and PTANo fractureSkull fractureNo fractureSkull fracture

Risk

1 in 31 3001 in 67001 in 811 in 291 in 1801 in 51 in 271 in 4

1990 British Medical Journal, 300: 363-367

limit (in anterior fossa fractures), or bruising over themastoid process (Battle's sign) in fractures of the petrousbone. Petrous fractures can damage the middle or innerear and may have associated bleeding from the externalmeatus, deafness, dizziness or facial nerve palsy. If thedura underlying a base of skull fracture is torn, there maybe a CSF leak through the nose or the ear, or air manyenter the subarachnoid space (pneumocephalus). In eitherevent there is a risk of bacterial meningitis. If the duraltear does not heal within 1-2 weeks, surgical repair isusually indicated. Recently published guidelines do notrecommend prophylactic antibiotics for a CSF leak.

The main significance of a skull fracture is that itindicates a greatly increased risk of the patient harbour-ing an intracranial haematoma that requires surgicalremoval. Table 19.3 illustrates the risks that form thebasis for guidelines on the early management of headinjuries. Table 19.4 lists the criteria for referral of a headinjury to hospital. Further guidelines on the indicationsfor a skull radiograph, admission to hospital, a CT scan,and referral to a neurosurgeon can be found in theScottish Intercollegiate Guidelines Network (SIGN)publication entitled 'Early management of patients witha head injury (No. 46)', published in August 2000.

Brain damage

Brain damage or dysfunction is the subject of most con-cern following a head injury. Concussion, seizure activity,mechanical compression and ischaemia, may all renderpart of the brain dysfunctional, that is, the axons do notconduct or the synapses do not transmit. Such dysfunc-tion may be reversible with appropriate treatment overtime. 'Brain damage' is the term used to indicate irreversible

Table 19.4 Indications for referral of a headinjured patient to hospital

A head injured patient should be referred to hospital ifany of the following is present:

Impaired consciousness (GCS <15/15) at any time sinceinjury

Amnesia for the incident or subsequent eventsNeurological symptoms, e.g. severe and persistent

headache, nausea and vomiting, irritability or alteredbehaviour, seizure

Clinical evidence of a skull fracture (e.g. CSF leak,periorbital haematoma)

Significant extracranial injuriesA mechanism of injury suggesting:

a high energy injury (e.g. road traffic accident, fallfrom height)

possible penetrating brain injurypossible non-accidental injury (in a child)

Continuing uncertainty about the diagnosis after firstassessment

Medical comorbidity (e.g. anticoagulant use, alcoholabuse)

Adverse social factors (e.g. no-one able to supervise thepatient at home).

From Scottish Intercollegiate Guidelines Network (SIGN)Publication Number 46 'Early management of patientswith a head injury', August 2000.

dysfunction, which generally equates with disruption ofthe structural integrity of the neurons.

Primary brain damage is that which occurs at the time(or very soon after) a head injury. By definition, no treat-ment will reverse this. The aim of management is toprevent further damage, the causes of which are listed inTable 19.5.

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Table 10.5 Causes of secondary brain damage

Ischaemiahypoxaemia

airway obstructionchest injury

hypotensionextracranial injuriesother causes of shock

Intracranial haematomaBrain swelling/oedemaSeizuresInfection (meningitis, abscess)Metabolic/electrolyte disturbance

Hypoxaemia and hypotension are two of the mostcommon causes of secondary brain damage that can betreated (or prevented) by a non-specialist. Hence theemphasis in all guidelines regarding the management ofhead injuries on the 'ABC' of resuscitation - the airwayand breathing (i.e. adequate blood gases) always takepriority, followed by treatment of circulatory disturbances.Treatment of an obstructed airway, or a tension pneumo-thorax, or bleeding from a ruptured spleen always takesprecedence over a possible intracranial haematoma.

Intracranial haematomas

An intracranial haematoma is the complication that mostpeople associate with a head injury, but haematomasrequiring surgical treatment are in fact uncommon. Theclinical characteristics of such a lesion are severe head-ache and vomiting, decreased conscious level, contralateralhemiparesis and (a late sign) an ipsilateral unreactivedilated pupil (see Fig. 19.1). Treatment of a significanthaematoma will usually be surgical evacuation via acraniotomy. An extradural haematoma (i.e. between theskull bone and the dura) generally carries a better prognosisbecause it is less often associated with contusions orlacerations of the brain substance. An intraduralhaematoma is commonly a mixture of subdural blood,brain contusions or intracerebral haematoma, althoughpure subdural or intracerebral haematomas do occur.

Chronic subdural haematoma (CSDH)

CSDH is a relatively common but poorly understoodcondition. The typical history is of a minor head injury inan elderly patient, followed weeks or months later by agradual onset of signs of a cerebral hemisphere lesion.Classically the conscious level fluctuates. Confusion alone

is a common presentation and may often be put down toother causes, such as dementia or stroke. Often there isno history of a head injury. An overdraining ventriculo-peritoneal shunt can also result in a CSDH.

Intracranial haemorrhage

Intracranial haemorrhage is subdivided into parenchymal(intracerebral) haemorrhage and subarachnoid or intra-ventricular haemorrhage. Pure intracerebral haemorrhagemay present in the same way as a cerebral infarct (withsudden onset of neurological signs) although is five timesless common. Hypertension is the commonest cause andsurgery is rarely indicated.

Haemorrhage primarily into the subarachnoid spaceor ventricles, or intraparenchymal haemorrhage thatruptures into the CSF spaces, presents with a very severesudden headache, sometimes referred to as thunderclapheadache. There may be accompanying neurologicaldeficits and/or a decreased conscious level or coma.

Subarachnoid haemorrhage (SAH) is the most com-mon type of intracranial haemorrhage that concerns theneurosurgeon. The usual cause is a ruptured intracranialaneurysm. Other uncommon causes include arteriovenousmalformations, tumours and blood dyscrasias. About12% of all patients with SAH have no cause found.Usually, such patients are relatively well following thebleed, make a full recovery in time and rarely rebleed.

The diagnosis of subarachnoid haemorrhage is madeon the history of sudden severe headache. Some patientsliken the onset to being hit on the back of the head witha baseball bat. A CT scan will show subarachnoid bloodin 90% of cases scanned within 24 h of the haemorrhage.A cerebral angiogram will demonstrate an aneurysm ifpresent (Fig. 19.2).

Treatment is directed towards preventing a rebleed.The aneurysm may be approached through a craniotomyand a small metal clip placed across its neck to exclude itfrom the circulation. Alternatively, platinum coils may bepacked into the aneurysm sac using angiographictechniques. It is unclear which method gives the bestlong-term results.

Aneurysmal subarachnoid haemorrhage is a seriouscondition with a high initial mortality and morbidity. Inpatients who survive the initial haemorrhage, the risk ofrebleeding is 25% in the first 2 weeks and 60% within6 months, with a mortality of 60%. Therefore earlyreferral and assessment of patients with suspected SAHis important. A common cause of litigation concerns

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Fig. 19.2 Anteroposterior (AP) view of a right internalcarotid angiogram showing an anterior communicatingartery aneurysm arising in the midline between the twoanterior cerebral arteries (A). A smaller aneurysm can alsobe seen at the bifurcation of the middle cerebral artery (B).

patients with a minor SAH (who remain relatively well)misdiagnosed as migraine or viral meningitis, only toreturn a week later with a devastating rebleed.

Intracranial neoplasms

Intracranial tumours form a large part of the neuro-surgical workload. There are many pathological types oftumour and detailed discussion of each is not possible.However, tumours can be grouped broadly into intrinsictumours (those that arise within the brain substance) andextrinsic lesions. The most common adult intrinsictumours are gliomas (astrocytomas, oligodendrogliomas,etc.) and metastatic carcinomas. The most commonextrinsic tumours are meningiomas, which arise from thearachnoid membrane on the internal aspect of the dura.In children, the most common neoplasms are medullo-blastomas and ependymomas, both intrinsic tumoursarising in the posterior fossa.

Depending on their position, size and rate of growth,tumours can present with virtually any neurologicalsymptom or sign. Headache, seizures and confusion arethree of the most common. The key feature of neoplasticlesions is that the presenting signs will usually be ofgradual onset and progressive. Diagnosis is by CT orMRI scan, although skull radiograph may give a clue insome cases. It is often possible to diagnose with a reason-

able degree of certainty the pathological type of tumourbased on the CT scan appearance. However, gliomas inparticular can have a varied appearance and can some-times look like a metastasis, an abscess, an infarct or aresolving haematoma. Biopsy is often required.

The management of intracranial tumours depends onmany factors but the key principle of management is toweigh the likely benefits of the proposed treatmentagainst the possible morbidity or mortality arising fromtreatment. Factors that tend to increase the risk of surgeryare older age, poor clinical condition, location within orclose to an 'eloquent' (i.e. functionally important) area ofbrain, and close involvement of important intracranialarteries or veins.

The usual classification of extracranial tumours intobenign or malignant is not so helpful or relevant withintracranial tumours. Most meningiomas, for example,are pathologically 'benign' and have a clear plane ofcleavage from normal brain. However meningiomas caninvade the dural venous sinuses or bone around the baseof the skull, making total removal impractical. Further-more, meningiomas may have 'atypical' features (such asmitotic figures) or be frankly malignant, and in all suchsituations there is a higher chance of recurrence.

The feature of the majority of gliomas, from lowgrade to malignant, is that they invade normal brain. It iswell established that even if the CT scan shows anapparent clear margin to the tumour, tumour cells extendat least 2 cm beyond the margin into brain substance.Most gliomas respond little to radiotherapy and even lessto chemotherapy, and therefore a cure is not possible.The aim of management must be to try and relieve thepatient's symptoms and extend the length of good qualitylife. Attempts at radical resection of the glioma are rarelyjustified if this means that the patient is to be left evenmore disabled postoperatively. Conservative manage-ment is often appropriate.

Secondary tumours within the brain are often multipleand most are not referred to a neurosurgeon because theyare terminal. Patients with a solitary metastasis in anaccessible area and who are generally well may benefit inthe short-term from surgical excision.

Intracranial infection

Meningitis

Viral meningitis rarely comes to the attention of theneurosurgeon unless there is suspicion of some other

169

diagnosis such as subarachnoid haemorrhage. Likewise,most cases of bacterial meningitis will be managed per-fectly adequately outside a neurosurgical unit. Diagnosisis by lumbar puncture.

Meningitis is seen most often by neurosurgeons as acomplication of an open head injury or followingintracranial surgery. Treatment is with the appropriateantibiotics. Occasionally, bacterial meningitis, especiallytuberculous meningitis, can cause hydrocephalus, whichrequires ventricular drainage of CSF. Therefore a patientin coma, or who fails to respond to antibiotic treatment,should have a CT scan.

Brain abscess and subdural empyema

A brain abscess (or subdural empyema) may occur as aresult of direct spread from infected sinuses, otitis mediaor a penetrating wound, or by the haematogenous route(Fig. 19.3). Haematogenous brain abscesses are morelikely to be multiple and are thought more likely in patientswith a cardiac septal defect that allows the normalbacterial filtering action of the lung to be bypassed.

170 Fig. 19.3Axial computerised tomography (CT) scanshowing an abscess in the region of the thalamus.

Congenital lesions

Congenital lesions of the CNS may occur in isolationor in association with other abnormalities as part of arecognised syndrome. Some lesions are obvious at birth(e.g. spina bifida), and others cause no symptoms andremain unrecognised throughout life (e.g. temporal lobeagenesis). Others, for example, craniosynostosis andaqueduct stenosis, are only diagnosed when they producesymptoms or signs.

Craniosynostosis

This refers to premature fusion of one or more of theskull sutures resulting in abnormalities of the skull shape.

Synostosis may be part of a more generalisedabnormality such as Crouzon's or Apert's syndrome, inwhich case there will be facial, dental and ophthalmicabnormalities to consider, and a multidisciplinary teamapproach is required.

Surgery consists of resecting the faulty suture line(s)and allowing the skull vault bones to 'spring'. Brain growthwill then hopefully mould the skull to a more normalshape and size. Surgery may also be required to the orbitsand facial bones.

Spina bifida

This term covers a range of abnormalities from asymp-tomatic spina bifida occulta to large, open, posteriorspinal defects with total loss of cord function. Opendefects need to be closed soon after birth. Less major(closed) spina bifida defects may only become apparentas the child grows and develops problems with walking.An MRI scan is the investigation of choice.

Arnold-Chiari malformation

In this condition, the cerebellar tonsils are prolapsedthrough the foramen magnum. The posterior fossa isoften abnormally shallow. In more pronounced forms thelower brain stem will also be herniated.

Mild forms are common and often asymptomatic.Symptoms may range from cough impulse headache tosigns of brainstem compression. Chiari malformationsmay be associated with spina bifida and aqueduct stenosis.Treatment of symptomatic cases is by bony decompressionof the foramen magnum.

Aqueduct stenosis

This can give rise to an obstructive hydrocephalus andmay present at any age. Ataxia is often an early symptomand headaches are frequently mild or absent even in thepresence of papilloedema. Treatment is by insertion of aCSF shunt or by making a fenestration in the floor of thethird ventricle.

Hydrocephalus

CSF is actively secreted in the colloid plexus of thelateral third and fourth ventricles at a rate of 20 mL perhour. There is a gentle pressure gradient that causes CSFto flow, in a pulsatile manner, through the aqueduct intothe fourth ventricle and then out of the fourth ventricleinto the basal subarachnoid space. The flow continuesover the cerebral hemispheres to the superior sagittalsinus, where CSF is absorbed through the arachnoidgranulations by a passive process dependent on differen-tial pressure between the CSF and the venous sinus.Hydrocephalus refers to the situation where there is animbalance between CSF production and absorption,causing the ventricles to enlarge. In acute hydrocephalusthis causes severe pressure on the brain, decreasedcerebral perfusion, herniation through the tentorial hiatus,brain stem pressure and, eventually, death. In more chronicforms there is progressive stretching, ischaemia anddestruction of white matter tracts around the enlargingventricles.

Hydrocephalus occurs as a result of a congenitalabnormality (e.g. aqueduct stenosis) or as a complicationof some other intracranial pathology. Almost any intra-cranial pathology can cause or be associated with hydro-cephalus and it is one of the commonest problems inneurosurgery.

The term 'active hydrocephalus' implies a continuingimbalance between CSF production and absorption,leading to ongoing raised ICP. Compensated or arrestedhydrocephalus refers to the condition of large ventricles(ventriculomegaly), suggestive of previous activehydrocephalus but with no continuing raised pressure.Arrested hydrocephalus is common in the communityand although such individuals may have no neurologicaldeficits they might have large heads and enormousventricles on CT scan. It is important to treat the patientand not the CT scan.

Active hydrocephalus usually requires surgical treat-ment. The best management in obstructive hydrocephalus

is to remove the cause of the obstruction if possible. As atemporary or holding measure a ventricular drain may beinserted to drain CSF into an external reservoir. A shuntconsists of a silastic ventricular catheter connected to asubcutaneous valve and reservoir, in turn connected toa tube into the peritoneal cavity (ventriculoperitonealshunt) or atrium (ventriculoatrial shunt).

The disadvantages and complications of shunts arelegion and include blockage, infection and over drainage.Each significant shunt complication requires furthersurgery; such patients can become very dependent onhospital services.

Vascular compression syndromes

Paroxysmal trigeminal neuralgia (PTN)

This is a relatively common condition characterised byvery severe episodes (paroxysms) of shooting painsaffecting one side of the face. The diagnosis is made onthe history alone and the characteristics are listed inTable 19.6.

In most so-called idiopathic cases of PTN the cause isa blood vessel compressing the trigeminal nerve at theposition where it enters the pons. There is evidence thatthe vessel leads to focal demyelination and ephaptictransmission. MRI scanning will usually demonstrate thecompressing vessel.

Treatment is by carbamazepine or other anti-convulsant drugs in the first instance. If the patient stillexperiences pain on the maximum tolerated dose ofanticonvulsants, it is possible to explore the trigeminalroot entry zone via a small posterior fossa craniectomy.Separating the compressing vessel from the nerve usually(80% of cases) cures the pain. However, there are caseswhere no compressing vessel is evident or, if present,decompression does not alleviate the symptoms. Clearlythere are other possible causes.

Table 19.6 Features of trigeminal neuralgia

Gradual worsening of severity and frequency of attacksover the years

Periods of remissionNo neurological deficits or sensory disturbanceOften aggravated by chewingA trigger spot where light touch or cold sets off the painResponds to carbamazepine 171

Fig. 19.4 Treatment for trigeminal neuralgia. The lateralskull X-ray shows a needle entering the foramen ovale anda Fogarty balloon inflated with contrast in the trigeminalcistern.

In patients not suitable for the above procedure (i.e.the elderly or unfit) a destructive procedure can be carriedout to the nerve. This may be a peripheral nerve blockusing alcohol or a cryoprobe (usually carried out by oralphysicians), or an injection into the trigeminal ganglionvia the foramen ovale under X-ray control. The ganglionmay be partially denervated by heat (thermocoagulation),chemical (glycerol) or mechanically (balloon compression;Fig. 19.4). The initial success rate of these destructiveprocedures is high, but so is the recurrence rate.

Patients with multiple sclerosis commonly develop anidentical syndrome to idiopathic trigeminal neuralgia.Presumably the origin is a demyelinating plaque some-where on the course of the nerve root. Vascular decom-

pression procedures will not help but ganglion injectionprocedures are effective.

Occasionally, a tumour in the cerebellar pontineangle, such as an acoustic neuroma, petrous meningiomaor epidermoid cyst may present with PTN. Removal ofthe tumour is usually curative.

Glossopharyngeal neuralgia (GPN)

This is a similar syndrome to PTN except the pain is inthe distribution of the glossopharyngeal nerve that is theposterior tongue and pharynx on one side. Typically, thepain of GPN occurs on swallowing and that of PTN onchewing. Open surgical treatment is highly effective andthere is usually a compressing vessel at the glosso-pharyngeal root entry zone into the brainstem. If there isno vessel, or the vessel is technically difficult to separate,unilateral section of the glossopharyngeal nerve and theupper roots of the vagus is curative and produces hardlyany neurological deficit.

Hemifacial spasm

This is the third of the curious cranial nerve vascularcompression syndromes. Most people have seen some-one with involuntary contractions of muscles on one sideof the face. The syndrome usually starts with blepharo-spasm but tends to progress over the years to involve thewhole of the side of the face in dystonic contractions.The patient may effectively lose the use of one eye andthe cosmetic effect is distressing.

Once again there is in most cases a blood vesselcompressing the facial nerve at its root entry zone. Aposterior fossa craniectomy and decompression of thenerve is usually successful in abolishing the spasm.

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Temporomandibular jointinvestigation and surgery

IntroductionThe most common condition affecting the temporo-mandibular region is temporomandibular dysfunction, ormyofascial pain dysfunction. This may be associatedwith a clicking of the temporomandibular joint. This is adisorder characterised by pain and masticatory musclespasm and limited jaw opening, which is treated byconservative measures such as soft diet, analgesics,occlusal splint therapy or physiotherapy. Intransigentcases may respond to psychotropic therapy.

Conditions affecting the temporomandibular joint(TMJ) that might require surgery are listed in Table 20.1.A detailed knowledge of the anatomy of the TMJ isnecessary and an overview of this follows, with aspectsof the history and examination of the patient and detailsof the investigations that are a prerequisite to appropriatesurgical care. This is followed by a discussion of theprocedures available for the surgical management ofTMJ disorders (Table 20.2).

Anatomy of thetemporomandibular joint(TMJ)The TMJ is a synovial joint with articular surfaces madeup of fibrocartilage. Fibrocartilage is adapted to takeshearing forces, rather than the compressive forces thatact on the hyaline cartilage in the knee joint. The TMJhas an upper and a lower compartment separated by acartilaginous meniscus. The non-articular surfaces arelined by a synovial membrane, which produces the synovialfluid that lubricates the joint and nourishes the cartilage(Fig. 20.1).

The only time that the joint is loaded is when eatingor clenching. When speaking or relaxed the teeth are

Table 20.1 Surgical conditions of thetemporomandibular joint

Internal joint derangementRecurrent dislocationTraumatic injuryArthritic conditionsAnkylosisTumours

Table 20.2 Surgical procedures for thetemporomandibular joint (TMJ)

ArthrocentesisTMJ arthroscopyMeniscal plicationMeniscectomyEminectomyDautrey procedureCondylotomyCondylectomyTMJ reconstruction

Fig. 20.1 The anatomy of the temporomandibular joint.A, bilaminar zone; B, condylar head; C, mandibulareminence; D, glenoid fossa.

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apart. When the jaws are closed much of the force istransmitted through the teeth into the facial bones butsome of the forces will go into the jaw joints.

The joints are supported by ligaments, which sur-round the joint capsule. Movement is by the action of themasticatory muscles and information from proprioceptorsin the mouth and particularly in the periodontal ligamentallow coordination of all components when chewing orspeaking. Injury or damage to any of these componentsaffects jaw function.

InvestigationsInvestigations of the temporomandibular joint includehistory, examination and special investigations, and theseare discussed in turn.

Palpation of the TMJs may cause pain and, on move-ment, clicking or crepitations may be felt or even heard.

On intraoral examination the patient may have limitedopening (normal interincisal opening 40-50 mm). Theremay be deviation of the jaw to one side when asked toopen widely due to limitation of movement from thatside (normal lateral movement 10 mm to each side).

Palpation of the masseter muscles and the pterygoidmuscles should be carried out. To palpate the pterygoidmuscles the patient should be asked to deviate the jaw tothe side being examined to allow a finger to be passedalong the upper buccal sulcus backwards between theramus of the mandible and the tuberosity of the maxilla.Behind the tuberosity are the pterygoid plates - theorigin of the pterygoid muscles. This site is often tenderin TM dysfunction, due to muscle spasm and fatigue.

History

The patient's presenting symptoms should be noted.Symptoms might include pain, swelling, clicking,crackling in the preauricular region and limitation of jawopening. There may also be an accompanying generalisedfacial ache or a numb sensation over the massetermuscles. When asked about pain, if a patient points to thepreauricular region then the pain is likely to be in theTMJ, but if the patient puts a hand over the side of theface as the area of pain then it is likely to be muscular pain.There is often a combination of both in arthromyalgia.TMJ symptoms must be distinguished from otherconditions in the orofacial regions.

Previous symptoms, duration and potential causes ofthe symptoms such as trauma should be elicited from thepatient. Any activity that exacerbates or relieves the con-dition should be noted. Chewing, yawning or parafunc-tional habits can aggravate TMJ disease.

A full medical and drug history should be taken, aswell as a family and social history. Of particular relevanceare traumatic life events such as bereavement, a house orjob move or a divorce. Stress is a common factor in TMdysfunction.

Examination

A general examination of the head and neck should becarried out, paying particular attention to tenderness inthe sternomastoid and temporal muscles. The angle ofthe jaw may be tender where the medial pterygoid muscleis attached.

Special investigations

The special investigations which may be considered arelisted in Table 20.3.

Plain radiographs include an orthopantomogram, andtranscranial and transpharyngeal views of the TMJ. Theseimages give information about the bone structure. Openand closed views will give some indication about jawmobility.

Arthrography is an invasive investigation using aradiopaque dye, which is injected into the upper jointcompartment, the lower joint compartment or a com-bination of both. This technique can provide informationabout the internal structures of the joint. The cartilaginousmeniscus is outlined. The procedure is usually carriedout under videofluoroscopy so that the joint can be imagedin motion. Disc displacement and perforations can beidentified. However, extravasation of dye into surround-ing tissues will spoil the investigation. With newerimaging techniques this method is now less frequentlyused.

Computerised tomography (CT) scanning can give alot of information about the bony relations and bone

Table 20.3 Investigation of temporomandibularjoint pathology

Plain radiographsArthrographyCT scanMRI scan174

quality of the TMJs. It gives axial views and computer-generated coronal views; it can also give three-dimensional images. This method is very helpful inproviding information about trauma to the joint, bonydisease in the joint and ankylosis.

Magnetic resonance imaging (MRI) images the softtissues and is helpful in identifying disc position. It candemonstrate disc perforation and joint effusions. It mayalso pick out adhesions within the joint. It does giveinformation about the bone but it is not as good as a CTscan.

Surgical managementArthrocentesis

Arthrocentesis is a method of flushing out the TMJ byplacing a needle into the upper joint compartment usinglocal or genera] anaesthesia. Ringer's lactate (see Ch. 5)is injected into the joint. This compartment will take upto 5 mL of fluid. By filling under pressure, any minoradhesions are broken down or lysed. A second needleplaced into the same joint compartment allows through-flow of fluid to be achieved. This allows thoroughwashing or lavage of the joint. The process is referred toas 'lysis and lavage' and can produce good therapeuticoutcomes. It has a particular roll in cases of acute closedlock. In this situation, the meniscus is usually jammed infront of the condyle, preventing translatory movement.By ballooning-up the joint the potential space becomesreal and the meniscus may have room to reduce to itsnormal position. The lavage will wash-out products ofinflammation, creating a better environment for healing.Sodium hyaluronate can be injected at the end of theprocedure to improve joint lubrication.

TMJ arthroscopy

TMJ arthroscopy can be used both as a diagnostic tooland as a treatment modality. The synovium, joint andminiscal cartilage can be visualised.

The standard technique for TMJ arthroscopy is via alateral approach. The upper joint compartment, wheremost of the translatory movement occurs, is entered witha 21 gauge needle posteriorly. After insufflation of thejoint with Ringer's lactate, through-flow of fluid isestablished via a second 19 gauge needle placedanteriorly in the joint space. A trochar and cannula arethen introduced into the space created by the fluid in the

joint. The trochar is removed and replaced by the arthro-scope. An outport second cannula may be insertedanteriorly into the joint for instrumentation - the workingcannula. The upper joint compartment can then beexamined for synovitis, displacement of the meniscus,adhesions between meniscus and the joint fossa andother pathology.

If adhesions are seen they can be divided with verysmall scissors inserted through the working cannula. It ispossible in some cases to reduce a dislocated meniscus,biopsy cartilage or synovium, remove loose bodies (frag-ments of cartilage floating in the joint) and reduce thejoint eminence with rotary instruments. Drugs such ascorticosteroids or sodium hyaluronate may be injected intothe joint to reduce inflammation and improve lubricationrespectively.

Splint therapy, soft diet and analgesics are used as partof the postoperative management. The patient is alsoinstructed in gentle jaw stretching exercises.

Meniscal plication

When conservative management has not causedimprovement after a period of 4-6 months, andarthrocentesis or arthroscopy have failed to correctmeniscal dislocation, then open arthrotomy should beconsidered.

The usual approach is via a preauricular incision (Fig.20.2). Once the joint is exposed, entry is made into theupper joint compartment and the position of the meniscusidentified. Any adhesions are released and the meniscusis repositioned and fixed with sutures from the lateralaspect of the cartilage and posteriorly into the temporalmuscle and fascia. Some surgeons will also enter thelower joint space to increase the mobilisation of themeniscus and remove a wedge of retrodiscal tissue, stitchor plicate the defect created with retrodiscal sutures,repositioning the meniscus more posteriorly. Sometimesthese procedures are combined with an eminectomy toincrease joint space.

Postoperative management is similar to that of arthro-scopy. Physical therapy is important as there is inevitablya degree of scarring following this surgery.

Meniscectomy

This procedure is not commonly performed in the UKbut there have been reports of successful outcomes inpatients suffering from internal joint derangement by this

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Fig. 20.2 Preauricular incision for exposure of thetemporomandibular joint.

method. Essentially, the approach is the same as that formeniscal plication. Once the meniscus is identified thecartilaginous part is excised. There is uncertainty aboutlong-term effects this may have on the joint.

Eminectomy

This procedure is used for recurrent jaw dislocation. Theapproach is the same as for the plication procedure. Thejoint eminence, which lies anteriorly to the fossa, has tobe well exposed. The eminence is then excised by a com-bination of bur cuts and a fine osteotome (Fig. 20.3). The

theory is that by taking away this eminence over whichthe joint head sticks, the joint head has no obstruction toprevent its return into the fossa.

Dautrey procedure

This procedure is another method of stopping TMJ dis-location. The approach is again exposure of the joint viathe preauricular incision. The eminence is again exposedbut in this procedure the anterior part of the eminence,which is attached to the zygomatic arch, is incised in amore vertical direction (Fig. 20.4). This anterior portionis fractured-off and, still attached anteriorly to the zygo-matic arch, is swung downwards and wedged against theremaining eminence to augment the eminence. In theory,because of the increase in eminence height, the condyleis unable to dislocate. Other methods of eminence aug-mentation have been described, for example bone graftaugmentation.

Fig. 20.3 Eminectomy. The hatched line indicates thebony incision line.

Fig. 20.4 The Dautrey procedure to increase the height of the eminence.176

Condylotomy

This technique for treating painful TMJs originally useda blind external approach using a Gigli saw. Nowadaysthis procedure is carried out via an intraoral approach.The lateral aspect of the ramus of the mandible isexposed and a cut is made below the condyle with anoscillating saw. It may be subcondylar or subsigmoid(Fig. 20.5). This causes reduced pressure on the meniscusand anterior movement of the condylar head, whichreduces pain and often allows reduction of the displacedjoint meniscus.

Condylectomy

Condylectomy is usually performed when there is eitherankylosis or pathology of the TMJ. A preauricularapproach is used and, once the condyle is well exposed,it is cut at the neck of the joint and removed. This pro-cedure is generally combined with joint reconstruction.

TMJ reconstruction

On rare occasions the TMJ requires reconstruction. Todate no replacement adequately replaces the normalTMJ. Indications for joint reconstruction are listed inTable 20.4.

The goal of treatment is to restore the mandible andTMJ to as near normal an anatomical state. Partial ortotal TMJ reconstruction may be required; partial recon-struction may be indicated. There are fossa prosthesesbut these are usually used in conjunction with condylarreplacement.

Various synthetic materials or alloplasts have beenused for meniscus replacement (e.g. Teflon®). Thesematerials can cause a foreign body giant cell reaction,which is relentless in its destruction of surroundingtissues. For this reason, these materials are now rarelyused. Autogenous grafts such as auricular cartilage anddermis are sometimes used. Potential complications fromthese grafts are disruption or displacement, cyst formationwith the dermal graft and fibrous ankylosis.

Ankylosis may be treated with a temporalis muscleflap, gap arthroplasty or total joint reconstruction.

The usual method in gap arthroplasty is by parallelcuts approximately 1 cm apart from the sigmoid notch tothe posterior ramus (Fig. 20.6). Interpositional materialcan be placed to reduce union. Alloplasts such as Silastic®

or a chrome–cobalt cap prosthesis have been used.

• • • • Two types of incision on vertical ramusof the mandible for condylotomy

Fig. 20.5 Two types of incision (subcondylar andsubsigmoid) on the vertical ramus of the mandible forcondylotomy.

Table 20.4 Indications for temporomandibularjoint reconstruction

AnkylosisJoint destructionTraumaInfectionTumoursPrevious surgeryRadiationDevelopmental deformity

Suturing medial pterygoid and masseter muscles togetherabove the ramus stump is a biological interpositionalgraft.

Most surgery for ankylosis is carried out through thepreauricular approach but when joint replacement isrequired a submandibular incision is used for accessto the ramus for a combined approach. A method ofbiological reconstruction of the TMJ is the use of aninferiorly based temporalis muscle flap, which is rotatedanteriorly beneath the zygomatic arch as an inter-positional material (Fig. 20.7).

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Fig. 20.6 Gap arthroplasty. The hatched area is the bonyexcision.

178 Fig. 20.8 A costochondral rib graft fixed with mini boneplates.

Fig. 20.7 Finger flap of the temporalis muscle rotatedanteriorly under the arch of the zygoma into the glenoid fossa.

Total joint reconstruction is required where there is nofunctional joint plus loss of ramus height. This may benecessary where there has been severe trauma, ankylosis,tumour resection or a developmental abnormality suchas hemifacial microsomia. Costochondral grafts or vas-cularised free bone grafts such as the second metatarsalbone from the foot could be used in combination with aninterpositional temporalis muscle graft. The most satis-factory method of total joint reconstruction is the com-bination of the temporalis muscle flap and an autogenouscostochondral rib graft (Fig. 20.8).

Several prosthetic joint replacement systems havebeen devised to replace both glenoid fossa and condyle.Some have had problems from chronic foreign bodygiant cell reactions to the synthetic materials.

Surgery is not the endpoint of treatment. The post-operative phase, as in all surgery, is very important andneglect in this area is often a reason for failure. Analgesicand anti-inflammatory medications are usually indicatedand physical therapy is essential, with jaw opening exer-cises plus lateral and protrusive movement exercises.

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PART II ORALSURGERY

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Introduction

The oral surgery section of this text focuses on thoseareas of surgical practice that are routinely encounteredin general dental practice. Certain procedures, such asuncomplicated extraction of teeth, will fall within thearea of competence of every dental practitioner whereasother procedures, such as removal of cysts and certainwisdom teeth, might be performed only by those whohave an interest in surgical dentistry and who havedeveloped the necessary competence, through training, toperform those more complex procedures. Regardless, alldental practitioners must have a detailed knowledge ofthe subject areas covered within the 'oral surgery'sections of this book because they will encounter patientsroutinely who present with signs and symptoms thatrequire a comprehensive knowledge to diagnose them.Thus, even if referral to a specialist is the management ofchoice, a dentist must be equipped with the knowledge to

make a competent referral and to fully inform the patientof the nature of the problem, the scope of the treatmentand the likely prognosis.

This section therefore covers those areas wherepractical knowledge is core information, whereas thepreceding section – 'special surgical principles' - wasconcerned with areas where theoretical rather thanpractical information is more important.

References to Part I of this book are extensive, thusminimising duplication of core information relating tobasic principles such as homeostasis, surgical sepsis andcross infection control.

The subsequent chapter details the process of historytaking and examination and also importantly covers theissue of the patient consent. Further chapters describespecific areas of oral surgical interest.

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History and examination

IntroductionIn oral surgical practice, the same approach to historytaking and examination should be adopted as for generalhistory taking and examination. The process should bemore focused, however, to the oral region and, forexample, a full systemic history and examination is notusually required.

History takingThe elements of the clinical history are shown inTable 22.1.

Introduction to the patient

Introduction to the patient is a most important moment,as discussed in detail in Chapter 2. This allows a rapportto develop with the patient that will facilitate the rest ofthe interview and enhance the possibility of achieving anappropriate diagnosis and treatment plan. Patient contactat a social level is an important prerequisite to obtainingthe rest of the history and is important before examiningthe patient. Premature physical examination of a lesionmay not only reduce the patient's confidence but alsounnerve the surgeon if the diagnosis is not immediatelyapparent with visual examination.

As discussed subsequently, consent to history takingand examination is usually implicit, but nothing shouldbe taken for granted and all of one's questions andexaminations should be fully explained.

The presenting complaint

The patient should be allowed to describe the complaintin his or her own words, and then a full history of thepresenting complaint should be established. This shouldbe carried out using searching questions that do not lead

Table 22.1 Elements of the clinical history

History of the presenting complaintPast medical history including drug historyFamily historyDental historySocial history

the patient into giving false information. Patients wishingto avail themselves of the best medical attention willusually wish to please and will therefore tend to agree,using a positive response, to any direct question asked.This problem can be overcome by providing the patientwith alternatives: 'Is the pain constant?' is more likely tobe answered accurately if the patient is asked 'Is the painconstant or not?'. Several features of the presentingproblem should then be elicited:

• When was the problem first noted?• What is the location?• Are the symptoms continuous or intermittent?• Does anything make the problem' better or worse?• Is the problem getting better or worse?

A common presenting symptom in oral surgical practiceis that of pain, which requires further specific interrog-ation to establish its full nature and extent. Key elementsto be ascertained are shown on Table 22.2.

Past medical history including drug history

The importance of obtaining a medical history is para-mount not only because it allows the surgeon to enquireabout other general aspects of the patient's wellbeing thatare associated with the presenting complaint but alsobecause it allows the surgeon to ascertain informationrelating to the patient's medical status that might have aninfluence on the treatment planning.

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Table 22.2 Key features in a history of pain

Principle site affectedRadiationCharacterSeverityDurationFrequency and periodicityPrecipitating and aggravating factorsRelieving factorsAssociated features

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A number of systemic diseases have a bearing onsurgical practice and these will be discussed below. Inaddition, however, a number of standard questions shouldbe asked relating to the patient's past medical history.The use of a preprinted questionnaire for this purpose ishelpful because patients are likely to produce truthfulresponses when filling in 'their own' questionnaire, andalso because it also provides written confirmation thatthese questions have been considered (Fig. 22.1). How-ever, the questionnaire should always be verified by theclinician and this information should always be includedin the written history that is recorded in the patient's caserecord.

Cardiovascular system

The cardiovascular status of the patient is particularlyimportant when general anaesthesia is required. Amyocardial infarction within the previous 6 months is acontraindication to general anaesthesia and surgery,unless this is vital (see Ch. 35).

Similarly, patients at risk of endocarditis shouldreceive antibiotic prophylaxis and it should also beremembered that many at-risk patients are also onwarfarin; their management must take this into account(see Ch. 35).

The respiratory system

An upper respiratory tract infection is a relative contra-indication to surgery and treatment should be deferreduntil the infection has been cleared. Patients with chroniclung disease may need special care. The history of aproductive cough should be elicited, together with sputumproduction, which may suggest a current pulmonaryinfection that requires active treatment before generalanaesthesia and surgery.

A history of smoking should alert the clinician to thepossibility of chronic lung disease and the patient shouldbe advised to stop prior to any surgical treatment undergeneral anaesthesia.

Gastrointestinal system

A past history of liver disease, with or without jaundice,should alert the clinician to the possibility of hepatitis.Such patients also frequently have problems withcoagulation, which may require investigation.

Locomotive system

A history of arthritis, especially rheumatoid disease, isimportant. Such patients tend to have problems with thecervical spine and this may be important, not only for theanaesthetist if the patient requires intubation but also forthe oral surgeon treating the patient within a dental chair.Particular care should be taken in patients with Downsyndrome because of their tendency to have atlantoaxialdislocation.

Neurological system

Neurological symptoms are important to elicit particularlyif there is a history of trauma and these are discussedfully in Chapter 19.

Drug history

It is crucial to know about the drugs ingested by thepatient, including over the counter medication, beforecontemplating any surgery. A history of corticosteroidmedication and anticoagulant therapy is particularlyimportant (see Ch. 35). Care should be taken to ensurethat the patient's medication will not adversely interactwith any medication given to or prescribed for the patient.

Family history

The family history provides information regardinggenetic disease, such as haemophilia, and also providesan insight into disease susceptibility by enquiring aboutconcurrent family disease and causes of death in deceasedrelatives such as heart disease, stroke or cancer.

Social history

This provides information regarding home support forpatients postoperatively and should also include questionsabout smoking and alcohol consumption, as these

influence not only disease susceptibility but also willinfluence postoperative recovery.

ExaminationExamination of the patient is subdivided into three areas:first, related to the presenting problem; second, to assessthe patient's fitness for the proposed procedure and third,to detect any associated or coincidental disease.

The first is dealt with in appropriate chapters withinthis book. The last two can be dealt with by a system ofexamination (Table 22.3).

General assessment

All clinicians should look at their patients at the firstencounter to see whether they think the patient looks'ill'. This may mean the patient looks cachectic, flushed

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Fig. 22.1 Medical history questionnaire.

Table 22.3 System of examination for an oralsurgery patient

General assessmentHandsFaceNeckOral cavity

and feverish, exhausted, pale or jaundiced, or that otherfeatures are apparent. If the patient looks ill, do nothesitate to ask if he or she feels ill.

When assessing a patient for oral or dental surgery, aquick and easy check can be performed as describedbelow.

Hands

Examination of the nails can demonstrate finger clubbing(suggestive of chronic lung disease or even lung cancer),koilonychia or nail spooning (may suggest iron deficiencyanaemia), white nails (may suggest liver disease) andcyanosis or bluish discoloration (may suggest heart orlung disease).

Examination of the palms of the hands may showpalmar erythema (red and mottled, associated with liverdisease), Dupuytren's contracture of the ring and fifthfingers (associated with liver disease and epilepsy), pallorof the palm creases (associated with anaemia) and jointdeformity and swelling will indicate arthritis and itsnature.

The pulse can now be felt recording the rate and anyarrythmia.

Face

Jaundice will be obvious from examination of the colourof the face and conjunctivae. This is a very important signfor the surgeon. Such patients have associated disordersof blood coagulation due to clotting factor deficienciesand are prone to sepsis. If the jaundice is related to viralhepatitis, the patient may be a major risk to the surgeonand the theatre staff.

Examination of the conjunctivae will not only demon-strate jaundice but they may also be very pale, indicatinganaemia.

Examination of the eyes may show arcus senilis, aring of cholesterol deposit around the iris of the eyeassociated with cardiovascular disease.

Skin rashes may be most obvious on the face asso-ciated with allergies, acne, dermatitis, psoriasis, and otherdisorders. Lichen planus is more typical on the wrists andflexor surfaces of the arms.

Facial paralysis may suggest a previous stroke or alower motor neuron palsy such as Bell's palsy. A palsy ofone side of the face results in the face being pulled to theopposite side because of unopposed muscle action.

Again this examination can take place while talking tothe patient and in only a matter of seconds.

Examination of the salivary glands, temporo-mandibular joints and muscles of mastication should becarried out when indicated.

Neck

Neck inspection is best performed from the front andpalpation from behind. It may reveal an obvious goitreespecially visible or palpable on swallowing.

Patients receiving treatment for known heart failuremay have distension of neck veins, which suggests thatthe failure is not fully controlled.

Enlarged lymph nodes may be visible and palpableand may be associated with infection, malignancy, orother less common disorders. These usually need to beinvestigated before any other treatment is instituted.

It is important to remember to inspect the sides of theneck especially in the region of the ears and parotidgland.

Scars in the neck should alert one to previous surgery(e.g. thyroidectomy) and enquiry should be made aboutthis if not mentioned by the patient during the historytaking.

Swelling of the neck or elsewhere in the orofacialregion is often a presenting feature and should beexamined in a rehearsed fashion in order to elicit theimportant clinical features (Table 22.4).

Oral cavity

The oral/dental surgeon has the great advantage of beingable to inspect the oral cavity closely and hence to detectassociated diseases that may be apparent here. This is inaddition to the presenting problem. The clinical featuresrelating to specific oral disease are detailed in the sub-sequent chapters.

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Table 22.4 Important clinical features of aswelling

PositionSizeShapeColour and temperatureTendernessMovementConsistencySurface textureUlcerationMarginAssociated swelling

A full cardiovascular, respiratory, abdominal andneurological examination does not come under the remitof the oral/dental surgeon. Suspicion of underlyingdisease may be detectable from a clear history andclinical examination as outlined above. Such a historyand examination should alert the oral/dental surgeon toan underlying or potential problem and in this situation,specialist advice should be sought before progressingwith treatment. The patient's GP will often be aware ofthe underlying problems and be able to advise on risksand whether further referrals, investigations and manage-ment are necessary. If there is any doubt, advice shouldbe sought before any oral surgical or dental treatment isperformed.

Conse'ntThe patient must consent to all procedures after fullexplanation of the options and consequences. Consent toanswer questions and to be subjected to routineexamination is usually implied. Consent to proceduresunder local anaesthesia is commonly obtained verballyas patient cooperation is a prerequisite to completing theoperation. The consequences, for example, of extractionof an impacted wisdom tooth, may be lip numbness,and it is therefore prudent to fully explain the possibleimplications and record this in the notes.

Although most dentists will not work on patientsunder general anaesthesia - most refer patients forgeneral anaesthesia and so hence have the responsibilitiesof the referring dentist, detailed below - they do havecontinuing responsibility for their patients postoperativelyand so must have detailed knowledge regarding theirresponsibilities surrounding such referrals.

A detailed discussion about the ethical and legalobligations upon clinicians is not included here but it isimportant to consider the principles of obtaining consentto treatment.

The use of the term 'informed consent' has led tomuch confusion amongst healthcare professionals aboutthe nature and extent of the information that should beimparted to a patient. Many clinicians have interpretedthis concept of informed consent as a process that has tobe undertaken to avoid possible legal actions and, as aresult, it is often carried out in a ritualistic way. Thisapproach is most commonly reflected in cursory clinicalnotes recording, for example, 'warning given regardingpossible nerve damage' in association with third molarsurgery.

It may be that the term 'informed consent' is amisnomer and that the process of obtaining consent totreatment should, by definition, incorporate all of theinformation that a patient requires to make an informeddecision on whether or not to proceed with the proposedtreatment. Rather than thinking in terms of obtaininginformed consent, a clinician may benefit from consider-ing the process to be undertaken to obtain valid consent.The concept of obtaining valid consent is one that:

• recognises a patient's right of autonomy• requires an assessment of the patient's competence to

give consent• imparts information to the patient in a way that is

understood• considers the patient's expectations and aspirations• obliges the clinician to obtain and assess all

information necessary to allow appropriate treatmentto be undertaken safely, including sufficientinformation about the patient's dental condition, thetreatment options and the material risks and/orcomplications arising from the condition itself, orassociated with the patient's medical condition

• requires disclosure of the material and relevant risksassociated with the treatment options underconsideration

• permits discussion about the implications of refusalof treatment by the patient or withholding oftreatment by the clinician

Before the process of obtaining consent can be broachedwith the patient, the clinician must undergo a process ofobtaining all relevant clinical information and recordingthe details in the patient record. The patient record is aninvaluable and permanent source of information and it

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must be possible to rely upon it for accuracy and contentat any time in the future. The patient record should alsocontain the information listed in Table 22.5. The prudentclinician will also record the information listed inTable 22.6.

Following a structured approach to patient assessmentand recording, the details in the patient record providethe clinician with all of the information necessary tofacilitate meaningful discussions with the patient aboutthe clinical situation. The imparting of all relevant infor-mation that the patient needs to make a valid decision onwhether or not to proceed with the treatment as proposedis then readily available.

Competence to give consent

The efficient delivery of dental care and/or treatmentrelies on the fact that the law recognises that consent toevery procedure need not be written or even explicitlygiven. The medical and dental professions rely on thefact that a patient implies consent by cooperating withtreatment. However, consenting to treatment is more thansimple acceptance or submission. The principles of obtain-ing or giving consent involve voluntariness, knowledgeand competence:

• Voluntariness requires the patient freely to agree totreatment (or not).

• Knowledge requires disclosure of sufficientinformation in a comprehensible way to allow thepatient to make an informed choice.

• Competence means that the patient must havesufficient ability to understand and make an informeddecision. Competence to give consent is aprerequisite to obtaining valid consent.

Put simply, the ability to give consent is a function of thepatient's age and mental or intellectual capacity. A patientmust be able to do the things listed in Table 22.7.

Patients who are not able to make such autonomousdecisions are young children (due to their lack of maturity),adults with cognitive difficulties and unconsciouspatients. These will be considered in turn.

Children

The Family Law Reform Act (1969) in England andthe Age of Legal Capacity (Scotland) Act, as amended,confirm that a patient aged 16 years and over could givevalid consent to treatment and, by implication, could also

Table 22.5 Essential information contained inthe patient record

Patient's personal detailsCurrent medical historyHistory of presenting complaint or reason for referralSymptoms experiencedPatient expectations and/or aspirations

Table 22.6 Desirable information included in thepatient record

Charting of teeth presentPeriodontal assessment and chartingOral cleanlinessSigns and symptoms noted including extra-oralSpecial tests undertaken and resultsAssessment of radiographsDiagnosis and treatment optionsAssessment of complications and sequelaeDefinitive diagnosis and treatment plan

Table 22.7consent

Requirements for the ability to give

Understand the informationRemember or recall that informationRelate the information to 'selfMake a judgement on whether or not to proceedCommunicate that decision

withhold consent. Although the law does permit a youngperson over 16 years to give valid consent, the prudentclinician undertaking a major procedure on a patientbetween 16 and 18 years should consider involving theparents, but only with the patient's consent.

For young children the consent of the parent orguardian is sufficient and must be obtained.

For older children, the Children Act (1989), the judge-ment in the Gillick Case and the Age of Legal Capacity(Scotland) Act, as amended, effectively permit a patientunder the age of 16 years to give legally valid consent ifhe/she has sufficient intelligence and maturity to fullyunderstand the nature and consequences of the proposedprocedure.

Although the law does permit a child under 16 yearsto give consent, it is subject to an assessment by theclinician of the patient's level of understanding, andpractitioners should always attempt to confer with the

parents of patients under 16 years unless the patientdeclines parental involvement.

Mental capacity

There are varying degrees of mental capacity/under-standing that affect a patient's ability to understand thenature and purpose of the treatment and to give validconsent. Where an adult patient is unable to give consentthen, in an emergency, the law relies upon the 'principleof necessity'. If emergency treatment is considerednecessary to preserve the health and wellbeing of thepatient then the clinician can proceed without formalconsent. To proceed with treatment on an elective basisfor such patients, a clinician would be wise to take advicefrom his/her defence organisation.

Unconscious patients

In the case of temporary incapacity, such as unconscious-ness, it is recognised that treatment can be carried outwithout consent provided that such treatment is clinicallynecessary and in the patient's best interests.

General anaesthesia

As a result of guidance issued by the General DentalCouncil, the availability of general anaesthesia for dentaltreatment has been removed from the general dentalpractice setting. There will be a continuing demand, albeita reducing one, for general anaesthesia in the secondarycare sector and an increasing requirement for sedationfacilities, and it is therefore important to define theobligations on dental practitioners.

The referring dentist

The General Dental Council places the followingobligations on a dentist who refers a patient for treatmentunder general anaesthesia:

• to assess the patient's ability to cooperate• to describe the various methods of pain control,

including an assessment of the relative risksassociated with each

• having decided that the patient requires treatmentunder general anaesthesia, or by sedation, to providea written referral specifying the following:- the patient's details

- the relevant medical and dental history- details of treatment to be undertaken- confirmation that the patient assessment has been

undertaken and specification of the reason forreferral.

The referring dentist is also required to ensure that theprovider to which the patient is referred complies withthe General Dental Council guidelines on staff, equip-ment and facilities for the safe delivery of care.

The operator dentist

Operator dentists are required to ensure that the treat-ment to be undertaken is not beyond their level ofexpertise and knowledge and that the facility complieswith General Dental Council requirements on anaestheticand support staff, equipment and drugs and that there isa protocol in place for the care of the collapsed patient.Staff training in monitoring of the patient and in dealingwith emergency situations is mandatory and should beundertaken regularly. Before embarking on the provisionof care the operator should:

• confirm the identity of the patient• confirm the nature and extent of the treatment to be

undertaken• assess the need for diagnostic radiographs if not

provided• assess the patient's level of cooperation and reinforce

the alternative methods of pain control• obtain written consent - following an assessment of

the patient by the anaesthetist, including anevaluation of the medical history - if generalanaesthesia is deemed necessary

• give appropriate advice about postoperativecomplications or sequelae.

When a patient is referred for treatment under generalanaesthesia the consent process is dependent on:

• the patient disclosing all relevant information• the referring dentist undertaking an assessment of the

patient, including the level of cooperation as well asthe treatment required

• the operator confirming the need for treatmentand the appropriateness of the request for generalanaesthesia

• in concert with the anaesthetist, obtaining writtenconsent following an assessment of the patient'sfitness for anaesthesia.

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Postoperative care

It could be difficult for the patient to find out-of-hours care after a referral for treatment under generalanaesthesia, and this is particularly true if the provider is

some distance from the referring practice. The referringpractitioner retains overall responsibility for the care ofthe patient and should therefore ensure that the patient, ora responsible person or carer, is informed of the arrange-ments for the provision of emergency care.

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Basic oral surgicaltechniques

IntroductionThe majority of oral surgery skills can be learnt bymost with good practical training, an awareness of basicprinciples of surgery (see Part 1), knowledge of theanatomy of the region and careful preparation for theprocedure. Whatever surgical operation is being under-taken, the operator must have considered the followingpoints (Table 23.1).

Preoperative considerationsThe surgeon must consider if the procedure is necessary.For example, oral surgeons over recent years have lookedmore critically at the removal of impacted wisdom teeth,given the unpleasant short-term effects and, moreimportantly, the longer-term possibility of inferior dentalor lingual nerve damage. In the light of more carefulscrutiny of these aspects, many surgeons are now

Table 23.1 Preoperative considerations

Equipment for oral surgeryOperative techniques

incisionraising a flapbone removaltooth divisionelevatorsdebridementsuturingtypes of suture

Postoperative carepostoperative instructionsanalgesiaprevention of infectionpostoperative bleeding

Follow-up

advising an increasing number of patients not to havethese teeth removed unless quite strict criteria arefulfilled (see Ch. 27).

The patient must be made aware of other possible,perhaps non-surgical, treatments. A good example of thisis the treatment of periapical infection by surgical meanswhere endodontic alternatives may be considered moreappropriate.

The short-term and long-term consequences of theoperation must be explained to the patient, particularlyin relation to known risks. Many surgeons now preferto prepare information leaflets on the more commonprocedures, such as removal of impacted wisdom teeth,so that verbal preoperative warnings are reinforced withwritten information.

The most appropriate measures for control of pain andanxiety during the procedure must be considered.Practically, there must be a decision on whether localanaesthesia, local anaesthesia with some form ofsedation, or general anaesthesia is the preferred method.Patients have an important contribution to make whenreaching such a decision but the operator may advisesedation or general anaesthesia where the procedurewould take an unacceptably long time, where accessmight prove difficult in the fully conscious patient, orwhere postoperative care would benefit from the expertiseof skilled nurses.

Patients should be urged to accept local anaesthesia,with or without sedation, for straightforward proceduresgiven that the additional risk of general anaesthesia,although small, should be avoided where possible (seeCh. 10). Only when these issues have been fully addressedwith the patient will he or she be in the position of beingable to give informed consent to the operation. Several ofthe points above can be supplemented with preoperativeexplanatory literature and the patient's signature is finallyrequired for documented consent. This is mandatory

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es

where sedation or a general anaesthetic is employed butis implied in many centres where local anaesthesia is usedalone. Informed consent is discussed fully in Chapter 22.

Equipment for oral surgerySurgical instruments

Although there may be individual preferences forparticular surgical instruments, there is a general con-sensus on basic items that are commonly used. Figure23.1 shows a typical oral surgical kit. In oral surgerythere is almost invariably a need for a hand-piece anddrills and, when soft tissue surgery is being carried out, abipolar diathermy unit can be invaluable. The use of thevarious instruments will be discussed later in this chapterand the importance of instrument sterilisation has alreadybeen discussed in Chapter 7.

Good lighting is essential to oral surgery and multi-focal surgical lamps reduce dark spots and minimise thehead or shoulder shadow of the operator or assistant. Darkprotective spectacles reduce the patient's discomfort fromthe glare of a good light, in addition to protecting theireyes from any possible debris or instruments.

Suction

Suction should be low volume and aspirator heads or tipsshould be narrow bore. This combination allows maxi-mum efficiency without undue soft tissue obstruction ofthe system.

Radiographic viewing screens

Most oral surgical operations require good radiographsand adequate viewing facilities within the operatingroom.

Assistance

Competent assistance is extremely valuable in oralsurgery. Good assistants realise that they can materiallyaid the operator's access and vision of the operative siteand are aware of the importance of their role in reducingtissue damage by careful retraction. They should be fullyaware of the objectives of the surgery being undertakenand operative problems that might be encountered.

Operative techniquesIncision

For most minor oral surgery, a Swann-Morton number 15blade is the most common choice for incision of themucoperiosteum (Fig. 23.2). The operator should have aclear picture preoperatively of the access that will beattained, and the incisions will be made appropriate tothis need. Scalpel blades should be new for each patient

190 Fig. 23.1 Typical oral surgery kit.

Fig. 23.2 Swann-Morton scalpel blades number 11 (left)and number 15 (right).

and, given that the cutting edge can be rapidly blunted bypressure onto a bony surface, they can and should berenewed as necessary intraoperatively. The cut should bemade at right angles to the underlying bone surface suchthat the epithelium on each side of the incision is notchamfered but each edge should lie as close as possibleto 90° to the basement membrane. This will maximisethe chance of good healing when the tissues arereapposed. Any laxity in the soft tissue that is a feature ofthe free rather than the attached gingiva can be tensedand hence be more stable by a finger stretching the sulcusand holding it firmly against the underlying bone. Thescalpel should move at uniform speed and with sufficientfirmness to cut through not only the mucosal surface butalso the periosteum overlying the bone. It should bemade, ideally, with one movement, avoiding redefiningor chopping actions, which produce ragged margins.

Raising a flap

This is undertaken with periosteal elevators such as theAsh pattern or Howarth elevators. Other instruments thatcan be used are the small blade end of a Mitchell'sosteotrimmer where the tissues are particularly adherentto the bone beneath, or the reverse side of the right or leftWarwick James' elevators for careful raising of inter-dental papillae. The term 'raising a flap' is probably notwell chosen, for it implies that the tissues are lifted upactively from the bone surface. In fact. the periostealelevator should be firmly pushed at approximately30-45° to the surface of the bone such that theperiosteum is stripped from it. It is important to try toraise both mucosa and periosteum in one layer and thisdoes require a considerable force to be applied. Eachpush of the periosteal elevator should only be designedto achieve a movement of about 5–10 mm, with theemphasis on the sharp edge of the instrument being kepton the actual surface of the bone. Occasionally, a dry,sterile swab can be interposed between the periostealelevator and the bone, particularly where muscle fibreattachments are very adherent to the periosteum. Thismeasure can more effectively clean the bone surfacetotally of overlying soft tissue.

Most mucoperiosteal flaps are buccally situated andare designed to have one horizontal and one verticallyarranged limb. The vertical cut is often known as therelieving incision. For this reason many refer to thisconfiguration as 'L'-shaped. For virtually all flaps the

horizontal arm should extend from the distal forward tothe operative site, with the vertical limb anteriorlyplaced. This ensures that when the flap is taken back andretracted, it is being held away from the operator's line ofvision, thus increasing access and visibility. From time totime there may be a need for a distal (posteriorly) placedvertical limb in addition to the anterior one, and this canbe an advantage where there is a more marked convexityto the curvature of the arch such as in the lower anteriorsegment. In general, however, the second vertical cut isavoided because the flap is never as stable when replacedin such circumstances. Palatal flaps do not require anyvertical relief whatsoever, as the concave configurationputs no requirement for it whether in the dentate oredentulous mouth.

In the edentulous patient, horizontal incisions aremade along the crest of the ridge or where there is anyinstability due to resorption of the underlying bonyalveolus, slightly to the buccal aspect of the crest.Incisions around standing teeth require care to avoidundue damage to the gingival cuff both for buccal orpalatal flaps. The vertical incision needs to be carriedfrom the attached into the free gingiva to a varyinglength, depending on the access needed. It should beangled forwards such that the base of the flap mustalways be longer than its free margin, thus ensuringadequacy of the blood supply to it. Only the mental nerveis at risk from a vertical cut in the oral cavity. Careshould always be taken to avoid the mental foramen witha vertical incision and even the horizontal incision mayneed to be swung to the lingual side around this areawhere, in the edentulous patient, there has been grossalveolar bone atrophy and the foramen is lying forpractical purposes on the crest of the ridge.

Finally, in the edentulous ridge, it may be possibleto increase the length of the horizontal (crestal) limb ofthe incision such that the need for a vertical relieving cutis obviated. This is sometimes known as an 'envelope'flap and it certainly reduces postoperative discomfortas movement of the lips and cheeks tends not to pulldirectly on it, and also where a denture is being insertedthis can be worn more comfortably. This principle (i.e.increasing the length of the horizontal incision to allowaccess without any vertical relief) can also be used indentate patients as, for example, in the removal of wisdomteeth (see Ch. 27).

Buccal retraction can be effected with a variety ofdesigned retractors. Some of these contain a rake edge,containing multiple teeth, which should be held against

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the bone but which can cause considerable damage to theundersurface of the flap if its teeth are allowed to rotateand tear into the flap. This might happen if the assistanttires later on in the procedure. Many prefer, therefore,to use periosteal elevators, one held by the operator andthe other by the assistant. The main objective of goodretraction is to protect the soft tissues from damageduring the procedure and this includes not only themucoperiosteal flap but also the lips and cheeks, whichare particularly liable to frictional burning from burshanks if the operator and/or the assistant is not dulyvigilant.

Bone removal

Many dentoalveolar procedures require bone to beremoved to allow access to a buried root, unerupted tooth,cyst, or whatever pathological condition is being treated.This can be done by a variety of methods.

Thin or weakened bone can often be removed withhand instruments such as osteotrimmers, curettes or evenelevators. Under local anaesthesia this may be a lessalarming method for the more nervous patients and canin some cases eliminate the use of drills. Bone rongeurs(bone nibblers) can also be used to enlarge existing bonedefects, as for example round cysts, in addition to theiruse for trimming sharp edges on completion of theoperation.

A hand-piece and drill is the most frequently usedmethod for bone removal. For most dentoalveolarsurgical purposes an engine with a capability of 40 000revs per minute and with good torque is needed, either airor electrically driven. As oral surgery techniques utilisedirect visualisation, a straight hand-piece is inevitablythe instrument of choice. High-speed air rotors do notgive the same desirable sense of feel to cutting bone andrun the risk of air escape into the wound causing airemphysema. Air introduced at pressure can be a mostalarming occurrence to both patient and operator as itcauses immediate swelling. Palpation of the resultantswelling will elicit characteristic crepitus, a creakingsensation that tends to 'move about', not always beingfelt at the same point of the swelling.

A variety of different burs are available but round bursand fissure burs are most commonly employed. For mostprocedures where bone alone is being cut, steel is a goodmaterial but where tooth sectioning is likely, tungstencarbide burs have faster cutting potential and can reducethe time spent cutting through enamel, as, for example,

when dividing a tooth. Removal of bone and how muchto remove is a skill learned by experience but, in generalterms, sufficient bone should be removed to allowadequate further instrumentation to achieve the desiredresult. Ideally, bone removal is kept to the minimumconsistent with the provision of satisfactory access.During the cutting, sterile water or saline should act as acoolant and aid the successful aspiration of any loosebony fragments, thus maintaining maximum visibility.

Chisels can be used as hand instruments or with ahammer. When the latter is employed, the patient wouldnormally be under a general anaesthetic as the procedurewould be unduly alarming to the conscious patient. Themost common use of the hammer and chisel is in theremoval of lower third molars where the lingual plate issplit (split bone technique) allowing the tooth to berotated lingually to effect its removal (see Ch. 27). Thebone must not be unduly brittle as this will increase thechance of uncontrolled splitting of the bone and jawfracture. It is therefore confined to young patients and,although the split of the bone may be less controlled thanusing a drill and hand-piece, it can be a very quick andremarkably atraumatic technique in skilled hands.

Tooth division

Division of an impacted tooth is usually carried out toreduce the amount of bone removal that would otherwisebe required to effect its elevation and delivery. Divisionof a tooth is normally carried out with a hand-piece andbur, the latter often being a fissure bur. Teeth may bedivided in any way appropriate to their position, but mostoften this involves sectioning of the crown from the rootcomplex. There are instances where, for example, in amesioangular impacted lower third molar there are twoclearly separate roots on radiograph, the tooth may moreeasily be divided longitudinally to separate the mesialroot and its adjacent crown from the distal root andcrown. The additional benefit of division of a tooth is theresultant reduction in its resistance to elevation.

Separation of the roots of a multirooted tooth willalso reduce the mechanical advantage of its resistance toremoval and some teeth do require sectioning of crownfrom roots, followed by root from root separation.Although this clearly requires more use of the drill, theforces that have to be applied with elevators are con-sequently reduced and this more than compensates forthe alarm that patients might experience as a result ofexcessive forces being used during elevation.

Elevators

A variety of elevators are available for removing teeth orroots from their sockets: Coupland's chisels (originallydesigned as hand-held bone chisels), Warwick James'elevators, Cryer's elevators and dental luxators (Fig. 23.3).Dental elevators work either on the principle of 'blockand wedge' or 'wheel and axle', and should never be usedas crow-bars (Fig. 23.4). Hence, a dental luxator with itssharp edge is pushed between the root of a tooth and itsalveolar bone via the periodontal space. This wedgingeffect should cause the root to be moved from its socket

Fig. 23.3 Elevators left to right Coupland's chisel,Warwick James' left, straight and right, Cryer's left andright.

Fig. 23.4 The correct application of an elevator betweenthe bone and the tooth.

as the elevator is advanced. Coupland's chisels can beused in a similar fashion and are more effective in thisway if their edge is well maintained and sharp.

The other method is accomplished by rotating theelevator along its long axis such that its edge exerts adisplacing force on the tooth or root. The straightWarwick James', Coupland's chisels, and, with theirpointed blades, Cryer's elevators are used in this way.Great care should be exercised to avoid using an adjacenttooth as a fulcrum for elevators except where severalteeth are to be extracted, when movement of the adjacenttooth will not be a problem and may indeed be desirable.

Elevators should be applied to teeth with an aware-ness of the most advantageous point of application so thatthe tooth will move along the line of its least resistance.Hence, as most roots in the lower molar region curvedistally, elevation from the mesial aspect is more likely tobe successful. Similarly, elevation from buccal ratherthan lingual is technically more practicable when usingthe rotation principle.

Debridement

Following the completion of any surgical procedure it isimportant to ensure that there are no impediments to goodhealing. These can take the form of loose bone spiculesor fragments insufficiently attached to periosteum tomaintain an adequate blood supply, dental fragmentslying loose or hidden under the flap, or infected softtissues such as infected follicular tissue around theremoved crown of an impacted tooth. Bony or dentalfragments should be carefully aspirated with thoroughirrigation paying particular attention to spicules hiddenunder the retracted flap. Soft tissues should be curettedor removed with tissue forceps such as 'mosquito' orFickling's forceps. Any sharp bony edges can be nibbledwith rongeurs or smoothed with a larger 'acrylic' bur.

Suturing

Inserting sutures into a mucoperiosteal flap allowsaccurate repositioning of the soft tissues to their pre-operational site. In many cases, this will re-establish theanatomical position of the flap but in certain circum-stances the flap may be moved for good reason. Such asituation arises where a buccal flap is pulled across anoroantral fistula to be attached to the palatal aspect of thesocket. This is known as a buccal advancement flap and,as will be discussed later in Chapter 26, it does require

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periosteal release by incising the periosteal layer at thebase of the flap to allow sufficient elasticity to move thetissues across the defect. In the majority of cases, how-ever, sutures hold the soft tissues in the desired healingposition and prevent the wound opening, with theconsequent exposure of bone beneath and encouragehaemostasis.

Materials required

A suturing kit is shown in Figure 23.5 and involves thefollowing:

Needle holder

These instruments come in a variety of sizes and designand operators tend to choose one that suits them, havingtried various forms. In general, they will be either ratchetor non-ratchet designed, the former allowing the needleto be locked into the beaks of the instrument whereas thelatter requires the operator to actively hold the needlewithin the beaks.

Tissue forceps

Sometimes known as dissecting forceps, the importantrequirement is that they hold the soft tissues atraumati-cally so avoiding crushing and with little chance ofslippage. This is achieved by a rat-toothed design, which,although possibly causing tiny puncture points, is idealfor the purposes of suturing and holding soft tissuesgenerally (Fig. 23.6). The use of non-toothed forceps will

result in crushing of the tissues as, to prevent tissueslippage from grasp, the instrument must be held tootightly.

Soft tissue retractor

The relevance of this instrument is obvious but it doesindicate that an assistant is necessary during suturing tohold the soft tissues aside to allow access and to use theaspirator.

Needles

These are made of stainless steel and, for oral surgicalpurposes, are usually a curved shape from three-eighthsto one-half the circumference of a circle; on cross-sectionthey are triangular. A full description of suture needlesand sutures appears in Chapter 3. The length of theneedle varies but between 18 and 26 mm is a reasonablerange for intraoral work. The triangular cross-sectionalview of the needle either has the apex of the trianglefacing inwards (i.e. on the concave side) or outwards.The former (i.e. inward pointing) is known as the cuttingneedle and the latter as a reverse cutting needle. Thesedesigns allow minimal soft tissue trauma during needleinsertion as they cut a path through the soft tissues and donot therefore require excessive force on the part of theoperator.

194 Fig. 23.5 Suturing kit containing a Kilner's needle holder,Gillies toothed tissue forceps, suture scissors and suture.

Fig. 23.6 The head of Gillies toothed tissue forcepsshowing the interdigitating nature of the points.

Suture material

There is a wealth of choice of material for suturingpurposes (see Ch. 3) but most commonly in oral surgerymaterials such as silk, catgut (now in its softgut format)vicryl and nylon are used. Sutures are available either asnon-resorbable (e.g. silk and nylon) or resorbable (e.g.catgut or vicryl). The gauge or thickness of the chosenmaterial must be determined and this is denoted by Ogradings. As the thickness of the material decreases, theO grading rises. Hence 2/0 is thicker than 3/0, which isthicker than 4/0 and so on. Most intraoral suturing iscarried out with 3/0 or 4/0 gauge material but onextraoral skin surfaces, finer gauge is preferred such as6/0 or even finer. This helps reduce scar visibility.

Types of suture

Different designs of suture usage can be chosenaccording to the particular needs of the clinical situation(Fig. 23.7). These vary from the simplest, such as theinterrupted suture, to more complex mattress designs tocontinuous sutures placed either over the wound or,particularly with skin surfaces, beneath it. These lattercontinuous sutures are sometimes known as subcuticularsutures. The vast majority of intraoral sutures will besimple interrupted sutures.

Mattress sutures have particular advantages in certainclinical situations. The horizontal mattress is oftenhelpful in reducing the surface area of a bleeding lowermolar socket and exerting pressure on the overlying

mucoperostium. It can also be a useful suture in closingan oroantral fistula where it encourages eversion of themargins of the wound, thus ensuring better connectivetissue contact and discouraging epithelial contact whichwould prevent healing by primary intention.

The vertical mattress suture also helps the appositionof connective tissue surfaces and hence trouble freehealing. One example of its application is the interdentalpapilla particularly of an anterior tooth where accurategingival repositioning of the flap is desired (see Ch. 29).

Suture technique

Flaps are normally 'L'- or inverted 'L'-shaped. Mostoperators prefer to suture the angle of the 'L' first as thiswill correctly align the vertical and horizontal limits ofthe flap. The tissue of the flap should be held firmly bythe tissue forceps and the needle passed through themucoperiosteum about 3 mm from the margin, more ifthe flap is friable because of chronic infection. Theneedle is then pushed through the corresponding tissueon the other side of the incision, again about 3 mm fromthe margin. The suture is pulled through such that thereare only a few centimetres from its entry point to the endof the suture. The knot should be tied as in Fig. 23.8 andthe ends cut. Where possible, the knots should be drawnto lie to one or other side of the line of incision and thetissue should not be drawn too tightly together (which isusually seen by blanching) as it causes the thread to'cheese cut' through the flap and produce a painful ulcer.

Fig. 23.7 Diagram showing types of suture: (a) interrupted; (b) mattress; (c) continuous; (d) subcutaneous continuous.195

Fig. 23.8 Suture tying: the suture is wound round the needle holder clockwise (a) before pulling the free end through (b) tocreate the first tie (c); the suture is then wound counter clockwise to complete the knot (d).

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Sutures placed intraorally are normally removed 5-7days postoperatively. Surface anaesthetic can be veryhelpful if the stitch has become embedded. In theremoval of sutures, normal dental tweezers such ascollege tweezers should grasp the free ends of the threadand the suture should be cut by sharp scissors or a sutureblade close to the knot. The suture should then be pulledthough in its entirety.

Postoperative careThe responsibility of the surgeon to a patient under treat-ment does not stop as the last suture is placed. Successfulhealing can be enhanced by regimes designed tominimise pain, prevent infection and reduce the chanceof bleeding. This involves not only necessary prescriptionof drugs to patients but also appropriate instruction asto the measures patients can follow to encourage fewerpostoperative problems.

Postoperative instructions

These can be given orally or by printed instruction sheets;both compliment each other because oral instructionsgiven immediately on completion of treatment areseldom retained fully by patients who have just comethrough what to most of them has been an ordeal. Figure23.9 outlines the information that should be given topatients. The list of instructions should not be over-detailed and their design should bear in mind the abilityof the patient to understand them. A contact telephonenumber is useful and instructions on where to get helpduring 'non-office' hours is reassuring even if notneeded.

Analgesia

As far as most patients are concerned, control of post-operative pain is the most important factor during theearly phase of healing.

Fig. 23.9 Postoperative instructions leaflet.

Local anaesthesiagiven penoperatively, normally at the start or the

Many operators now administer local anaesthetics to procedure, and many now prefer to use longer-actingcontrol immediate postsurgical pain. Under local agents such as bupivacaine. It is obviously important toanaesthesia with or without sedation, the necessary inform patients that the area in question will be numbinjections are given and tested presurgically as a matter when they first recover consciousness, and this isof course. Under general anaesthesia local anaesthetic is particularly important when they have been warned

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preoperatively of the possibility of nerve damage as aconsequence of the procedure. Even if longer-actinglocal anaesthetics are not used, some operators reinforceanaesthesia with the usual agent on completion of thesurgery, whether under local or general anaesthesia. Itdoes appear that immediate control of pain for the firstfew hours postoperatively seems not only to have anearly benefit but may also reduce the discomfortthroughout the several days following surgery.

Systemic analgesia

The normal agents employed following minor oralsurgery are non-steroidal anti-inflammatory drugs orparacetamol. Recourse to narcotics is seldom needed,other than codeine-containing preparations. Opiates maybe needed after more extensive surgery but these patientswill generally be inpatients under the supervision ofskilled nursing personnel. There may be an advantage inprescribing drugs with an anti-inflammatory action aswell as an analgesic effect. However, certain groups ofpatients, such as asthmatics or those with a history ofpeptic ulceration, are at risk from these drugs and the useof paracetamol with or without codeine is more prudent.

All patients should be prescribed adequate analgesics,and given instructions on their correct usage. Thereseems little doubt that, whatever drug is prescribed,patients should be instructed to take the analgesic beforethe local anaesthetic effect has worn off. Some suggestthat analgesics are best started preoperatively, to ensurethat there is an adequate plasma level of the drug whenthe local anaesthetic begins to wear off. Many patientshave their 'favourite' preparation and in these circum-stances should be encouraged to use a drug that has aproven success for them.

Prevention of infection

Antibiotics

Prescription of antibiotics as a prophylactic measure inthis context remains a contentious issue. The evidencefor their use is far from convincing and it is true to saythat most surgeons rely on their clinical experience whenmaking the decision of whether or not to use them. Manyoperators justify their use based on the presence ofinfection in the surgical field (see Ch. 8) or the removalof substantial amounts of bone during the procedure. Theblood supply in the maxilla is more profuse than in the

mandible and infection is consequently a more uncommoncomplication and most antibiotics are therefore prescribedfor procedures carried out on the mandible.

Arguments against antibiotic use are based on theiroverprescription resulting in increasing numbers ofbacteria that have developed resistance to these drugs,and in some cases multiresistant organisms such as themethicillin-resistant Staphylococcus aureus (MRSA)that now poses such serious problems. The possibility ofmore and more organisms having multiresistance is with-out question a serious and potentially disastrous scenarioof which both the medical and veterinary professions arebecoming increasingly aware. There is good cause, there-fore, for all clinicians to consider carefully the perceivedadvantages and disadvantages of antibiotic prescription,particularly where they are being used for prevention ofpossible infection rather than the actual treatment ofexisting infection. Many clinicians now reduce the lengthof time for which antibiotics are prescribed because thismeasure in itself will reduce the chance of the emergenceof resistance in bacterial colonies. Amoxicillin or metroni-dazole are probably the most commonly prescribedantibiotics when the postoperative risk of infection isconsidered significant. Their use for patients with areduced capability of coping with infection, such as thosewith a reduced immune response (for example, poorlycontrolled diabetics, HIV-positive patients or those onimmunosuppressive drugs) in whom the results ofinfection can be correspondingly serious, is thereforeuncontroversial. A further discussion of the use of anti-biotics in surgery is given in Chapter 8.

Mouthwashes

Patients are universally advised on the use of mouth-washes and they undoubtedly play an important role inmaintaining wound cleanliness if used frequently.

Chlorhexidine

This is an antiseptic mouthwash which is effective incontrolling plaque but may also have positive benefits forwounds. With inability to use toothbrushes in the areas ofthe surgery, both plaque control and local antiseptic actionare needed and this mouthwash is commonly prescribedas a routine post-operatively. Use of chlorhexidine isprobably best restricted to 2 or 3 times per day with theintervening periods covered with simple saline rinses.Pre- or perioperative use of a chlorhexidine mouthwash

has been shown to reduce the risk of post-operativeinfection and reduce the incidence of 'dry sockets'.

Saline mouthwashes

These should be made up with approximately oneteaspoonful of salt to one tumbler of warm to hot water.They are the mainstay of wound cleanliness and shouldbe encouraged. Their use should initially be gentle ratherthan vigorous but, as the days progress, a more vigoroususe should be encouraged. In addition to increasing theuse of mouthwashes after the first 24 h, patients shouldalso be encouraged to keep their mouths moving so thatstagnation of saliva does not result, as this can encourageinfection. Mouthwashes upwards of six times per dayshould be discontinued only if bleeding from the wound

Postoperative bleeding

Bleeding from intraoral wounds is seldom due to a defectin the haemostatic mechanism or in the clotting process(see Ch. 6) but is more commonly due to leakage fromsmall vessels in bone or periosteum. It is more frequentlyseen within a few hours of surgery and may in somecases be reactive bleeding resultant upon the dilatationof vessels previously constricted by local anaestheticcontaining adrenaline (epinephrine). Another contributoryfactor may be inappropriate exploration of the wound byfingers or tongue and by mouth rinsing too soon after thesurgery.

Control of such bleeding is usually affected by useof local haemostatic agents such as regenerated oxidisedcellulose, further suturing of the wound and direct masti-catory pressure via a suitably placed swab.

Secondary haemorrhage caused by wound infection ischaracteristically seen around 10 days postoperativelybut is very uncommon in dentoalveolar wounds.

Follow-upFollowing surgery, most patients will be seen between5 and 7 days later to ensure that healing is progressingsatisfactorily. Sutures are removed when necessary anddebris may need to be irrigated from the wound area if thepatient's oral hygiene measures have been inadequate.For some patients, results of histological examination oftissue can be explained and, if necessary, further appoint-ments arranged. For many patients, however, there is nofurther need for follow-up and they can be discharged.For routine removal of wisdom teeth or retained roots,for example, and where resorbable sutures have been usedin the surgery, some operators see only those patientswho have continuing problems. Where this format ofmanagement is used, a full postoperative leaflet is issued,which indicates the particular problems that could occurand might need further consultation. The requiredcontact telephone numbers are a necessary inclusion insuch a leaflet.

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Local anaesthesia

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IntroductionAchieving good local anaesthesia is a prerequisite forvirtually all dental surgery, and in oral surgery theconfidence this gives is mandatory from both thepatient's and the operator's point of view. The ability toadminister a comfortable local anaesthetic to any patientis a fundamental skill that dental surgeons should striveto achieve. This will allow stress levels in both giver andreceiver to be greatly reduced, and technique must beconstantly reviewed and revised to this end.

Not only is the actual injection of local anaestheticimportant, the operator must give the drug adequate timeto block nerve transmission and must have confidencein his or her ability to recognise the subjective changesit will bring about before testing its adequacy. One ofthe most common faults is testing the effect of localanaesthetic before reasonable time has elapsed, whenlack of necessary depth of anaesthesia causes discomfort.This immediately results in loss of confidence by thepatient, who becomes more apprehensive and may there-fore be far more difficult to convince that adequateanaesthesia, even after further administration, is finallyattained.

Patients must be told before the testing of ananaesthetic that all sensation is not, and will not, be lost,and that it is specifically pain that will be abolished. Thisis particularly true in oral surgery practice, where theprocedure may often involve causing a very real feelingof pressure that can be alarming to patients who have notbeen fully briefed on what the local anaesthetic can andcannot do. If patients are asked to report 'feeling any-thing' during the testing procedure they might truthfullysay that they feel something, and this could lead tofurther, and possibly unnecessary, administration of localanaesthetic. Finally, awareness that good local anaesthesiais one of the most important criteria by which patients

judge their operator makes this subject worth studyingand knowing well.

Uses of local anaesthesiaThe uses of local anaesthesia are listed in Table 24.1 andthese are discussed in turn.

Diagnostic use

Administration of local anaesthetic can be a useful wayof finding the source of a patient's pain. An example ofthis is the pain of a pulpitis, which can be very difficultfor both the patient and the dentist to isolate because ofits tendency to be referred to other parts of the mouth orface. Particularly useful is the infiltration technique,which achieves a localised action and can discriminatebetween maxillary and mandibular sources, and evenbetween individual upper teeth provided they are notimmediately adjacent. Another example is the patientwith myofascial pain who is convinced that an uppertooth is causing the problem. Local anaesthesia may helpthis patient and the surgeon in this situation to eliminatethe tooth as the cause of pain and may thus avoid itsunnecessary treatment.

Table 24.1 Uses of local anaesthesia

Diagnostic: to isolate a source of painTherapeutic: to reduce or abolish the pain of a

pathological conditionPerioperative: to achieve comfort during operative

proceduresPostoperative: to reduce postoperative pain

24

Therapeutic use

Local anaesthetics can, in themselves, constitute part of atreatment regimen for painful surgical conditions. Theability of the dentist to abolish pain for a patient, albeittemporarily, is a therapeutic measure in its own right.The use of a block technique to eliminate the pain of drysocket (localised osteitis) (see Ch. 26) can be immenselyhelpful to the management of this very painful condition,particularly in the first few days. Inferior dental blocks oflong-acting local anaesthetics such as bupivacaine cangive total comfort for several hours, allowing patients tocatch up on lost sleep and perhaps reduce the use ofsystemic analgesics to avoid overuse. Moreover, thepatient can return for further local anaesthesia if the painonce more becomes too demanding. Although it wouldbe impossible to keep administering local anaestheticblocks, there is enough, albeit anecdotal, evidence tosuggest that when the pain returns after the block wearsoff, it is not at the same level of intensity.

Blocks of the inferior dental, mental or infraorbitalnerves can also be used for the treatment of trigeminalneuralgia when pain breakthrough, despite medicationsuch as carbamazepine, has become unacceptable. Long-acting local anaesthetic in this context seems, in somepatients, not only to give comfort during the duration ofthe anaesthetic but also to break the pattern of break-through in the longer term.

Perioperative use

The provision of pain-free operative surgery is by farthe most common use of local anaesthetics, and providesan effective and safe method for almost all outpatientdentoalveolar oral surgical procedures. It can, in con-junction with sedation techniques, allow more difficultor protracted procedures to be carried out without theadditional risks of general anaesthesia, and this may beparticularly of value in patients with significant cardio-vascular or airway disease (see Ch. 11).

Additionally, however, local anaesthetics are oftengiven to patients undergoing oral or maxillofacial surgeryunder general anaesthesia. This serves several purposes:

• It reduces the depth of general anaesthesia needed.• It reduces the arrhythmias, which are noted on

electrocardiogram (ECG) during the surgery whensignificant afferent stimulation is taking place. Thiscan be seen, for example, when a tooth is beingelevated.

• It also provides local haemostasis to the operative siteand provides immediate postoperative analgesia.

Postoperative use

After surgery with either local or general anaesthesia, thecontinuing effect of the anaesthetic is a most beneficialway of reducing patient discomfort. It helps to reduceor even eliminate the need for stronger (often narcotic)systemic analgesics, which have their own drawbacks.Many operators now use longer-acting agents, such asbupivacaine, to prolong the immediate postoperativeanalgesia. There is some evidence to suggest that thismeasure, allied to early prescription of systemicanalgesics, can more effectively control pain and that thisearly benefit may well be sustained throughout the daysfollowing surgery.

Local anaesthetic agentsTable 24.2 shows the commonly used local anaestheticagents. In oral surgery there is a distinct advantage inusing a local anaesthetic with adrenaline (epinephrine),which, by its vasoconstrictive action, improves thevisibility of the surgical site by reducing small-vesselbleeding.

Action

Both lidocaine (lignocaine) and prilocaine hydrochlorideare good local anaesthetic agents and account for the vast

Table 24.2 Commonly used local anaesthetic agents

Anaesthetic drug

Lidocaine (lignocaine) hydrochloride 2%Prilocaine hydrochloride 3%Bupivacaine hydrochloride 0.5%

Vasoconstrictor

Adrenaline (epinephrine) 1 :80 000Felypressin 0.03 international unitsAdrenaline (epinephrine) 1 :200 000

Duration (ID block)

2.5-3 h2.5–3 h6–8 h

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majority of local anaesthetic administrations in oralsurgery. They are both tertiary amines that form hydro-chloride salts for use in solution. When injected into thetissues, these agents dissociate into cationic quaternaryamides with a positive chemical charge, although someremains in the uncharged base form. It is this unchargedlidocaine (lignocaine) or prilocaine that passes throughthe nerve membrane to once again dissociate into thecationic form. These intracellular cations of the anaes-thetic agents are believed to be primarily responsible forblocking the sodium channels in the membrane, which inturn blocks the rapid sodium inrush to the cell duringnerve impulse propagation. Distortion of the axonmembrane by uncharged local anaesthetic also appears tohave a role in blocking this transmission.

pain breakthrough, and that for oral surgical purposes therelatively bloodless field they produce is a significantadvantage.

In general terms, the maximum safe dose can beexpressed as 4.5-5.0 mg per kg body weight of lidocaine(lignocaine) with 1:80000 adrenaline (epinephrine) and3 mg per kg body weight of prilocaine. When translatedinto millilitres of 2% lidocaine (lignocaine) with adrena-line (epinephrine) or 3% prilocaine with felypressin in afit 70-kg adult patient this means that a maximum of sixcartridges of lidocaine (lignocaine) (or four of prilocaine),each of 2.2 mL, is well within the safe limit. The pre-occupation with volume is misleading as it tends to causeunthinking administration, and not consideration of eachpatient's individual situation allied to safe technique.

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Maximum safe dose

Local anaesthetics such as lidocaine (lignocaine) andprilocaine are extremely safe given their extensive use inboth medicine and dentistry. The addition of adrenaline(epinephrine) to lidocaine (lignocaine)and of felypressinto prilocaine reduces the rate of uptake from the site ofinjection, thus reducing the possible toxic effects ofthe local anaesthetic agent and increasing, in theory, thevolume that can therefore be used. Apart from the actualamounts used, three other considerations should be takeninto account: (1) the avoidance of intravascular injectionby use of an aspirating syringe; (2) the rate of adminis-tration of the local anaesthetic - a slow rate reduces thechance of overload and hence possible toxic effects; and(3) the status of the patient. Extremes of age, physicalsize and medical background should be determined foreach individual patient, all of which may modify whatcould be considered a safe quantity.

Most authorities do now acknowledge that the toxiceffects of the local anaesthetic agents - which mainly arisefrom central nervous system depression, and in particularrespiratory depression - must be balanced against thepossible undesirable effects of adrenaline (epinephrine)where that is included in the solution. The action ofadrenaline (epinephrine) on the heart (causing increase inmyocardial excitability, rate, force of contraction, andstroke volume) is potentially undesirable, particularly inpatients with known heart disease. It is in this group ofpatients that many operators prefer to use adrenaline(epinephrine)-free local anaesthetics. Others argue thatlidocaine (lignocaine) and adrenaline (epinephrine)provide a more profound anaesthesia with less chance of

Local anaesthetictechniqueThere are a variety of techniques used in localanaesthetic administration and these will be discussed inturn (Table 24.3).

Infiltration

This can be used to achieve anaesthesia of upper teethand lower anteriors. It is achieved by depositing thesolution around the apex of a tooth on its buccal aspect inthe sulcus. The porosity of the bone allows it to diffusethrough the outer plate of bone to affect the apical nerveor nerves. It normally achieves anaesthesia within 1-2 minand has the added surgical advantage (where adrenaline(epinephrine) is in the solution) of small-vessel vaso-constriction, which provides reduction in bleeding and

Table 24.3 Local anaesthetic techniques

InfiltrationBlock anaesthesia

inferior dental blockmental nerve blockposterior superior alveolar blockinfraorbital blockgreater palatine blocknasopalatine block

Other injection techniquesperiodontal ligament blockintraosseous injectionintrapulpal injection

increased visibility as a consequence. Administrationshould be considered as a two-part technique:

1. needle insertion2. deposition of local anaesthetic.

Needle insertion

To achieve minimal discomfort, topical local anaestheticshould be applied 2-3 min before the injection. Theindex finger or thumb of the 'free' hand should pull thelip or cheek such that the sulcus tissues are taut, as thiswill minimise discomfort on introduction of the needle.The tip of the needle needs to be advanced only 3-4 mminto the tissue adjacent to the tooth to be anaesthetised(Fig. 24.1).

Deposition of local anaesthetic solution

The solution should be deposited slowly because thelumen of a dental needle is very fine and undue force ofthe solution being injected can lead to unwanted pain andtissue damage. This therefore takes time and patience butis essential in reducing discomfort.

For palatal anaesthesia, the greater palatine (or naso-palatine) nerve anteriorly supplies the mucoperiosteum.

Fig. 24.1 Position of the needle for the infiltration of localanaesthetic to achieve anaesthesia of an upper lateralincisor.

Only a small quantity of local solution should beintroduced and use of topical anaesthesia and strongfinger-pressure adjacent to the point of entry of theneedle can help to reduce this notoriously unpleasantinjection. The injection is normally given adjacent to thesurgical site but many consider that the area midwaybetween the midline of the palate and the gingival marginof the tooth is less tightly bound down to the underlyingbone, and is therefore less uncomfortable.

Another technique is to achieve buccal anaesthesia inthe usual way, then pass the needle from buccal to palatalthrough both the interdental papillae (anterior andposterior) of the tooth under treatment. This does appearto reduce discomfort even if an additional palatal injectionis necessary to be quite sure of adequate anaesthesia.

Block anaesthesia

Several block injections of nerve trunks can be used fororal surgical purposes. By far the most common is theinferior dental block, but others include the mental block,the posterior superior dental block and the infraorbitalblock. The hard palate can be anaesthetised by greaterpalatine and nasopalatine blocks if more extensive areasof palate require to be anaesthetised.

Inferior dental block

Several techniques have been suggested but only two willbe described here, the first being a standard block and thesecond a closed-mouth technique that can be very usefulif restricted opening is a problem.

The nerves affected are: (1) the inferior dental nerve,which provides sensation to the pulps and periodontalmembranes of first incisor to third molar, the boneinvesting the teeth, the buccal gingivae and the sulcusfrom premolars to incisors, lower lip and chin; and (2)the lingual nerve, which supplies the anterior two-thirdsof the tongue, the floor of mouth and the lingual gingiva.

Technique

The precise technique will vary but the following willserve as a guideline for administering an inferior dentalblock injection.

The patient should be seated with good head and necksupport and with the neck slightly extended such that thelower occlusal plane will be approximately horizontal onfully opening the mouth. With the mouth widely opened,

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the finger or thumb of the 'free' hand should pass alongthe lower buccal sulcus until it rests posteriorly in theretromolar triangle, which lies between the (external)oblique line of the mandible and the continuation of themylohyoid ridge or internal oblique line.

The pterygomandibular raphe should then be identifiedas an almost vertically running soft tissue line. This takesits origin from the pterygoid hamulus and runs down-wards to its insertion on the lingual aspect of the mandiblein the third molar region. The raphe gives rise to muscleattachments running laterally (buccinator) and medially(superior constrictor).

The syringe should be introduced from the lowerpremolar teeth of the other side parallel to the lowerocclusal plane such that the needle penetrates the tissueslateral to the pterygomandibular raphe and at a levelhalfway up the finger or thumb lying in the retromolartriangle (Fig. 24.2).

The 'long' dental needle (3.4 cm) should be advancedabout 2.5 cm until bone is touched lightly. The needleshould then be withdrawn a millimetre or two andaspiration performed. If blood in the form of a smoky redtrail is noted in the cartridge, the needle should bewithdrawn a millimetre or so before reaspirating.

The local anaesthetic should then be deposited slowly,using most of the 2.2 mL cartridge and with the localanaesthetic being deposited on slow withdrawal to

204 Fig. 24.2 Position of the needle for an inferior dentalblock.

'catch' the lingual nerve, which lies anteromedial to theinferior dental nerve.

This technique introduces a local anaesthetic solutionto the inferior dental nerve as it enters the mandibularforamen on the medial aspect of the ramus. In patientswho, for a variety of reasons, have trismus and cannotopen sufficiently to allow this technique, a closedtechnique can sometimes be useful.

The patient should be seated such that the occlusalplane is approximately horizontal. The cheek should beretracted with the index finger or thumb of the 'free' handand the needle advanced horizontally at about the level ofthe gingival margins of the upper molar teeth. The needleshould penetrate to a depth of 1–1.5 cm before aspiration.Slow deposition of most of the 2.2 mL cartridge isnormally required.

This technique leaves the local anaesthetic solution ata level higher than the standard technique, which meansthat it is deposited above the mandibular foramen but stillbelow the level of the mandibular notch.

Determination of adequate anaesthesia

As mentioned in the introductory paragraph, it isimportant not to embark on surgery until full anaesthesiais achieved. This is normally done by asking the patientwhat subjective changes he or she feels in the lower lipand chin of the affected side. A feeling of pins and needlesor a tingling sensation denotes early-stage changes, whichwould normally progress to a numb, swollen, thick orrubbery sensation. At this point the area can be testedobjectively with a sharp probe passed between the toothto be extracted, or operated upon, and the attachedgingiva. Patients must be told that the sensations oftouch, and especially pressure, will not be totallyabolished, although pain should not be felt. Patientsshould always be advised that, once the surgery begins,they must immediately indicate if there is any painbreakthrough because more local anaesthetic can begiven.

Buccal injection

The sulcus region in the lower premolar and molarregions may have innervation from the buccal nerve andthis must be covered by a separate injection.

The buccal injection can be given more comfortablyby waiting for the inferior dental block to becomeeffective. Rather than a single block given in the cheek at

the level of the crown of the third molar at the anteriorborder of the ramus, many operators simply infiltratearound the surgical site, for example, in the sulcus of thethird molar region where an impacted third molar isbeing treated since this will have the added benefit ofhaemostasis of the flap.

Complications of inferior dental block

Systemic complications such as allergy, fainting orinadvertent intravascular injection with cardiac or centralnervous system effects are rare, with the exception offainting, which can usually be averted by placing thepatient in the supine position. Specific to this injection,however, are certain local complications and these arelisted in Table 24.4.

Facial nerve paralysis (palsy) occurs when theinjection is given too far distally and the parotid gland ispenetrated, allowing diffusion of the local anaestheticthrough the loose glandular tissue, which then affects allfive terminal branches of the facial nerve. The effect isseen in the lack of the corrugation of the forehead,inability to close the eye or blink, and inability to raisethe corner of the mouth or puff the cheeks. Patients mayfeel that something is wrong but be unable to identifyexactly what the problem is, and it is usually the operatorwho notices these specific changes. Patients should beinformed, reassured as to the transitory nature of thepalsy, and the eye should be protected with a loose padsuch that the cornea is protected until the protective blinkreflex returns. Recovery often occurs in a relatively shorttime (within an hour), unlike the inferior dental nerveitself, which can take up to 3 h.

Postinjection trismus may also arise. The diagnosis ofthis distressing complication is normally fairly easy inthat the trismus occurs within hours of the injection. It isbelieved to be due to damage to the medial pterygoidmuscle, resulting in its spasm and consequent inability ofthe muscle to relax and allow opening. It is not painfulbut many patients are extremely anxious and do needreassurance. In terms of technique, it may be attributed toan injection at too low a level and perhaps using too

Table 24.4 Complications of inferior dental block

Facial nerve paralysisPostinjection trismusProlonged anaesthesiaVisual impairment

much force to deliver the anaesthetic solution. If undueresistance to any injection is felt (as when in a musclebed) excessive force should be avoided and the needlewithdrawn. The free-running of the cartridge plungershould be checked and the needle reinserted at a higherlevel. Trismus can also occur after the extraction of teeth,unrelated to the anaesthetic technique. This is especiallyso with mandibular third molar teeth (see Ch. 27).

If the problem does occur, some prescribe a benzo-diazepine to try to alleviate muscle spasm. The mainstayof management, however, is reassurance and encourage-ment to the patient to try to gain further opening. Use ofwooden spatulae may be a convenient method for thepatient to measure progress. The trismus may last forweeks and even months, and resolution may occur slowlyor quite dramatically over a day or two after even aprolonged period of limitation.

Prolonged anaesthesia is a rare and poorly documentedcomplication. It can affect the inferior dental nerve orlingual nerve, and very occasionally both. It mayrepresent physical trauma to the nerve by the needle or anidiosyncratic reaction to the local anaesthetic. Prognosisis difficult to judge as there is little evidence of outcomeand resolution appears unpredictable.

Visual impairment is a reported complication but isvery rare. Its cause is unknown although vasospasm hasbeen suggested as a possible factor. Any impairment ofvision warrants immediate referral to an ophthalmicspecialist.

Mental nerve block

This injection will anaesthetise the pulps and periodontalmembranes of the lower incisors, canine, first premolarand variably the second premolar. For surgical procedures,it must be remembered that the lingual mucoperiosteumwill require separate infiltration as the mental blockanaesthetises the teeth through the incisive branch of theinferior dental nerve and the peripheral distribution of themental nerve.

Technique

In dentate patients, the mental foramen lies below andbetween the apices of the lower premolar teeth, approxi-mately half way between the cervical margins of theteeth and the lower border of the mandible. The injectionis similar in all respects to an infiltration injection, andthe objective is to deposit the solution at or near the

205

206

Fig. 24.3 Position of the needle for a mental nerve block.

foramen (Fig. 24.3). No attempt should be made to 'feel'the distally facing foramen because this is totallyunnecessary and often causes haematoma formationthrough damage to the mental blood vessels.

In edentulous patients, the foramen may lie nearer thecrest of the ridge as a result of alveolar resorption anddue allowance for this should therefore be made beforethe injection is given.

Posterior superior alveolar (dental) block

This block is intended to anaesthetise the posteriorsuperior dental nerve as it penetrates the posterolateralaspect of the maxillary tuberosity before it pierces bone.As such, a close relationship exists between the site ofthe injection and pterygoid venous plexus lying laterallyand above and which can easily therefore be entered bythe needle. This can cause an immediate and alarminghaematoma visible both in the sulcus and externally inthe face just below the zygomatic arch.

Technique

The technique, which is in effect high infiltration, isseldom, if ever, really necessary as diffusion ofanaesthetic from the conventional infiltration is almostalways effective. If it is considered necessary, then the

needle should be angled inwards towards the buccal plateas much as possible, given that the opening of the mouthwill restrict this. The other angle to remember is thealignment of the needle at approximately 45° to theocclusal plane after entering the sulcus in the secondmolar region.

Infraorbital block

This injection, although given infrequently, can be a veryvaluable technique for achieving anaesthesia in theanterior part of the maxilla. The local anaesthetic solutionis deposited around the infraorbital foramen, where it candiffuse back along the infraorbital canal to affect theanterior and, where present as a separate nerve, the middlesuperior dental nerve. Ideally, therefore, in addition toanaesthesia of the soft tissues of the upper lip, side ofnose, cheek and lower eyelid, the upper incisors, canineand premolars will be affected together with the adjacentsulcus and gingivae.

For oral surgery purposes this injection can be givento avoid injecting into inflamed tissues in the incisor orcanine region, but can also achieve a more dependableand profound anaesthesia for larger lesions such as cysts.Use of a long-acting agent such as bupivacaine to achievecontrol of trigeminal neuralgic pain breakthrough alsomakes knowledge of this technique valuable.

Technique

Although several techniques can be used, the mostcommonly employed, which uses the upper first andsecond premolar as the key landmark, is described.

The buccal sulcus is tensed with the finger or thumbof the 'free' hand in the premolar region. Some operatorssuggest that a finger be placed over the infraorbitalforamen on the face to 'feel' the local anaesthetic as it isadministered and ensure that it is in the correct location.In practice, however, this is often not a realistic measure.The needle is introduced such that it is parallel to thelong axis of the premolars; it penetrates the lateral aspectof the sulcus about 1–1.5 cm from the buccal bone surfaceand it is advanced upwards approximately 1.5 cm into thetissues (Fig. 24.4). After aspiration, the local anaestheticis slowly introduced to the tissues when 1.5–2.0 mL ofthe preferred solution is normally sufficient.

Alternative techniques include direct injection throughthe skin to the foramen. The lower orbital margin rim

Fig. 24.4 Position of the needle for an infra-orbital block.

should be palpated carefully before injecting about 1 cmbelow this landmark, and at the midpoint of the infra-orbital bony margin. Administration of local anaestheticin this way can be alarming to a patient, and carefulexplanation of what is being done is necessary. The eyeshould be protected by the fingers of the 'free' hand, withone finger carefully palpating the lower orbital bonymargin.

Other injection techniques

Periodontal ligament injection

This technique introduces local anaesthetic directly intothe periodontal space and, as the force required is quitesubstantial, specialised syringes are available to achievethis. In oral surgery, the intraligamentous injection ismost frequently used if pain is being felt despite thenormal techniques of infiltration or block anaesthesia.This can occur when a tooth is 'hot' through acutepulpitis or apical infection. It may also be of value iflimitation of jaw mobility makes block injection difficultor impossible. One of its advantages is the small volumeof local solution needed, but it is often uncomfortable toadminister and will cause a bacteraemia which should be

prophylactically covered with appropriate antibiotic in anendocarditis at-risk patient.

Intraosseous injection

This technique will achieve excellent anaesthesia limited,however, to the immediate locality of the injection. Thelocal is administered through a trephined hole bestprepared with a specially designed bur through the outercortical plate of bone. Initial infiltration anaesthesia ofthe area is hence a prerequisite and, after the entry is cut,a short needle is introduced into the medullary spacebefore injecting a small quantity of solution. The diameterof the trephined hole should ideally be matched to theneedle to prevent leakage. Again, the advantages of thetechnique are the small quantity of local anaesthetic usedand the ability to achieve a good depth of anaesthesiawhere access may be limited through trismus.

Intrapulpal injection

This injection is normally used where, despite apparentlygood anaesthesia by other conventional means, the toothremains painful on manipulation. This again is a featureof some pulpal or apical infections. In oral surgery, thetooth is normally being extracted and either the pulpcanal(s) are already accessible or can be accessed usinga small round bur. The technique is imprecise and escapeof the solution is almost invariable. It can, however, beremarkably successful if sufficient local can be intro-duced. Discomfort during its administration is often areliable indication that it will prove of benefit.

Difficulty in obtaining anaesthesia

The above techniques can all be helpful in achievingsufficient anaesthesia where prior, more conventional,methods have been unsuccessful. One other measure isthe use of a stronger local anaesthetic solution, such as4% prilocaine. The higher concentration appears in somecases to obtain a more profound depth of anaesthesia. Ifan inferior dental block fails to allow surgical comfortdespite all the subjective features of adequacy, it may beuseful to consider giving a second block with thestronger anaesthetic solution rather than simply repeatingthe procedure with the same agent.

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Extraction techniques

IntroductionTeeth are extracted for a number of reasons, includingcaries, trauma, periodontal disease, impactions andorthodontics. Tooth extraction techniques improve withclinical experience. Two aspects of tooth extraction areimportant in successful completion of the operation:equipment and technique.

Equipment

208

Most teeth are extracted with dental forceps of which avariety of types are available.

Lower forceps have their blades at 90° to the handlesand upper forceps have the blades either angled slightlyforwards or straight in relation to their handles (Fig. 25.1).Forcep design has developed over many years and isbased around the principle of creating a displacing forceon the roots of the tooth, not the crown. When teethfracture during extraction it is most commonly the resultof poor forceps placement. Forceps are therefore designedaround the root morphology of the tooth they are intendedto remove (Fig. 25.2). The appropriate forceps choice isoutlined in Table 25.1.

Root forceps that have smaller beaks for smaller teethor fractured roots are available. There are other specificforceps with more limited application, such as upper thirdmolar forceps, which have an elongated 'gooseneck' foraccess to the posterior maxilla.

Elevators may be used as an alternative method ofmobilising or extracting teeth, and these are discussed inChapter 23. There has been a recent increase in the use ofinstruments known as luxators to assist with extractions.Luxators are designed to help the operator gain space forapplication of the forceps. They are very sharp-bladedelevators that are used to increase the gap between thetooth and the surrounding bone, thus loosening the tooth

and producing more space for forcep application. Theycan be very helpful but care must be taken due to thepotential soft tissue damage. They should be used to'unscrew' the tooth, not to elevate it.

TechniqueEvery clinician will develop specific techniques for toothextraction, but all follow the same basic pattern (listed inTable 25.2), and these will be discussed in turn.

Application

Having chosen the forceps that best fit the rootmorphology of the tooth to be removed, surgeons mustfirst position themselves and the patient to achieve goodaccess and vision, as well as allowing the surgeon to

Table 25.1 Types of forcep

Forcep

Upper universalsUpper straightsUpper molars (R/L)Lower universals

Lower molarsCow-horns

Tooth

Upper incisors and premolarsUpper caninesUpper molars (R/L)Lower incisors, canines and

premolarsLower molarsLower first and second molars

Table 25.2 Extraction technique

Application of forceps

Consolidation of gripDisplacement of toothPostdelivery care

25

Fig. 25.1 Upper (left) and lower (right) universal extraction forceps.

Fig. 25.2 Blades of universal forceps (left) and lower molar forceps(right) applied to the roots of an incisor and lower molar, respectively.

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Table 25.3 Operator–patient position forextraction

Quadrant

Upper right and upper leftLower leftLower right

Patient

SupineUprightUpright

Operator

In frontIn frontBehind

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put appropriate force on the tooth. For a right-handedoperator this is outlined in Table 25.3. It is usual practiceto remove lower teeth before upper teeth, and posteriorteeth before anterior teeth, to avoid blood obscuring theoperator's view if a number of teeth are to be extracted.

The patient's head should be at the level of thesurgeon's elbow. The next stage is to position thesurgeon's non-dominant hand. This is important becauseit improves access by retracting soft tissues and allowsthe surgeon to place a counterforce on the jaw to assisttooth extraction. For example, when buccally expandingan upper molar it is necessary to have an opposing forceprovided by the operator's passive hand. It is conventionalto place a finger and a thumb on either side of the toothto be extracted.

Application of the forceps is the most important stageand the basic principle of tooth removal must always beborne in mind: application of the beaks of the forceps tothe root rather than the crown of the tooth. It shouldusually be as easy to remove a tooth fractured at gingivallevel as a fully intact tooth because the forcep blades areplaced on the root face not on the enamel of the tooth.

This application involves the placing of the bladesunder the gingivae, taking care to minimise soft tissuedamage. The forceps should then be pushed apically,completing this stage of the procedure. This may requireconsiderable force.

There are exceptions to these general rules, forexample, cow-horn forceps fit into the bifurcation of lowermolars and, because of their unique design, produce anupwards force. Their application is therefore different.

Consolidation

To remove the tooth efficiently, the forceps must bepushed together firmly to engage on to the root surface,with the handles of the forceps being gripped with thepalm of the hand with an apical force applied at the same

time as forcing the handles together. This avoids thebeaks of the forceps sliding around the root of the toothon rotation rather than the efficient transfer of forcesfrom operator to tooth.

Displacement

Displacement depends on root morphology. Teeth can beremoved in two ways: by rotational movement or buccalmovement (expansion).

Upper incisors and lower premolars can be rotated.All other teeth are best removed by controlled buccalexpansion. Upper first premolars are an exception as theyoften present with two thin roots. The best extractiontechnique is a combination of gently wiggling the teethand slight expansion, both bucally and palatally.

Rotational movement involves increasing destructionof the periodontal ligament by a circular movement bothclockwise and anticlockwise. Buccal expansion involvesthe enlargement of the bony socket allowing toothdelivery. This is usually a staged process where the toothis forced bucally and, with sustained pressure on thebuccal alveolar bone, the tooth is extracted.

There are variations of the above basic movements:lower molars can often be removed efficiently by acombination of rotation and buccal expansion (a figure-of-eight movement is often suggested); also lower thirdmolars can be expanded lingually where the lingual plateis thinner than the buccal bone.

Postdelivery

The extraction socket usually heals without incident,even when multiple extractions have produced a large,open wound. Healing can be aided by a number ofprocedures: sockets that have been expanded should besqueezed to replace the bone to its original position;sharp pieces of bone can be removed and the patientshould be instructed to bite on to a damp piece of gauzeto aid haemostasis. Once haemostasis has been achieved,postoperative instructions should be given (Ch. 23). Post-operative instructions should include leaving the socketundisturbed for 4-6 h and then gentle rinsing with hotsaline mouthwashes after each meal. Patients should alsobe advised of control measures if bleeding occurs post-operatively and how to contact the appropriate emergencyservice in case of complications.

Risk assessment in toothextractionTeeth should be assessed preoperatively to anticipatepotential difficulties with extractions. Preoperative assess-ment can be carried out using the history, examinationand special investigations.

Examination

Clinical examination will reveal gross caries, which canmake forceps placement very difficult. Imbrication orcrowding can make forceps placement and delivery ofthe tooth difficult. Wear facets, indicating increasedocclusal load, increase supporting bone strength makingextractions more difficult.

History

A history of difficult extractions or postoperativecomplications can give an early indication of potentialproblems. The age of the patient is also important: thebone of older patients is less flexible than that of youngerpatients, making standard techniques such as buccalexpansion more difficult.

Radiography

Radiographs are helpful in showing the number, shapeand relationship of the roots of the tooth. They also revealwhether the roots of a lower molar tooth are convergentor divergent. Radiographs can also indicate areas of hyper-cementosis and bony pathology that may complicate theextraction.

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Complications of extractions

212

IntroductionComplications can arise during the procedure of extrac-tion or may manifest themselves some time following theextraction. These will be discussed in turn. Problems oflocal anaesthesia are discussed in Chapter 24.

Immediate extractioncomplicationsThese occur at the time of the extraction and are listed inTable 26.1.

Fracture of the crown of a tooth

This may be unavoidable if the tooth is weakened eitherby caries or a large restoration. However, the forceps mayhave been applied improperly to the crown instead of tothe root mass, or the long axis of the beaks of the forcepsmay not have been along that of the tooth. Sometimes,crown fracture arises from the use of forceps whose beaksare too broad (see Ch. 25) or as a result of the operatortrying to 'hurry' the operation. The management of thiscomplication is to remove all debris from the oral cavityand review the clinical situation. Surgical extraction of theremaining fragment may then be necessary (see Ch. 23).

Fracture of the root of a tooth

Ideally, it should be possible to ensure that the wholetooth is removed every time an extraction is carried out.However, when a root breaks a decision about manage-ment of the retained piece of root has to be made.

Further management depends on the size of the rootfragment, whether it is mobile, whether it is infected, how

Table 26.1 Immediate extraction complications

Fracture of tooth:crownroot

Fracture of alveolar plateFracture of mandibleSoft tissue damageInvolvement of maxillary antrum:

oroantral fistulafractured tuberosityloss of root (or tooth) into antrum

Loss of tooth or root:into pharynxinto soft tissues

Damage to nerves or vesselsDislocation of temporomandibular jointDamage to adjacent teethExtraction of permanent tooth germ with deciduous

toothExtraction of wrong tooth

close it is to major anatomical structures such as the maxil-lary antrum or inferior dental canal, patient cooperationand the ability of the surgeon to successfully completethe procedure taking into account the constraints of time,equipment and surgical expertise.

If the decision is made to leave the root then this mustbe written in the case notes and the patient fully informed.If the procedure is deferred, the root fragment shouldhave the pulp removed and a dressing placed.

If a deciduous tooth is being removed, it must be keptin mind that the roots are usually being resorbed with theroots being pushed towards the surface by the permanenttooth. It is often prudent therefore to leave these frag-ments, as injudicious use of elevators can cause damageto the underlying permanent tooth.

26

Fracture of the alveolar plate

This is a common complication and is often seen whenextracting canine teeth or molars. If the alveolar plate haslittle periosteal attachment and is hence liable to lose itsblood supply then it should be carefully removed bystripping off any remaining periosteum with a periostealelevator. If, however, it is still adequately attached to theperiosteum, a mattress or simple suture over the socketmargin will stabilise the plate and allow its incorporationinto the healing process.

Fracture of the mandible

This is an uncommon complication of dental extraction,which is usually heralded by a loud crack. The mostimportant thing is to stop the extraction and reassessthe situation. The patient should be informed of thepossibility that his or her mandible might be broken anda radiograph should be taken. If a jaw fracture is con-firmed then the patient should be referred to a maxillo-facial centre as an emergency. It would be advisable toadminister another inferior dental block injection. If thisinvolves a significant delay, then further analgesia shouldbe provided and appropriate antiseptic mouthwashes andantibiotics prescribed.

Soft tissue trauma

Soft tissues must not be crushed. For example, the lowerlip is at risk from the handles of the forceps whenremoving maxillary teeth. It should be ensured thatrecently sterilised instruments are not too hot and thepatient's eyes should be protected from instruments andfingers using safety spectacles. Soft tissue damage ismore likely to be encountered when the patient is undera general anaesthetic and cannot communicate. Careshould be exercised to avoid application of the beaks offorceps over the gingival soft tissues, especially linguallyin the lower molar region where the lingual nerve may bedamaged. Protective finger positioning is required whenusing elevators that may slip and damage the tongue,floor of mouth or the soft tissues of the palate. The softtissues at the angle of the mouth may also be damaged byexcessive lateral movement of forceps particularly whenextracting an upper tooth when an ipsilateral inferiordental block has been administered or where the patientis having general anaesthesia.

Involvement of maxillary antrum

Oroantral fistula (OAF)

The roots of the maxillary molar teeth (and occasionallythe premolar teeth) lie in close proximity to, or evenwithin, the maxillary antrum. When the tooth isextracted, a communication between the oral cavity andthe antrum may be created. The operator may be awareof this possibility from the study of a pre-extractionradiograph (Fig. 26.1) or may suspect the creation of anOAF by inspection of the extracted tooth or the socket.An upper molar may have a saucer-shaped piece of boneattached to the trifurcation of the roots, indicating thatthe floor of the antrum has been detached. The socketitself may show abnormal architecture such as loss of theinterradicular bony septae. To confirm the presence of anOAF the patient can be asked to pinch the nostrilstogether and blow air gently into the nose. The operatorcan then hold cotton wool in tweezers under the socketand look for movement of the fibres. Sometimes, theblood in the socket can be observed to bubble or the noiseof the air moving through the fistula can be detected.Some operators favour inspection of the socket withgood lighting and efficient suction using a blunt probe toexplore the integrity of the socket. The noise of thesuction often becomes more resonate if a communicationexists between socket and sinus.

Once confirmed, an OAF can be treated in two ways:if small, the socket can be sutured and a haemostaticagent such as Surgicel® can be used to encourage clotformation. Strict instructions should be given to avoidnose blowing because this can increase the intrasinuspressure and break-down the early clot that covers thedefect. The patient should be prescribed an antibiotic

Fig. 26.1 Radiograph of the upper molar region showingthe close association of the maxillary antrum to the uppermolar roots. On the right side a root apex has beendisplaced into the maxillary antrum.

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214

Fig. 26.2 A buccal advancement flap: (a) and (b) show abuccal flap, which is inelastic due to the underlyingperiosteum; (c) and (d) show the flap advanced to coverthe fistula after incising the periosteum.

because of the risk of infection, which would prevent thesinus healing and lead to a chronic oroantral fistula. Thepatient should be reviewed 1 week later to check pro-gress and then 1 month later to ensure that the socket hashealed.

If the OAF is large then it should be closed im-mediately by means of a surgical flap. Most commonlythis is done by means of a buccal advancement flap. Thisis a U-shaped flap with vertical relieving incisions takenfrom the mesial and distal margins of the socket. The flapis mucoperiosteal, which means that the periosteum lieson its inner aspect. Periosteum is a thin sheet of osteo-genic soft tissue that has no elasticity and must thereforebe incised to allow the whole flap to be advanced to thepalatal margin of the socket (Fig. 26.2). The incision ismade horizontally along the whole length of the base ofthe flap; it need not be deep because the periosteum isrelatively thin. Some surgeons reduce the height of thebuccal plate of bone to reduce the length of the advance.Horizontal mattress sutures encourage wound margineversion and aid primary healing. A prophylacticantibiotic would normally be prescribed and the patientasked to avoid nose-blowing.

Fractured tuberosity

The maxillary tuberosity is the posterior part of thetooth-bearing segment of the maxilla. Occasionally,during extraction of a maxillary molar tooth a segment ofbone becomes mobile. As with the fractured mandible,

the operator should stop the extraction and assess theproblem, as continuing to extract the tooth will lead totearing of the soft tissues and displacement of the frac-tured segment. Assessment can be carried out clinicallyby palpating the area to gauge the size of the bonefragment. This can be confirmed by taking radiographsincluding periapicals, oblique occlusals or panoramicfilms. It must be decided whether to retain the fracturedpiece of bone or to remove it with the associated tooth, orteeth. The principal consideration is size of the defectthat will be left when the segment is removed, as this cancomplicate future denture provision. If the decision ismade to remove the tooth and the bone, then a muco-periosteal flap should be raised and the segmentdissected out carefully. The soft tissues can then besutured and the wound closed completely. As there is abreach of the maxillary antrum, antibiotics and analgesicsshould be prescribed for the patient.

The more common management is to retain the toothand bone in position and allow the fracture to heal. First,the segment must be reduced if it is displaced, and thiscan normally be done with digital pressure or throughforceps on the tooth. The tooth that has been giving riseto pain will have to have appropriate pulp extirpationor obtundent dressing. The next stage is to take animpression for construction of an appropriate splint tohold the fractured segment in position and protect it fromtrauma from the mandibular teeth. Alternatively, a seg-ment of preformed arch bar can be wired to the buccalaspects of the fragment, extending forwards as far as thecanine. Orthodontic wire can be used in much the sameway, either using brackets or more simply attached withcomposite. The patient should be prescribed analgesicsand antibiotics. The splint should be kept in place forapproximately 4 weeks, after which time healing shouldbe assessed. If the fragment is firm and there is no signof infection, the tooth should be removed surgically byraising a flap, removing buccal bone and dividing thetooth into separate roots to avoid applying lateralpressure to the relatively weak tuberosity segment.

Loss of the root (or tooth) into the antrum

Another complication involving the antrum is pushingpart or all of a tooth into the antral cavity. Normally theoperator should arrange for the removal of this root as thepatient is again at risk of the development of maxillarysinusitis with or without an oroantral fistula. The patientshould have radiographs taken to confirm the presence of

the root in the antrum and the operator should then raisea buccal flap from the mesial and distal margins of thesocket. Access to the antrum should then be increased bybone removal with bone nibblers and drills. The root canthen be removed from the antrum by a variety of tech-niques including suction, the use of small caries exca-vators or direct removal by tweezers. If these methodsare unsuccessful then the antrum can be flushed-out withsterile saline in an attempt to 'float' the root out, or theantrum can be packed with ribbon gauze, which mightdislodge the root when it is removed. Once the root hasbeen removed from the antrum, the resulting defectshould be closed with a buccal advancement flap, as inthe closure of an oroantral fistula. In the rare circum-stances where a whole tooth is dislodged into the maxil-lary antrum, its removal is often paradoxically easier.

Loss of tooth/root

Occasionally, during removal of a tooth, parts of thetooth can be dislodged and disappear. If this happens, asearch should be instituted, using good suction. Thepatient may be aware of swallowing the tooth, or part ofthe tooth. If the tooth or root cannot be located then aradiograph, first of the abdomen, should be arranged tocheck whether the tooth or root has been swallowed,which is most likely. It is important to ensure that theobject is not in the patient's airways.

Roots that are elevated incorrectly can occasionallybe pushed through a very thin bony plate overlying thesocket and disappear — bucally or lingually — into the softtissues. This is more problematic when a root (often anadditional third root) is pushed through the lingual platein the lower third molar region, because these can be verydifficult to recover.

Damage to nerves or vessels

This complication applies more commonly to the sur-gical removal of teeth rather than simple extractions butone must always be aware of difficulties when operatingin the region of the inferior dental, lingual or mentalnerves.

Dislocation of the temporomandibular joint

Occasionally, a patient will open the mouth so widelyduring an extraction that the mandible is dislocated; orthe operator might apply force to an unsupported man-dible, causing it to dislocate. In this event, the operator

should try, as quickly as possible, to reduce the dislocationby pushing the mandible downwards and backwards. Ifthis is not done relatively quickly, muscle spasm of thepowerful elevator muscles of the mandible will ensue andthe patient will require sedation, or indeed even a generalanaesthetic, to reduce the dislocation. When extractingteeth under general anaesthesia the mandible can dis-locate due to the loss of muscular tone. It is important toensure the mandible is repositioned before the patientrecovers from the anaesthesia. Recurrent dislocation ofthe temporomandibular joint is discussed in Chapter 20.

Damage to adjacent teeth

When extracting teeth, fillings from adjacent teeth maybecome dislodged and this should be dealt with appro-priately. Inexperienced operators sometimes damage teethin the opposing jaw when the tooth being removed comesout of its socket rather more quickly than expected. It isimportant to recognise that damage has been caused andto deal with it appropriately.

Extraction of a permanent tooth germ alongwith the deciduous tooth

When extracting deciduous teeth there is occasionally asignificant amount of soft tissue attached to the apex ofthe deciduous root. It is often difficult to ascertainclinically whether this is a granuloma or abscess, orwhether it is the permanent tooth germ attached to theroot. If there is concern, the specimen should be sent forhistopathological investigation to confirm whether thepermanent tooth germ has been removed.

Extraction of the wrong tooth

Extraction should be considered to be an irreversibleprocedure and therefore extreme vigilance should beemployed to ensure that the correct tooth is extracted.The most vulnerable clinical situation is where one isextracting teeth for orthodontic reasons and the teethhave no obvious clinical problem. Extracting the wrongtooth is medicolegally indefensible.

Postextraction complicationsPostextraction complications can occur a variable lengthof time after the extraction. They are listed in Table 26.2and will be considered in turn.

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Table 26.2 Postextraction complications

HaemorrhageDry socketOsteomyelitisSwelling, pain, echymosisSequestraTrismusProlonged anaesthesiaActinomycosisChronic oroantral fistulaInfective endocarditis

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Postextraction haemorrhage

Haemorrhage is one of the complications that cliniciansworry about most and it can seriously complicate theextraction of teeth. Prevention of haemorrhage isdesirable. To achieve this, the patient must be questionedcarefully as to any previous history of excessive haemor-rhage particularly in relation to previous extractions (seeCh. 6). If a history of postextraction haemorrhage iselicited it is important to try and ascertain for how longthe bleeding continued and what measures were used tostop the bleeding on previous occasions. It is also im-portant to discover when the bleeding started in relation-ship to the time of the extraction. General questionsregarding a history of prolonged bleeding after trauma orother operations, or a family history of excessivebleeding or known haemorrhagic conditions may berelevant. It is also important to question the patient aboutthe use of drugs, such as anticoagulant drugs. If there isany doubt regarding the existence of a haemorrhagicabnormality the patient should be investigated asdiscussed in detail in Chapter 6.

A postextraction haemorrhage is first dealt with byremoving any clot from the mouth and establishing fromwhere the bleeding is originating. The patient can then beasked to apply firm pressure by biting on a gauze pack for10–15 rnin. It is advantageous to infiltrate local anaestheticwith a vasoconstrictor into the region, as this will makeany manipulation of the socket more comfortable and thevasoconstrictor in the local anaesthetic will also aid inreducing the haemorrhage. Suturing is essential in themanagement of a postextraction haemorrhage and ahorizontal mattress or interrupted sutures should be usedto tense the mucoperiostem over the underlying bone sothat the haemorrhage can be controlled (see Ch. 23). Theuse of haemostatic agents such as Surgicel® is helpful.Agents like bonewax can help to stop bleeding from the

Table 26.3 Predisposing factors in dry socket

InfectionExtraction traumaBlood supplySiteSmokingSexSystemic factors, e.g. oral contraceptives

bony walls of the socket. Although postextraction haemor-rhage can be dramatic, significant blood loss is unusual.Patients should, however, be assessed for evidence ofshock if bleeding appears significant (see Ch. 4).

Dry socket

Dry socket is also known as focal or localised osteitis andmanifests clinically as inflammation involving either thewhole or part of the condensed bone lining the toothsocket (lamina dura). The features of this are a painfulsocket that arises 24-72 h after extraction and may lastfor 7-10 days. Clinically, there is an empty socket withpossibly some evidence of broken-down blood clot andfood debris within it. An intense odour may be evidentand can be confirmed by dipping cotton wool into thesocket and passing it under the nose. The overall incidenceof dry socket is about 3% but this figure is much higherif the definition of postextraction pain is used as the solediagnostic criterion.

The aetiology of this condition is incompletely under-stood but many predisposing factors exist and these arelisted in Table 26.3.

Infection

This could occur before, during or after the extraction.However, many abscessed and infected teeth heal with-out leading to a dry socket. The oral flora in some patientscan be shown to be haemolytic and these individuals maybe more susceptible to recurrent dry sockets.

Extraction trauma

Excessive force may be associated with an increase in theincidence of dry socket. This is not always the case andit may occur after very easy extractions. The difficulty ofextraction may be important, as the bony wall of the socketmay be burnished during the extraction, crushing smallbony blood vessels and so impairing the repair process.

Blood supply

Vasoconstrictors in local anaesthetics may predispose toa dry socket by interfering with the blood supply to thebone and dry sockets certainly occur more frequentlyafter extractions with local anaesthetic than after thoseusing general anaesthetic.

Dry sockets are much more common in the mandiblethan in the maxilla. The relatively poor blood supply ofthe mandible predisposes to the development of thisproblem and food debris also tends to gather in the lowersockets more readily.

Site

The incidence of dry sockets increases further back in themouth with the highest incidence in the mandibularmolar region. The most common tooth involved is thelower third molar, where the incidence may be signi-ficantly more than 3% (see Ch. 27).

Smoking

Tobacco use of any kind is associated with an increase indry socket. This may occur, in part, due to the significantvasoconstrictor effect of nicotine on small vessels thatoccurs in smokers.

Sex

Dry sockets are significantly more common amongfemales.

Systemic factors

It has been suggested that systemic factors are involved,although these have not been elucidated. Oral contra-ceptive use is associated with an increased incidence ofdry sockets.

In an attempt to reduce the incidence of this painfulcondition, the teeth to be extracted should be scaled toremove any debris and preoperative flushing with 0.2%chlorhexidine may reduce the incidence. The operatorshould use a minimum amount of local anaesthetic andthe teeth should be removed as atraumatically as possible.Where patients have a consistent history of this problem,some clinicians advise prophylactic use of metronidazole.

Management

Management of a dry socket firstly involves the relief ofpain and secondly resolution of the condition. The socket

should be anaesthetised and irrigated gently and alldegenerating blood clot and food debris should beremoved. A dressing should be inserted into the socket toprotect it from further irritation by food debris. The mostappropriate dressing is a matter of personal choice butWhitehead's varnish pack, a zinc oxide pack or the use ofproprietary agents such as Alvogyl® are commonly used.Analgesics are an essential part of the management, as isthe use of regular mouthwashes to keep the area clean.It is important that the patient is reviewed regularly toensure that healing is progressing. When pain is intoler-able, long-acting local anaesthesia such as bupivacaineblocks may afford relief and allow patients to sleep.

Osteomyelitis

This rare complication is often a result of an immune-comprised state or a reduction in the blood supply, usuallyof the mandible following radiotherapy. The patient isusually systemically unwell: there is an increase intemperature and severe pain. Often the mandible, whichis more commonly involved, is tender on extraoral palpa-tion. The onset of disturbance of labial sensation after anextraction is characteristic of acute osteomyelitis. Thepatient will often be admitted to hospital for managementof this condition. The principles of treatment are thedrainage of pus, the use of antibiotics and the laterremoval of sequestra once the acute infection has beencontrolled. Prevention is best achieved, in a predisposedpatient, by ensuring primary closure of the socket bybone trimming and suturing (see Ch. 33).

Swelling, pain, echymosis

Some swelling, pain or bruising can be expected afterany surgical interference and it is important for theoperator to realise that if the soft tissues are not handledcarefully these features can be exacerbated. The use ofblunt instruments, excessive retraction or burs becomingentangled in the soft tissue all predispose to increasedswelling and discomfort. If sutures are tied too tightly,postoperative swelling due to inflammatory oedema orhaemotoma formation can cause the sutures to cheese-cut through the soft tissues, causing unnecessary pain. Itis helpful for the patient to bathe the area with hot salinemouthwashes in an attempt to reduce debris around thewound. Surgeons must be aware of the possibility ofwound infection and be prepared to institute drainage andconsider antibiotic therapy.

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Sequestra

There will be occasions when small pieces of bonebecome detached and cause interruption to the healingprocess. The patient will return, complaining of somethingsharp in the area of the socket and may feel that theoperator has left a root fragment behind. These sequestracan be dealt with either by reassuring the patient andawait shedding of the piece of bone or by administeringsome local anaesthesia and removing the piece of loosebone with tweezers. In some cases, granulation tissuemay be apparent with pus discharging especially on probingthe socket. This will respond well to a curettage of thesocket, thus removing the sequestrum in the curettings.

Trismus

Trismus is a common feature after the removal ofwisdom teeth (see Ch. 27) and may be associated withother extractions. It can also be related to the use ofinferior dental block local anaesthesia (see Ch. 24). It isimportant to ascertain the cause of the trismus and thento manage it appropriately. On most occasions thetrismus will resolve gradually over a period of time,which will vary depending on whether the condition isdue to inflammatory oedema or perhaps direct damage tothe muscles following local anaesthesia. The manage-ment is discussed in Chapter 24.

Prolonged anaesthesia

This is usually a feature of the removal of difficult orimpacted teeth, particularly wisdom teeth, and isconsidered in detail in Chapter 27.

Actinomycosis

This is an uncommon chronic suppurative infectioncaused by Actinomyces israelii and classically charac-terised by swelling in the neck with multiple sinus forma-tion and widespread fibrosis. The common site ofpresentation following extraction is the region around theangle of the mandible. Extraction wounds from lowerteeth or fracture of the mandible provide pathways forthe entry of the organisms. A detailed consideration ofcervicofacial actinomycosis is given in Chapter 33.

Chronic oroantral fistula

This complication arises when a communication betweenthe socket of an upper molar (or more rarely premolar)

and the maxillary air sinus has not been noted at the timeof extraction and infection both in the socket and the airsinus occurs. The patient may present with a variety ofsymptoms and signs either within a week or two follow-ing the extraction or many months (and even years) later.Common to all, however, is failure of the normal healingprocess and persistence of the socket. As infection of theair sinus becomes acute, symptoms of diffuse unilateralmaxillary pain, nasal stuffiness, bad taste and intraoralpus discharge may occur; these can be intermittent incharacter.

On examination, the socket can appear empty or befilled with granulation tissue. Occasionally, distinctlypolypoidal tissue can grow down from the opening,reflecting the sinus origin of the tissue. In other cases, thesocket can appear almost totally closed, with only a verysmall opening into the sinus. Diagnosis by carefulprobing is normally straightforward and an occipito-mental radiograph will show the extent of infectionwithin the sinus.

The management involves two stages. First, the acuteinfection must be controlled, then the opening should beclosed surgically. Initially, any accumulation of pus inthe sinus should be drained. This often requires excisionof the infected granulation tissue and polyps fromthe socket to allow free drainage and also to ensure his-tologically that the formation of the fistula is not relatedto downgrowth of an antral neoplasm. Nasal decon-gestants and antibiotics also help to control more acuteinfections.

Once the acute phase is controlled, most fistulae canbe closed using the buccal flap advancement. Themargins of the opening must be freshened by excising arim of soft tissue, because epithelium will often havegrown-up into the opening and, if not removed, willprevent healing. Where infection is limited to theimmediate vicinity of the fistula, a limited curettage iscarried out. However, where the whole sinus is filled withpolypoidal granulation tissue, a more thorough explorationof the sinus may be required, and this often is performedunder general anaesthesia.

Infective endocarditis

Infective endocarditis may arise in susceptible patientswith cardiac lesions who are not given appropriateantibiotic prophylaxis. A detailed consideration ofantibiotic prophylaxis for dental procedures is given inChapter 35.

Wisdom teeth

IntroductionThird molars are the last teeth to erupt in the humandentition and are popularly known as wisdom teeth. Theyfrequently give rise to problems when they are eruptingand the management of these problems has becomecolloquially known as the 'bread and butter' aspect of thespeciality of oral surgery. Through evolution, the humanjaws are occasionally no longer large enough to accom-modate all of the permanent dentition and therefore thelast ones to erupt are short of space. Most of the problemsassociated with wisdom teeth occur between the ages of18 and 25 but adults of any age can have problems.

A consideration of the criteria for removing wisdomteeth will be followed by discussion of pericoronitis. Theclinical assessment and management of impacted wisdomteeth will then be outlined, including preoperativeassessment, the procedures used to remove wisdom teeth,postoperative care and - finally - complications of surgery(Table 27.1).

Criteria for removal ofwisdom teethOver recent years there has been debate over theadvisability of removing symptom-free wisdom teeth orleaving them in place. The trend in recent years has beento be conservative in the management of these teeth andthis has been driven, to some extent, by the incidence ofcomplications associated with their surgical removal, andparticularly the small, but measurable, risk of damage tothe inferior dental nerve or the lingual nerve.

The controversy surrounding wisdom teeth has led tothe publication of guidelines, the most recent of whichare 'Management of unerupted and impacted third molarteeth' a National Clinical Guideline from the Scottish

Table 27.1 Management of impacted third molars

Criteria for removal of wisdom teethPericoronitis

spread of infection from pericoronitistreatment of pericoronitis

Clinical assessmentRadiographic assessmentClinical management

preoperative informationtechniques

lower third molarsupper third molars

Postoperative careComplications of surgery

Table 27.2 Indications for removal of wisdomteeth

Infectionpericoronitisuntreatable cariesuntreatable pulpal or periapical pathologyperiodontal disease

Cystic changeExternal or internal resorptionWisdom tooth in tumour resection

Intercollegiate Guidelines Network (SIGN) and'Removal of wisdom teeth' guidance from the NationalInstitute for Clinical Excellence (NICE). These guide-lines inform the decision on whether to remove wisdomteeth.

Surgical removal of impacted third molars, it isrecommended, should be limited to patients withevidence of pathology. These are listed in Table 27.2 andwill be discussed in turn. Further possible indications tobe considered are listed in Table 27.3.

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27

hTable 27.3 Further possible indications forremoval of third molars

TransplantationFractured mandibleAtrophic mandibleDenture or implant designAccess to dental careMedical conditionOrthodontic considerationsOrthognathic surgery or reconstructive surgeryUse of general anaesthesiaAge of patient

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Infection

Pericoronitis

The most common reason for recommending removal ofwisdom teeth is that patients have experienced significantinfection associated with them. This usually manifestsitself as pericoronitis and a discussion of the clinical fea-tures and management of this will follow. Pericoronitis isonly an indication for extraction if the first episode is veryacute or there has been more than one episode.

Untreatable caries, pulpal or periapical pathology

Another common indication for removal of wisdom teethis the development of caries either in the wisdom toothitself or in the adjacent second molar. This occurs becausethe patient is unable to clean the distal aspect of thesecond molar or the area around the wisdom tooth, whichis often partially erupted. This leads to the accumulationof food debris and plaque and then caries of the adjacenttooth surfaces. This may lead to untreatable pulpal orperiapical pathology.

Periodontal disease

As a result of the unsatisfactory relationship between thesecond and third molars, the area is prone to periodontaldisease, which may compromise the second molar. Thiscan be improved by the removal of the third molar.

Cystic change

When third molars are unerupted they may be the sourceof a dentigerous cyst, which can enlarge considerablybefore giving rise to symptoms. The risk of developing

these cysts is low but is also unpredictable and gives riseto a clinical dilemma of how often radiographic assess-ment of unerupted third molars is necessary to diagnosea cyst before its size makes the management morecomplicated.

External or internal resorption

A less common reason for removal of third molars isexternal resorption of the second molar due to pressurefrom the unerupted third molar. As with the formation ofthe dentigerous cyst, this resorption can be extensivebefore the patient experiences symptoms. Internalresorption within the wisdom tooth is also an indicationfor removal.

Wisdom teeth in tumour resection

If an impacted wisdom tooth is associated with a tumourat the angle of the mandible, or is within the tumourresection margins, it should be removed.

Transplantation

When a patient presents with a heavily restored orcarious first molar tooth and a partially erupted thirdmolar tooth it is possible to transplant the third molar intothe socket of the first molar. This procedure is complicatedby the difficulty of removing the third molar withoutdamage and also because the root morphology of theseteeth is different, which causes problems accommodatingthe third molar in its new site. Once transplanted, the toothwill often require to be splinted for a period and, with alow success rate, this procedure is rarely carried out.

Fracture of mandible

If a fracture of the mandible through the angle occurs, anopportunity may arise to remove the third molar whensurgical access is being made to treat the fracture itself.Some authorities consider that unerupted third molarsshould be removed in those individuals who participatein contact sports like rugby and boxing, in whom the riskof mandibular fracture is increased.

Atrophic mandible

It has been argued that an unerupted third molar in analready atrophic mandible might be a potential site for

fracture and consideration should be given to removing itin a controlled manner before a fracture occurs.

Denture or implant design

Restorative dentists can request the removal of uneruptedthird molar teeth to facilitate denture design or theaccurate placement of implants.

Access to dental care

Where patients are in a situation where they do not haveeasy access to dental care, it is appropriate to considerthe removal of potentially troublesome third molar teeth.This could for example, include submariners or occu-pations that involve working in isolated areas wheredental help may be difficult to find. With modern meansof travel and communication, this reason for removingthird molar teeth has assumed less significance.

Medical conditions

Removal of third molars may be indicated in certainmedical conditions, such as prior to cardiac surgery or inthose scheduled to have radiotherapy of the jaw. Removalof third molars following radiotherapy increases thelikelihood of the development of osteoradionecrosis, andis therefore better carried out before such treatment (seeCh. 36).

Orthodontic considerations

Orthodontic treatment plans may include the removal ofimpacted lower and upper third molars in an attempt toprevent or reduce imbrication of the incisor teeth. Thereis no evidence, however, that third molars contribute tothis problem (see Ch. 31).

Orthognathic or reconstructive surgery

Third molars may also need removed when orthognathicsurgery is being planned, particularly with proceduressuch as sagittal split osteotomy (see Ch. 13).

General anaesthesia

More rigorous criteria for removal of lower third molarscan lead to further difficulties in determining whethersymptom-free third molar teeth on the other side of the

mouth should be removed when general anaesthesia orsedation is being used for the removal of a symptomaticthird molar tooth. The fact that the tooth is present is notsufficient reason to remove it while the patient isanaesthetised. However, as in all situations regardingthird molars, all four teeth should be subject to arisk-benefit analysis.

Age of patient

Finally, removing third molars in young fit patients andnot leaving them until an older age when the bone isdenser and more difficult to manage, and when thepatient may have medical problems related to older agegroups, is still a common point of view. Contrary to thisargument is the view that the small but significant mor-bidity following removal of wisdom teeth supports a moreconservative approach, and so removal for this reasonalone can no longer be condoned. The more conservativeapproach is now more commonly adopted but many oralsurgeons are mindful that they may be storing updifficulties for later years, both for their patients and fortheir surgical successors. Time alone will answer thisquestion

PericoronitisThis condition is characterised by inflammation aroundthe crown of a tooth and only occurs when there is com-munication between the tooth and the oral cavity. Thetooth is normally partially erupted, and hence visible, butoccasionally there may be little evidence of communi-cation between it and the oral cavity and careful probingof the gingiva immediately distal to the second molarmay be necessary to demonstrate some communication,however small.

The patient's main complaint will be pain, whichinitially may be of low intensity. As the conditiondevelops the pain increases in intensity. Swelling overthe affected site may develop and this will cause furtherdiscomfort when the patient occludes with the opposingteeth. As the swelling increases, the pain on occludingbecomes more severe and the patient will be discouragedfrom bringing the teeth together. The 'lid' of gum overthe involved tooth is known as the operculum and thismay show evidence of trauma from the cusps of theopposing maxillary teeth. There may be pus formationand a bad taste. There will be marked inflammation in the

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tissue adjacent to the affected tooth and this can lead totrismus and difficulty in swallowing. The patient may begenerally unwell, with lymphadenitis and pyrexia. Therewill often be marked halitosis.

Spread of infection from pericoronitis

On occasion, pus associated with an impacted lowerwisdom tooth will track buccally forwards above thebuccinator attachment forming a sinus in the region ofthe first permanent molar. This may lead to some con-fusion as to the source of the infection and can lead tounnecessary removal of the first permanent molar. Thiscondition is referred to as a migratory abscess.Pericoronitis can also be associated with acute ulcerativegingivitis causing marked halitosis and gingivalsloughing and ulceration. Spread of infection can occurin various directions (Table 27.4), including laterally intocheek, or distobuccally under the masseter muscle to giverise to a submasseteric abscess characterised by profoundtrismus. It can also spread to the sublingual or sub-mandibular region and also into the area around thetonsils and parapharyngeal space (see Ch. 33). Lesscommonly, it can ascend through the anterior pillar offauces into soft palate causing marked dysphagia. Earlyand competent management of acute pericoronitis willhopefully limit this spread.

Treatment of pericoronitis

The management of pericoronitis is similar to the man-agement of any acute oral infection. It is essential toprovide drainage for any pus. Once drainage is adequateit is important to clean the area beneath the operculum.

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Table 27.4 Spread of pericoronal third molarinfection

Region

Migratory abscess of sulcus

Soft tissue of cheekSubmassetericSublingual spaceSubmandibular spaceParapharyngeal spaceSoft palate

Direction of spread

Forwards, bucally abovebuccinator

LaterallyDistally and bucallyLingually above mylohyoidLingually below mylohyoidDistally and linguallyUpwards through anterior

fauces

This can be carried out mechanically by irrigation withwarm chlorhexidine or saline solution. This shouldremove any accumulated food debris and plaque.Application of antiseptic or mildly caustic solutionsunderneath the operculum may be beneficial. Examplesinclude Talbot's iodine and trichloracetic acid. Theseagents are astringents and will cause soft tissue damage,and must therefore be used with caution. If the maxillarythird molar has overerupted and is causing trauma to theoperculum, the single most effective treatment is itsremoval. This can be carried out easily, even in thepresence of some degree of trismus, and often leads toresolution. The patient's general condition needs to beassessed and a decision made regarding the prescriptionof an antibiotic (see Ch. 33). The patient should beencouraged to use regular hot saline mouthwashes anddiscouraged from applying heat to the cheek area extra-orally. Arrangements should be made for early review ofthe patient's condition (within 2-3 days), when someresolution should have occurred.

Clinical assessmentOnce the symptoms of pericoronitis have settled thepatient needs to be assessed fully regarding the futuremanagement of the wisdom teeth. It is important to con-sider all four third molars as a unit and to make a decisionon each of them. A general assessment of the mouthshould be made, including caries activity and the level ofperiodontal disease. The patient's oral hygiene should bechecked with particular reference to the accumulation ofdebris around the third molars. The eruption status of eachof the four third molars is made using three categories -unerupted, partially erupted or fully erupted. Note shouldbe taken of the patient's age because the management ofthird molars can be significantly influenced by thisfactor. It is also important to assess the surgical access tothe third molar region by asking the patient to openwidely and to note the space available between the distalaspect of the second molar and the vertical anterior borderof the ascending ramus. This is particularly importantwhen removal of these teeth under local anaesthesia isbeing contemplated.

Radiographic assessmentRadiographs are an essential part of the assessment of apatient's wisdom teeth. When removal is contemplated it

is important that the entire tooth and the surroundingbone can be seen clearly using a panoramic view of theoral cavity. A periapical radiograph may be helpful iflack of detail in the panoramic view compromisesassessment of the root morphology or its proximity to theinferior dental canal.

Table 27.5 lists the information which should beavailable from the radiographs.

Most operators initially assess the depth and theposition of the impacted tooth. The simplest method ofdepth assessment can be made by looking at the positionof the crown of the impacted tooth relative to the secondmolar (Fig. 27.1). A crown-to-crown relationshipindicates a superficial impaction, crown-to-crown-and-root of the second molar indicates intermediate depth andcrown of wisdom tooth to the roots only of the secondmolar implies a deep position. The angulation should beassessed by comparing a line joining the mesial anddistal images of the cusps of the wisdom tooth with thecurve of Spee formed by joining the cusps of the pre-molar and molar teeth. If the lines are parallel then thewisdom tooth is vertical in position. However, if thewisdom tooth line, when extended posteriorly, wouldmeet the Spee line then the tooth is mesio-obliquelyimpacted (Fig. 27.2). Conversely, if the wisdom toothline when extended posteriorly would never meet thecurve of Spee, then it is disto-oblique in position. Themost common position is mesio-oblique and the mostdifficult to remove is the deep disto-angular impaction,because its path of removal impacts into the ramus of themandible and there is often little space to elevate thetooth from its mesial aspect.

The crown may show evidence of distal bone loss orfollicular enlargement, which is indicative of chronicpericoronal infection and often facilitates removal of thetooth.

The crown of the impacted tooth should also beexamined for evidence of caries, as caries will tend toweaken it and make fracture more likely on elevation.Paradoxically, a carious crown is also more difficult tosection and split than an intact crown. The size, numberand shape of the roots, and how they relate to each other,is fundamental to the assessment of difficulty in removal.Fused roots tapering to the apex present little difficulty inelevation and removal compared to converging ordiverging roots with apical dilacerations.

The relationship of the roots to the image of theinferior dental canal should be scrutinised carefully(Fig. 27.3). Features likely to indicate close proximity

Table 27.5 Information obtained fromradiographs of wisdom teeth

Angulation of the wisdom tooth (for examplemesioangular, distoangular, vertical or horizontal)

Depth of the wisdom toothThe relationship to the inferior dental canalCrown featuresThe root morphologyThe texture of the surrounding boneAny associated pathology (e.g. dentigerous cyst)Surgical accessThe state of the second permanent molars (including

root morphology, presence of caries or extensiverestoration)

Fig. 27.1 Depth assessment of an impacted wisdomtooth on a radiograph: (a) superficial impaction;(b) intermediate depth; (c) deep position.

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Fig. 27.2 Angulation of a wisdom tooth on a radiograph: (a) vertical: theintercuspal line of the wisdom tooth is parallel to the line of Spee; (b) mesio-oblique:the intercuspal line of the wisdom tooth is converging with the line of Spee; (c) disto-oblique: the intercuspal line of the wisdom tooth is diverging from the line of Spee.

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include narrowing of the canal as it passes across theoutline of the root, loss of continuity of the radio-opaqueroof of the canal or deflection of the normal arc of thecanal as it passes across the root(s). Additionally, theapices of the roots may show severe dilacerations as theyapproach the outline of the canal. Although less reliable,any radiograph that shows the root image crossing that of

the canal may indicate anatomical closeness. Conversely,it is important to understand that separation of the imagesof roots and the inferior dental (ID) canal with interposedbone on any radiographic view indicates lack of closeapproximation because, if the root(s) were anatomicallyclose, such a separation could not be shown radio-graphically, regardless of angulation.

Fig. 27.3 Radiographic features likely to denote close proximity between root(s) and inferior dental canal.

Finally, the morphology of the roots and distalrestorations present in the second molar should be notedas forces carelessly applied to the third molar may causemovement to this tooth or risk dislodging the restoration.

Clinical managementOnce the decision has been made to remove a patient'swisdom tooth, the options for anaesthesia should then beconsidered. Consideration of either local anaesthesiaand sedation or general anaesthesia may be indicated.Decisions regarding the form of anaesthesia used willdepend upon the patient's anxiety about the procedure,the number and the degree of difficulty of removal of thewisdom teeth and the availability of patient-care options.

Preoperative information

Before treatment commences, the patient should be giveninformation regarding the possible complications of theremoval of wisdom teeth. This is best done not onlyverbally on a one-to-one basis with the clinician but alsoby the use of written information, which the patient canstudy and discuss with the surgeon before the procedure.The information provided to the patient should include a

description of the discomfort that follows removal ofthese teeth and the associated swelling and difficulty inopening the mouth for a short period. Bruising of the faceat the angle of the jaw can cause alarm. Dry socket ismore frequently experienced when lower wisdom teethare removed than other teeth (see Ch. 26). The mostserious complication is numbness of the tissues suppliedby the inferior dental or lingual nerves. It is mandatorythat the patient is advised of this possible complicationprior to their procedure. Around 15% of patients whohave lower wisdom teeth removed will experience sometemporary alteration in sensation along the distributionof the lingual or inferior dental nerves but permanentnumbness occurs in under 1%. It is important that thecase record is fully documented with the information thathas been given to the patient regarding the possible com-plications and also to indicate whether written informationhas been given to the patient.

Techniques

Lower third molars

Access to the tooth is gained by lifting a buccalmucoperiosteal flap (Figs 27.4 and 27.5). Raising theflap lingually can lead to stretching of the lingual nerve,

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Fig. 27.4 Flap design for removing an impacted wisdomtooth: (a) occlusal view; (b) lateral view; unerupted; c)partially erupted.

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Fig. 27.5 Envelope flap (no vertical relief) for removing animpacted wisdom tooth.

which is anatomically close to the lingual aspect of thelower wisdom tooth and, in many cases, can be avoidedif sufficient visibility and access are gained without it.

Once the lower wisdom tooth is adequately exposed,consideration should be given to bone removal tofacilitate delivery of the tooth. Bone removal is mostcommonly achieved using drills and burs and is carriedout on the buccal aspect of the tooth and onto the distalaspect of the impaction. The intention is to create a deep,

Fig. 27.6 Removal of pericoronal bone.

narrow gutter around the crown of the wisdom tooth (Fig.27.6), and not a shallow, broad gutter. Bone should beremoved to allow correct application of elevators on themesial and buccal aspects of the tooth. The operator canthen assess the possibility of removing the tooth in itsentirety with the use of elevators or a combination ofelevators and forceps. If it proves impossible to removethe tooth in this way and adequate bone has beenremoved, sectioning the tooth using burs is carried out(Fig. 27.7). Most commonly, the crown of the tooth issectioned from the roots and the crowns and roots arethen removed as individual items. Further separation ofthe roots with burs may also be necessary. Where theroots are separate, the tooth may be sectioned longitudi-nally, allowing removal of the distal portion of the crownand distal roots, followed by elevation of the mesial halfof the tooth.

In younger patients under general anaesthesia, thelingual wall of the third molar socket may be removedusing a hammer and chisel (the split bone technique).This often allows the tooth to be delivered in one pieceby rotating it lingually. Clearly, this technique doesrequire a lingual flap to be reflected but in skilled handsit can be a very successful and rapid technique.

When tooth removal is completed, any debris iscleaned out and any follicular tissue - especially thathidden behind the second molar - is curetted free. Aftersmoothing any sharp bone, irrigation of the socket iscarried out with saline. The flap is then sutured usingeither resorbable or non-resorbable materials.

Fig. 27.7 Methods of sectioning an impacted wisdom tooth.

Fig. 27.8 'Anatomical' closure of a flap after surgicalremoval of an impacted wisdom tooth.

Although it is possible to suture the flap across thesocket to the lingual side, many operators prefer to returnthe flap to its original position, leaving a socket that ismore easily kept clean by the patient postoperatively, andmay well also reduce swelling (Fig. 27.8).

Upper third molars

These teeth are generally easily removed by elevationfrom the mesiobuccal aspect using a curved WarwickJames elevator or Coupland's chisel. If undue resistanceto elevation is encountered then excessive force cancause fracture of the posterior aspect of the tuberosity,and forceps should be used if possible in this circum-stance. If this is not possible due to only partial eruptionof the tooth, a buccal flap can be raised with appropriatebone removal.

Upper third molar removal should not be under-estimated and access to grossly carious, partially erupted

examples with diverging roots in large patients can bemore than a little challenging.

Postoperative care

The overuse of antibiotics is being recognised and, inparticular, there is controversy about their use prophy-lactically in the removal of wisdom teeth. Some routinelyprescribe antibiotics to the patient whereas others with-hold antibiotics and use them only if infection occurs. Noclear evidence is available to support either viewpoint.Some operators provide antimicrobials where there is ahistory of repeated episodes of pericoronitis or if therehas been a recent acute episode. Others prescribe ifextensive bone removal is necessary or there is extremedifficulty in removing the tooth.

The antibiotic may be administered preoperatively,perioperatively or immediately postoperatively. Regimesand choice of antibiotic vary but the most commonlyused are amoxicillin or metronidazole, and they shouldbe prescribed for as short a period as possible. The use ofcorticosteroids during the removal of wisdom teeth ismore evidence-based and more clinicians are now usingthem to reduce postoperative swelling. The provision ofpostoperative analgesia is an integral part of treatment.Chlorhexidine mouthwashes twice daily and frequent hotsaline rinsing is beneficial. Patients should be encour-aged to keep moving the jaw, despite the swelling anddiscomfort, as this reduces stagnation and consequentinfection.

Complications of surgeryThese can be considered under perioperative and post-operative complications.

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Perioperative complications are similar to those oc-curring with any other dentoalveolar surgery and includeexcessive bleeding (see Ch. 26). Certain complicationsare more specific to the third molar region and includefracture of the mandible, loss of a root in the lower jawinto the lingual space or in the upper jaw displacement ofthe tooth into the maxillary air sinus or into the pterygoidspace (see Ch. 26). Direct trauma to the inferior dentalneurovascular bundle may occur and can be difficult toavoid where anatomically the roots are intimately relatedto the canal tissues. The most obvious example of this isthe rare situation where the inferior dental canal actuallypasses through the root. Even here, it may be possible tosplit the root around the neurovascular bundle leaving thebundle relatively undamaged.

Postoperatively, the majority of patients will haveswelling at the angle region, trismus and discomfort. Thisgenerally peaks after 48 h and will resolve within a week

to 10 days. Infection in the form of localised osteitis (drysocket) can occur and should be managed in the usualsymptomatic way (see Ch. 26). Occasionally, the woundmay become infected with pus production and this ismore likely if there has been haematoma formation in thecheek or other adjacent soft tissue spaces.

Anaesthesia (complete loss of sensation), paraesthesia(partial loss) or dysaesthesia (an altered sensation oftenpainful to the patient) are more worrying sequelae. Wherelingual nerve damage has been sustained taste perceptionis also frequently altered and can be an additional dis-tressing symptom. The prognosis for resolution is goodbut a small number of patients have to accommodate topermanent loss or alteration of sensation in the distri-bution of the particular nerve. Recovery of normalsensation may take from a few days to several months,but after a year little improvement will occur.

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Cysts of the jaws

IntroductionA cyst, by definition, is a pathological cavity that isusually lined with epithelium and which contains fluid orsemi-fluid.

The vast majority of cysts of the jaws form withinbone and grow slowly. They may therefore attain arelatively large size because they are often initially

symptom free. Diagnosis of a cyst is not uncommonlymade when the cyst becomes acutely infected, or it isfound by chance on routine radiography of the dentition.Table 28.1 shows a list of the cysts found in the jaws.Several are very rare. The most common will be con-sidered in more detail here, discussing their clinicalfeatures, diagnosis and treatment.

Table 28.1 Features of cysts of the jaws

Type

Radicular (apical ordental)

Dentigerous

Keratocyst

Periodontal

Nasopalatine

Nasolabial

Solitary bone cyst

Staphne's idiopathicbone cyst

Aneurysmalbone cyst

Site

Any non-vital tooth

Unerupted teeth

Angle of mandible butanywhere possible

Periodontal pocket

Midline anteriorhard palate

Nasolabial fold(not intrabony)

Mandibular body

Mandibular body onlingual aspect

Usually mandible

Epithelial source

Debris of Mallassez

Reduced enamelepithelium

Dental lamina

Debris of Mallassez

Epithelium nests atnasopalatinefissure

Possibly epitheliumfrom thenasolacrimalduct

Not epithelium lined

Not cystic butsubmandibularsalivary glandinclusion

Not cystic

Frequency

Most common of all

Relatively common

Relatively common

Uncommon

Uncommon

Very rare

Rare

Very rare

Rare

Radiographicappearance

Round or ovalradiolucency

Radiolucency aroundcrown of uneruptedtooth

Multilocular when large

Round or ovalradiolucency

Midline palatalradiolucency, laminadura of centralsintact

May cause depressionof nasal lateral wall

Radiolucency oftenscalloped aroundroots of lowermolars

Small round shadowbelow inferior dentalcanal

Multilocular, soap-bubble apearance 229

28

Radicular cysts

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A radicular cyst is by far the most common cyst of thejaws. Its synonyms are dental cyst, periapical cyst or sim-ply apical cyst. From time-to-time the teeth responsiblefor the formation of a radicular cyst may be extracted butthe cyst remains and may well increase in size sub-sequent to the extraction. In this circumstance the nameresidual cyst is commonly used.

A radicular cyst develops when epithelial debris ofMallassez in a granuloma at the apex of a non-vital toothis stimulated to proliferate. The epithelium forms a ballor mass of cells, which may break down centrally, perhapsdue to lack of nutrients, to form a liquefied central area.Alternatively, the epithelium cells may form strands andsheets that encompass part of the granuloma, with asimilar resulting breakdown of the enclosed granulomatouscontent to form the fluid centre of the cyst. Whichevermethod occurs, the effect is the formation of an epithelialsemipermeable lining to the cyst content that allowsfluids to enter the lumen by osmosis and leads to itsgradual enlargement. This whole process is sometimesknown as cystic degeneration.

Clinical features

Initially, the cyst will be contained within the alveolarbone around the apex of the non-vital tooth. At this stagethe bone increases its density peripherally around thelesion in an attempt to wall it off. This is possible due toits slow rate of growth and explains why, radiographically,there is a sharp radio-opaque line surrounding theradiolucent shadow of the cyst.

With continued growth, the cyst eventually approachesthe surface of the alveolar bone and as the apices of mostteeth lie closer to the buccal than the palatal or lingualplates, it is the buccal plate which is usually first affected.Lying on the surface of the bone is the periosteum, andthis layer of osteogenic tissue in turn reacts to theencroaching cyst by laying down new bone over itsadvancing front. The first real evidence of a cyst istherefore a bony swelling, known as bony expansion, inthe buccal sulcus. Occasionally, especially with an upperlateral incisor, the expansion may be palatal, reflectingthe palatal inclination of the apex. This expansion willfeel hard to palpation and its presence may be convincingonly on comparison with the contour of the bone on theother side of the jaw. With further growth, thisenlargement will continue until the periosteum can no

longer lay-down bone sufficiently rapidly and the cysterodes through an ever-thinning bony buccal coveringuntil it presents as a soft fluctuant (fluid-filled) swellingin the sulcus, which often appears slightly blue in colour.When the overlying expanded bone is very thin,palpation may elicit the characteristic eggshell cracklingthough this is rarely felt in practice.

Acute infection can supervene at any time during thisprocess of evolution and this will convert the cyst, as faras its clinical features are concerned, into those of anacute apical abscess. If the acutely infected cyst burstsand discharges into the mouth, the continued dischargemay lead to formation of a sinus.

Loosening or tilting of adjacent teeth is onlyencountered in very large cysts, and resorption of rootsusually results from repeated infection of the cyst and isrelatively uncommon.

Unless a radicular cyst becomes infected, it willremain painless and vital structures will be gently movedaside to accommodate it. This can be seen clearly inlarger mandibular cysts, which push the inferior dentalcanal downwards to the lower border of the mandible. Noanaesthesia will be noted of the lip or chin unless thepressure within the cavity rises rapidly as with an acuteinfection. With large cysts occasionally the toothresponsible for the lesion elicits a rather hollow note onpercussion.

Diagnosis

As mentioned above, many radicular cysts are foundeither by chance radiographically or because of acuteinfection. However, other clinical features may present.Expansion of bone is usually buccal and hard to pal-pation. Later it is soft, fluctuant, and bluish in colour.The tooth will be non-vital. Radiographic features willshow the classic appearance of a round or oval-shapedradiolucency (Fig. 28.1) surrounded by a sharplydelineated thin white line of increased bone density. Theaffected tooth will show loss of its apical lamina dura.Very occasionally there may be evidence of resorption ofadjacent teeth and this reflects repeated acute episodes ofinfection within the cyst. Similarly, such infection cancause a haziness in the sharp radio-opaque delineationsof the margin of the cyst. In larger mandibular cysts theremay be clear evidence of the inferior dental canal havingbeen displaced downwards by the advancing lesion.

Aspiration of the cyst contents may be possible inlarger cysts with little or no bony covering. Classically,

Fig. 28.1 A radicular cyst associated with a lateral incisorshowing as a round radiolucency.

the fluid appears as straw-coloured in which a shimmermay be seen due to its cholesterol content. However, ifthe cyst has been infected, this characteristic appearancemay be lost and the fluid may well consist of pus orblood-stained pus. Many authorities have alluded to thedifference between the higher soluble protein content ofthe radicular cyst and the dentigerous cyst compared withthe lesser amount contained in odontogenic keratocysts.Such analyses are in practice seldom, if ever, carried outbecause of their cost and due to the fact that thedifferences between aspirates are visible to the naked eyeand the use of a simple cytological smearing of suspectedkeratocysts makes such expensive tests unnecessary.

With very large cysts, especially in the mandible, itmay be prudent to obtain some lining for histopatho-logical examination, as this may allow differentiationbetween a large radicular (or residual) cyst, a keratocystor a cystic ameloblastoma, especially when consideringthe differential diagnosis of a radiolucency of the angleof the mandible.

Treatment

There are two main methods of treatment for cysts:enucleation (removal of the lining in total) andmarsupialisation (creation of a permanent opening intothe cyst cavity). The vast majority of cysts are treated by

enucleation, with marsupialisation tending to be reservedfor certain categories of patients, usually with largercysts.

Enucleation

This is suitable for all small to moderate-sized cysts andthe majority of large cysts.

Root-treating and conserving the tooth causing thecyst may be worthwhile and surgery may therefore bepreceded by endodontic treatment.

A standard mucoperiosteal flap is raised buccally withthe vertical relieving incision placed anteriorly (seeCh. 23). The thin bone is then removed with bone rongeurs(nibblers) or burs to allow surgical access to the fluid-filled sac. The cyst lining is then separated with peri-osteal elevators or curettes from its bony wall and 'shelled'out. The lining should be sent for histopathologicalinvestigation. After irrigating with sterile saline the flapis sutured back to its anatomical position. If the tooth hasbeen root filled, an apicectomy should be performed atthe same time with retrograde sealing of the canal ifappropriate.

The operation is for all but very large cysts usuallycarried out under local anaesthesia with or without sedationaccording to the patient's preference. Postoperative com-plications are rare, although breakdown of the wound inlarge mandibular cysts can occur. The patient is normallyrecalled about 4-6 months postoperatively, when a radio-graph should show evidence of bony infilling of the cystcavity.

Marsupialisation

As the name implies, marsupialisation means creating apouch. The rationale of this treatment is the permanentdestruction of the integrity (wholeness) of the cyst. This,in effect, depressurises the cyst cavity, stops its continuedexpansion and encourages a shrinkage of the lining bynew bone formation around its periphery. It is moresuitable for large cysts where enucleation may endangervital structures such as the inferior dental nerve or thereis a risk of fracture during enucleation. The limited surgeryinvolved is very suitable for outpatient care under localanaesthesia and it can therefore be particularly appro-priate for elderly or medically compromised patientswho would be at risk from a general anaesthetic. Anydecision to marsupialise a cyst cavity should be precededby histological evidence that confirms the lesion as a cyst

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and this involves a small incisional biopsy or retrievingtissue from the cyst cavity at the time of the procedure.

Marsupialisation may be achieved most simply byextraction of the tooth responsible for the cyst, aspiratingthe contents through the socket, then irrigating the cystlumen before packing the opening with a surgical pack.Sterile ribbon gauze soaked in Whitehead's varnish isexcellent for this purpose, as the antiseptic content willprotect the cyst cavity from infection. The pack is latersubstituted for a partial denture with a root-shaped acrylicbung extending into the cyst cavity from the socket. Thepatient is then given syringes with which to irrigate thecyst cavity with warm saline on a twice-daily basis. Withthe lining no longer complete, the bone heals inwardsaround the cyst, reducing it progressively in size. Someoperators remove the cyst by enucleation when it hasreduced to a more manageable size.

If no tooth is involved - as in a large residual dentalcyst - then a small semilunar flap is raised over the mostexpanded part of the cyst to allow part of the lining to beexcised, and the cyst contents to be aspirated and washedout. The flap is then turned into the cyst and sutured toits lining, and the opening maintained initially with asurgical pack and later by a denture or prosthesis with anacrylic bung.

Marsupialisation of a large cyst may take manymonths for healing to occur and the onus is therefore onthe patient to maintain cleanliness by frequent irrigationsof the cyst cavity, as described above.

Dentigerous cystsThese cysts are developmental odontogenic cysts, whicharise when cystic degeneration occurs in the reducedenamel epithelium (dental follicle). They are seen aroundunerupted teeth and are therefore most frequently foundin the third molar areas, both upper and lower, the uppercanine region and, less frequently, around lower secondpremolars. They may also arise in relation to super-numerary or supplemental unerupted teeth.

Clinical features

These cysts grow slowly and have the same effect asradicular cysts on surrounding bone. A bony expansionoccurs initially and at a later stage a soft fluctuant swellingover the area of the unerupted tooth will develop. Aswith radicular cysts, dentigerous cysts are usuallyasymptomatic until infected.

Diagnosis

Radiographic imaging and aspiration are often fairlyconclusive (Fig. 28.2). A very large dentigerous cyst inthe lower third molar area can displace the wisdom toothand may require to be differentiated from other lesionssuch as a keratocyst or ameloblastoma. Although boththese lesions are classically described as beingmultilocular radiolucencies on radiograph, it must beremembered that unilocular lesions do exist. Aspirationmay not be sufficient to differentiate a dentigerous cystfrom a keratocyst, particularly if there has been infection.Similarly, an ameloblastoma may have within it areas ofcystic degeneration, even in the more solid tumours, anda variant of the ameloblastoma – known as the cysticameloblastoma – can be very similar to the dentigerouscyst in its clinical appearance, radiographic image andaspirated fluid content. If any doubt exists, then biopsy ofa small portion of the lining will be diagnostic in mostcases, although in the cystic ameloblastoma the tumourmay only be evident histologically in a small area of thecyst lining and the sample taken may therefore bemisleading.

Fig. 28.2 Radiograph of a dentigerous cyst in the lowerthird molar area showing downward displacement of theinferior dental canal.

Treatment

Treatment will either be enucleation along with extrac-tion of the unerupted tooth or marsupialisation.Marsupialisation is the method of choice if it is hoped toencourage eruption of the buried tooth, but it isremarkable how seldom the involved tooth is in a satis-factory position in terms of its angulation and depth tomake this the preferred choice. The vast majority,therefore, are enucleated with the unerupted tooth.

Keratocysts (odontogenickeratocysts)Keratocysts are believed to be derived from remnants ofthe dental lamina. They can be found anywhere in thejaws but the most common site is at the angle of themandible. Unlike other cysts of the jaws, their epitheliumis a keratinising stratified squamous epithelium and theircontents are therefore filled with desquamated squamesand keratin, which form a semisolid material that hasbeen likened to cottage cheese. Their mode of growth isalso different from the other cysts in that the liningappears to be more active, with passive fluid ingress oflittle significance. Keratocysts are also characterised bythe formation of microcysts or satellite cysts which pro-trude into the surrounding fibrous tissue and tend to beleft behind during enucleation. This increases the risk ofrecurrence and dictates a different managementapproach.

Clinical features

The active growth of keratocysts appears not to be evenlydistributed, so the cyst does not expand uniformly as asphere or oval-shaped lesion. Different rates of activitywithin areas of the lining probably account for the forma-tion of locules, which, once the cyst has achieved amoderate size, will give rise radiographically to the typicalmultilocular appearance. They appear to grow selectivelywithin the looser medulla of the jaw initially andalthough eventually the outer cortical plates do showexpansion, the cyst may be by that time a considerablesize. Lingual as well as buccal expansion is often noted.

Infection often only occurs when the cyst is quitelarge and where soft tissue trauma allows ingress ofbacteria. It is not infrequent to find that with expansionthe cyst communicates with the surface through the

periodontal space of an adjacent tooth. It is important torealise that, unless infected, these sometimes very largelesions are painless and do not exert sufficient pressureon vital structures such as the inferior dental nerve tocause anaesthesia of the lip and chin. When infected,however, they can become very painful, cause anaesthesiaand may discharge into the mouth, with consequent badtaste and bad breath as additional clinical features.

Diagnosis

As with other cysts, the diagnosis is based on clinicalfeatures, radiographic findings and the results of aspirationand biopsy. Two extraoral radiographic views at rightangles to each other, such as an orthopantomogram andposteroanterior mandibular view, may be required withlarge keratocysts. Classically, the appearance is of amultilocular radiolucency with marked expansion of bothbuccal and lingual plates. Unerupted wisdom teeth maywell be pushed into bizarre ectopic positions such asinverted high into the ramus of the mandible. The inferiordental canal may be difficult to see and may reflect themore active growth of these cysts around the canal withless evidence of significant repositioning as is seen withradicular cysts. Displacement or tilting of the teeth canbe a feature, as can resorption of roots, although this isagain probably a result of infection. Infection within acyst also accounts for many becoming symptomatic.

As previously indicated, the soluble protein content ofthe aspirate obtained from a keratocyst is lower than thatof other cysts and this is due to the fact that keratin is aninsoluble protein. Aspiration will yield a 'dirty' cream-coloured semisolid material composed of keratinisedsquames. These can be confirmed histologically andprovide good evidence that the lesion is a keratocyst.

As the differential diagnosis may well includeodontogenic tumours such as ameloblastoma, manysurgeons prefer to make a small flap incision and removesome lining of the cyst to confirm the diagnosis.

Treatment

Keratocysts have a higher recurrence rate than other cystsand especially when they are large and multilocular.

Enucleation is suitable for most keratocysts but maybe difficult in large ones where, for example, they extendupwards into the vertical ramus of the mandible. Surgicalaccess may be difficult and with the multilocular patternof growth it may be impossible to ensure that the whole

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lining is removed. It is known that small clusters ofepithelium known as microcysts, or satellite cysts can lieoutside the epithelial lining and within the fibrous wall,and leaving even a small amount of this fibrous wall maywell account for eventual recurrence. For this reason,some operators have in the past used chemicals such asmercuric salts or, more recently, cryotherapy techniques(particularly liquid nitrogen sprayed around the bonycavity) to try to ensure that no viable soft tissue remnantsremain (see Ch. 38).

Marsupialisation can be used particularly with largekeratocysts where it can be very effective (Figs 28.3and 28.4). It has the same advantages as mentionedpreviously with radicular cysts and probably reduces thechance of recurrence. Again, it may be appropriate in

some cases to use the technique to reduce the size of thelesion before enucleating it. Whatever method is used,follow-up is required for years to ensure that there is norecurrence, and this is mainly radiographic.

Gorlin-Goltz syndrome

Gorlin-Goltz syndrome, or multiple basal-cell naevisyndrome, is an inherited (autosomal dominant) conditionin which multiple keratocysts of the jaws form part of theoverall syndrome. Other aspects in these patients are thepresence of many skin lesions in the form of basal-cellnaevi or carcinomas, and skeletal abnormalities affectingthe vertebral column and the ribs. Calcification of thefalx cerebri is also a noteworthy feature.

234Fig. 28.3 Marsupialisation of a large keratocyst showing (a) cyst cavity; (b) denture with extension.

Fig. 28.4 Radiograph of keratocyst at left angle ofmandible: (a) at presentation; (b) 6 months aftermarsupialisation.

Nasopalatine cystsThese cysts arise from epithelial remnants within or nearto the nasopalatine foramen. They are not odontogenicbut are classified as fissural cysts, and they represent byfar the most common example of fissural cysts of thejaws.

Fig. 28.5 A radiograph of a nasopalatine cyst causingdisplacement of incisor roots.

Clinical features

These cysts cause swelling of the anterior aspect of themidline of the hard palate. They may become infectedand cause pain and overlying tenderness and can, onoccasion, discharge forming a sinus. However, as withmost cysts, they are painless unless infected and maygrow to a considerable size.

Diagnosis

Presence of a midline anterior palatine swelling is theonly usual clinical finding. However, many are againdiagnosed through chance by radiographs of the teeth inthis region. It can be difficult when such radiolucenciesare found on routine radiographic assessment of thecentral incisors, to know if the image seen is withinnormal anatomical limits of the nasopalatine foramen. Aradiolucency of approximately greater than 8 mm indiameter is more likely to represent cystic degenerationbut, where doubt exists, a further radiograph 6 months to1 year later may be more conclusive. The normal radio-graphic image is a round or inverted pear-shapedradiolucency with sharp radio-opaque margins (Fig.28.5). When they are large, they can cause separation ofthe central incisor roots, but the laminae dura of the teethremain intact. If there is doubt whether the cyst is aradicular cyst related to one or other incisor, pulp testingcan be carried out and close examination of the apicesradiographically should show an intact lamina dura.

Treatment

These cysts should be enucleated - never marsupialisedbecause marsupialisation in this area can lead to a

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Fig. 28.6 Palatal flap raised to expose a nasopalatinecyst.

permanent cavity that will show no evidence ofrestoration of the normal contour. Normally, enucleationis carried out with a palatal flap taken around the gingivalmargins of the premolars on one side to the premolars ofthe other (Fig. 28.6). After enucleation, interdentalinterrupted sutures are used to replace the flap and inlarger cysts. It is sometimes useful to have constructed apalatal plate from preoperative impressions to supportthe flap and prevent the formation of a painful haematoma.

Other cysts

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The other cysts of the jaws are very uncommon and, asthey are so rare, it is only necessary to know a few factsabout them.

Nasolabial cyst

This is a fissural cyst that is thought to form by cysticdegeneration of epithelium from the lower part of thenasolacrimal duct during embryological development.Clinically, they may present as painless swellings in thenasolabial fold, where they may be palpated eitherexternally on the skin surface or intraorally high in thebuccal sulcus anteriorly. Radiographically, although theyare not intrabony cysts they may, if they attain areasonable size, cause a depression of the radio-opaquemargin of the floor and lateral wall of the nose, which isbest viewed by an oblique anterior occlusal radiograph.

This bony surface is normally very gently convex inappearance but may show concavity where the cyst hascaused saucerisation of the bone in this region.Confirmation may be obtained by aspiration and thenormal treatment would be surgical enucleation.

Solitary bone cyst

This used to be known as a traumatic bone cyst or ahaemorrhagic bone cyst. It is usually found in themandibular body and appears radiographically as aradiolucency that not infrequently shows scallopingaround the roots of the lower molar and premolar teeth.It causes no expansion of the bone and even onradiographic examination the outline of the radiolucencyis less well defined than would be obtained from othercysts. This cyst is not a true cyst in so far as it has noepithelial lining and, in fact, the majority have apparentlyno content whatsoever. When surgically explored, theytend to heal spontaneously after the surgery.

Staphne's idiopathic bone cyst

Although usually discussed with cysts of the jaws, this isnot in fact cystic at all. It consists of submandibularsalivary gland tissue that occupies a recess on the lingualaspect of the mandibular body. These cavities are usuallyfound by chance on routine radiography of the lower jawwhere they appear as round or oval-shaped radiolucencies

Fig. 28.7 Staphne's idiopathic bone cyst.

lying below the image of the inferior dental canal (Fig.28.7). Surgical exploration is not advised and mostclinicians would take a further radiograph 6 months to1 year later to confirm that the shadow of this cavityremains unchanged.

Aneurysmal bone cyst

This is discussed in Chapter 36.

Globulomaxillary cyst

This cyst was originally thought to be a separate clinicalentity. It was believed to be a fissural cyst formedbetween the upper lateral and canine teeth, but many nowconsider it to be a radicular cyst derived from the lateralincisor.

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Periradicular surgery

IntroductionThe term 'periradicular surgery' has superseded the olderterm of 'apicectomy' and reflects the fact that the surgerymight not always be related to an apical problem but canaffect the side of the root, as when a post has perforatedinto the periodontal space. Virtually any tooth can betreated in this way although anterior teeth, beingstrategically and aesthetically more important, are morecommon. The indications for periradicular surgery willbe discussed, followed by a consideration of surgicaltechniques and post perforations.

Indications for surgeryIn general, too many teeth are treated by periradicularsurgery and this is a direct result of inadequate endo-dontic techniques. There are, however, several indicationsfor periradicular surgery, including endodontic failure,which may be unavoidable. These will be discussed inturn (Table 29.1).

Endodontic failure

Obstructions to instrumentation, such as calcified rootcanals, dilacerated (hooked or curved) roots, brokenendodontic instruments or root fractures may occur; root-

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Table 29.1 Indications for periradicular surgery

Endodontic failure:canal obstructionproblems with root fillingother, e.g. canal number and shape

PathologyPost-crowned teeth

filling problems may also arise. Underfilling of the canaloften reflects preparation of the root canal short of thetrue apex with necrotic tissue perpetuating the infection(Fig. 29.1). Overfilling of the canal may occur and thematerial used and the quantity of material through theapex will determine the likelihood of the need for sur-gery. A small amount of relatively non-irritant material,provided the patient is symptom-free, can often be left(Fig. 29.2). An open apex may require both endodonticand surgical sealing if the apex is funnel-shaped.

Miscellaneous examples of endodontic failure includesignificant lateral canals, often near the apex, poornatural drainage and difficult canal morphology. This canlead to difficulty in controlling infection and may needapical surgery in addition to endodontics.

Fig. 29.1 Radiograph of an underfilled root canal.

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Fig. 29.2 Radiograph of an overfilled root canal (andlateral perforation).

Fig. 29.3 Lateral perforation of a root with a post.

Pathology

The presence of a radicular cyst requires enucleationafter endodontic sealing of the canal. Also there may beassociated pathology such as infection from an upperlateral incisor spreading to the follicle of an uneruptedcanine.

Post-crowned teeth

Post-crowned teeth can fail due to any of the abovereasons and there may be additional considerations inthe decision to carry out periradicular surgery. Often, thecorrect treatment would be to root treat the tooth again,but this would involve destroying the existing crown andremoving the post. This may be unattractive to thepatient, especially if the crown is good functionally andaesthetically. The pragmatic solution may therefore be toleave the crown and post undisturbed and carry out thesurgery, unless the endodontic filling is very poor.

Minimising the risk of post perforations and theirmanagement will be discussed later (Fig. 29.3). It is,however, likely that the infection is initiated by theacidity of the cement used to retain the post causingtissue necrosis in the periodontal space and this sub-sequently becoming infected.

Surgical techniquePeriradicular surgery is a simple minor procedure and isoutlined in Table 29.2.

Anaesthesia

Infiltration with an adrenaline (epinephrine)-containingsolution is preferable and significantly improves visibilityby its haemostatic effect. Even where a block anaestheticis given, additional infiltration is wise. Palatal or lingualinfiltration is needed for full gingival margin flaps toallow suturing but may be necessary for larger lesions inany case, e.g. upper lateral incisor where the infectionhas eroded palatal bone.

Table 29.2 Periradicular surgical technique

AnaesthesiaFlap designBone removalApex removalCurettageRetrograde root fillingWound closureFollow-up 239

Flap design

An 'L' or inverted 'L'-shaped flap from the gingival mar-gin is the flap of choice (see Ch. 23). Only one verticalincision is normally required and the access afforded isexcellent (Fig. 29.4). The only perceived disadvantagemay be gingival recession postoperatively, but this can beminimised by careful suturing.

The older semilunar flap avoids the risk of recessionbut has several disadvantages (Fig. 29.4). It gives lesssurgical access, is more difficult to suture accurately and,by cutting across the gingivae, can lead to dysaesthesia(painful altered touch sensation) of the gingivae, whichmay be long lasting.

Bone removal

It may be necessary to remove bone over the apex of thetooth to gain surgical access. This is relatively easy whenthe pathology has destroyed bone, but accurate assess-ment of the location of the apex is required when the areaof infection is smaller, and good radiographs may be veryhelpful. The apical third of the root should be found byusing a fast-rotating round bur with good suction andlight, and bone then removed over the apex and suf-ficiently above it to allow access.

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Removal of apex

Normally, 3 mm of apex is removed using a narrow-tapered fissure bur. Ideally, the cut across the root shouldbe at right angles to the long axis of the root and thisstage should be carried out early in the procedure to clearthe field for curettage of the existing infection.

Curettage

Large to medium-sized caries excavators are ideal forcurettage. The cavity should be clean but it is probablyunnecessary to spend too much time removing everyfragment of soft tissue. Ideally, curettings should be sentfor histopathology.

Retrograde root filling

The vast majority of teeth treated require retrogradesealing of the root canal. This need may be obvious fromthe outset with good radiographs but visual inspection

and probing will almost inevitably indicate therequirement.

The root canal needs to be prepared and cleansed to adepth of 3 mm (Fig. 29.5). In practice, this can be accom-plished with a small rose head bur (a small contra-anglehand-piece may be helpful) or by ultrasonic preparationusing specially designed tips.

After drying the canal, various sealants can be used,including zinc oxide and Eugenol® preparations, ethoxybenzoic acid cement (EBA) and, more recently, mineraltrioxide aggregate (MTA). No material will produce ahermetic seal, although this must be regarded as theultimate objective of the procedure. Excess filler shouldbe removed carefully to reduce foreign body reactions.

Wound closure

After thorough irrigation with sterile saline the woundshould be closed. In the anterior region, especially, afiner gauge of suture and smaller needle may facilitate aneater result. Great care should be exercised to ensurethat the interdental papillae are repositioned accurately.

Fig. 29.4 Flap design for apicectomy: older L-shapedflap.

Fig. 29.5 Retrograde sealing of a root canal.

In many cases, the knot can be tied over the contact point,allowing the suture to act as a pulley in this context (Fig.29.6). Where there is no contact point, a verticallyarranged mattress suture can be very helpful in holdingthe papilla firmly on either side of the tooth. Time spentin the closure of these wounds is well spent as theaesthetics of the end result can depend largely on accuratesuturing.

Follow-up

Sutures are usually removed 5-7 days postoperativelyand patients are normally seen 3-6 months after this toassess the longer-term results. Absence of pain, tender-ness of the sulcus sinus formation and undue mobility areindicative of success. Radiographs should show theretrograde seal in good position and a reduction in theradiolucency compared with the preoperative film.

Reasons for failureThe reasons for failure of periradicular surgery are listedin Table 29.3.

The procedure will fail if the apical seal is inadequateand release of toxins and bacteria continues. The sealmay be poorly placed at surgery or it can be displacedwhen, for example, a new post is being prepared for thetooth. The possibility of extra root canals or bifid rootapices may be missed and hence not sealed.

Inadequate support may cause undue movement ofthe tooth and may cause reinfection. This may result

Fig. 29.6 Suturing of an L-shaped apicectomy flap.Suture between 23 is interrupted and tied over the contactpoint. The suture between 12, having no contact pointinterdentally, is a vertically arranged mattress suture.

Table 29.3 Reasons for failure of periradicularsurgery

Inadequate apical sealInadequate tooth supportVertical tooth fracture

Fig. 29.7 The root of a tooth supporting a post crownshowing a vertical split.

from an existing periodontal lesion, undue forces actingon the tooth or overzealous removal of the root apex.

A vertical split in the tooth may be the result ofexcessive forces acting on a large post (Fig. 29.7). Avertical fracture may be suggested if the post has had tobe recemented on several occasions and the radiolucencyevident on the radiograph may correspond with the postrather than the apex of the tooth. If a vertical fracture isdiagnosed, the tooth must be extracted.

Post perforationsThe risk of post perforation during preparation of the rootcanal for the posts can be minimised by ensuring thepreparation is carried out without local anaesthetic. If aninadvertent perforation occurs, the patient will feel painand bleeding may be evident from the canal. In addition,root-filling material should be removed carefully usinghand-driven non-dentine cutting instruments. Finally,good quality radiographs should always be available.

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Perforations which do occur should be gentlyirrigated, dried and the correct alignment re-established.The false channel should normally be sealed on fillingthe canal.

Diagnosis

This may be obvious if the post has perforated mesiallyor distally, when the rarefaction can readily be seen onperiapical radiograph (Fig. 29.3). If the perforation hasbeen labial or palatal (or lingual) then the use of a'profile' (i.e. lateral) periapical radiographic view may beuseful. The site of the radiolucency can be a valuableclue, as it will generally appear on the lateral side of theroot at the level of the top of the post. This appearancecan also be seen where there is a vertical split.

Management

To curette the abscess and seal the perforation from thesurgical aspect will normally be unsuccessful in the long

term. Better results demand removal of the post andthorough cleansing of the false channel. Root fillershould then obliterate this channel and, as excess fillermay be extruded into the abscess cavity, curettage shouldbe arranged very soon afterwards. Sealing the defect canlead to complete healing and resolution of the defect. Ifthe original post is otherwise satisfactory, it may bereduced in length before recementing, or a new postcould be fitted along the correct line of the root canal.Surgical access is achieved in the usual way, the cavitycuretted of infected tissue together with any excess rootfiller. If the perforation is directly palatal or lingual,access may be virtually impossible and the prognosiswill hence be poorer.

Some clinicians have extracted inaccessible perforatedroots, sealed the perforation outside the mouth andreimplanted it with appropriate splinting. This is clearly'last chance' treatment but can be remarkably successful,at least in the short term.

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Preprosthetic surgery

IntroductionIn the normal course of events, the extraction of teethwill be the final surgical procedure undertaken before theprovision of a prosthesis, whether this is a full or partialremovable appliance or a fixed system. The presence of'hidden' pathology in the form of unerupted teeth orroots, or residual infections or cysts, should also beascertained and dealt with appropriately before prostho-dontic work is undertaken, as this may well avoidembarrassing complications at a later date, which mightcompromise the prosthesis. However, certain situations -often anatomical rather than pathological - will benefitfrom minor surgical modifications, which can greatlyimprove the provision of a more stable and comfortableprosthesis. Additionally, dental implants have opened upnew horizons for increased stability and hence patientacceptability of both fixed and removable crowns, bridgesand dentures, and this topic will be discussed in moredepth in Chapter 38.

Preprosthetic surgery can conveniently be dividedinto three subtopics: extraction of teeth; soft tissuesurgery and bone surgery (Table 30.1), and these will bediscussed in turn.

Extraction of teethStanding teeth

Standing teeth should be extracted with an awarenessthat preservation of the bony socket and attached gingivawill materially promote healing by preserving themaximum amount of tissue on or within which futurereplacement of the lost unit(s) will be based. Goodtechnique ensures that soft-tissue damage by forceps isminima], as does firm digital support of the alveolusduring extraction. Compression of expanded buccal plate

Table 30.1 Preprosthetic surgical procedures

Extraction of teethstanding teethunerupted teeth

Soft tissue surgeryfraenal attachmentsvestibular denture-induced hyperplasiapalatal hyperplasialeaf fibromafibrous tuberositiesflabby ridges

Bone surgeryalveolectomy or alveolotomybony exostoses and bone undercutssharp bony ridgestorus palatinustorus mandibularissharp mylohyoid ridgegenial tuberclesridge augmentation and vestibuloplasty

and judicious use of sutures over the socket margins, orwhere minor soft tissue tears have occurred, can alsobenefit the healing process.

It is clearly beneficial that teeth are extracted withoutroot fracture, but this may be unavoidable. Surgicalremoval of any such roots requires awareness by theoperator that the ridge form can be influenced by thetechnique employed to remove the fragment. It is unwiseto persist in attempting to elevate a root through thesocket if this causes damage to the soft tissue margins ordestroys bone in an uncontrolled fashion. A mucoperiostealflap can often not only preserve soft tissue health but alsoreveal the underlying root in such a way as to minimisebone loss. In some cases, bone may be preserved aroundthe coronal aspect of the socket by gaining applicationpoints for elevators further apically, in a manner similarto bone removal for apicectomy. This will help to

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preserve the ridge height. Careful wound debridement isessential and the flap should be sutured back anatomi-cally to maximise ridge form. Drawing a buccal flap overthe socket on completion will effectively reduce bothridge height and also the stronger attached gingiva, whichis better able to cope with future prostheses. In somesituations, periodontal bone loss and gingival recessionmay combine to leave spurs of interradicular bone lyingproud to the socket margin, and careful trimming withbone rongeurs will allow the blood clots to cover all theunderlying bone.

Unerupted teeth

Before provision of any prosthesis, it must be ascertainedthat no buried teeth that could compromise longer-termsuccess are present. The most commonly found arewisdom teeth, upper canines and lower premolars, and anorthopantomogram is an ideal radiograph to reveal suchpotential problems. A judgement is needed as to whetherit is likely that an unerupted tooth could, within thelifetime of either the patient or the proposed prosthesis,cause a problem that would prejudice the appliance. Thisassessment may be relatively easily made where there isrelated pathology such as dentigerous cyst formationaround the crown or evidence of communication, how-ever minimal, with the surface. In many cases, however,it may well be in the patient's best interests to leave sucha tooth, especially where its depth makes it improbable -even with resorption over many years - that it will everinterfere with a prosthesis. Further, its surgical removalmight risk damage to nerves or involve a considerableamount of bone removal resulting in a poorer ridge form.If removal is deemed necessary, planned removal of bonein which sectioning of the tooth may well reduce thisneed can better preserve the ridge contour and height.So-called osteoplastic flaps can, in a limited number ofsituations, help to preserve bone. This technique usuallyinvolves hinging the buccal plate (with its periosteumintact) from the underlying tooth to gain surgical access,and then suturing the intact plate of bone, still with itsblood supply through the periosteum, back to itsanatomical site.

Soft-tissue surgerySeveral soft-tissue impediments to provision of a good,stable prosthesis can be rectified surgically and arerelatively minor surgical procedures.

Fraenal attachments

These anatomical fraenal bands are composed not ofmuscle but of fibrous tissue. They may form an attach-ment on the ridge, which is near the crest, and causeinstability to removable appliances when adjacentmuscles are in function and they become tense.

Surgically, they may be excised (see Ch. 31) or theirattachment to the ridge may be incised close to thealveolar ridge and a surgical pack sutured over to preventreattachment. Alternatively, if the patient has an existingprosthesis, this may be lined with gutta percha or a zincoxide-based periodontal pack to hold the incised fraenumaway from the ridge during the healing phase.

Vestibular denture-induced hyperplasia

Several forms of denture-related hyperplastic soft-tissuelesions are recognised but they all arise as a result of lossof denture fit and are therefore more often seen in the'old denture' wearer, who is often the satisfied denturewearer.

Aetiology and clinical appearance

The most common form is the result of alveolar resorptionover a considerable number of years. This causes theperiphery of the flange of the denture to impinge on thesulcus depth or adjacent lip or cheek tissue. As this is avery gradual process, the tissues have time to react to theirritation by a protective hyperplastic reaction. Thisresults in a characteristic sausage-shaped roll of excesstissue, which can lie in function either on the outer aspectof the flange or between the flange and the alveolar ridgewhere there is a space (Fig. 30.1). This can result, onoccasion, in two parallel rolls of tissue lying across thesulcus region, and sometimes - when progressive loss offit causes trauma further into the lip or cheek - in severalflaps of redundant tissue. Hyperplasia of this kind canoccur anywhere along the periphery of a denture, andeven along the line of the post-dam, but it is mostcommon in the lower labial anterior sulcus, reflecting themore extensive resorption of alveolar bone in this region.

A less common but distinctive group of patients withthis problem are the immediate denture wearers, whosedentures have not been adjusted appropriately for themore rapid loss of fit that is caused by initial resorption.These patients often complain of pain - in markedcontrast to the 'old denture' wearer - because the tissues,

Fig. 30.1 Denture-induced hyperplasia of the lower labialsulcus in a patient with a loose-fitting denture.

having had less time to react to the loss of fit, ulcerate inaddition to forming a hyperplastic protective overgrowth.

Management

In the established denture wearer, the roll of tissue isusually composed of very mature connective tissue,which, even if the flange is trimmed back, will not shrinkappreciably and resolve. However, trimming of the flangeshould always be carried out at the time of presentation,with or without the use of a tissue-conditioning lining tomaximise the retention of the prosthesis. Surgical trim-ming of the excess tissue is almost always needed andthis is usually done under local anaesthesia. The surgeoncan manipulate the roll of tissue better by passing asuture through the lesion, allowing accurate incisionalong its margins. When the incision on the outer andinner aspects of the role of tissue is completed, its basecan often be simply lifted and separated using a scalpel.It is undesirable to cut down to deeper tissues, as this cancause excessive scarring on healing thus reducing sulcusdepth. When the base of the wound extends into lip orcheek, superficial 'tack' sutures can be used after carefulundermining of the margins, but in some cases the baseis left open and covered by a surgical pack, or thepreviously trimmed old denture lined over the woundwith gutta percha or a zinc oxide-based periodontal pack.

In the more 'acute' immediate denture hyperplasia,denture adjustments with appropriate soft lining can oftenobviate the need for surgery, because the hyperplasia is

often oedematous and elimination of further traumaproduces a dramatic resolution.

In both cases, provision of new dentures is the ulti-mate aim.

Palatal hyperplasia

Aetiology and clinical appearance

This reactive condition results from movement and lossof even contact of the upper denture base on the palatalepithelium and underlying connective tissues. Theclinical appearance can vary between a multitude ofsmall papillary projections, to an appearance of cobble-stones, to areas of surface hyperplasia with slit-like cleftsbetween the 'blocks' of hyperplastic mucosa. This latterform is more commonly seen under partial dentures. Thisclinical appearance represents a hyperplastic type ofdenture stomatitis (Newton's classification Type III) andis infected with Candida. The tissues may be significantlyred and inflamed.

Management

Treatment of the candidal infection involves:

• leaving the denture out during sleep• thorough scrubbing of the fitting surface of the

denture• leaving the denture in Milton's solution (sodium

hypochloride) or, in the case of metal-based dentures,in chlorhexidine solution overnight

• brushing the palatal soft tissue with a toothbrushnight and morning

• the use of systemic antifungals, such as fluconazole.

The dentures should be lined with tissue conditioner fordaytime use.

Total resolution by such means is unusual andremoval of the hyperplastic tissue either with diathermyloop or laser may be needed. The resultant raw surfacecreated by surgery is best covered with the denture linedwith a zinc oxide-based periodontal pack.

Leaf fibroma

Aetiology and clinical appearance

This lesion is not, as its name implies, a true neoplasmbut is again the result of chronic frictional irritation of thepalatal soft tissues by movement or irregularity of the

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palatal coverage of an upper denture. Were it not coveredby the denture, it would grow evenly as a roundedexophytic non-ulcerated swelling but, because of itsposition, it is flattened into a leaf shape by the denture. Itis a perdunculated lesion, which means that it has a stalk-like attachment, and on occasion can be of considerablesize, having lain unseen in the vault of the hard palate(Fig. 30.2). Gentle probing can often cause it to lose itsadhesion to the true vault and it then hangs from itsnarrow attachment and is very obvious.

Management

Excision biopsy under local anaesthesia is very simple.Bleeding can be a problem from its feeder arteriole,which may need to be cauterised.

Fibrous tuberosities

Aetiology and clinical appearance

These excess masses of fibrous gingival enlargement ofthe upper molar regions are usually bilateral, althoughoften asymmetrical. They may be so bulky that theycontact the lower alveolar process in edentulous patientsand hence prevent provision of adequate dentures.Grossly enlarged tuberosities may be due to bonyovergrowth rather than fibrous tissue and it is importantto ensure by clinical examination and radiographs whichtissue is present in excessive quantity. Fibrous over-growth may often be moveable on palpation, unlike bonyovergrowth, but if doubt exists as to the extent of the softtissue component, a sharp probe can be used for assess-ment after appropriate local anaesthesia has been given.

Management

Surgical reduction can be undertaken in which a wedgeof soft tissue is excised through an elliptical surfaceincision (Fig. 30.3).

After removal of this wedge of tissue, the marginsrequire to be undermined by further cuts and 'filleting' oneither side of the original excision to allow the edges tobe approximated and sutured without undue tension.

'Flabby' ridges

Aetiology and clinical appearance

Flabby ridges are the result of fibrous replacement of thebony ridge. This is most commonly seen in the upper

Fig. 30.2 Leaf fibroma: (a) lying against hard palate;(b) demonstrating pedunculated attachment.

anterior segment where a full upper denture is opposedby natural lower teeth but with free end saddles notcompensated with a partial lower denture. The resultanttipping action induced by the protrusive chewing actionresults in bony resorption and fibrous replacement of theridge. The ridge becomes excessively mobile reflectingthe lack of underlying hard tissue.

Management

Surgery is seldom indicated, as most prosthodontistswould prefer more rather than less of this tissue giventhat the bone is by then lost. In the grossest situation it

Fig. 30.3 The treatment of fibrous tuberosities: (a) wedge excision removing an ellipse of fibrous tissue; (b) cross-sectionshowing undermining of the wedge to allow suturing without tension from 'A' to 'B'.

can be 'tightened' by a wedge excision similar to thefibrous tuberosity reduction.

Bone surgeryAlveolectomy or alveolotomy

Aetiology and clinical appearance

The indications for these procedures are rare but may beof value where excessive anterior projection of the ridgein the upper premaxillary area might pose problems forfuture denture aesthetics or stability. Class II, division Imaloclusions are therefore most likely to benefit fromsuch surgery.

Management

Alveolectomy involves reduction in both the height andwidth of the ridge and is mainly accomplished byreduction of the labial plate. The mucoperiosteum is bestraised with a 'U'-shaped incision to allow access. Bonerongeurs or larger 'acrylic' burs can be used to reduce thelabial plate prominence and, on occasion, also the inter-dental septae. The bony margin is then smoothed with afile and the wound closed with sutures.

Transeptal or interseptal alveolotomy reduces thelabial prominence but maintains the height of the ridge.Following extraction of the incisors and canines, theinterdental septum is removed between each socket andthe labial plate is then fractured inwards with firm digitalpressure. A vertical cut may be needed over the canine

prominence labially to facilitate this fracture. The labialplate will still be attached to its overlying periosteum andshould therefore remain viable.

These operations may be facilitated by cooperationwith the prosthodontist, who can provide the surgeonwith a template of acrylic that is made on the casttrimmed to the desired contour. Unless the patient desiresan aesthetic change, these procedures are becoming lessfrequent.

Bony exostoses and bone undercuts

Aetiology and clinical appearance

Surgery is indicated where the bony morphology, eitherthrough localised excessive growth or as a result ofunusual resorption of the ridge, gives rise to impedimentsto denture construction.

Management

A simple mucoperiostial flap is taken, the bone impedi-ment is reduced with rongeurs or burs, and the flap isclosed with sutures.

Sharp bony ridges

Aetiology and clinical appearance

These are usually found in the lower anterior regionwhere resorption of bone has produced a pointed, oftenrazor-sharp, bony ridge, described as a knife-edge orfeather-edge ridge.

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Management

The incision to gain surgical access is often best made onthe buccal aspect of the crest of what is often a very thinline of attached gingiva forming the soft tissue crest ofridge. This allows the underlying bone to be smoothedbut prevents undue disruption to the stability of the over-lying soft tissues when the wound is closed.

Torus palatinus

Aetiology and clinical appearance

This presents with a midline bony swelling (Fig. 30.4)which is normally symmetrical and, unless traumatised,symptom free. The overgrowth is composed of normalbone but its presence may make palatal coverage with adenture impossible or, if a denture is made over, it cancause fracture of the denture. In some dentate patients,repeated trauma caused by the swallowing action on itsposterior aspect may result in ulceration of the overlyingsoft tissues and this would merit surgical reduction.

Management

A preoperative impression allows construction of apalatal splint in dentate patients or the existing denture, ifavailable, can be used as a postoperative covering. Anincision is made anteroposteriorly along the midline ofthe torus and relieving 'Y'-shaped incisions are made atthe anterior and posterior extensions (Fig. 30.5). Theoverlying mucoperiosteum should be reflected with careas it is often very thin. The bony mass is then divided

with one anteroposterior fissure bur cut and crossed byseveral lateral cuts. This conveniently divides the massinto smaller blocks, which can be chiselled free. A finalsmoothing with a round 'acrylic' bur precedes woundclosure. Some soft tissue reduction of the margins maybe needed, as there will be excess soft tissue. Suturingmay be difficult and the prior construction of a plate tocover and hold the flap is very helpful, as this will reducethe chance of a painful palatal haematoma and will helpthe patient to eat in the first few days after the operation.Large palatal tori are better removed under generalanaesthesia or at least under local anaesthesia withsedation.

Torus mandibularis

Aetiology and clinical appearance

Mandibular tori present on the lingual aspect of thealveolar process in the premolar region (Fig. 30.6). Oftenbilateral, they may or may not be symmetrical and theexcess bone may be a single dome-shaped mass or several

Fig. 30.5 Incision to allow surgical trimming of a palataltorus.

Fig. 30.4 A torus palatinus. Fig. 30.6 Bilateral torus mandibularis.248

protuberances. Surgical reduction is only indicated ifthey impede denture design.

Management

In the edentulous patient, a straight incision over the crestof the ridge with no relieving incision is needed. Thisallows the raising of the mucoperiosteum from the torus.The excess bone can then be trimmed using a com-bination of a narrow fissure bur with a chisel or simplywith a flame-shaped acrylic smoothing bur. Flap retractionshould be combined with protection of floor of mouthand underlying soft tissue. The flap is then sutured backwith no need for trimming.

In dentate patients, the procedure is essentially thesame but surgical access caused by the presence of teethin the area can make for difficult surgical access.

Sharp mylohyoid ridge

Aetiology and clinical appearance

With continued alveolar resorption in the lower molarregion, most of the alveolar process may eventually belost, with the denture base then being constructed overmore basal bone. On the lingual aspect of the molarregion, the mylohyoid ridge of bone can be covered bythe lingual flange of a denture, which may cause dis-comfort and even overlying soft tissue ulceration due toits sharp upper surface.

Management

If the denture cannot be relieved adequately to reducepressure on the ridge it may be surgically reduced.

A straight-line incision over the crest of the ridge,extending back into the retromolar pad from the premolarregion, allows a lingual flap to be raised to expose thesharp upper aspect of the ridge. Often, minimal smooth-ing using a bur, or even a hand file, without stripping themuscle off the affected area is successful and can bejudged by running a finger over the ridge. If musclestripping is thought necessary, this will undoubtedly

increase postoperative swelling and haematoma formationis more likely. Patients require to be warned pre-operatively of this possibility.

Genial tubercles

Aetiology and clinical appearance

Gross alveolar resorption following extractions can causethe upper tubercles to be traumatised by the lingual flangeof a lower denture in the midline. Recurrent ulceration,hyperplastic tissue formation or simply discomfort maybe the stimulus to surgery.

Management

An incision along the midline of the crest of the alveolarridge allows a lingual flap to be raised to expose the bonytubercle. Simple smoothing with a bur is normallysufficient, and stripping of the genioglossus should beunnecessary because it is important to maintain thefunction of this muscle.

Ridge augmentation and vestibuloplasty

These minor surgical procedures can be of great benefitto the patient. It will be apparent that many problemsarise as a result of alveolar resorption and surgeons havein the past devised many surgical procedures to makegood this loss of ridge, either by augmenting the ridge orby deepening the sulcus (vestibuloplasty). Augmentationusing bone, hydroxyapatite or allelograft materialoften failed due to infection or the inability of the softtissues to accommodate the increased ridge bulk.Vestibuloplasties were probably more successful in thatthey increased sulcus depth rather than trying to increasethe resorbed bony ridge. In recent years, however, suchoperations have largely been superseded by the use ofdental implants. The success rate with implants is highand involves relatively minor surgical operative pro-cedures. This rapidly growing field will be discussed inChapter 37.

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Orthodontics and oral surgery

IntroductionWhen jaw relationships such as severe skeletal baseabnormalities result in a malocclusion that is beyond thescope of orthodontic treatment, orthognathic surgery ordistraction osteogenesis should be considered to effectcorrection. These are described in Chapter 13.

Dentoalveolar surgery may be required, often inconjunction with orthodontic treatment, to deal withspecific localised problems of eruption or crowding.Where several options exist, the risks of surgery, andperhaps general anaesthesia, must be weighed against thebenefits of a successful outcome. It is for the surgeon andorthodontist together to explain the options and advisewhen a surgical approach is in the best interest of thepatient.

The most common orthodontic problems with surgicaltreatment options are crowding, failed eruption, spacingand ankylosis. The orthodontist may have several treat-ment options so it is important for the surgeon to have agood appreciation of the orthodontic problem. A goodhistory is essential. Clinical and radiographic examinationreveal the nature of the malocclusion or orthodonticproblem and the state of oral and dental health. Discussionof the surgical aspects with the patient and parents revealstheir attitude to treatment, and helps to finalise the 'treat-ment plan.

Some causes of the orthodontic problems alluded toabove are listed in Table 31.1.

Treatment optionsA number of surgical treatments exist for orthodonticproblems and these should be considered as part of thetreatment-planning exercise. These include extractions,surgical removal of teeth, surgical exposure of teeth,fraenectomy and tooth transplantation.

Table 31.1 Causes of orthodontic problems

Crowding and impactionteeth relatively large for arch sizeearly loss of deciduous teeth allowing mesial driftsupernumerary and supplemental teethodontomes

Failed eruptioncrowding or early loss of deciduous teethretained deciduous teethcongenital absencesupernumerary teeth/odontomesfibrous tissue (scar) due to previous trauma, surgery

or infectionectopic development or dilaceration due to traumacysts and other pathologycleft palatecleidocranial dysostosisDown syndrome or hypothyroidismgingival hyperplasia or fibromatosis

Spacingtooth size/arch size disproportionsmall teethprominent fleshy frenumproclined incisorspartial anodontia

Ankylosistraumainfection

Non-surgical extractions

Extractions are the most common requirement for reliefof crowding. There may be an indication for generalanaesthesia in very young or nervous children, and thosewith learning difficulties. Local anaesthesia, with orwithout sedation, should be used wherever possible,bearing in mind that in most cases orthodontic treatmentis elective. In some cases, it is better to delay treatmentuntil the patient is more cooperative. On the other hand,

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correct timing of extractions can be a significantadvantage, often removing the need for later orthodonticappliance treatment. For example, timely removal ofcarious or heavily restored or hypoplastic first permanentmolars may not only relieve crowding but also removesteeth of doubtful long-term prognosis.

Surgical removal of teeth

Surgical removal may be indicated when a tooth isunerupted. There is no need to remove a buried toothunless there is a positive indication such as interferencewith the orthodontic movement of other teeth, or asso-ciated pathology such as cyst formation, or resorption ofan adjacent tooth.

Surgical exposure of teeth

Surgical exposure is used to encourage eruption or toallow access for orthodontic traction. It involves removalof overlying soft tissue, bone and scar tissue. It isimportant to use a technique that will result in goodgingival contour and minimise postoperative scarring.Adequate exposure is important otherwise the tissueswill cover the tooth again. Orthodontic traction using agold chain bonded to the exposed tooth can also be used.

Fraenectomy

Fraenectomy may be requested when there is adiastema or a localised periodontal problem. Upper labialfraenectomy or lingual fraenectomy are the most commonof these procedures. A prominent fraenal attachment cancause a diastema, which is most common where there isa thick, fibrous, upper labial fraenum. When this is present,blanching of the palatal gingiva when the lip is pulled upto create tension confirms the need for fraenectomy, asdoes the presence of 'V notching interincisally on amaxillary anterior occlusal radiograph. A radiographshould always be taken to exclude a midline super-numerary tooth or any other pathology. A tight lingualfraenum can pull on the gingival margin and cause apocket or contour defect together with tongue restriction.

Tooth transplantation

Tooth transplantation can be considered when ortho-dontic movement cannot achieve the desired result, or

sometimes to expedite the outcome in impacted caninecases. There are, however, inherent problems in the trans-plantation of teeth.

A transplanted tooth must not be left in traumaticocclusion or it will quickly fail. Unfortunately, trans-plants have a high failure rate. After a promising startmany develop internal and external resorption after about4 years. This often progresses to abscess formationdespite root canal therapy. Root treatment soon aftertransplantation is advocated by some but the failure rateis still high. Alveolar bone is removed when the socket iscreated and abscess formation can cause further damage.The resulting depression in the alveolus causes a cosmeticproblem with a subsequent denture or bridge, and leavesinsufficient bone for an osseointegrated implant. For theabove reasons, transplantation is now rarely the bestoption. It is often better to temporise and consider anadhesive bridge or implant later. Autotransplanation,where a tooth is extracted from one site, such as a lowerpremolar, and inserted into the upper central region aftertraumatic loss, has a good success rate, however, andshould be considered.

Surgical management ofspecific orthodonticproblemsThe aforementioned treatment options can be appliedto several teeth with orthodontic problems related tocrowding and impaction. The problems of spacing andankylosis will also be discussed followed by a consider-ation of the individual surgical procedures.

Incisors

Maxillary central incisors may be impacted. There maybe lack of space but trauma is the most common factor.Young children often fall onto their deciduous incisors,causing displacement or damage to the permanent toothgerms. The tooth may subsequently develop in an ectopicposition and the crown or root may be deformed. Also,trauma to the alveolar mucosa or bone may result in scartissue, which later prevents eruption. Supernumerary teethand odontomes are another common obstacle to eruption.Scar tissue formed following their surgical removal mayalso result in eruption problems. Further space can belost by drifting of adjacent teeth if eruption is delayed.

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Occasionally there are systemic factors such ascleidocranial dysostosis, Down syndrome or chemo-therapy to cause a delay in eruption. Also, gingival over-growth due to hereditary fibromatosis, or secondary todrugs such as phenytoin or cyclosporin may inhibiteruption.

Scar tissue or a supernumerary tooth frequently holdsthe incisor in a fairly normal pre-eruptive position, butfollowing intrusion trauma it is more often displacedupwards and forwards and lies horizontally under theanterior nasal spine. Very occasionally there is a palatalinclination. It is important to realise that a tooth will onlyerupt through attached mucosa. If gingival mucosa hasbeen lost through previous trauma or the tooth isattempting to erupt under the unattached sulcus mucosa,surgical exposure will be required.

The choice of treatment depends on the position of thetooth, the space available and patient cooperation. If thepatient is unlikely to accept appliance therapy, or if oralhygiene is poor, it may be better to accept the space andconstruct a partial denture. Alternatively, the space couldbe allowed to close as far as possible and the defectdisguised by building up, by restorative means, adjacentteeth. The tooth can be left in situ unless there is anyassociated pathology, but surgical removal is oftenindicated.

Ideally, the incisor should be aligned unless radio-graphs suggest that the tooth is hypoplastic, markedlydilacerated or in an unfavourable position. Surgicalexposure is performed to encourage eruption and createorthodontic access. This would normally be by a labialflap, either apically repositioned, or replaced after attach-ment of a gold chain.

Removal of supernumerary teeth normally requires apalatal flap as they are almost always palatally situatedrelative to the permanent incisors.

Canines

Impacted maxillary canines have a prevalence of about1.7% in Caucasians. Ideally, they should be detectedbefore the teenage years, as timely interception can reducethe severity of the problem. Canines can be palpated inthe labial sulcus at around 10 years of age. Eruption isexpected at about 12 years of age in girls and 13 yearsof age in boys. Any deviation from this normal patternwarrants investigation. Extraction of the deciduous caninecan encourage the successor to resume a normal path oferuption in more than 60% of cases depending on several

factors such as canine height, inclination, mesiodistalposition and crowding.

Unfortunately, resorption of the roots of adjacentpermanent incisors can occur and it is claimed that theincidence may be as high as 12% for incisors adjacent toectopic canines. It would not be practical or defendableto remove every buried canine for this reason and the bestadvice is to be vigilant. Root resorption, if it is going tohappen, generally occurs at 10 or 11 years of age and itis rare for this complication to occur after 14 years ofage, unless there is a general delay in dental development.

The management of the unerupted upper canine canbe in one of four ways.

No surgery

The most common option is to leave the buried caninealone. The first premolar can be disguised by reducingthe palatal cusp or by its orthodontic alignment providedthis is not obstructed by the unerupted canine. Thedeciduous canine may be kept and often lasts for manyyears where alignment of the permanent tooth is notfeasible. Later, an adhesive bridge or implant can beconsidered, although overeruption of an opposing toothcan cause difficulty.

Surgical exposure

Surgical exposure may be requested where space isreadily available or where it is decided this will providethe optimum aesthetic result. The position of the toothmust be ascertained by clinical examination and radio-graphy. The tooth may be palpable on the buccal orpalatal aspect and the position and inclination of adjacentteeth often gives guidance. For example, the lateralincisor may show undue prominence of its root outlineon the labial aspect and be almost retroclined due to thepalatal presence of the canine crown exerting pressure onit. A panoramic film is most useful but other radiographssuch as periapical or occlusal views may be required forlocalisation. It can be difficult to know whether the canineis inclined buccally, palatally or lies in the line of thearch. Parallax methods may help localisation but clinicalassessment is often more reliable. Approximately three-quarters of impacted canines lie with crowns palatal tothe arch line.

The principle of parallax is that the image of twoparallel objects will alter with differing angulations ofradiographic views. If, on comparing the image of the

unerupted canine relative to the lateral incisor on apanoral film with its position on an oblique occlusal film,the canine appears to move upwards, then it is palatal tothe lateral incisor. Put more simply, if the buried toothmoves with the position of the tube (i.e. the source of theX-rays), then it is palatal. The depth and inclination arerelevant not only to the difficulty of surgery but also tothe prospect of successful orthodontic alignment inreasonable time. Availability of space and overeruption ofopposing teeth must also be considered.

Surgical removal

Surgical removal is required when the buried canine isnot suitable for alignment and there is an indication, suchas interference with proposed orthodontic treatment, orassociated pathology, such as dentigerous cyst formationor resorption of the roots of the incisors. Often, a first orsecond premolar would need to be extracted to makespace for alignment of the canine and the patient mayprefer to avoid more prolonged appliance therapy byaccepting space closure. As with exposure, the positionof the tooth must be assessed by clinical and radiographicexamination. Difficulties such as dilaceration of the rootand proximity of adjacent teeth must be assessed.

Reimplantation

Reimplantation of canines is another option. If space isavailable or can be created and the impacted canine canbe removed intact and with minimal trauma, it may bereimplanted into a surgically prepared socket. Thetransplanted tooth may need to be stabilised with acemented splint or an orthodontic bracket. This techniqueis usually successful in the short term, although it is oftendifficult to place the canine in the optimum positionunless additional space to that previously occupied by thedeciduous canine is obtained preoperatively by ortho-dontic means. Commonly, the lower canine has over-erupted and this can also lead to difficulty in positioningfree of occlusal contact. As described previously, thefailure rate is high and transplantation is seldom thepreferred option.

Premolars

In the maxilla the second premolar is occasionallyexcluded from the arch due to crowding. It is usuallyfound in the palate, where it may remain harmlessly or

eventually erupt. The tooth can be left unless it interfereswith orthodontic treatment or if it erupts and becomesa threat to periodontal health by encouraging foodtrapping.

In the mandible, premolars may be impacted due tocrowding and can be buccal, lingual or in the line of thearch. The second premolar is usually lingually inclined,in which case it can be left in situ or removed if there isa good indication. Surgery on the lingual aspect of themandible can be awkward because of difficulty of accessand of reflection of the delicate lingual mucosa. Generally,therefore, a lingually inclined premolar is removed via abuccal approach.

If lower first permanent molars have been lost early,the adjacent premolars have a tendency to drift backwardsand may even become horizontally impacted against theroot of the second molar. Surgical exposure and ortho-dontic alignment may be appropriate in a well-motivatedpatient.

First and second permanent molars

If one or more carious first permanent molars requireextraction it is often beneficial to carry out balancingextractions. Ideally this should be done in childrenaround the age of nine years.

Removal of second permanent molars at anappropriate time during development is still accepted asa method of encouraging wisdom teeth to erupt into afunctional position but this is not always successfulespecially where there is severe crowding. Removal ofsecond molars in late adolescence to allow eruption ofwisdom teeth is not wise, as the eruption of third molarsis unreliable and these teeth may be of poor quality.

Third molars

Imbrication of lower incisors often occurs around20 years of age but prophylactic removal of third molarsis no longer regarded as effective in preventing loweranterior crowding. There are only rare occasions whenwisdom teeth should be removed for orthodontic reasons.Possible indications are proposed distal movement ofsecond molars or orthognathic surgery involving themandibular ramus.

Guidelines advise that the risks of damage to inferioralveolar or lingual nerve, as well as the trauma ofsurgery, should be undertaken only when there are validindications. In our present state of knowledge it is not

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possible to predict the behaviour of lower third molars. Ifit were possible to predict which ones would needremoval, this could be done much more easily during theteenage years, before their roots are fully formed anddifficult impactions have developed.

Removal of lower third molar tooth germs at around12 years of age, before calcification of enamel and dentine,used to be fairly common practice. This procedure, knownas lateral trepanation, was fairly simple but a generalanaesthetic was required. There is no evidence that thisoperation was worthwhile. Extraction of third molars isconsidered further in Chapter 27.

Spacing

Spacing is normal in the deciduous dentition and as thejaws increase in size to accommodate the permanentteeth. Spacing of permanent teeth may be due to smallteeth or partial anodontia. There are usually restorativetreatment options but implants may also be indicated.

Ankylosis and submerged deciduous teeth

Although most commonly seen in the upper incisors,ankylosis of other teeth also occurs. The causes aretrauma and infection.

Upper incisors are frequently traumatised andankylosis is especially common after reimplantation. Anankylosed tooth does not move as jaw growth progresses,so that, if reimplantation occurred at an early age, thereimplanted tooth is significantly palatally and apicallydisplaced by adulthood. The tooth can function normallyfor many years, but frequently internal and externalresorption results in abscess formation or complete lossof the root. An implant should be considered if no simplerestorative option is available.

Submerged deciduous molars are also a result ofankylosis. Some children have submerged teeth in severalareas, the cause of which is often unknown. It has beensuggested that there is a lack of growth potential in theseareas. The ankylosed tooth remains static while alveolarbone growth continues, so that it may become completelyburied. The adjacent permanent teeth erupt and oftenthe submerged tooth becomes impacted between them.The submerging tooth is prone to caries and eruption ofthe permanent successor is prevented. Removal becomesmore difficult as they become more deeply embedded soit is better to extract them early.

Failure of a permanent molar to erupt may be due toankylosis. The cause is again unknown but trauma to the

Table 31.2 Orthodontic surgical procedures

Upper labial fraenectomyRemoval of supernumerary teethExposure of incisorsExposure of palatal caninesExposure of buccal caninesRemoval of impacted premolars

area by a mouth gag during dental extraction or othersurgical procedures under general anaesthesia is apossibility, as is primary failure of eruption. Surgicalexposure is sometimes successful if there is soft tissueobstruction or a small odontome preventing eruption, butresults are poor if there is true ankylosis or long delayafter normal eruption time. These teeth are often partiallyerupted and develop caries and surgical removal is thenindicated. Cyst formation can also occur.

Several of the surgical procedures discussed above aredescribed in other chapters. Some, however, are specifi-cally used only as an adjunct to orthodontic treatment(Table 31.2) and these are described below.

Surgical proceduresUpper labial fraenectomy

When the lip is pulled upwards, a fibrous band betweenthe inner surface of the upper lip and the crest of themaxillary alveolar ridge can be palpated just underneaththe mucosa. An incision is made around the fibrous bandand the fraenal attachment on the ridge. The incision issuperficial on the lip and fraenum but extends down tobone between the central incisors. The fraenum isgrasped with forceps and detached by sharp dissectionfrom the lip. The fibres entering the bone are detachedwith a small excavator or curette. Some operators millthe crestal bone surface with a bur.

When the fraenum has been removed, further dis-section is required to recontour the sulcus. A Z-plasty canbe performed but this can cause excessive swelling. It issimpler and kinder to hitch the midline of the incision tothe periosteum overlying the anterior nasal spine with aresorbable suture. The fatty tissue on the anterior aspectof the alveolus is mobilised by inserting scissors super-ficial to the periosteum and opening the blades. Thisallows the bulky tissue to be displaced laterally so that agood sulcus depth can be achieved when the suture is

placed. The incision is then closed with interrupted sutures.A Whitehead's varnish pack may be placed between theincisors and this will also cover the adjacent small defectin the alveolar mucosa, but this is often unnecessary.

Removal of supernumerary teeth

Supernumerary teeth may occur anywhere in themaxillary or mandibular alveolus but it is most commonto find one or two in the midline of the anterior maxilla.They are almost always on the palatal aspect. A parallaxview should confirm the position, but occasionally alateral radiograph of the anterior maxilla is helpful.

It is better to wait until there is some root formationin the permanent centrals before surgery than to riskdamage to the tooth germ. Bear in mind that many super-numeraries erupt and a surgical approach is then avoided.There is no need to remove those that have no associatedpathology and are not in the way of orthodontic toothmovement.

The normal surgical approach is by a palatal flapusing a gingival margin incision. The incisive vessels andnerve can usually be preserved. Larger supernumerariesare usually easy to find due to altered bone contour.Small ones can be very difficult to find, especially if thefollicle is small or the enamel is hypoplastic. It is a mis-take to look too high because the root of an invertedsupernumerary is often found between the roots of thecentrals, near the amelocemental junction. Bone over-lying the buried tooth is removed with a chisel or bur,creating a window large enough for its elevation.

If there is an associated buried incisor, a decisionshould be made on whether surgical exposure isindicated. It may well be opportune to avoid a furtheranaesthetic but many orthodontists prefer to wait foreruption, as the gingival contour may be uneven follow-ing surgical exposure. Healing after removal of a largesupernumerary often produces a barrier of scar tissue,however, and patients may require surgery if the incisorfails to erupt.

Exposure of incisors

Upper permanent centrals are usually on the labial aspectof the alveolus. The object of surgery is to leave a portionof the crown exposed to allow natural eruption or ortho-dontic traction. Alternatively, if the tooth is high andsimple exposure is not possible, an attachment such as agold chain can be cemented via a surgical approach.

A labial flap with parallel sides is taken. Thehorizontal arm of the incision must include attachedmucosa, as this will be used to form the gingival marginwhen the flap is repositioned. The flap is carefullydissected away from any bulky follicle or scar tissue.Soft tissue and bone are removed from around the crown.It is sometimes necessary to excise a wedge of palatalmucosa and follicle to ensure that the incisal edgeremains exposed. The flap is then repositioned apicallyand sutured in position. It is important to place the flaphigh enough to ensure that the tissues do not heal overthe tooth. In this situation, the flap can be inverted so thatthe attached mucosal edge of the flap is brought close tothe amelocemental junction of the incisor. A resorbablemattress suture placed high in the vertical incision willusually stabilise the flap. The flap will have less tendencyto slide back over the crown if this suture enters and exitson the mucosal surface, as this helps to invert the margin.

When the above technique is not feasible a gold chainmay be attached. There are alternatives, such as bracketsor wire loops, but these are less effective. Gold chain isused only because stainless steel chain is not readilyavailable. A small circle of stainless steel mesh is weldedto one end of the chain to facilitate bonding to the enamel.Corrosion between gold and stainless steel can result indetachment of the chain and so it is better to add a ligatureof fine wire around the weld.

Attachment of the chain is easy if the enamel surfaceis isolated. A section of a surgical rubber glove makes aconvenient sterile 'rubber dam'. The enamel is etched inthe normal way and the surface is irrigated with sterilewater and dried using the surgical suction. The mesh isattached to the tooth using a light-cured orthodonticbonding agent. After testing the bond with a gentle tug,the flap is replaced with the chain emerging in the pro-posed path of eruption (usually at the crest of the ridge).

With normal healing, orthodontic traction can beginafter a couple of weeks. If there is a long delay, scartissue forms around the chain and makes alignment moredifficult. Patients should be warned that traction mighttake many months.

Exposure of palatal canines

The hard palate is covered by keratinised mucoperiosteumso that it is not necessary to preserve and reposition a flapto achieve a gingival margin.

If the surgeon is confident that the crown of theunerupted tooth lies palatally, an ellipse of overlying

mucoperiosteum can be excised. The amount of furthertissue to be excised becomes clear as the operationproceeds. Alternatively, a palatal gingival margin flap israised and an ellipse of tissue is excised after the toothhas been uncovered. Overlying bone is removed with abur or hand chisel, taking care not to uncover rootdentine or damage adjacent teeth. The amount of softtissue and bone removal should be sufficient to preventmucosa reforming over the canine. The crown of thetooth should be visible within a saucerised cavity.

There may be brisk haemorrhage from the palatalaspect. Digital pressure or artery forceps will control thisduring the procedure. A suture should be placed aroundany identified vessel if bleeding persists at the end. AWhitehead's varnish pack is held in place using non-resorbable sutures. The pack is left in situ for 1-2 weeks,depending on the extent of the surgery. The orthodontistoften waits for some eruption before commencingappliance therapy.

An alternative method is to attach a gold chain oncethe tooth is uncovered and replace the palatal flapwithout excising the overlying mucoperiosteum. This istechnically more challenging due to difficult access andhaemorrhage, which makes creating a dry field for attach-ment of the chain more problematic.

Exposure of buccal canines

It is sometimes difficult to get a good result, particularlyif the tooth is high in the buccal sulcus. Ideally, an

apically repositioned flap should be carried out, as forburied incisors. Unfortunately, the only attached mucosamay be the gingival margin of the lateral incisor, but thiscannot be used as it would leave an unsightly defect. Ifthere is a gap, however, sufficient mucosa may be avail-able on the ridge.

Overlying mucosa in the sulcus may be excised and apack inserted, but often the tissues close over or the toothis tethered by unsightly scar tissue. A better option is totake a normal flap and attach a gold chain as describedabove or simply to close the flap over the surgicallyexposed crown.

Removal of impacted second premolars

The impacted maxillary premolar is normally palatallyplaced and may be removed by raising a palatalmucoperiosteal gingival margin flap. Elevation is thenoften sufficient to remove the tooth but occasionally bonemay need to be removed to gain adequate elevation.

Impacted lower premolars are usually linguallyinclined and, if sufficiently erupted, can be removed bygentle elevation and forceps. Fine beaked upper forcepsare often ideal for this purpose. If a surgical approach isneeded, a buccal flap is raised and bone removed toexpose the crown buccally and several millimetres of theroot. The crown can then be sectioned and deliveredlingually and the root subsequently elevated into thespace vacated by the crown.

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Tissue sampling and softtissue lesions

IntroductionA biopsy is defined as a procedure whereby tissues aresampled from a patient for the purpose of histopatho-logical, microbiological, or other laboratory analysis.Results from such investigations may confirm a pro-visional diagnosis or establish one. They may also helpin the determination of a prognosis, which in turn isdefined as a likely outcome of the disease encounteredand is based on previous knowledge.

The word biopsy may have unwanted connotationsfor many patients, who regard this procedure as a testfor malignant disease, and it may be better avoided orexplained more fully. Any abnormal tissue removed fromthe mouth should undergo routine analysis, with thepossible exception of caries or periodontally infectedteeth, where selection of particular cases may at timesalso be worthwhile. If a surgeon considers that removalof soft tissue is indicated even though the nature of thepathological process is certain, this is best confirmed withappropriate histological examination. Various methodsmay be used to sample tissue and some representativeexamples will be discussed (Table 32.1). This will befollowed by consideration of individual soft tissuelesions.

Table 32.1 Tissue sampling techniques

Aspiration techniquesbloodpuscystsradiolucenciesfine-needle aspiration

Surgical biopsyexcisionincisionpunchfrozen sections

Tissue samplingAspiration techniques

Aspiration of blood, cavity fluids and solid tissue can allprovide diagnostic information, as discussed below.

Blood

A venous blood sample can yield a vast amount ofinformation on disease processes relevant to oral surgicalpractice. Most common is the full blood count, whichindicates total numbers of red cells, white cells andplatelets. The differential count of white cells will indicatethe numbers of neutrophils, lymphocytes and eosinophilswithin the white-cell population. The haemoglobin levelis also included in this analysis.

Blood serum can also be examined to determine bio-chemical parameters such as electrolytes, proteins andenzyme levels, which may alter significantly in disease.Within the globulin fraction of the serum, antibody levelsmay be determined, which may reflect a patient's previousexposure to viral or bacterial infection. Glucose levels,if raised, may raise suspicion of diabetes mellitus andindicate further investigation.

Aspiration from pathological lesions

The most common example of this is the aspiration of anabscess presenting either in the soft tissues of the sub-mandibular or submental regions, or intraorally in thebuccal sulcus or palate. The advantage of aspirating a pussample is that the technique avoids gross contaminationof the aspirate by other organisms, especially in the mouthwhere there is a commensal population. Additionally,by drawing the pus into the partial vacuum of a sterilesyringe, the viability of the anaerobic bacteria is protectedand they are therefore more likely to grow in the labora-

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32

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tory. Anaerobes are extremely common in dentoalveolarinfections and their survival from any sampling proce-dure is important, allowing a more accurate assessmentof the antibiotic sensitivity of the infection.

Cystic lesions are also often easily aspirated to deter-mine both their fluid nature and contents. Keratocysts,which contain keratin and shed epithelial squames, canbe differentiated from inflammatory or other odontogeniccysts, which contain a proteinaceous fluid. More sophisti-cated assessment of the contents of keratocysts and ofother cysts involves assessment of soluble protein content(the keratocyst has less than the dental cyst) although, inpractice, this is seldom needed (see Ch. 28).

Aspiration of radiolucent areas of the jaw may alsoindicate that a presumed pathological cyst cavity is not,in fact, cystic. If no fluid is present then the aspirationwill yield nothing, which may indicate a need for anincision biopsy of the tissues within the cavity becausethe implication is that the lesion is solid. Occasionally, inthe maxilla, air may be aspirated from a radiolucentimage. This might indicate that the maxillary air sinushas been penetrated and incorrectly diagnosed as a patho-logical cavity. Very occasionally blood may be aspiratedfrom a lesion, which may indicate the presence of anintrabony haemangioma or arteriovenous shunt.

Fine needle aspiration biopsy

This technique, which aspirates cells from solid lesions,can be useful in less accessible swellings or lumps suchas in salivary glands or the neck. Cytology is moredifficult to interpret than an incisional biopsy but it canbe a valuable guide as to the nature of a swelling.

Surgical biopsy

Two types of biopsy can be taken from abnormalities ofthe soft tissues of the mouth: the excision biopsy and theincision biopsy, using either a scalpel or a punch biopsy.

Excision biopsy

This procedure removes all the clinically abnormal tissuethat is evident. It is therefore normally carried out onrelatively small swellings or lumps for which the clinicianwould have normally made a confident provisional diag-nosis. Lesions such as papillomas, fibrous hyperplasticovergrowths and mucocoeles are common examples oflesions normally removed in total by this means.

Incision biopsy

A representative piece of tissue is removed from a lesionwhose total removal would not be practicable as an out-patient procedure, either because of its size or because itsnature is not known and requires to be identifiedhistologically to allow a correct treatment plan to beformulated. Such lesions as widespread erythroplakia orleukoplakia, larger swellings either arising as soft-tissuelumps or within bone are examples of the appropriate-ness of this technique.

Punch biopsy

This may be a useful way of sampling a lump beforedeciding on its definitive treatment. The punch is a hollowtrephine of 3-4 mm in diameter, which can remove asmall 'core' of soft tissue with minimal damage and doesnot normally require suturing.

Sample disposition

Accurate orientation of the sample may be importantwhen sending the specimen to the histopathology labora-tory, especially if the lesion is thought to be neoplastic.Correct disposition into 10% formalin is also needed topreserve the tissues in the best possible condition andundue trauma during the surgery should be avoided forthe same reason. All relevant clinical information shouldbe included on the specimen form for the information ofthe pathologist.

In widespread lesions it may be prudent to take morethan one biopsy sample, especially where there is aclinical variation in the appearance in different areas ofthe abnormal tissue. An example of this would be a whitepatch but within which there are areas of rednessdenoting atrophic epithelium or superficial ulceration.

At one time, it was considered necessary to providean incision biopsy that contained the transitional areabetween clinically normal and abnormal soft tissue. Thisis now considered of less importance than providing anuntraumatised, representative sample of the lesion itself.

Where there are extensive areas of soft tissue abnor-mality and there is therefore a choice of site for incisionbiopsy, certain areas should be avoided. The orifices ofthe parotid and submandibular ducts may cause fibrosisand contraction if surgically traumatised, and this in turnmay lead to obstruction of salivary flow and resultantswelling with or without ascending infection. The tip of

the tongue is very sensitive and should, where possible,be avoided, as should areas close to larger blood vesselsor nerves such as in the region of the mental foramenor the deep lingual veins on the ventral surface of thetongue.

Almost instant histopathological assessment can beachieved by freezing the specimen rapidly rather thanfixing it in formalin. This is known as a frozen sectionand can provide information to the clinician withinminutes. It can be a very appropriate way of ensuring thatmargins of tumour excision are clear during the operationand can therefore be acted on while the patient is stillanaesthetised. However, the clarity of the preparedspecimen may not be as good as the paraffin preparedsections. For this reason, frozen sections are notindicated for routine diagnostic biopsies. Immuno-fluorescence cannot be performed on formalin-fixedtissue and so fresh tissue for frozen sections is requiredfor immunopathology using fluorescent techniques.

Soft tissue lesionsSoft tissue lesions that may present on the buccal mucosaor gingivae are listed in Table 32.2. Oral carcinoma isdiscussed further in Chapter 17 and denture-inducedhyperplasia is considered in Chapter 30. Minor salivarygland swellings are considered in Chapters 14 and 34.

Fibrous epulis

An epulis may be defined as a swelling or lump arisingfrom the gingivae, and the fibrous epulis is the mostcommon type. The lesion is basically a hyperplasticresponse to irritation to the attached gingivae. In somecases, the stimulus or irritant is very obvious, such as anoverhanging restoration or subgingival calculus. Inothers, however, it may be more difficult to detect andonly careful examination may reveal a small develop-mental defect in the enamel or dentine of the tooth at thegingival margin. Clinically, they present as smooth-surfaced, rounded swellings, normally pink in colour andoften pedunculated in attachment (Fig. 32.1). In older,more mature lesions, the surface may show stipplingreflecting the attached gingival origin of the overgrowth.Treatment is by surgical excision, with removal of anyirritant focus found. The base of the wound is oftendressed with a periodontal pack or if larger with a ribbongauze impregnated with Whitehead's varnish. This maybe sutured over the raw surface.

Table 32.2 Oral soft tissue lesions

CarcinomaDenture-induced hyperplasiaFibrous epulisFibrous overgrowthGiant-cell epulisHaemangioma and lymphangiomaLipomaPregnancy epulisPyogenic granulomaSquamous cell papillomaSalivary gland lesions

Fig. 32.1 A fibrous epulis.

Fibrous overgrowth

Fibrous overgrowths or fibroepithelial polyps arerelatively common in the mouth and are usually the resultof trauma or frictional irritation. By contrast, fibromas,which are benign neoplasms, are extremely rare. Theyare most often seen in the cheeks or lips where suchirritation from the dentition can be encountered. Some-times known as polyps, they may be semi-pedunculatedor sessile in their attachment and are similar in colour tothe surrounding normal tissue unless they have beentraumatised frictionally, when they may show a whitenedkeratinised surface. They do not, however, have the cauli-flower hyperkeratotic surface of the papilloma, beingsmooth-surfaced and hence easily distinguished fromthe papilloma (Fig. 32.2). Treatment is simple surgicalexcision. As, histologically, they are simple hyperplasias,there is no requirement to remove a margin of normaltissue nor to extend the excision deeply into the under-

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Fig. 32.2 A fibroepithelial polyp of dorsum of tongue.

Fig. 32.3 A giant cell epulis.

260Fig. 32.4 A haemangioma of cheek.

lying tissues. A suture may be needed to ensure adequatehaemostasis in the larger lesions.

Giant cell epulis

This epulis is sometimes known as a peripheral giant-cellgranuloma and, as its name implies, the tissue consists ofa mass of multinucleated giant cells in a vascular stroma.Many are seen in teenagers or adolescents and areusually found in the anterior regions of the mouth. Theymay represent an overgrowth of osteoclasts derived fromthe resorptive process encountered during the loss of thedeciduous dentition. They can, however, arise in theolder patient. These lesions are typically deep red or evenpurplish in colour and are often quite broadly based,unlike the paler coloured, often pedunculated fibrousepulis (Fig. 32.3). If suspected of being a giant-celllesion, radiographs should be taken to ensure that it isa peripheral and not a centrally, i.e. bony, originatinglesion, which would appear as a radiolucent area (seeCh. 36). If it is a peripheral epulis then surgical excisionwith curettage or cautery to its base is normally curative.The base of the lesion can be covered by a periodontalpack if small, or a Whitehead's varnish packing may beused for larger lesions. If a central giant-cell lesion isevident on the radiograph, it must be distinguished fromthe brown tumour of hyperparathyroidism by appropriateassessment of blood calcium, phosphate and para-thormone levels (see Ch. 36).

Haemangioma and lymphangioma

These lesions, which may appear in any of the softtissues of the mouth, are regarded as hamartomata. Theyare developmental overgrowths of either blood vessels orlymphatic vessels. In some patients they may achieve aconsiderable size, particularly in the tongue. Typically,however, the haemangioma will appear as an exophyticmultilobular swelling, deep blue in colour, and oftenlikened to a small bunch of grapes (Fig. 32.4). Gentlefinger pressure on the surface of the haemangiomaempties the blood-filled vessels leaving the swelling flatand pale in colour. If the malformation is likely to be,or has been, traumatised repeatedly, it may either beremoved surgically or treated by cryotherapy. This lattermethod may be very successful but, as no pathologicalconfirmation of the diagnosis is possible, the clinicianmust be quite sure of the diagnosis before treatment iscarried out in this way (see Ch. 38). Provided they are

symptom free and not subject to direct trauma, some aresimply kept under observation.

Lipoma

This is a benign neoplasm of fat; true intraoral lipomasare quite rare. They may present with a soft swelling,which is often pale or yellow in colour, and they arenormally sessile. These lesions may, on occasion, growinto muscle layers and be quite difficult to dissect outsurgically. The treatment, however, is normally that of

Pregnancy epulis

This lesion is histologically indistinguishable from thepyogenic granuloma, being essentially a vascular over-growth of granulation tissue. It may be related to anobvious focus such as calculus but it may equally arisefrom an extraction socket. Hormonal changes duringpregnancy are believed to enhance the reactive tissueresponse to irritation and although many lesions remainsmall and do not require surgical intervention, some cangrow alarmingly fast and attain considerable size even tothe point of being traumatised by the opposing teeth.These lesions are therefore surgically excised withappropriate curettage or diathermy to their bases. If smallthey tend to resolve following the pregnancy.

Squamous cell papilloma

This is not an uncommon lesion of the oral mucosa andmay arise at virtually any site, but more commonly onpalate, buccal mucosa or lips. It is a benign neoplasm ofepithelial tissue and most squamous cell papillomatapresent as pedunculated (stalked attachment) lesions withcharacteristic white, hyperkeratinised, crenated surfaces,which can be likened to a cauliflower (Fig. 32.6). Theyare normally small, usually less than 0.5 cm in diameter.Treatment is simply excision at the base of the stalk

Fig. 32.5 A pyogenic granuloma.

Pyogenic granuloma

The pyogenic granuloma is a lesion that arises from afailure of normal healing causing an exuberant over-growth of what is essentially granulation tissue. Theymay grow in relation to extraction sockets or fromtraumatic injuries to soft tissues, most often tongue orpalate. They can be regarded as reactive lesions andobvious irritational factors may be evident clinically orfrom the patient's history. Foreign bodies related toextraction sockets, such as fragments of filling materialor indeed of small bony sequestra, may form the stimulus,whereas in soft tissues there is occasionally a historyof self-medication with a variety of remedies that couldbe attributed as causal. Clinically they appear as red orspeckled-red overgrowths of tissue that closely resemblegranulation tissue on visual examination (Fig. 32.5).Treatment is surgical excision with curettage or diathermyto the base of the lesions where appropriate. Fig. 32.6 A squamous cell papilloma of the soft palate.

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attachment. A very similar lesion may be attributed to aviral origin and is sometimes known as a viral wart. Inthese cases it is sometimes possible to see finger warts

that have clearly been responsible for transmitting thevirus to the oral cavity. These can also be treatedeffectively with cryotherapy (see Ch. 38).

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Pyogenic dental infectionand its spread

IntroductionDental disease, both caries and periodontal disease, is aninfective process occurring in a bacterial oral environ-ment. It is therefore not surprising that pyogenic dentalinfections are common. The most common causes of pus-producing infection in the mouth are listed in Table 33.1.

A dental abscess, otherwise known as an apicalabscess or periapical abscess, arises from an infectedpulp, which is most commonly the result of caries butmay also be due to trauma, either physical or chemical.A periodontal abscess arises from a periodontal pocketand may involve the bifurcation or trifurcation of molarteeth. Pericoronitis results from infection involving thefollicle and overlying gingivae (operculum) of a partiallyerupted and usually impacted tooth. This infection wasdiscussed in Chapter 27. Salivary gland infection isusually the result of obstruction to a major salivary gland,most commonly the submandibular gland. The infectionis said to be 'ascending' from the oral cavity along theduct. Management was discussed in Chapter 14.

Dental abscessThe dental abscess accounts for the majority of pyogenicinfections in the mouth. Acute infection may arise directlyfrom spread of acute pulpal infection or it may representre-ignition of an existing chronic abscess or granuloma

by more virulent bacterial contamination or through alowering of the patient's natural resistance as, forexample, after influenza. Dental abscesses are normallypolymicrobial. This means that there are severalorganisms present and anaerobic bacteria predominate.

Clinical features

Pain

The dominant symptom is pain, which can be describedvariously as throbbing, unremitting or unresponsive tosimple over-the-counter analgesics. Unlike pulpal-derivedpain, thermal irritation tends not to be a feature. Severityis usually sufficient to cause sleep loss. In function, thepain is made worse as the abscess will be under consider-able pressure because of the acute inflammatory reaction.Interestingly, the pain may be slightly reduced by gentleocclusal pressure from the opposing tooth and this maybe due to pressure increasing to the point that nerveendings become non-functional. When the abscess hasachieved sufficient size, it breaks out of the bone into thesoft tissues and at this point the pain reduces dramaticallyas the pressure eases.

As the soft tissue reacts to the infection, acute inflam-mation within these tissues will eventually again causepain as swelling in the soft tissues increases and pressureeven in the more lax soft tissue spaces rises. This maytake up to 2-3 days to occur.

Table 33.1 Common pus-producing oralInfections

Dental abscessPeriodontal abscessPericoronitisSalivary gland infection

Swelling

Early abscesses are confined within the unyieldingalveolar bone and at this stage no swelling is evident. Itis only when the abscess bursts through alveolar bonethat swelling may become apparent, together withredness and surface tenderness. The site of the swellingvaries and may be intraoral and/or extraoral. The sulcus

33

on the labial or buccal aspect of the tooth is the mostcommon intraoral site of swelling because the apices ofmost teeth are closer to the buccal plate surface. Theminority of upper lateral incisors have apices closer tothe palatal bone surface and can therefore present aspalatal swellings. In later presentations, the sulcusswelling may become soft and fluctuant, or even havedischarging pus through a sinus, and this heraldsreduction in both swelling and pain.

Spread of infection

When dental abscesses escape the confines of alveolarbone, the infection passes into soft tissues and in turnprovokes in these tissues an acute inflammatory reactionand eventually pus formation. Where this happensdepends largely on the anatomy of the region in whichthe apex or apices lie. The length of the root is thereforerelevant, and how it relates in certain cases to muscleattachments. In acute abscesses of deciduous teeth, there-fore, the short roots often dictate that the infection passesnot into the facial structures but intraorally, forming a so-called 'gumboil'. Where spread of infection causes facialor cervical swelling it is often characteristic of thequadrant of the mouth involved, and these will beconsidered in turn.

Maxilla

Anteriorly from incisor to canine, the patient may showupper lip swelling, obliteration of the nasolabial fold andpuffiness of the lower eyelid. In extreme cases, the eyemay be almost totally closed with oedematous swelling(Fig. 33.1).

Posteriorly, the swelling will be evident in the upperpart of the cheek, with swelling around the eye occasion-ally but will not distend the nasolabial fold or causesignificant lip swelling (Fig. 33.1). Spread upward frommolar or premolar infection seldom passes into themaxillary air sinus. The buccinator muscle attachmentsin the molar region may determine whether the infectionpasses above it into the cheek or below into the sulcus,although both are frequently present, as this muscle willform only a partial barrier.

Mandible

Spread from incisors or canine teeth may cause mental orsubmental swelling (Fig. 33.2). Lower canine infections

Fig. 33.1 Facial swelling and closure of the eye due toinfection spreading from an upper incisor.

Fig. 33.2 Mental abscess arising from infectionassociated with a lower incisor.

do sometimes pass into the floor of mouth, resulting inswelling here in addition to the swelling of the chin.

Posterior teeth infections may pass either buccallyor lingually through the bone, and the attachments ofbuccinator laterally and mylohyoid lingually will have abearing on the direction of spread. If buccal spreadoccurs above buccinator, the swelling will largely be seenin the sulcus but, if below, it will cause swelling on thelateral aspect of the jaw externally, which may gravitatedownwards into the upper part of the neck. Occasionally,infection may spread deep to the masseter muscle. Thisusually arises from a pericoronal infection around awisdom tooth, as described in Chapter 27. If the infectionpasses lingually, the swelling will be in the submandibularspace if below the mylohyoid or in the floor of mouthif above this muscle. Although the muscles direct theroute of spread into the various tissue compartments, it is

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important to be aware that both intraoral and extraoralspread can occur from any tooth. It is therefore notunusual to see swelling in both the sublingual and sub-mandibular space from a lower molar tooth or, for thatmatter, both sulcus swelling and facial swelling from anupper tooth.

When infection spreads into whichever of the softtissue spaces, the initial reaction of these tissues will bean acute inflammatory reaction. The fluid exudate of thisreaction causes the early swelling, which is thereforemainly oedematous, and this phase can be known as acellulitis complicating the original bony abscess. Asthe soft tissues continue to react to the infection, pus willbe formed, which may collect within the compartment,giving rise to, for example, a submandibular or a sub-mental abscess (Fig. 33.3). A well-recognised compli-cation of lower jaw dental infection is the rapid spread ofsubmandibular and sublingual infection across themidline of the neck. This is a life-threatening situationknown as Ludwig's angina and requires immediatehospital admission for appropriate drainage and intensiveantimicrobial therapy.

Pus within the soft tissues of the upper part of the faceseldom presents as a facial external abscess but usuallycollects within the upper buccal sulcus.

Management

Management of the acute dental abscess is shown inTable 33.2.

Drainage

Provision of drainage remains the most importantmeasure where pus has formed.

Extraction

Extraction of the tooth is usually carried out if it isunconservable or if the acuteness of the conditionwarrants it. This provides excellent drainage, especiallyin upper teeth. If the abscess is still confined to thealveolar bone, or even where spread to soft tissues is inits early oedematous phase, extraction is often sufficientto allow resolution. There is no justification whatsoeverin delaying the extraction on account of swelling becausethis is one of the best ways of achieving good drainage,and thereby speeding resolution.

Fig. 33.3 A submandibular abscess.

Table 33.2 Management of an acute dentalabscess

Drainagetooth

extractionroot canal drainage

incisionintraoralextraoral

Removal of source of infectionendodontic treatmentextractionperiradicular surgery

Supportive antibiotic therapysevere spreading infectionsystemic toxicitymedically compromised

Root canal drainage

Opening of the root canal can, in the early intrabonyabscess, be sufficient in itself. When opened and pus isobtained, it is prudent not to close the canal immediatelybut allow sufficient time for adequate drainage to occur.This may take only 12–24 h but gross contamination andeven caries within the root canal can occur if the tooth isleft open for too long.

Incision of intraoral abscesses

The presence of pus is usually detected by a palpable'bounce' in the swelling within the buccal sulcus. Local

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anaesthesia within the outer wall only of the abscessis normally sufficient to allow incision with a pointedscalpel blade (number 11), which should be used with astab action and a cut of suitable size made on withdrawal.If the pus is deeper, fine artery forceps may be introducedto explore the abscess and gently open it to encouragefree flow of pus. This may require more extensive localanaesthesia. Palatal abscesses may require excision of asmall ellipse of soft tissue or insertion of a small drainafter incision as this mucoperiosteum tends to reboundand seal following the release of pus, thus preventingfurther free drainage.

Incision of extraoral abscesses

This is usually carried out by a specialist surgeon and,unless the abscess is very superficial, under generalanaesthetic. Provision of a general anaesthetic for someof these patients is a skilled procedure when trismus is amarked feature and laryngeal oedema masks the normalanatomy (see Ch. 10).

The presence of pus is confirmed clinically by elicitingfluctuation on careful palpation of the swelling. Fingerpressure of one hand on one side of the swelling causesfluid movement to be detected by the pulps of the fingersof the other hand. This can be difficult to determine,especially in deeper lying pus collections. Generally, theabscesses requiring such treatment will be submental orsubmandibular.

The key points of treatment are that the skin overlyingthe abscess should be prepared with surface antisepticand isolated with sterile drapes. A wide-lumen needleshould be introduced into the abscess cavity to obtain anuncontaminated sample, and it may also help to 'find' thepus. An incision is made below the maximum convexityof the swelling, parallel to the lower border of themandible, if possible using a skin crease line to minimiselater scar visibility (see Ch. 15). The incision should bethrough skin only and normally an incision of about 2 cmis sufficient. Blunt dissection is then carried out withblunt scissors or Hilton-type forceps into the cavity,which should be explored thoroughly with the bluntinstrument or a finger. A drain is then inserted into theabscess and sutured to the skin surface. A dry steriledressing is finally taped over the drain. This allowsfrequent assessment of the continuing discharge. Thedrain is removed after the dressings are seen to containno further pus.

Removal of source of infection

This will be accomplished immediately if the tooth isextracted in the process of gaining drainage but may be alater procedure in the form of either endodontic treat-ment or periradicular surgery.

Supportive antibiotic therapy

The decision to prescribe antibiotics for acute abscesseswill depend upon a number of factors and is notinvariable. Extraction of a maxillary tooth or incision ofa well-localised sulcus abscess may well be sufficient toallow resolution of the acute infection without antibioticsupplemental treatment. Clinical experience is invaluablebut some features may well influence the decision toprescribe an antibiotic (Table 33.3).

The swelling may encroach on the airway as, forexample, in a submandibular or sublingual infection.Difficulty in swallowing normally implies that the tongue,floor of mouth or parapharyngeal spaces are affected. Ifincision and drainage have yielded poor quantities ofpus, this suggests that management may be inadequatewithout antibiotics. Regional nodes are often late to reactto acute dental infection or are masked by the swelling.If present, this is good evidence of spreading infection,which would require supplemental antibiotic treatment.If the patient is medically compromised, and particularlyif the immune system is compromised, patients may nothave the capability to respond adequately to this typeof infection. Patients with conditions such as diabetesmellitus, HIV infection, or who are receiving treatmentwith corticosteroids or cytotoxic drugs, can be includedin this group. Where infection is evident in the floor ofthe mouth, there appears to be an increased likelihoodof rapid spread. The patient may feel unwell, with anelevated temperature and a tachycardia, signifyingsystemic toxicity. Most severe infections will cause a

Table 33.3 Factors influencing antibiotic therapyin the management of acute dental abscess

AirwayDysphagiaLack of drainageMedically compromisedSite of spreadSystemic toxicityTrismus266

degree of trismus by simply stretching the soft tissues,but profound trismus often implies infection affectingmuscles either directly or indirectly involved in jawmovement.

The choice of antibiotic is initially empirical, as theresults of antibiotic sensitivity testing will not be avail-able. The penicillin group is often chosen in non-allergicpatients, with the wider-spectrum amoxicillin being acommon choice. Metronidazole is becoming more popularas a first choice antimicrobial because anaerobes are thepredominant pathogens. Cephalosporins, erythromycinand, where antibiotic sensitivity indicates, clindamycinare all possible useful agents. In severe acute infections,it is sometimes considered necessary to prescribe two ormore antibiotics. Metronidazole and amoxicllin haveproved to be a popular choice where two antibiotics aredeemed necessary.

Finally, management of the acute abscess requiresmeticulous follow-up to ensure that the treatment ishaving the desired effect. In the early stages, this may beas an outpatient and require daily assessment until it isevident that resolution is being achieved. If the dentist,from the initial presentation, feels that the infection isvery severe, early referral to a specialist is appropriate,because a number of patients will require admission tohospital for appropriate drainage and perhaps intravenousantibiotic therapy.

Complications

A number of complications may arise from a dentalabscess as listed in Table 33.4.

Cavernous sinus thrombosis

Spread of infection through emissary veins from theperiorbital region and upper face can, in theory, causethrombus formation within the cavernous sinus. Withmodern antibiotics, this complication is seldom seennowadays.

Table 33.4 Complications of dental abscess

Cavernous sinus thrombosisLudwig's anginaNecrotising fasciitisOrofacial sinusOsteomyelitisSepticaemia

Ludwig's angina

This severe complication has been described above andrequires immediate admission to hospital for drainageand appropriate intravenous antibiotic therapy.

Necrotising fasciitis

This combination of virulent pathogens can cause massivesoft tissue necrosis with formation of multiple sinuses.It can arise from a dental infection.

Orofacial sinus

This complication arises when the pus has dischargedonto the face or neck, either through lack of treatment orinadequate treatment (Fig. 33.4). If the condition remainsuntreated it can cause disfiguring soft tissue fibrosisaround the intermittently discharging sinus. Epitheliumfrom the skin can grow into the sinus, complicating thetreatment in that surgical revision of the opening may benecessary. The dental source must be removed as soon aspossible.

Osteomyelitis

This is very rare and may be an indication of an immuno-compromised state or previous irradiation of the jaw,which has reduced the blood supply to the bone (seeCh. 36).

Fig. 33.4 An orofacial sinus arising from a lower premolar 267abscess.

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Septicaemia

This is discussed in Chapter 8.

Periodontal abscessThis arises from a periodontal lesion and the clinicalfeatures are therefore different from the apical lesion.

Clinical features

Pain and swelling

The swelling in this type of abscess being further coronalthan the apical abscess normally discharges eventuallythrough a periodontal pocket or through a sinus in thealveolar process. Spread to soft tissues is thereforerelatively rare but can involve particularly the floor ofmouth.

Mobility of the affected tooth

This feature may not be particularly helpful in diagnosisif other teeth also have mobility reflecting a generalisedperiodontal loss of bone. The tooth in question, however,will be uncomfortable on testing its firmness.

Vitality

The tooth in question will normally be vital to pulptesting.

Management

Extraction is often the logical treatment. This providesgood drainage and also removes the source of infection.Occasionally, if the abscess involves a strategicallyimportant tooth and the patient's general periodontalcondition is considered capable of control, then curettageand root planing may be appropriate.

Less common pyogenic oralinfectionsLess common infections that produce pus are cervico-facial actinomycosis and submandibular staphylococcallymphadenitis of childhood. Although these infections

are rare, they are important to recognise and managesuccessfully. Both are somewhat unusual in that they aredue to one organism rather than the polymicrobial natureof most pyogenic oral infections.

Cervicofacial actinomycosis

Different species of actinomyces microorganisms can befound in mixed dental abscesses related to infected teeth,and do not require particular management other thanappropriate drainage with additional antibiotic therapy ifconsidered necessary. Cervicofacial actinomycosis is adistinct clinical entity and arises subsequent to eithermandibular extractions or jaw fracture.

Aetiology

The infecting organism is the strictly anaerobicActinomyces israelii. This microorganism is found indental plaque and appears to gain access to the softtissues through an extraction socket or fracture throughthe tooth-bearing area of the mandible.

Clinical features

Most commonly, a swelling forms either at the lowerborder of the mandible or in the neck. It classicallypresents a week or so (and up to 6 weeks) after thewound in the mouth, which will normally appear to havehealed well. Severe pain is not a feature and, if nottreated, the infection may develop with several swellingsand skin sinus formation. The related skin is said to havea dusky, bluish tinge. Tissue planes are not followed andthe tissues respond by forming a granulomatous reactionaround the infected area. If a sinus is active, closerexamination of the pus may reveal small, yellow, seed-like granules in the discharge. These are known assulphur granules.

Diagnosis

Microscopic analysis of a granule by crushing it betweenglass slides and Gram staining shows typical Gram-positive branching mycelia with related pus cells.Anaerobic culture will later reveal the typical 'molartooth' colonies of Actinomyces israelii on blood agar.Occasionally, another small Gram-negative bacillus maybe found: Actinobacillus actinomycetemcomitans.

Management

Where pus is formed, incision and drainage should becarried out. Antibiotics should be prescribed for 6 weeksbecause they take a considerable time to penetrate thegranulomatous fibrous tissue reaction in the soft tissues.Shorter courses may result in a recurrence of the infec-tion and it is therefore important to stress to the patientthe importance of continuing the antibiotic for the fullprescribed period. Actinomyces israelii is sensitive tomost commonly used antibiotics and, being a narrow-spectrum antibiotic, penicillin is a sensible choice. Ifcervicofacial actinomycosis presents late or is treatedinadequately, it can gravitate from the neck into themediastinum, and this is clearly a serious complication.Less serious but disfiguring is the scarring that resultsfrom the fibrotic reaction in the neck.

Acute submandibular staphylococcallymphadenitis

This acute infection occurs in children between the agesof 2 and 12.

Aetiology

The cause of the infection is Staphylococcus aureus,which probably arises from the nasal passages or from

infection of the skin hair follicles and which passes downthe lymphatics to settle in submandibular lymph node.The child may not have been previously exposed to astaphylococcal infection and, the immune reaction beinginsufficient to deal with this challenge, the node is over-whelmed and becomes an abscess itself.

Clinical features

This is similar to any acute inflammatory swelling at thelower border of the mandible. There may be surfacereddening and it will be tender to palpation; thetemperature may be elevated. Dental examination showsno carious focus and this generally will raise suspicionsof a staphylococcal infection. There may be evidence ofinfection of a hair follicle on the face on that side or ahistory of recent nasal congestion such as a head cold.

Management

If there is evidence of accumulation of pus, such asfluctuation, then incision and drainage is necessary.Aspiration prior to the incision, will allow an accuratemicrobiological analysis. If no pus is formed, then abeta-lactamase-resistant form of penicillin, such asflucloxacillin or erythromycin, may be effective inallowing resolution.

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Salivary gland diseases

IntroductionSurgery of the major salivary glands has already beendiscussed in Ch. 14, but there are some conditions thatare treated by minor surgery within the oral cavity. Theseprocedures are mainly related to pathology of the minorglands but, where the major gland ducts are involved, itis often possible to treat the condition by less radicalsurgery intraorally.

When the major gland ducts are involved, it is oftenpossible to treat obstructive sialadenitis intraorally.Obstruction of the minor salivary gland ducts can alsobe managed by minor surgery and these conditions areconsidered here, after a review of their applied anatomy.

Applied anatomyAn awareness of the location of the minor glands and theanatomical course of the ducts of the major glands isneeded and these will be considered in turn. The grossanatomy of the major glands has been discussed inChapter 14.

Submandibular duct (Wharton's duct)

This duct is between 5 and 6 cm in length. It originatesfrom the deep surface of the gland just behind theposterior limit of the mylohyoid muscle. It runs upwardsand forwards between mylohyoid and hyoglossus, andthen between the sublingual gland and the genioglossusmuscle, before ending on the sublingual papilla besidethe fraenulum of the tongue and just behind the lowerincisor teeth. Its important relation is the lingual nerve,which crosses its lateral surface on its earlier coursebefore running upward on its medial side where the nerveis already beginning to divide into its smaller terminalbranches. As the duct runs forwards, it becomesprogressively more superficial.

Sublingual ducts

The sublingual gland lies fairly superficially beneath themucosa of the floor of the mouth, which it raises to formthe sublingual fold. It has many ducts (around 12), someof which run directly up to open onto the floor of mouth,whereas others may join the submandibular duct.

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Parotid duct - (Stenson's duct)

This duct is approximately 6 cm in length and is formedwithin the anterior part of the gland by the joining of twomain branches. After emerging from the gland it runshorizontally forwards over the surface of the massetermuscle to the anterior border of that muscle and thenturns inwards, passing through the buccinator and buccalpad of fat, before ending in a slightly raised papillaadjacent to the upper first or second molar tooth on thebuccal mucosa. The accessory parotid gland lies closelyrelated to its initial third and the buccal branches of thefacial nerve may be in close relationship to it.

Minor salivary glands

Around the mouth are aggregates of minor salivaryglands, which are mucus secretors. They lie superficiallyin the submucosal regions and are most easily felt bypassing the tongue along the inner aspect of the lower lip,where they are felt as a multitude of small lobules. Theyare most numerous in the lower lip but are plentiful in theupper lip, buccal mucosa and floor of mouth. In lessernumbers, however, they may also be found in the palate,the posterior aspect of both the hard palate and softpalate, and also on the ventral surface of the tongue. Theyopen onto the surface of the mucous membrane by tiny

34

ducts and their secretion is an important contribution tothe lubrication of the soft tissues.

Obstructive sialadenitisObstructive sialadenitis in a major gland is due either toa stone or, less commonly, stenosis of the duct. Minorgland obstruction gives rise to a mucocoele.

Major gland obstruction

Aetiology

Obstruction to the free passage of saliva from a majorgland can clearly cause problems to a patient. The mostcommon cause of this is blockage of the duct by a stonethat is sometimes known as a sialolith. This is relativelyuncommon in the parotid gland and is more frequentlyseen close to the orifice of the duct. In the submandibulargland, the stone may form either within the duct or thegland itself, but duct stones are more common. A certainnumber of obstructions within the duct are poorlycalcified, if at all, and are referred to as mucous plugs.

Other less common causes of obstruction are stenosis(probably a developmental occurrence) and pressureeffects from space-occupying lesions, such as malignantdisease, arising either from the epithelium of the floor ofmouth or within the gland itself. In the parotid gland,there may be another cause related to the trapping ofthe duct as it pierces the buccinator muscle, and this hasbeen described as more often occurring in children oradolescents.

Submandibular duct stones are relatively commonand their presentation may vary from patient to patient.

Clinical features

Characteristically, the stone may become apparent byswelling and discomfort in the submandibular glandregion. The swelling is palpable at the lower border ofmandible in the submandibular triangle. It is often madeworse at meal-times and, typically, pain may last for acouple of hours. Although this can occur at each meal-time for several days, it often settles and the patient mayreport being quite symptom free for weeks or months. Itis not unknown for large stones occupying most of thefloor of mouth to present with no history whatsoever ofdiscomfort or swelling in the gland.

More dramatically, however, infection may supervenebecause the duct is not being 'washed out' with saliva.Bacteria from the mouth may pass along the duct andgain access to the gland around the obstruction. This isknown as ascending infection and it can give rise to acutesialadenitis of the submandibular gland. When this occurs,the patient experiences severe pain and swelling of thegland, which becomes extremely tender with dysphagiaand, often, high temperature. Pain is made worse onattempting to eat or drink and the patient may complainof a bad taste in the mouth. Intraorally, the floor of mouthmay be severely swollen with a raised, red, wheal-likeline along the length of the duct. Small amounts ofpus may be expressed from the orifice of the duct onoccasion.

Diagnosis

This is made fairly straightforward with a clear historybut clinical examination by visual inspection of the floorof the mouth may show a yellowish coloured, rounded orfusiform-shaped lump of varying size along the line ofthe duct. This is more often seen when the stone is closeto the orifice of the duct or is fairly large. If it cannotbe seen, bimanual palpation of the floor of the mouthwith the 'outside' hand pushing the floor of the mouthupwards while the line of the duct is palpated with theindex finger of the 'inside hand' may reveal a hard lump.Saliva from the orifice of the duct may be absent, sparse,or slightly turbid in appearance.

Radiographs are usually confirmatory with a lateralview (lateral oblique jaw or orthopantomograph) andocclusal view, the latter being most useful (see Fig. 14.4).If no stone is noted on the radiograph, it may indicate thatthe obstruction is not calcified. In these circumstances, asialogram – where a radio-opaque dye is passed along theduct prior to the radiograph being exposed - may revealthis type of obstruction and also strictures within the duct(see Fig. 14.5).

In the acute presentations, the clinical features arefairly conclusive but radiographs should be taken toallow accurate location of the stone.

Management

Acute sialadenitis should be treated vigorously withaspiration, incision and intraoral drainage if possible, andantibiotics. Amoxicillin is commonly prescribed with a

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high initial dosage, and this can usually be administeredorally. Clindamycin may be appropriate in casesunresponsive to more commonly described antibiotics, asit is secreted through the salivary glands and perhaps hasa more direct effect.

Removal of the stone may often be done on anoutpatient basis with local anaesthesia. However somepatients have great difficulty in relaxing their tonguesufficiently to allow the surgery, particularly if the stoneis further back in the mouth. Large stones are normallyeasy to treat but some small stones can be very difficulttechnically. The nearer to the duct orifice the stone lies,the less difficult it will prove to remove. Anaesthesia isbest carried out with a lingual nerve block, as infiltrationcan often distort the surgical site and with small stonesmay obscure them from easy vision and palpation.

The technique involves passing a suture behind theobstruction underneath the duct and tightening thissufficiently to prevent the stone being pushed inadvertentlybackwards during the procedure. There is often dilatationof the duct up to the point of the obstruction and thisdisplacement therefore is a real possibility, with theadded complication that it may pass from the duct intothe gland itself.

An incision is then made over the stone parallel to theduct and slightly lateral to it. A blunt dissection is thencarried out to expose the duct. An incision is made in theduct over the stone, which is removed. There is often arelease of pus and saliva at this point. The wound shouldnot be sutured. It is accepted that the saliva may not 'use'the duct but may form a false opening through the wound.Suturing may additionally cause excessive fibrosis onhealing, which may itself cause obstruction. Patientsshould be encouraged to rinse copiously postoperativelyand a free flow of saliva should be encouraged with citrusdrinks.

Mucocoeles

Mucocoeles are the most common cause of minorsalivary gland problems. Neoplasms arising from minorsalivary glands are relatively uncommon but both benignand malignant varieties can be found. They can occur atany site where minor glands are found but the mostcommon intraoral location is at the junction of the hardand soft palates. Swellings in the upper lip are usuallyneoplastic rather than mucocoeles, which are rare in theupper lip.

Aetiology

Mucocoeles are caused either by damage to the minorduct leading to leakage of saliva into the submucosallayer (mucous extravasation cyst) or by blockage of theduct, normally by a mucus plug (mucus retention cyst).By far the more common is the extravasation cyst.

On occasion, small stones can cause obstruction tominor salivary glands. This is more commonly seen onthe upper lip or buccal mucosa and secondary infectionof the gland can occur, causing a localised raised tenderswelling. On the top of this dome-shaped swelling it maybe possible to see or feel the small stone. Treatment issimply surgical excision of the lesion.

Clinical appearance

Clinically, mucocoeles present as soft, bluish, fluid-filledswellings that often burst or leak, only to reform, andpatients normally are little inconvenienced by them. Themost common site is the lower lip (Fig. 34.1), probablyreflecting its greater tendency to trauma and ductaldamage, but the floor of mouth is also quite a commonsite.

In the floor of mouth, they may be related to the sub-lingual gland and can rapidly assume quite a large size.The ballooning lesion in the floor of the mouth may bedescribed as a ranula (frog's belly) and may be anuisance to the patient, although they frequently rupture.

Fig. 34.1 A mucocoele affecting the lower lip.

More precisely, however, a ranula merely implies asublingual swelling regardless of aetiology.

Diagnosis

The diagnosis is very straightforward, as the history isusually typical. Occasionally, mucocoeles resemble minorsalivary gland tumours, especially if they have becomefibrosed and more walled off. Their bluish colour canmake them similar to a superficial haemangioma but theytend not to deflate on sustained digital pressure, as wouldmost haemangiomas.

Management

The majority of mucocoeles are surgically excised butsome in the floor of mouth may be marsupialised.

Excision is carried out under local anaesthesia. Anincision over the swelling must be executed with care orthe lesion will burst and the subsequent removal may bemore complicated. Extravasation cysts do not haveepithelial lining and, if the cyst is ruptured, it may bedifficult to visualise. A blunt dissection around the cystfrees it very simply if it remains intact and minor glandsat its base are usually also removed. One or two suturesmay be needed to close the wound.

Marsupialisation of a larger floor of mouth mucocoeleis preferable to dissecting the lesion out and removing it.This may be done by passing a suture through the lesionto lift it. A small incision can then be made over themaximum convexity and the contents aspirated. Sterileribbon gauze is then packed into the now empty cavitythrough the small incision to 'reconstitute' the swelling,and the mucosal roof can then be removed with scalpelor scissors. The opening into the cavity must be keptpatent by suturing its margins to the oral mucosa, or thepack may be soaked in Whitehead's varnish and suturedto the side walls. The aim, whichever technique is used,is to prevent the opening sealing up and closing. Despite

this, some do recur as the floor of mouth wound doesclose over rapidly. If floor of mouth mucocoeles dorepeatedly recur, it may be necessary to remove thesublingual gland, (see Ch. 14).

Minor salivary gland biopsyIn Sjögren's syndrome, it has become established that thelymphocytic aggregates around minor glands are a directreflection of the pathology in the major glands thatcauses the reduction in saliva production. Histologicalexamination of minor salivary glands therefore avoidsthe more invasive major gland biopsy. An incision ismade in the mucosa of the lower lip - along the lines ofthe mental nerve branches rather than across them, tominimise nerve damage. The minor mucous glands willextrude through the open wound and can be excisedbefore wound closure (Fig. 34.2).

Fig. 34.2 An incision in the lower labial mucosa showingthe minor salivary glands protruding through the wound.

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Oral surgery in the medicallycompromised patient

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IntroductionPatients who require an oral surgical procedure will havetheir medical status questioned as a matter of routineduring the history taking. Certain conditions have a directbearing on the management and treatment of thesepatients, which may have to be altered or modified as aresult. Thus the treatment plan may have to be modifiedfor the patient's safety.

Most medical conditions do not interfere with minororal surgical procedures carried out under local anaes-thetic. The major problems are with patients who havebleeding tendencies, allergies, are on corticosteroids orhave cardiac disease.

Those requiring general anaesthetic will be treated inthe secondary care system under the supervision of aconsultant anaesthetist.

Not only can systemic disease influence the oralmanagement of a patient, but systemic disease may arisefrom the mouth, usually as a result of infection. Anexample of this is infective endocarditis arising in apatient with valvular or other cardiac disease; immuno-compromised patients, such as those taking cytotoxicchemotherapy, are also at special risk of infection. More-over, a number of acute medical emergencies may arisewhile oral surgical procedures are being carried out andthe surgeon must have the necessary agents available forthe appropriate management of the patient. The mainsystemic diseases that impact on the practice of oralsurgery are listed in Table 35.1, and these will bediscussed in turn.

Blood disordersHaematological disease, particularly anaemia, is notuncommon. Except in severe cases and those requiringgeneral anaesthesia, anaemia is not a significant problem

Table 35.1 Systemic disease and oral surgery

Blood disorders: haemorrhagic diseaseCardiovascular diseaseEndocrine diseaseLiver diseaseNeurological diseasePregnancyRadiotherapyRenal diseaseRespiratory disease

because blood loss during minor oral surgical proceduresshould be controlled and not excessive.

A number of bleeding disorders can occur (seethe discussion in Ch. 6) and the specific management ofpostextraction haemorrhage is considered in detail inChapter 26. In addition, it should be noted that aspirinis being taken by an increasing number of patients forprophylaxis against thrombotic disease such as coronaryartery disease or cerebrovascular thrombotic incidence.Normally, a dose of 75 mg daily is prescribed, whichhas the desired effect of reducing platelet adhesiveness.In theory, this should also cause more bleeding after oralsurgery, but in practice it seldom seems to have asignificant effect. Occasionally, continued oozing mayprompt haemostatic measures such as suturing or use ofregenerated oxidised cellulose but in most cases firmpressure is all that is necessary.

When patients are taking higher doses of aspirin forchronic pain (e.g. patients with osteoarthritis or rheum-atoid arthritis), then more major oral surgery may requirethe use of alternative analgesics for about 2 weeks beforesurgery, as the effects on platelets might prove moretroublesome in these circumstances.

Patients taking anticoagulants, such as warfarin, forcardiac arrythmias or those with prosthetic heart valves,

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should have their INR (International Normalised Ratio)estimated on the day of surgery. A higher INR can beaccepted before minor oral surgical than before generalsurgery (Ch. 6). Some suggest that an INR of <4 can beaccepted, but most oral surgeons would wish the INR tobe between 2-3 for elective procedures other than singletooth extractions. Haemostasis should be secured withlocal measures including Surgicel®, suturing and pressurepacks.

Surgeons must also be aware of the effect of prescribeddrugs on anticoagulated patients. Most antibiotics andsome antifungals will enhance the anticoagulant effect ofwarfarin, and non-steroidal anti-inflammatory drugs suchas aspirin not only enhance the activity of warfarin butrisk more severe bleeding from the stomach by theiraction on the gastric mucosa.

a consequence of its effects on the valves. Althoughdamage is not invariable, these patients are regarded as'at risk' unless there is proof to the contrary. This shouldinclude those with developmental septal defects and thosewith prosthetic heart valves following cardiac surgery.Patients with cardiac pacemakers are not at risk and anti-biotic therapy is not required. The remainder are at riskof endocarditis as a result of bacteraemia, which will beresultant upon oral surgery. Antibiotic cover is, therefore,a preoperative requirement and the regime is dependenton whether the patient is being treated under local orgeneral anaesthesia, whether the patient is allergic topenicillin and whether penicillin has been prescribed onmore than one occasion in the previous month. Patientsat a particular high risk are those who have had aprevious episode of endocarditis. The appropriate regimefor managing these patients is listed in Table 35.2.

Cardiovascular diseaseFrom an oral surgical viewpoint, patients with cardio-vascular disease can be considered in two groups.

Those with vascular disease

Hypertension is probably the most common consequenceof peripheral vascular disease. Patients may be taking avariety of medications, ranging from diuretics to beta-blockers, calcium-channel-blockers or angiotensin-converting-enzyme (ACE) inhibitors. In general terms,treatment of the hypertensive patient will be largelyunaltered other than under a general anaesthetic. Mostdentoalveolar surgery can be carried out with noproblems under local anaesthesia, although adrenaline(epinephrine)-containing local anaesthetics are known tocause a reduction in the blood potassium level and, inpatients taking potassium-losing diuretics, an adrenaline(epinephrine)-free local anaesthetic may be preferred.This is a theoretical risk.

Those with cardiac disease

Those with cardiac disease can be conveniently consideredunder two headings.

Valvular disease

Although rheumatic fever is now extremely rare, valvulardisease of the heart is still seen in the older population as

Ischaemic heart disease

Patients at particular risk are those with severe hyper-tension, those with angina or those who have had aprevious myocardial infarction. Anxiety or pain can causean outpouring of adrenaline, which can increase the strainon the heart and also precipitate dangerous arrhythmias.The patient should, therefore, be exposed to minimumstress and prescribed sedation if required (see Ch. 11).

The most effective agent for local anaesthesia islidocaine (lignocaine) 2% with adrenaline (epinephrine)(see Ch. 24). Doses of local anaesthetics should be keptto a minimum and treatment sessions should not beprolonged.

If it is unavoidable, general anaesthesia should begiven by an expert anaesthetist in a hospital setting,because cardiovascular disease is the chief risk of deathunder anaesthesia.

A number of measures should be considered whentreating patients in an outpatient environment underlocal anaesthesia. Patients should be advised to continuetheir normal medication before and after procedures.Patients should bring their glyceryl trinitrate (GTN)spray to the surgery, if they use one, because they maywish to use it prophylactically. Oxygen should beavailable on a continuous flow delivery system and staffshould be trained in the appropriate care for thecollapsed patient.

Where possible, surgical treatment is best deferred for3-6 months after myocardial infarction, depending on

Table 35.2 Prevention of endocarditis1 in patients with heart-valve lesion, septal defect, patent ductus, orprosthetic valve

Dental procedures2 under local or no anaesthesia, patients who have not received more than a single dose of apenicillin in the previous month, including those with a prosthetic valve (but not those who have had endocarditis), oralamoxicillin 3 g 1 h before procedure; CHILD under 5 years quarter adult dose; 5–10 years half adult dose

patients who are penicillin-allergic or have received more than a single dose of penicillin in the previous month, oralclindamycin3 600 mg 1 h before procedure; child under 5 years quarter adult dose; 5–10 years half adult dose

patients who have had endocarditis, amoxicillin + gentamicin, as under general anaesthesia

Dental procedures2 under general anaesthesia, no special risk (including patients who have not received more than asingle dose of a penicillin in the previous month), either i.m. or i.v. amoxicillin 1 g at induction, then oral amoxicillin500 mg 6 h later; CHILD under 5 years quarter adult dose; 5–10 years half adult dose

or oral amoxicillin 3 g 4 h before induction then oral amoxicillin 3 g as soon as possible after procedure; CHILD under5 years quarter adult dose; 5-10 years half adult dose

or oral amoxicillin 3 g + oral probenecid 1 g 4 h before procedure

Special risk (patients with prosthetic valve or who have had endocarditis), i.m. or i.v. amoxicillin 1 g + i.m. or i.v.gentamicin 120 mg at induction, then oral amoxicillin 500 mg 6 h later; CHILD under 5 years amoxicillin quarter adultdose, gentamicin 2 mg/kg; 5–10 years amoxicillin half adult dose, gentamicin 2 mg/kg

patients who are penicillin-allergic or who have received more than a single dose of a penicillin in the previous month,

either i.v. vancomycin 1 g over at least 100 min then i.v. gentamicin 120 mg at induction or 15 min before procedure;CHILD under 10 years vancomycin 20 mg/kg, gentamicin 2 mg/kg

or i.v. teicoplanin 400 mg + gentamicin 120 mg at induction or 15 min before procedure; CHILD under 14 yearsteicoplanin 6 mg/kg, gentamicin 2 mg/kg

or i.v. clindamycin3 300 mg over at least 10 min at induction or 15 min before procedure then oral or i.v. clindamycin150 mg 6 h later; CHILD under 5 years quarter adult dose; 5–10 years half adult dose

1 Reproduced from the British National Formulary (March 1997), with the permission of the British Medical Associationand the Royal Pharmaceutical Society of Great Britain.

2 Dental procedures that require antibiotic prophylaxis are: extractions, scaling and surgery involving gingival tissues.Antibiotic prophylaxis for dental procedures may be supplemented with chlorhexidine gluconate gel 1 % or chlorhexidinegluconate mouthwash 0.2%, used 5 min before procedure.

3 If clindamycin is used, periodontal or other multistage procedures should not be repeated at intervals of less than 2 weeks.

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the severity of the attack and the patient's rate and degreeof recovery.

Endocrine disordersA number of endocrine disorders can complicate themanagement of the patient undergoing minor oralsurgery. The most prevalent of these conditions is diabetesmellitus, which can occur in the insulin-dependent formor in the non-insulin-dependent, maturity-onset form. Inaddition, an increasing number of patients take corti-costeroid drugs for the management of autoimmuneconditions. The management of these groups of patientswill now be discussed.

Diabetes mellitus

If oral surgery requires a general anaesthetic, the require-ments of preanaesthetic starving and the difficulties withpostoperative food intake will need appropriate manage-ment. This needs to be carried out on an inpatient basisin cooperation with the patient's physician and using abalance of dextrose infusions and soluble insulin.

Under local anaesthetic, patients should be encouragedto maintain their normal regime with regard to eating andinsulin injections. Effort should be made not to delaytreatment such that the normal dietary intake is disrupted.

Diabetic patients have a compromised response toinfections. Certain procedures may, therefore, warrant anantibiotic prescription to cover them over the initial

healing period. For the straightforward extraction in awell-controlled patient, however, this is not necessary,particularly where good oral hygiene can be relied upon.

Certain non-steroidal anti-inflammatory drugs havean effect on blood sugar levels and paracetamol, with orwithout codeine, may be a wiser analgesic choice.

Corticosteroid treatment

Corticosteroids have important effects when given insufficiently large doses, and these include depression ofadrenocortical function, which will lead to collapse understress. Depression of the inflammatory and immuneresponses may lead to an increase in opportunisticinfections and impaired wound healing.

The need to give additional steroids for those patientstaking systemic corticosteroids, or having used them inthe previous 2 years, is controversial. Where clinicalconcerns exist regarding the risk of hypotensive shock,patients should be treated by increasing oral steroid therapyor by intravenous or intramuscular hydrocortisone.

Liver diseaseNormal liver function is essential for production ofseveral blood-clotting factors and for the metabolism anddetoxification of many drugs. Viral disease also hasimplications in terms of cross-infection (see Ch. 7). It isimportant to assess coagulation defects preoperatively toensure that adequate haemostasis will occur (see Ch. 6),and to be aware of the possibility of reduced drug break-down when administering or prescribing agents. TheBritish National Formulary contains valuable informationon prescribing for such patients and should be consultedappropriately.

Neurological diseaseThe most significant neurological problem presentingroutinely in minor oral surgical practice is that of grandmal epilepsy.

Most patients with epilepsy will be taking antiepilepticdrugs such as carbamazepine or phenytoin for the controlof the seizures. Oral surgery can be carried out underlocal anaesthesia without any problems if control issatisfactory and patients should be advised to continuetheir normal antiepileptic drug unchanged. If general

Table 35.3 Oral surgical considerations inpregnancy

Risk to motherincreased gingivitis and epulis formationrisk of hypotension if supinerisk of hypertensionvomiting especially with general anaesthesiaaspirin may cause neonatal haemorrhage

Risk to fetusradiography hazardousrespiratory depression with sedativestooth staining with tetracyclinesprilocaine rarely causes methaemoglobinaemiasome drugs are teratogenic

anaesthesia is required, the anaesthetist should be madeaware of the history to allow for the use of appropriatevolatile agents for anaesthetic maintenance.

PregnancyMinor oral surgical procedures can be carried out duringpregnancy, which, it should be remembered, is a physio-logical state. The potential risks to the mother and fetusare outlined in Table 35.3.

In the later stages of pregnancy, patients shouldnormally receive treatment in a more upright positionrather than supine because the weight of the fetus anduterus can interfere with blood return via the inferiorvena cava.

Although radiographs in the region of the jaws do notcause direct irradiation of the abdominal area, theseshould be restricted to clinical necessity, as should allradiographs. Patients who have non-acute problemsshould defer radiographic imaging until after pregnancy.Protective shielding where radiographs are neededshould be used as much for reassurance as for their actualbenefit. In acute conditions, radiographs will often benecessary and patients should be reassured that the risk isminimal.

Prescription of drugs should be carefully consideredand reference to the British National Formulary isnecessary to allow a choice of drugs that have beenproven safe during this period. Lidocaine (lignocaine)plus adrenaline (epinephrine) is an appropriate anaestheticand some clinicians prefer to avoid prilocaine withfelypressin, which may (in theory) have a mild oxytocic 277

effect. During the first trimester of pregnancy, particularcare should be taken with any prescription as this is thetime when drugs administered to the mother can have themost serious consequences on the child's development.

Necessary dental treatment should continue duringpregnancy, especially such measures as extraction ofunrestorable, grossly carious teeth where delay couldlead to acute pain and spread of infection. Prompt treat-ment under local anaesthesia may well avoid the need forlater use of antibiotics and painkillers, and even the needfor general anaesthesia where gross infection precludesthe use of a local anaesthetic. For less urgent surgery,such as removal of wisdom teeth or periradicular surgery,it is better that the surgical treatment is carried out duringthe middle trimester of pregnancy or deferred until afterthe pregnancy.

Most pregnancies are trouble free, but if there arerelated problems surgeons should communicate with theconsulting obstetrician if there is any doubt as to theappropriateness of dental treatment.

RadiotherapyRadiotherapy in the head and neck region may not onlycause mucosites and xerostomia but also reduces thevitality of bone, which increases susceptibility toosteoradionecrosis. This is discussed in Chapter 36.

Renal diseaseRenal disease is becoming more important to the dentalsurgeon as more patients are now receiving renal dialysis

or renal transplantation. Patients receiving regular haemo-dialysis are heparinised before dialysis and haemostasisis impaired for 6–12 h thereafter. These patients are alsoat greater risk of carrying hepatitis viruses. Furthermore,the permanent fistula formation that is required forhaemodialysis is susceptible to infection and antibioticcover should be provided for these individuals.

In addition, the kidney is a major organ of excretionand many drugs may have reduced elimination leading topossible toxic effects if renal function is impaired. TheBritish National Formulary should be consulted beforeprescribing drugs for any patient with a history of renaldisease.

Respiratory diseaseLong-standing or severe obstructive pulmonary diseaseposes general anaesthetic problems not only because ofthe compromised gaseous exchange but also because ofthe possible related right-sided heart failure problems.The conditions most likely to cause chronic obstructivepulmonary disease are bronchitis, bronchiectasis andasthma.

Treatment that is to be carried out under localanaesthetic should be staged to reduce stress and fatigue.Asthmatic patients should be counselled to bring theirsalbutamol or corticosteroid inhalers to the surgery andto use them if the need arises. Salbutamol and oxygenshould be kept in the surgery, with a suitable method ofdelivery as an emergency measure.

Worsening of asthma can be related to non-steroidalanti-inflammatories and caution should be exercised intheir prescription.

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Diseases of bone

IntroductionThe health of the bone of the jaws is important to theintegrity of the oral cavity and the teeth. Among them, anumber of conditions, primarily of bone, exist whichmay be genetic, metabolic or due to some otheraetiology. Often, however, bone disorders have a mixedaetiology which makes their classification problematic:cherubism is a genetic condition but is also a fibro-osseous metabolic bone disease. A list of bone disorders,categorised according to their known aetiology is shownin Fig. 36.1. These will be discussed in turn.

AchondroplasiaAchondroplasia is the most common genetic skeletaldisorder and is characterised by failure of epiphysealcartilage growth. This leads to short limbs and a retrusivemiddle third of the face due to defective growth at thebase of the skull. The facial deformity leads tomalocclusion.

This very rare condition affects the mandible rather thanthe maxilla. It is characterised by expansion of themandibular inner and outer cortical plates with a veryvascular fibrous tissue that contains osteoclasts and areasof immature bone. The lesion may appear radio-graphically as multilocular radiolucencies with a soap-bubble type of appearance and with evidence of markedexpansion in larger lesions. Treatment is by curettagelocally and some operators prefer to freeze the peripheryof the bony cavity with liquid nitrogen. Occasionally,very aggressive aneurysmal bone cysts may require moreradical treatment in the form of local resection of theaffected part of the jaw.

Central giant-cell granulomaThe clinical appearance in the jaws of this lesion may beexactly the same as the brown tumour described later inhyperparathyroidism. However, it is not a parathyroid-related problem but appears to be an endosteally originat-ing resorptive process causing a cyst-like lesion filledwith a very vascular fibrous tissue rich in multinucleatedgiant cells.

Clinical presentation

There is normally a bony expansion of mandible ratherthan maxilla and there may be mobility of related teethand resorption of roots.

Diagnosis

Radiographically and histologically, the giant-cellgranuloma is indistinguishable from the brown tumour,and bone biochemical tests must be carried out toexclude hyperparathyroidism. The diagnosis is thereforemade on histological grounds supplemented by negativeserological findings of parathyroid disease.

Management

These lesions are treated conservatively by localcurettage. They do have a tendency to recur and manyoperators now freeze the bony walls of the cavity withliquid nitrogen after curettage in an attempt to preventthis recurrence. In children, where there may be quitegross deformity, the lesions may respond to calcitonininjections, which are given over a prolonged period suchas a year. When successful, such treatment may avoid theneed for extensive surgery and the consequent aestheticproblems that can, in turn, require later surgicalreconstruction in the form of bone grafting.

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Fig. 36.1 Diseases of bone according to aetiology.280

Cleidocranial dysostosisThis is also a very rare inherited disorder. It is charac-terised by partial or complete agenesis of clavicles, byfrontal bossing, ocular hypertelorism (excessive spacingbetween the orbital cavities) and late closure of skullfontanelles. Dentally, there may be multiple super-numerary teeth, lack of eruption of teeth generally andthin dilacerated roots. It would appear that normalresorptive activity during eruption is compromisedleading to the unerupted teeth lying in crypts coveredwith overlying bone which does not resorb. Dental treat-ment involves exposure of teeth and removal of obstruct-ing supernumeraries where these are impeding normaleruption. However, even after exposure, the teeth maynot erupt satisfactorily.

FluorosisExcessive intake of fluoride can lead to mottling of theteeth. Skeletal sclerosis can also occur and this ishistologically similar to Paget's disease.

Fibro-osseous lesionsThese form a group of lesions with diverse aetiologieswith a range of clinical presentations. Fibrous dysplasiais the most important.

Fibrous dysplasia

This condition affects children and is, as the nameimplies, a replacement of normal bone by an immaturebone not unlike woven bone with extensive vascularfibrous tissue elements. The abnormality may affectmany bones (polyostotic) or one bone (monostotic), andthe maxilla is far more commonly affected than themandible. Two rare variants are also identified, one beingcherubism and the other Albright's syndrome, which is aform of polyostotic fibrous dysplasia with additionalfeatures of skin pigmentation and precocious puberty infemales. Fibrous dysplasia is usually self-limiting andtends to 'burn out' on completion of skeletal growth. Itcan, however, cause quite marked disfigurement in severecases and in the polyostotic form can encroach on bonyforamina leading to compression of nerves.

Clinical appearance

In the monostotic form, the usual presentation is of apainless enlargement of the maxilla on the affected side.Buccal and palatal aspects of the alveolar bone may beenlarged and expanded and this may cause spacingbetween the teeth compared to the unaffected side. Theocclusion, however, is seldom significantly affected otherthan the spacing and the teeth erupt normally and are notunduly mobile. The overgrowth can usually be seen as afacial asymmetry with fullness of the cheekbone andnasolabial fold.

Diagnosis

The diagnosis is normally made on three grounds: theage of the patient and clinical features described; theradiographic appearance and the histopathology. Radio-graphs of the affected bone or bones typically show agranular appearance that has been likened to groundglass. There is an obvious excess of this abnormal boneand it merges with the normal appearance of bone with-out a clearly defined separation. A bone biopsy willgenerally show the typical histological picture of islandsof irregularly shaped bone with vascular fibrous tissueinterspersing.

Bone biochemistry is normally unhelpful, withcalcium, phosphate and alkaline phosphatase levelswithin normal limits. The alkaline phosphatase level,which is a measure of osteoblastic bone formativeactivity, may be raised if the sample is taken during anactive growth phase of the child, and its relevance istherefore almost impossible to determine.

Management

Unless there is unacceptable disfigurement, most sur-geons prefer to defer treatment until growth is complete.The surgery is normally in the form of recontouring ofthe excess bulk of bone. In more gross cases, surgerymay be needed at an earlier stage but may require to berepeated when maturity is reached.

Cherubism

This is regarded as a form of fibrous dysplasia that isfamilial and carried by a dominant gene. It is charac-terised by an increased width and fullness of the anglesof mandible bilaterally. The bone itself is immature in

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these regions with areas of vascular fibrous tissue. Radio-graphically, it appears as bilateral multilocular cyst-likeradiolucencies. Although normally seen in the mandible,the maxilla can be affected also. The condition is firstseen in childhood and becomes less active on maturity.

Cemento-ossifying fibroma

These rare lesions can grow to a considerable size. Theyare essentially fibrous overgrowths that become filledwith either a bony or cement-like calcification. They aregenerally painless and are found as swellings usually inthe buccal sulcus. They may be encapsulated but thesecapsules are not invariably present. Surgical removal ofthe lesion may be difficult as the boundaries of the lesionmay be almost impossible to ascertain. They are morecommon in the mandible and generally present in youngadults.

Cemento-ossifying dysplasia

This process is similar to fibrous dysplasia but lesionsresemble cemento-ossifying fibromas and probably arisein the periodontium. The condition may be multifocal orgeneralised. Single lesions are called cementomas andflorid lesions are termed gigantiform cementomas. Theyare more common in women and black patients andundergo progressive periapical calification. This leads todifficulties with extractions and the subsequent risk ofosteomyelitis.

Gigantism

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Excess growth hormones arising from a pituitaryadenoma will cause increased growth in height before theepiphyses are closed. Subsequent growth causesacromegaly with prognathism and increased soft tissuegrowth leading to coarse facial features and macroglossia.The bone quality is normal.

HyperparathyroidismThis may be primary and due to overproduction ofparathormone often by an adenoma in the parathyroidglands or secondary to conditions that reduce calciumlevels in the blood, such as chronic renal disease. Whereincreased levels of parathormone are present, calcium ismobilised from the bony skeleton to raise blood levels of

calcium. In the primary form of the disease, this leads tohypercalcaemia, and renal calculi may develop if theproblem is not identified. In the bone, however, where thejaws can be affected, cyst-like spaces known as 'browntumours' may develop. The bone in these tumours isresorbed by vascular fibrous tissue with multinucleatedgiant cells in profusion. This has given rise to the othername of this condition, osteitis fibrosa cystica. In thejaws, the mandible is more commonly affected by suchlesions than the maxilla.

Clinical features

In the mandible, the presence of a brown tumour maygive rise to expansion of the outer and/or the innercortical plates of bone. Occasionally, the soft tissue of thebrown tumour may grow through the upper border of thealveolar process and appear as a dark red or purple-coloured mass under the oral mucosa. The lesion isusually non-painful but may be tender to palpation.

Diagnosis

Radiographs will show a well circumscribed area ofradiolucency with a less defined lamina dura surroundingit than is normally found in a true cystic lesion. The out-line may have a scalloped margin and some authoritiesalso describe a lack of definition of the lamina duraaround all the standing teeth. This, in fact, is difficult todiscern and tends to be a rather subjective finding.

An incision biopsy of the lesion reveals the typicalhistological appearance of fibrous vascular tissue withlarge numbers of multinucleated giant cells.

Serum biochemistry will reveal elevated parathormonelevels and, in the primary form of the disease, this will beaccompanied by a raised serum calcium and loweredphosphate level.

Management

Primary hyperparathyroidism is normally treatedsurgically by removal of usually an adenoma of theparathyroid gland. The bone lesions usually resolvespontaneously following this surgery.

HypophosphatasiaThis rare recessive genetic disorder can be of early or lateonset. It is characterised by bony fragility and a rickets-

like condition. Defective cementogenesis can lead toshedding of the teeth.

Infective bone conditionsInfection in bone is relatively uncommon in the jawsgiven the large number of dental abscesses that occur andalso the amount of bone exposed by extractions that healwithout apparent problems. It is probably a reflection ofthe good blood supply in the mouth generally, and par-ticularly in the upper jaw, which seldom becomesinfected. The use of antibiotics also limits the occurrenceof bone infection compared with preantibiotic days.Osteomyelitis is so rare nowadays that most clinicianslook for underlying reasons for its occurrence. Conditionsthat have rendered the patient immunocompromised,such as diabetes mellitus, HIV infection, immuno-suppressive drug therapy and blood dyscrasias should beexcluded. Local factors, such as previous radiotherapy tothat region of the jaw or lack of a normal blood supply(as encountered in osteopetrosis), are also relevant aspredisposing factors. A number of distinct bony infec-tions can occur (Table 36.1) and these will be consideredhere.

that found in dental abscesses with anaerobes pre-dominating. It differs in this from osteomyelitis in a longbone, which is often of staphylococcal origin and is saidto be haematogenous, meaning that the bacteria havecirculated in the bloodstream from other sources such asskin infections.

Clinical features

These reflect the results of a sudden increase in pressurewithin the medulla of the bone in which the intactcortical plates do not allow any release in the earlystages. This rapid increase in pressure is brought aboutby the inflammatory reaction in response to the presenceof infection. Patients therefore complain of severethrobbing pain, trismus, swelling over the mandible andparaesthesia or anaesthesia in the distribution of themental nerve. More variably, a bad taste or dischargethrough sinus formation may be seen. In severe casesthere may be pyrexia with consequent malaise andanorexia. Lymphadenitis may be relatively late but maybe palpable and tender in the submandibular and uppercervical chain of nodes. Later features may include sinusformation on the skin and shedding intraorally ofnecrotic bone.

Localised osteitis (dry socket)

This is discussed in Chapter 26.

Acute osteomyelitis

By definition, this is an acute inflammatory reaction toinfection within the medulla of the affected bone. Itrarely affects the maxilla, which has a more profuseblood supply, being primarily a mandibular infection. Itis comparatively rare and may well be an indication ofother disease that reduces the normal defence mechanisms.The source of most mandibular osteomyelitis is dento-alveolar infection and the microbial profile is similar to

Table 36.1 Infective bony conditions

Localised osteitisAcute osteomyelitisChronic osteomyelitisChronic sclerosing osteomyelitisSubperiosteal osteomyelitisOsteoradionecrosis

Radiographic features

Initially, there may be little evidence of changes withinthe bone, other than possible dental foci of infection. Inthe later stages, areas of patchy radiolucency are present,within which there may be irregular areas of increaseddensity that signify bony sequestra (Fig. 36.2). Sequestraare areas of dead bone formed by thrombus formation inthe nutrient blood vessels to these areas of bone broughtabout by the increased pressure on these vessels. Theareas of necrotic bone further enhance the inflammatoryreaction, as the body attempts to shed them in the sameway as any foreign body.

Management

Initially, the management of osteomyelitis follows theprinciples of any acute pyogenic infection: incision anddrainage of any collection of pus together with appro-priate vigorous antibiotic therapy. If possible, pus shouldbe sampled by aspiration for culture and antibioticsensitivity testing but antimicrobial prescriptions shouldnot be delayed for this laboratory analysis. Commonly,metronidazole and amoxicillin are used together but

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Fig. 36.2 Radiograph showing acute osteomyelitis3 months after removal of an infected lower third molar.

these can be changed to reflect the bacteriological findingsif required. Clindamycin has good bone-penetratingqualities and is effective in many anaerobic infections, itis therefore a useful drug if there is a poor clinicalresponse. Once the acute phase has been brought undercontrol, surgical sequestrectomy, which removes anyareas of dead bone and curettage, is carried out. If sig-nificant loss of bone has occurred, bone grafting may beconsidered at a later stage but only after total resolutionof the infection.

Chronic osteomyelitis

Features of chronic infection are less florid that in theacute form, and hence pain is less marked, disturbance ofnerve transmission is much less likely and generally thepresentation is more subtle. Management is normally bysurgical means with sequestrectomy and curettage.

Chronic sclerosing osteomyelitis

This is a rare and ill-understood condition in which areasof bone in the mandible show radiographic evidenceof rarefaction often giving patchy round or ovalradiolucencies in the affected region. It does not appearto be due to bacterial infection although there is somedispute over this, and surgical curettage reveals chronicinflammatory changes but no histological evidence ofmicrobial presence. The condition may cause swelling

and pain that responds to non-steroidal anti-inflammatory drugs, which are often used together withantibiotics, although the latter are usually prescribedbefore any accurate diagnosis is made. Systemic cortico-steroids can also be helpful in controlling the acutesymptoms. Some investigators have suggested that thecondition, which is chronic and intermittent in character,may be related to excessive tooth clenching or grinding,and will therefore respond to interocclusal splinting ofthe teeth. Surgery often involves decortication of theouter lamellar bone and this is normally followed by anosteosclerotic reaction. The condition frequently remitsspontaneously with the affected region or regions show-ing increased radiodensity on radiographic examination.

Subperiosteal osteomyelitis

This is more commonly seen in children or young adultswhere infection usually through an infected tooth causespus to form under the periosteum of the bone. Theperiosteum is hence lifted off the bone and reacts byforming a layer of new bone known as an involucrum.Patients have a fairly hard bony swelling formed of thisnew bone beneath which pus may be trapped. Radio-graphically, this is often best illustrated by occlusal orposteroanterior mandibular views, which show the outercortical plate with a thin overlying wafer of new bonewhere the periosteum has been raised from the surfaceand formed new bone in an attempt to wall-off theinfection. Treatment consists of removal of the source ofinfection, normally a tooth, and curettage of the area withappropriate removal of the overlying involucrum bone.

Osteoradionecrosis

Irradiation to the jaws may occur as a result of radio-therapy for malignant disease of the mouth, pharynx orsalivary gland regions. Damage to the cells within thebone, the osteocytes, and to the nutrient blood vesselswithin bone, renders the bone less vital and hence moreopen to infection. In the blood vessels there is anendarteritis and periarteritis that significantly reduces theblood supply to the bone and this particularly affectsmandibular bone, which has a less profuse vascularnetwork than the maxilla. Where irradiation has beenextensive, which is now less commonly seen due tobetter zoning of the beam and protection of adjacenttissues, a form of avascular necrosis can occur withexposed bone failing to sequestrate normally and heal

with granulation tissue. Creation of a wound such as anextraction wound can, therefore, result in infection veryeasily, and this may be difficult to control. Added to thisproblem is a dry mouth and high caries rate if the salivaryglands have been affected by the radiation.

Management

Prevention is preferable to treating exposed or infectedbone and careful preradiation assessment of restorativeneeds is essential. Unrestorable teeth should be extracted,if possible 3 weeks before the start of radiotherapy. Strictoral hygiene measures should be stressed to reduce thechance of subsequent caries and tooth loss and thisshould be in conjunction with regular dental treatmentincluding preventive measures.

When extraction is unavoidable after radiation, mostclinicians use antibiotics for a week to 10 days after theextraction. Care should be taken to cover any exposedbone such as interradicular septa and, if necessary, suchuncovered areas need to be protected with a Whitehead'svarnish ribbon gauze pack or covered with a surgicalflap. More recently, hyperbaric oxygen therapy has beenused with some success in the management of theseproblems. The treatment involves the patient entering apressure chamber where the atmospheric pressure isincreased to about 2.5 atmospheres for a period of 90min. This has to be done daily for several weeks but doesappear to help the healing process significantly. It hasalso been shown that surgery to remove necrotic bonefollowing hyperbaric oxygen treatment increases thechance of successful healing. The success of hyperbaricoxygen therapy underlines the ischaemic cause of theproblem consequent to radiotherapy.

NeoplasmsNeoplastic disease

Neoplasms derived from bone itself are relativelyinfrequent in the jaws. The benign osteoma and themalignant osteosarcoma are very uncommon. However,the jaws may be affected by neoplasms of dental origin,such as odontogenic tumours, secondary metastaticdeposits in bone from primary tumours such as breast,thyroid or lung, or more commonly from direct invasionof the oral squamous cell carcinoma arising from theoverlying mucosal epithelium. Neoplasms in bone giverise to radiographic changes in the form of radiolucencies

Table 36.2 Neoplasm in bone

OsteomaOsteosarcomaCemento-ossifying fibromaOdontogenic neoplasms

and therefore bone loss unexplained from the more com-mon infective causes should always arouse suspicion. Inthese situations, a biopsy of the area is the only satis-factory method of eliminating the possibility of neoplasticdisease. The neoplasms to be discussed are listed inTable 36.2.

Osteoma

This is a benign tumour of bone and, unlike bonyexostoses, is very uncommon. It can arise from compactor cancellous bone in the form of a painless hard swelling.Radiographically, a round or oval-shaped radiodenseimage is seen and although a capsule is classically foundin benign tumours it is seldom seen clearly on suchradiographs. If the swelling is interfering with function itcan be surgically removed.

A more rare condition, Gardner's syndrome, ischaracterised by multiple osteomata of the jaws. Thecondition is important because the syndrome exhibitsmultiple intestinal polyposis and these polyps have thepotential for malignant transformation. Urgent referral toa gastroenterologist is therefore needed.

Osteosarcoma

This is - fortunately - a rare malignant tumour of thejaws. It is more common in young people under the ageof 30 but can occur in older patients and a small numberof people with Paget's disease develop osteosarcoma as arare complication. The age of presentation of the diseaseappears to be significantly older in the jaws than in otherbones, and it may affect maxilla or mandible. Jaw lesionsalso appear to differ from those in other bones in thatmetastases usually to lung or brain are less prevalent. Thepoor prognosis of the disease appears to be more relatedto local aggressive recurrence.

Clinical appearance

This varies according to the site of origin but normallyconsists of a fairly rapidly enlarging swelling, which can

be painful and cause loosening of related teeth. Anaesthesiamay also occur if the tumour grows in relation to theinferior dental canal or infra orbital canal causing alteredsensation peripheral to the point of tumour pressure orinfiltration.

Radiographs may show clear evidence of bonedestruction although areas of radio-opacity, which maybe quite dense, can be seen within the radiolucent region.The periphery is indistinct reflecting the rapid growthand both widening of the periodontal membranes andresorption of the roots of teeth may be evident.

Diagnosis

This is confirmed by incision biopsy of the lesion.

Table 36.3 Odontogenic tumours and odontomes

Epithelial in originAmeloblastomaCalcifying epithelial odontogenic tumour (Pindborg

tumour)Adenomatoid odontogenic tumour

Mesenchymal in originOdontogenic myxomaCementoma

OdontomesInvaginated odontome (dilated composite odontome

and 'dens in dente')Compound composite odontomeComplex composite odontomeGerminated odontome

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Management

The lesion is treated by radical excision of the affectedbone and wide margins of soft tissue are also removed.More recently, better responses have been claimed bypresurgical chemotherapy and, if necessary, postsurgicalchemotherapy or radiotherapy.

Cemento-ossifying fibroma

This neoplasm has been discussed in the section on fibro-osseous lesions.

Odontogenic neoplasms

This is a collection of neoplasms derived from tooth-forming tissue and may arise from epithelial ormesenchymal tissue. They are rare, although the mostaggressive of them - the ameloblastoma – is the mostcommon. At the other end of the spectrum of theseneoplasms are the odontomes, which are best consideredhamartomas (which means that they are abnormal tooth-like structures that generally do not continue to growonce their development is complete). There are manyhistological types of odontogenic tumour, the morecommon of these are listed in Table 36.3.

Ameloblastoma

The ameloblastoma is the most common of the odonto-genic tumours and can present at any time from child-hood to older age groups but is more often seen in themiddle-aged adult population. It occurs in both mandibleand maxilla but is far more common in the lower jaw,

with an approximate ratio of 3:1. In the lower jaw, theangle and ramus is the most frequent site, with overtwo-thirds of occurrences.

The tumour is variable in its aggressiveness andspreads by local destruction of bone. If untreated, it willeventually spread into soft tissues and this may make itvery difficult to eradicate surgically. It does not tend tometastasise other than the extremely rare malignantameloblastoma variant. There are several histologicalvariants of this tumour, the two most common being theplexiform and the follicular forms, but these differentappearances do not appear to produce differences inbehaviour or prognosis.

Clinical features

Gradual swelling of the jaw is the usual initial symptomof this tumour, although it may be diagnosed through aradiograph before this becomes apparent. Loosening anddisplacement of teeth can occur, although pain or alteredsensation is not usually reported. In the earlier stages, theswelling will be in the form of expansion of buccaland/or lingual cortical plates and is hence hard topalpation. With further growth, however, the swellingmay be softer but firm denoting that the lesion has erodedthrough the bone into the adjacent soft tissues.

Radiographs classically show a multilocular 'soapbubble' round or oval-shaped radiolucency with well-demarcated radio-opaque margins (Fig. 36.3). The sharpdelineation of the radiolucent areas reflects the slow rateof growth of these neoplasms. It may displace the outlineof the inferior dental canal and may also cause displace-ment and/or resorption of the roots of the teeth.

Fig. 36.3 Radiograph of an ameloblastoma showing(a) soap-bubble appearance; (b) expansion.

One recognised variant of the ameloblastoma is thecystic ameloblastoma, which most frequently occurs atthe angle of mandible. Radiographically, this is indis-tinguishable from a dentigerous cyst related to anunerupted wisdom tooth and is a fluid-filled cystic cavitywith nodules of ameloblastoma within certain areas ofthe lining of the cyst (Fig. 36.4). Even if an incisionbiopsy of the cyst lining is taken following aspiration of

Fig. 36.4 Radiograph of a cystic ameloblastoma.

the fluid content, it may not be taken in an area that isshowing neoplastic change and it is therefore importantthat, when any presumed cyst is enucleated, the wholepathological specimen is examined by a pathologist whois aware of such variations of the ameloblastoma (seeCh. 28).

Irrespective of histological differences in this neoplasm,most authorities advise total resection with around 1 cmclearance of the affected bone. In smaller lesions thismay still allow preservation of the lower border of themandible and this clearly has significant advantages withregard to aesthetics. The resultant defect may be filledwith a bone graft and, where necessary, supported by areconstruction plate.

Calcifying epithelial odontogenic tumour (Pindborgtumour)

This rare neoplasm can occur at any site in the upper orlower jaw but is most commonly found in the mandible.It causes painless expansion of the affected area and isfrequently related to an unerupted tooth. Radiographsshow a radiolucency, which may be multiloculated, andthere may be areas of radiodensity within the central areaof the radiolucency. Demarcation of the tumour fromnormal bone is not always clear. The lesion is locallyinvasive into the surrounding bone and is treated by alocalised resection with a small margin of normal bonearound it to reduce the chance of recurrence.

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Adenomatoid odontogenic tumour

This benign neoplasm is commonly found in the maxillaand is often related to an unerupted canine tooth. Radio-graphically, it can be indistinguishable from a dentigerouscyst around the crown of the unerupted tooth. Conser-vative curettage is its method of treatment.

Odontogenic myxoma

These slow-growing tumours are benign and are mostfrequent in the second and third decades. They occur ineither jaw but are more common in the mandible. Theyerode bone and enlarge to form multilocular, radiolucentregions that can be very difficult to differentiate fromother multilocular lesions such as ameloblastoma orodontogenic keratocysts. Treatment is conservative bythorough bony curettage. Recurrences can occur and,therefore, although the treatment is generally con-servative, follow-up is required. These tumours do notappear to metastasise.

Cementoma

These lesions are composed of cementum and may occursingly or may affect many teeth in the dentition. They area form of cemento-ossifying dysplasia. They are asymp-tomatic and are usually diagnosed by radiographic appear-ance. In the early stages they cause radiolucency, whichlater mineralises into cement-like tissue. The teeth affectedare vital throughout this process.

OdontomesOdontomes are relatively infrequent occurrences in thedentition but, when they do occur, they often impede thenormal eruption of adjacent teeth or, in the case of theinvaginated form, directly affect the vitality of the tooth.They are best regarded as malformations of developmentof the tooth from its dental lamina or as hamartomas,which cease their growth at completion of theirformation and do not alter thereafter.

Invaginated odontome

This malformation is most often seen related to the upperlateral incisor tooth. It is formed by an ingrowth ofenamel epithelium forming a blind-ending, enamel-linedpouch that is in direct communication with the surface of

Fig. 36.5 Radiograph of an invaginated odontome withrelated radicular cyst.

the tooth, most commonly at the cingulum. The labialsurface of the tooth may look entirely normal and theentrance to the invagination may be a minute pit, but theingress of saliva and bacteria usually results in pulpaldeath and the development of an apical lesion. Suchinvaginations may be so small as to be difficult to imageeven with good radiographs but in some cases the mal-formation may be so great that the whole clinical crownis taken up by the dilated nature of the ingrowth and theappearance on radiograph can then be likened to a toothwithin a tooth or 'dens in dente' (Fig. 36.5).

When the invagination is small the tooth may well beamenable to conventional root canal treatment and, wherean apical cyst has developed, periradicular surgery. How-ever, the malformation may be so gross that extraction isthe only practical solution.

Complex odontome

This developmental aberration results in a randomlaying-down of all the dental elements in a totallyhaphazard fashion. Radiographically, it gives rise to anirregular radiodense image. Enamel, dentine, cement andpulpal tissues are all represented and the radiographicimage obtained may well reflect these different tissues

Fig. 36.6 Radiograph of a complex odontome.

with varying degrees of opacity and radiolucency (Fig.36.6). Complex odontomes may obstruct adjacent teethfrom normal eruption and they are better removed asearly as possible to reduce this chance.

Compound odontome

In this abnormal manifestation of development, there ismore organisation of the dental tissues and the lesionconsists of numerous small denticles massed togetherwithin an outer capsule (Fig. 36.7). The odontome maybe small, with only a few tiny teeth, or it may be ofconsiderable size and contain many denticles. As withthe complex odontome, the compound form should beremoved where it is affecting normal eruption of thedentition.

Germinated odontome

This defect of development arises from either a completeor partial fusion of adjacent tooth germs or by a splittingor dichotomy of one germ. The result is a fusion of theresultant tooth that may affect only the crown or thecrown and root together. They can pose both aesthetic andorthodontic problems and, where extraction is necessary,they may cause difficulties due to the complex nature of

Fig. 36.7 Radiograph of a compound odontome.

the root form. Management of this problem will largelybe dependent upon aesthetic and orthodontic criteria.

Although not a developmental problem, fusion ofteeth by excessive production of root cementum can leadto what is referred to as pathological germination orconcrescence. The most common teeth to be joined inthis fashion are upper second and third molars, especiallywhere the upper wisdom tooth has developed with adisto-oblique angulation. Concrescence of teeth isfortunately very rare as they pose considerable problemsin removal since they are usually only detected atextraction.

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Osteogenesis imperfectaThis is a group of rare, usually autosomal dominantconditions of varying severity affecting the formation ofall bony tissue. The condition is sometimes referred to asbrittle-bone disease because the inherent weakness of thestructure of the tissue can lead to fracture of the bonewith even minimum trauma. The condition arises due todefective biosynthesis of type I collagen, leading toinadequate amounts of bone formation by osteoblasts. Inaddition to the weak nature of the bones, they tend to bethinner than normal, although growth may be relativelyunaffected. Multiple fractures can lead to deformity. Thesclerae of the eyes are typically a bluish colour and manycases also have a related defect in dentine structure,dentinogenesis imperfecta. This dentine is poorlyattached to the overlying enamel and this can lead torapid loss of the enamel and subsequent wear of theunprotected dentine. Patients may often therefore requireextractions, and these need considerable care in theirexecution, although fracture of the jaw during suchextraction is relatively uncommon.

OsteopetrosisThis inherited but very rare condition is sometimesknown as marble bone disease because of the density ofthe bone that encroaches upon medullary spaces and maytherefore compromise haemopoesis. The condition arisesdue to inactivity of osteoclasts. The problem can affectthe jaws where the lack of vascularity of the tissue maylead to infection. The avascular bone makes eradicationof infection by antibiotics difficult because adequatelevels of such antibiotics may not be effective in theaffected area because of the lack of blood supply.Similarly, surgical removal of affected bone can befollowed by very poor healing and the risk of reinfection.Extractions may not only be difficult, therefore, but mayalso lead to infection. Reduction of the medullary spacescompromises haemopoesis, which then takes place in theliver and spleen. Regardless, anaemia is progressivewithout marrow transplantation.

Osteoporosis

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This disorder is characterised by loss of bone density.The composition of the bone is normal and there are nodemonstrable metabolic changes. Physiological bone loss

Table 36.4 Risk factors for osteoporosis

Physiological

AgeingFemale sex

Early menopauseImmobilityUnderweightChildhood maturation failure

Pathological

AlcoholCorticosteroid drugs,

Cushing's syndromeMultiple myelomaDiabetes mellitus rareHypogonadism causesThyrotoxicosisSmoking

with increasing age accounts for the apparent increasingprevalence of this disorder. The risk factors for osteo-porosis are listed in Table 36.4.

Treatment is unsatisfactory. Prevention is preferredand hormone-replacement therapy (HRT) is effective inpostmenopausal women. Patients with osteoporosis haveincreased alveolar resorption if they are edentulous.

Paget's diseaseThis disease can affect the jaws but is normally more ofa problem in the weight-bearing bones. It is characterisedby irregular resorption of bone with subsequentredeposition and it therefore disrupts normal bonyarchitecture. During the resorptive phases, areas of bonemay be severely resorbed, leading to distortion undernormal weight bearing function. There may be pain inthe bones, large vascular regions in the medullary spacesand consequent problems in cardiac function due to'pooling' of blood in these areas. In the formative phase,occlusion of bony foramina can prove a problem and therelative avascularity following redeposition of bone canthen make infection in bone more difficult to manage.Paget's disease is essentially a disease of the elderly,although a juvenile form is recognised.

Clinical appearance

The skull can enlarge, as can the jaws and in particularthe maxilla. Deformity can result from vertebral columnand lower limbs being unable to deal with the forces anddeforming as a result. This deformation led to Paget'sdisease being known as 'osteitis deformans', but thisterm is now rarely used. Enlargement of the jaws, wherethey are affected, may result in loss of fit of prostheses

and the teeth themselves may show excessive deposits ofcement known as hypercementosis.

trimmed and covered by soft tissues with appropriatesuturing.

Diagnosis

Blood samples may show very high levels of alkalinephosphatase with normal values for calcium and phos-phate. Radiographs show patchy areas of radiolucencyinterspersed with radio-opaque density. The descriptiveterm 'cotton wool' has been used to describe thesechanges and is an accurate reflection of the radiographicchanges seen. Bone biopsy may show irregular areas ofresorption or evidence of previous resorption in the formof reversal lines. These are heavily staining haematoxilinlines, which denote the boundary of previous resorptiveactivity.

Management

In the general management of Paget's disease,bisphosphonates are the usual form of treatment. Thesedrugs appear to have a direct effect on hydroxyapatitecrystals, which make the bone less receptive to resorptiveactivity and hence reduce the rate of turnover. Dentalproblems may be encountered in the form of excessivebleeding if the area of the jaw affected is undergoingactive resorption, and infection can be a complicationwhere the bone has reformed and become relativelyavascular. Added to these problems may be hyper-cementosis of the roots resulting in large-rooted teeththat may be difficult to extract conventionally. Prophy-lactic antibiotics are often prescribed for extractions ifthe bone is sclerotic and areas of exposed bone such asprominent interdental or interradicular septa should be

RicketsRickets arises as a result of defective calcium andphosphorus metabolism during bone growth. Aftercessation of bone growth the condition causes osteo-malacia. It may occur in three ways (Table 36.5).

Biochemistry reveals a low normal calcium andphosphate (both maintained by parathyroid activity) andan increased bone alkaline phosphatase level. Treatmentis with oral vitamin D.

ScurvyScurvy is caused by vitamin C deficiency. This is nownot seen in clinical practice but, historically, caused bonedefects due to defective collagen formation, which alsocaused bone pains due to periosteal haemorrhage.

Table 36.5 Vitamin D deficiency

Reduced intake/ Poor dietary content ofabsorption vitamin D

Fat malabsorption -steatorrhoea

Skin synthesis impaired Lack of exposure to sunlightPigmented skin

Metabolism abnormal Impaired renal activation of25-hydroxyvitamin D to1,25-dihydroxy vitamin D;e.g. chronic renal failureInterference by anticonvulsantdrugs

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Dental implants

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IntroductionDental implants are now increasingly used to attachcrowns, bridges or dentures by anchorage to bone. Extra-oral implants are also available for attaching facialprostheses such as artificial ears or noses, and for boneanchored hearing aids.

Placement of implants requires careful patient selectionand treatment planning. Although the surgical techniquesare straightforward, they are exacting and practitionersshould only embark on implant treatment after appropriatetraining and experience.

Types of implantEarly implants were unreliable because the attachment tobone was by a layer of connective tissue. A variety ofpins, screws and blades were tried but epithelial down-growth frequently led to rejection. The resulting loss ofalveolar bone led to an even more difficult restorativeproblem.

Subperiosteal implants were less damaging butrequired a general anaesthetic to expose the bone surfacefor impression taking. Chrome-cobalt frames were con-structed in the laboratory and a further anaesthetic wasthen required for insertion. They were often in functionfor many years but epithelial downgrowth usually resultedin failure. Removal of failed implants was difficult dueextensive scar tissue.

Transmandibular implants appeared to have someadvantages but an extraoral incision was required and thesurgical technique was demanding. They were obviouslyunsuitable for routine use as they required specialistexpertise and hospital facilities.

The progression to modern implantology followed thediscovery of osseointegration, with the predictablesuccess of titanium implants. Osseointegration implies

Table 37.1 Osseointegrated dental implants

OsseointegrationIndications for implant treatmentPatient selectionTreatment planningSurgical techniqueAugmentation of boneComplicationsSuccess rates

contact between the implant surface and bone withoutany intervening connective tissue layer. It is, in fact, anankylosis of implant to bone and some prefer the term'functional ankylosis'. The bone does not recognise theimplant as a foreign body, which becomes, in effect, partof the bone. Thus an osseointegrated implant forms adirect bone anchorage for a prosthesis.

Osseointegration is therefore a prerequisite to success-ful implant placement and a consideration of the require-ments for this is followed by a description of the indicationsfor implant placement in dentistry. Discussion of patientselection and treatment planning will be followed by adescription of the surgical techniques involved in implantplacement including augmentation techniques, compli-cations and a consideration of success rates (Table 37.1).

OsseointegrationThe requirements for successful osseointegration of animplant are listed in Table 37.2. Suitable implant materialsare discussed below.

Implant materials

Ideally, an implant should be non-toxic, biocompatible,strong and aesthetic.

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Table 37.2 Requirements for osseointegration

Suitable implant materialMinimal surgical traumaPrimary implant stabilityAdequate bone volume and qualityDelayed loading (healing phase)

Metals such as nickel and chromium used in stainlesssteel are corroded in living tissue and taken into the blood-stream. There is concern about possible neurotoxicity.Titanium is also absorbed and may be detected in tissuesat very low concentrations, but there is no evidence oftoxicity.

Implant materials can be biotolerated, bioinert orbioactive. Stainless steel, chrome cobalt and other alloysare tolerated by bone but are linked by a connective tissuelayer rather than an intimate bond. Titanium implantsmake direct contact with bone but are regarded as bioinertbecause there is no chemical bond. Bioactive materialssuch as calcium phosphate and hydroxyapatite allow a truechemical bond to develop as the bone surface remodels.

The material should be able to withstand occlusal forcesand be capable of accurate machining into cylinders withscrew threads for initial stability in bone, and with suit-able abutment connections. Unfortunately, a bioactivematerial with adequate mechanical properties has not yetbeen developed.

Surface characteristics can modify the properties ofthe material. Correct pore size is important in osseo-integration of ceramics. Surface roughness may affect thereaction of tissues to implants enhancing osseointegrationas well as increasing the surface area in contact withbone.

Titanium

Titanium is the best material available at present. It is ahighly reactive metal that oxidises in the atmosphere toform an inert surface layer of titanium oxide. It has goodmechanical properties and can be machined. Implantfractures can occur but these are minimised by carefulimplant design and avoidance of a traumatic occlusion. Adisadvantage of titanium is its grey colour, which may bevisible at crown margins if there is recession and maydiscolour thin mucosa. The surface can be polished andanodised and surface roughness can be achieved byaddition or subtraction processes. In plasma coating,titanium powder is sprayed onto the implant as an inert

gas at high temperature in an electric arc. Plasma-sprayedimplants have a much greater surface area and mechanicalresistance to rotational forces. Abrasion of the surfacewith titanium pellets or grit blasting and acid etchingmay also achieve similar effects. Some workers claimthat these surface modifications promote a chemical andmechanical attachment to bone. Rough surfaces exposedto the mouth will be difficult to keep clean and plaqueformation will result in peri-implant disease. Transmucosalelements and abutments are therefore made smooth. A'gingival' cuff attachment is achieved by reorientation ofconnective tissue fibres and possibly by adhesion ofepithelial cells.

Ceramic

Ceramic implants had good biological and aestheticproperties but lacked mechanical strength. In practice theincidence of implant fracture was unacceptable and theyhave been discontinued. It is possible that better ceramicswill be developed.

Hydroxyapatite

Hydroxyapatite can be used as a coating on titaniumimplants because it is osteoinductive. It enhances, andreduces the time for, osseointegration. It is also used inparticle or block form to augment bone for placement ofimplants. It does have mechanical weakness and disrup-tion of the surface occurs in function, although thesemicrofractures do not seem to result in loss of implants.Fractures can also occur at the interface betweenhydroxyapatite and titanium.

Implant system

Many implant systems are available and many factorsneed to be considered when making a choice. These arelisted in Table 37.3.

Surgical principles

Initially an implant bed must be prepared by drilling ahole in the bone to receive the implant. It is essential tominimise tissue damage when preparing the implant bed.Mucoperiosteal flaps should be well designed, carefullyreflected and gently retracted, so that healing is optimal.Healthy soft tissue cover enhances osseointegration byproviding a barrier to infection and restoration of blood

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Table 37.3 Criteria affecting choice of implantsystem

Use commercially pure titaniumComponents proven to withstand masticatory loadPhysiological response of bone when loadedOne- or two-stage systemType of surface, i.e. plain, plasma sprayed, roughened

or hydroxyapatite coatedPlain cylinder, or threaded ± self-tappingDiameter and lengthEfficiency of drill systemImmediate or delayed loadingSuitability of abutments

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supply. With transmucosal systems, soft tissue is suturedaround the implant neck and a good seal is even moreimportant.

Bone preparation is carried out with the minimumheat production so that, as far as possible, the osteocytesnear the bone surface remain vital. If there is bonedamage the inflammatory reaction will produce a fibrousrepair resulting in a connective tissue layer betweenimplant and bone rather than osseointegration.

The requirements that -must be taken into accountwhen drilling bone to receive an implant are listed inTable 37.4.

Primary implant stability

The implant bed should be prepared accurately to con-form to the shape of the implant, so that there is maximumcontact with healthy bone. This good congruence alsoresults in primary implant stability, which is essentialduring the healing phase.

Screw threads are often used as they increase primarystability, enhance resistance to occlusal forces andincrease surface area.

Bone quality and quantity

Blood supply is essential for bone vitality so the maxillamight be thought to be better suited for implantplacement. In fact, there is a significantly better successrate in the mandible, which is likely to have a poorerblood supply especially in the older edentulous patient. Itseems, therefore, that a firmer bone structure is anadvantage. The cortical plate in the maxilla is often thinor absent and the cancellous bone is crumbly.

Table 37.4 Bone drilling for osseointegration

Use sharp drills (single or limited use)Use purpose designed drillsUse drills of smaller diameters first, rather than one-

stage cuttingUse slow drill speeds (<2000 rpm)Use cooling with copious chilled salineAvoid clogging of drill channels - repeated withdrawalThread tapping or self-tapping systems are available

Table 37.5 Methods of improving implantsuccess in the maxilla

Use additional implants to share loadUse connecting bars for bracingUse maximum length of implantConsider augmentation of ridge boneConsider sinus lift to extend available ridgeReduce occlusal table and eliminate traumatic occlusionAllow more time for osseointegration

The pattern of bone resorption and anatomicalstructures in the maxilla also cause problems. Resorptioncauses bone loss from the anterior and crestal surfaces,often leaving a narrow ridge in a retruded and highposition. Thus there is less bone and the implants have tobe placed in a poor position. The superstructures maythen be placed in a compromised position. The occlusalload on the implants may therefore be beyondphysiological tolerances.

Implants can still successfully be placed in themaxilla if allowance is made to avoid exceeding theabove limitations by the methods listed in Table 37.5.

Resorption in the mandible does not alter the antero-posterior implant position but there can be severe loss ofbone height. The alveolar bone has often been completelyresorbed and there is a pencil-thin mandible. Augmentationis rarely required, even in this situation, and two implantsmay be sufficient to stabilise a lower denture. This isfortunate, as denture instability is more of a problem inthe mandible.

Blood supply may be compromised by radiotherapybut, although this causes more failures in the mandible,there is still a reasonable success rate. In the maxillathere are many more failures after radiotherapy. A courseof preoperative and postoperative hyperbaric oxygentherapy, if available, may improve success in the maxillabut is not usually needed in the mandible.

Table 37.6 Classification of bone quality

I Cortical bone predominantII Dense cancellous bone and thick cortical boneIII Dense cancellous bone and thin cortical boneIV Porous cancellous bone and thin cortical bone

The quality of bone available is also important andthis can be assessed using the classification listed inTable 37.6.

Healing phase

It is a fundamental requirement that undue loading isavoided until osseointegration has occurred. This is oneof the main differences compared to previous implantpractice where there was immediate loading and osseo-integration rarely occurred.

In the mandible, 3 or 4 months are required forosseointegration, whereas in the maxilla 6 months isallowed. These rules have been relaxed in the anteriormandible only. If bone quality is good, depth is adequateand four or five (or possibly fewer) implants are placed,the superstructure may be fitted immediately. Theoreti-cally, function encourages bone formation and there issome evidence that controlled loading could bebeneficial. This is difficult to control in practice atpresent.

Indications for implanttreatmentThe availability of implants has expanded treatmentoptions for a number of restorative problems highlightedin Table 37.7.

Difficult edentulous cases

Poor retention of a mandibular prosthesis not onlyinterferes with eating but also inhibits social contact, aspatients are afraid that the denture will dislodge in speechor mastication. The attached mucosal ridge may be littlemore than 1 mm wide and the sulcus mucosa is prone topain or ulceration. Severe resorption often results inprominent genial tubercles or exteriorisation of themental nerves so that provision of a comfortable dentureis impossible. An implant-supported fixed prosthesis

Table 37.7 Indications for implant treatment

Difficult edentulous casesLong span bridgesFree end saddlesSingle tooth replacementSpecial indications

restores function and confidence. An implant-supportedremovable denture is a simple, cheaper and effectiveoption. Two implants with stud attachments or a bar canbe sufficient to stabilise a denture, which is then mainlytissue borne. Implants are always placed between themental foramina in edentulous cases.

Retention problems occur in the maxilla, althoughless frequently because the hard palate gives better sup-port and retention for a conventional denture. Resorptioncan lead to a flabby ridge and retrusion. Implants placedin the anterior maxilla will aid retention and stability butpoor bone quality requires placement of as many implantsas possible and a bar may be required for bracing.

Patients who are unable to tolerate a denture, due togagging, or who are unwilling to wear a removableappliance, can benefit from an implant-born bridge,although the lip will not be as well supported as with adenture flange. This problem should be explained to thepatient, who may then prefer a conventional denture.

If the patient decides on implant treatment, ridgeaugmentation may be necessary, especially in themaxilla. The available bone can also be increased by asinus lift where a bone graft or synthetic material isplaced in the maxillary antrum.

Long span bridges

Implants can be used where the span is too long for aconventional bridge or when abutment teeth are com-promised by bone loss, short roots or extensiverestoration.

In the maxilla, there may be limiting factors such asinadequate or poor quality bone. Resorption may resultin an unfavourable position or angulation of the implant,necessitating a long clinical crown or placement of therestoration well in front of the ridge. These aestheticproblems are noticeable with a short upper lip. Lip con-tour may be not be as good as that obtained by a dentureflange. Augmentation should be considered as inedentulous cases.

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In the mandible, the pattern of bone resorption is lessof a problem and the main constraint is the proximity ofthe inferior alveolar or mental nerves.

Free end saddles

Replacement of mandibular molars is difficult with con-ventional dentures. There is a risk of mental anaesthesiawhen placing implants in the posterior mandible so it isessential to allow a good safety margin when calculatingimplant length. Drill tips do not conform exactly to theshape of the implant so allowance must be made forthe additional depth of the implant bed. The maxillaryantrum limits implant placement in the posterior maxilla.

Single tooth replacement

It can be simple and cost effective to replace an incisortooth with an implant when there is adequate bone. Ifthere is a diastema, the difficulties in construction of anadhesive bridge or partial denture are avoided. Also,preparation of adjacent teeth is avoided and there are nodenture clasps. Unfortunately, the pattern of boneresorption can result in an unfavourable path of implantemergence in the maxilla (especially if there is a historyof previous replantation or transplantation of a canine orincisor). If there is crowding, the nasopalatine canal canbe large enough to prevent implant placement. This cansometimes be overcome by restoration of ridge form bybone augmentation.

Special indications

Implants may also be indicated under specialcircumstances that are not dental in nature. These arelisted in Table 37.8.

Patient selectionPatient selection is important when planning implanttreatment to avoid a poor outcome and complications.

Clinical history and examination

The clinical history and examination will reveal thepatient's caries and periodontal disease experience.Patient compliance can be an important indication ofsuitability. It is also important to ascertain the patient'sexpectations of treatment.

Table 37.8 Special indications for implanttreatment

Wind instrument players or singersDenture intolerance due to gaggingPsychological aversion to denturesXerostomia, e.g. Sjogren's syndromePhysical disability (e.g. cerebral palsy, stroke or

myasthenia gravis)

Table 37.9 Medical problems compromisingimplant success

Cardiac diseaseHaematological diseaseImmunological diseaseBone disordersOther systemic diseaseOral disease

Medical history

A detailed consideration of the patient's medical historyis essential because several conditions can compromiseimplant success by interfering with healing, or increasingthe risk of infection (Table 37.9).

Cardiac disease

Severe cardiac problems can present risk but many patientswith mild disease can benefit from implants. Simplequestions about exercise tolerance give an indication ofthe patient's ability to withstand a surgical procedure.Implant failure is more likely in a patient with severedebilitation. Patients who are at risk of endocarditis maybe suitable but regular monitoring and radiographs areadvisable, and any failing implant should be removedwithout delay. Implants are contraindicated in patientswho have had a recent myocardial infarct, a valve replace-ment, are in cardiac failure or who have had previousbacterial endocarditis.

Haematological disease

Treated or mild anaemias should not prevent implanttreatment. Patients with haemophilia and other signifi-cant factor deficiencies would not normally be suitable.Warfarin therapy is a relative contraindication, butsurgery may be possible in selected cases with carefulmonitoring of the international normalized ratio (INR).

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Immunological problems Oral disease

Prolonged corticosteroid therapy can present a risk butthe patient can be given steroid cover. Implant survivalmay be reduced in patients on corticosteroids and thisshould be balanced against the potential benefit to thepatient. Patients on chemotherapy and those with severeimmune deficiency should not be considered. Drugaddiction depresses immune responses and implies poorcompliance. Smoking has an adverse effect on implantsurvival and patients should be strongly advised to cease.Smoking most probably reduces the success rate bysignificantly reducing the bony blood supply, especiallyto the mandible.

Bone disorders

Most bone diseases are a contraindication. Osteoporosisis especially common in older females but the jaws areless affected and implants can still be successfullyplaced.

If a patient has undergone radiotherapy there will be apoor success rate in the maxilla although hyperbaricoxygen (HBO) has been used with some success. Fewerproblems are encountered in the mandible and HBO isnot essential.

Other systemic diseases

Many other medical conditions, such as renal or liverdisease, can compromise treatment and consultation withthe patient's physician is advisable if in doubt. Indi-viduals with well-controlled diabetes can be accepted,although they have a greater risk of peri-implant disease.Patients with psychiatric disorders should be acceptedwith caution, especially if they attribute their problems todental disorders.

Table 37.10 Available bone and space forimplants

6- or 7-mm ridge width (i.e. implant diameter + 2 mm)Proximity of adjacent teeth or foramina (incisive, mental)Adequate distance between implants for superstructureDepth of boneSafety margin for inferior alveolar nerve, floor of nose

and maxillary antrumUndercutsSufficient intermaxillary space for superstructure

It is important to ensure that the patient has a stableperiodontal condition and low caries rate at the time ofassessment, although many patients require implanttreatment as a result of previous neglect. Mucosaldisorders should be eliminated as far as possible. Bonequality and availability should be assessed (Table 37.6).

Treatment planningApart from appropriate patient selection, successfultreatment planning requires consideration of the avail-able bone and space within the mouth (Table 37.10) andthe associated anatomical structures (Table 37.11). Treat-ment planning also needs to be informed by appropriateradiographic examination and examination of articulatedstudy casts.

Radiographic examination

Conventional radiography, including an orthpantomo-graph (OPT) and periapical or lateral views whererelevant, is necessary. The OPT is most useful because itindicates vertical bone height and the position of allrelevant bone cavities and nerve canals. It is important tomake allowance for distortion and magnification whenusing an OPT. Transparent overlays are available butmore accuracy can be obtained by inserting a base platewith standard metal balls or strips of gutta percha overthe planned implant positions before taking the radio-graph. This latter method enables exact calculation ofavailable bone when implants are to be placed close tothe inferior alveolar nerve or other important structures.

Serial tomograms or computerised tomography (CT)scans may also be used where detailed mapping ofavailable bone and anatomical structures is required. CTscans are not always readily available and they involve a

Table 37.11 Anatomical structures important inimplant treatment planning

Maxillafloor of nosemaxillary antrumnasopalatine foramen

Mandibleinferior alveolar nervemental nerve 297

much higher radiation dose. Scatter due to metalrestorations can render the image unusable. CT imagescan be very helpful but can be disappointing unless theradiologist is familiar with dental requirements andsoftware.

Magnetic resonance imaging (MRI) is becomingmore readily available. It has no radiation dose and theonly known hazard is with ferrous metals in the magneticfield. It is likely to replace CT scanning and - eventually- most other X-ray investigations. New machines will beless likely to induce claustrophobia and noise levels arenow significantly reduced.

Study casts

Study casts are invaluable for demonstrating treatmentoptions. Duplicates can be used for a diagnostic wax-upso that tooth position can be planned. A template canthen be constructed with indicator holes drilled as an aidto the surgeon, so that implants are placed in the optimumposition at operation.

Other treatment options

After considering the factors relating to patient selectionand treatment planning, restorative options should beconsidered (Table 37.12).

Surgical techniqueFlap design

Mucoperiosteal flaps are usually taken along the crest ofthe ridge. Relieving incisions may be short, as it is notusually necessary to expose all the alveolar bone. If thereare adjacent teeth it may be necessary to release theinterdental papilla. Flaps should be handled carefully aspoor healing could compromise osseointegration.

With two-stage implants where the implant is buried,it used to be common practice to keep the incision away

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Table 37.12 Treatment options

Removable partial dentureFixed bridgeComplete dentureImplant-supported dentureImplant-supported bridgeNo prosthesis

from the crest so that the suture line was not directly overthe implant. This was technically more difficult and isnow less popular because of the risk of haematomaformation or flap necrosis.

When augmentation procedures are planned, a bevelledflap is taken so that mucosal cover of the membrane orgraft is achieved. A bevelled flap taken from the palatalaspect can also be used to improve the bulk of buccalinterdental papilla when uncovering a buried implant atthe second stage.

Bone drilling

Purpose-made sharp drills are essential. Many manu-facturers advise single use and supply prepacked steriledrill kits. It is essential to have an accurate indication ofdrill speed so that overheating is avoided by keepingbelow 2000 rpm. Thermal damage is also minimised byincremental drill stages up to the final diameter. Threadtapping, where required, may be hand driven or by veryslow drilling, preferably using a drill with a torque con-troller. Copious irrigation with chilled saline solution isessential. Drills must be withdrawn frequently to allowcooling and prevent clogging of the drill channels. It isimportant to maintain drill direction, or the implant bedwill be inaccurate.

Countersinking is used where the system requires thecover screw to be buried or where the transmucosalelement is to be submerged to improve aesthetics.

Insertion

Decontaminated and sterilised implants are individuallypacked in vials. Titanium forceps are used if handling ofthe implant is required, but this is not normally necessarydue to the design of manufacturer's delivery system. Afixture mount may be included in the package or attachedby the operator.

The implant should be placed with as little con-tamination as possible. Good flap retraction will reducecontamination by saliva and epithelial surfaces. Themethod of insertion varies but most implants are screwedin either by hand or using a drill with a torque controller.Irrigation is used to prevent overheating. Excessive forceshould not be used because heat will be generated, andthere is also a danger of damage to the implant or coldwelding it onto the fixture mount.

A cover screw is placed and the soft tissues are suturedover or around the fixture according to the system in use.

With two-stage systems, where the implant and coverscrew are covered by mucosa, it is important to ensurethat the cover screw is seated properly, as soft tissue orbone formation below the cover screw can be difficult toremove from the implant face at the second stage.

Abutment connection

Two-stage implants have to be uncovered to allow abut-ment placement. This is done through a small incision onthe crest of the ridge or by removing a circle of mucosausing a punch. Bone may have grown over the coverscrew and this is removed using the manufacturer's bonemill. Instruments are also available to remove any bonethat has formed on the implant face because of a loosecover screw. The implant face must not be damagedduring bone removal as the junction with the abutmentis accurately machined. A portal of entry for micro-organisms would cause problems with infection later.

A suitable abutment is chosen and screwed in, takingcare that it is seated correctly and avoiding crossedthreads. Selection of a suitable abutment at this stage canbe difficult because the soft tissue level will vary as themucosal cuff matures. Alternatively, a healing abutmentcan be placed and the final abutment is selected once thesoft tissues have healed.

Augmentation of boneWhen there is insufficient width or height of bone it maybe possible to gain additional bone either before or at thetime of implant placement.

Various methods of bone augmentation can be used,including onlay grafts, guided bone regeneration, sinuslift procedures or ridge expansion. Bone graft materialsmay be in block or granular form (Table 37.13).

Table 37.13 Bone graft materials

Autograft: patient's own bone, e.g. iliac crest, tibia orintraoral

Allograft: human donor (not used due to risk of cross-infection)

Xenograft: calcified matrix derived from biologicalmaterial, e.g. bovine bone or coral (no risk of cross-infection due to removal of protein?)

Synthetic material: e.g. hydroxyapatite, tricalciumphosphate, glass

Onlay grafts

Blocks of bone may be used for extensive defects.Cortical bone taken from the patient's iliac crest orcalvarium is preferred but harvest involves major surgeryand the risk of donor site morbidity. Implants are placedsome months later when the graft has taken.

Immediate placement is also advocated, as earlyloading may reduce resorption and the patient is spared asecond operation. However, there may be an increasedrisk of loss of fixtures and bone due to infection.

A reliable substitute for autologous block bone is stillawaited.

Guided bone regeneration

Healing by osteoblasts produces bone but, when a bloodclot is organised by fibroblasts, collagen formation ispredominant and scar tissue is formed. When a suitablemembrane is placed over bone, however, fibroblasts areexcluded and angiogenesis and osteogenesis occur in thecavity below. This is the basis of guided boneregeneration.

Membranes can be non-resorbable (e.g. polytetra-fluorethylene) or resorbable (e.g. collagen). The shape ofthe cavity can be maintained by using a reinforced mem-brane. Alternatively, the membrane can be supportedwith bone, bone substitute or a mixture of both. Smallsteel posts may also be used as supports. The peripheryof the membrane is stabilised by screws or pins, whichcan also be resorbable. Recent developments with the useof bone morphogenic proteins may revolutionise boneaugmentation in the future.

Sinus lift procedure

There is often insufficient bone height in the posteriormaxilla due to bone resorption and the presence of themaxillary antrum. Onlay bone grafts are prone to failureand may be unsuitable due to lack of intermaxillaryspace. The sinus lift procedure creates additional alveolarbone height within the antral space.

The antral lining is exposed by removing a window ofbone on the buccal aspect via a buccal mucoperiostealflap. The antral lining is carefully elevated intact and issupported by bone-grafting material. It is also possible toleave the bony window attached to the antral lining andsupport both with graft material or implants. Immediateimplant placement is only advised if there is sufficientbone for primary implant stability (about 6 mm in height).

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An alternative is to approach the antral floor usingosteotomes to enlarge a bur hole on the crest of the ridge.The antral lining can then be lifted and supported bybone graft material. When there is sufficient bone forprimary implant stability the lining can be lifted throughan implant preparation. If the preparation is stopped justshort of the antral floor the cortical plate can be tappedupwards with the lining. The cortical plate and theimplant then provide support for the lining.

Ridge expansion

Where there is sufficient bone depth but the ridge is toonarrow, the implant bed may be prepared by boneexpansion, provided that there is a cancellous layerbetween the cortical plates. The crest of the ridge isexposed leaving the rest of the alveolar bone attached tomucoperiosteum. The ridge is widened by D-shaped andround osteotomes between the cortical plates prior todrilling.

Success ratesThe patient's appreciation is a very good indicator ofsuccess but objective criteria are required to monitor theeffectiveness of osseointegrated implants (Table 37.14).Various criteria have been suggested but the most reliableway to obtain comparable data is to record removal rates.Cumulative survival rates are based on an actuarialcalculation that allows for the fact that implants in aseries will have been present for differing times. It isreasonable to expect that, in the maxilla, 90% of implantswill survive for 10 years. In the mandible a 95% 10-yearsurvival is expected.

A number of adverse events may complicate implantplacement (Table 37.15). Avoidance of these compli-cations can only be achieved by careful planning and anexacting surgical technique based on sound training andexperience.

Table 37.14 Criteria for evaluation of success

Patient satisfactionSurvivalSuitable positionMobilityAmount of bone lossHealth of adjacent soft tissues - pocketing and

inflammationInfections or radiographic evidence of peri-implant bone

pathologyOperative complications e.g. damage to nerves or

adjacent teeth

Table 37.15 Complications of implant treatment

Intraoperativeimplant in poor positiondamage to mucosa and adjacent teethbone damage, i.e. lateral perforation, fracture of

alveolar bone or mandibular fractureperforation into adjacent areas, e.g. lower border of

mandible, nasal cavity or maxillary antrumnerve damage, e.g. inferior alveolar nerveloose implant due to incorrect drillingcontamination of implant or boneimplant damage, e.g. crossed thread or surface defectprimary haemorrhage - especially floor of mouth,

possible airway compromisePostoperative

painswellingreactionary or secondary haemorrhageinfection of peri-implant soft tissue or boneexposed or loose cover screws

Latemucosal recessionbone resorptionmobilityimplant fracture

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Cryosurgery andlaser surgery

IntroductionConventional surgery has used the scalpel to cut or excisetissue during surgical procedures. The scalpel, however,has limitations as a surgical tool. When an area of tissueis excised haemorrhage may be difficult to control and askin graft or flap may be needed to cover the defect orprevent scarring. Cutting or coagulating diathermy causedamage to the adjacent tissues. The physical effects ofcold and lasers offer alternative methods of removing ordevitalising tissue. They work in different ways and theywill be considered in turn.

CryosurgeryCryosurgery relies on the fact that rapid freezing andthawing of tissues cause cell death and necrosis. Cryo-surgery is thought to cause ice crystals in and aroundcells, causing disruption of cell membranes and contents.These effects are enhanced by rapid freeze and thawcycles. Blood flow to the area is reduced so that a largerand colder 'iceball' is achieved at the next application.Vascular damage also results in ischaemic necrosis.Immune mechanisms may be altered with beneficial oradverse effects.

Oral lesions are often surrounded by abnormalmucosa. The operator must therefore consider the effectsof cryosurgery at the edges of treated area. If there isepithelial dysplasia it is possible that cryosurgery couldpotentiate malignant change.

Uses of cryosurgery

Cryosurgery can be used in a number of conditions andin several is the treatment of choice (Table 38.1).

Freezing can be used to treat surface lesions such aswarts or small tumours. It is particularly suitable for

Table 38.1 Uses of cryosurgery

Ablation of warts and small tumoursAblation of haemangiomasTreatment of bony cavitiesBlocking of nerves

haemangiomas around the mouth. Several applicationsmay be required but cryosurgery has the advantage thatthere is no haemorrhage and the surface may be leftintact. Viral warts necrose and vascular lesions regress.There is often significant oedema but postoperative painis unusual. With a deeper freeze the mucosa or skin maynecrose, but re-epithelialisation occurs as the lesionsloughs away and healing is usually good with minimalscarring.

Bone cavities may be treated to reduce recurrence oflesions such as odontogenic keratocysts or central giantcell granulomata. The bone is devitalised but still remainsfunctional until it is replaced by vital tissue. In themandible the inferior alveolar nerve may be spared asnerves regenerate surprisingly well after freezing.

Cryosurgery is also used to treat painful nerve lesionsbecause nerves can be blocked without causing thesecondary neuralgia that often follows nerve section,avulsion or alcohol blocks. Pain relief lasts for severalmonths but repeat treatments are often required. Theevidence-base for this application of cryosurgery islacking but it has a place when conventional treatmentsare ineffective. Infraorbital, mental or inferior alveolarnerves can be treated after surgical exposure. An intraoralapproach is used. The most common condition treated inthis way is trigeminal neuralgia that no longer respondsto therapy with drugs such as carbamazepine, or whendrug side-effects are severe. Neurosurgical options shouldalways be kept in mind. The surgical management oftrigeminal neuralgia is discussed in Chapter 19.

301

38

302

Cryosurgery has been advocated for ablation ofmalignant tumours either as a curative procedure or forpalliation. Incomplete ablation of the lesion is unaccept-able and could easily occur, as it is not possible to predictaccurately the extent of tissue destruction. Moreover,case reports of accelerated tumour growth followingincomplete treatment raise the possibility that hostimmune response is compromised. Malignant andpremalignant lesions are therefore better treated by othermethods.

Cryoprobes

Dermatologists apply liquid nitrogen to skin lesionsusing a stick but a more precise method is needed for themouth. A cryoprobe is a surgical instrument with a coldtip. The temperature is determined by the boiling pointof the refrigerant liquid. The freezing effect may beachieved by evaporation at normal pressure, as withliquid nitrogen applied directly with a stick or spray, orwithin the probe tip. Other probe tips rely on the JouleThompson effect, where a pressurised gas is forcedthrough a small orifice. The refrigerant properties of thevarious liquid systems are listed in Table 38.2.

Nitrous oxide units are commonly available in hos-pitals and are suitable for most oral applications. Theywork from a nitrous oxide cylinder so they are alwaysready for use. Liquid nitrogen machines are much morepowerful but must be filled with liquid nitrogen on eachoccasion. This can be inconvenient for routine use andhandling a liquid at –196°C is hazardous.

Probe tips come in a variety of shapes and sizes. Flator dome-shaped tips from 3 to 10 mm are useful in themouth (Fig. 38.1). Long, narrow, insulated probes areavailable for freezing nerves.

Cryosurgery techniques

Under local anaesthesia the probe is applied to the lesionand switched on. The probe is held firmly onto the lesionuntil an ice-ball forms and freezing is continued. The timeof application will usually be about 1 min. The probeshould not be pulled away because it will be adherent tothe lesion. For vascular lesions, the effect is enhanced bycompressing the lesion with the probe, which decreasesblood flow. On turning the machine off there should be arapid thaw and the probe is released.

One or two further applications are made after 1 minto allow a complete thaw. Experience is necessary to

Table 38.2 Refrigerant properties of liquidcryoprobe systems

Type

Liquid nitrogen probeNitrous oxide probeCarbon dioxide probeLiquid nitrogen spray

Boiling point

-196°C-89°C-78°C-196°C

Surfacetemperature

-150°C-75°C-50°C-196°C

Fig. 38.1 A variety of shapes and sizes of cryoprobe tips.

judge the amount of treatment and the extent of thefreeze. The size of the ice-ball produced in a glass ofwater gives an indication of the effects on tissue tem-perature but the blood supply will modify this effect inliving tissue.

If necessary, a specimen can be obtained for histo-pathology while the lesion is frozen. Haemostasis wouldthen be required and, of course, there would be a surfacedefect. Freezing fixes the tissue temporarily before transferto formal saline so that good sections are possible.

Some liquid nitrogen units have the option of probe orspray freezing. The latter is a very effective tool for useon wide areas or uneven surfaces. It produces a veryrapid deep freeze and is more effective than the probe forfreezing large soft tissue lesions.

When treating a bone cavity after curettage of a lesion,a water-soluble gel may be used to aid contact with thebone surface and, in this situation, a liquid nitrogen unit

Table 38.3 Advantages and disadvantages ofcryosurgery

Advantagesno haemorrhageminimal postoperative paingood recovery of nerve functionminimal scarringbone structure maintainedblood vessel recoveryadjacent normal tissues recoverexcellent for haemangiomaspossible treatment of painful nerve lesions

Disadvantagescannot be used to cut tissuesdifficulty in assessing extent of treatmentexcessive swelling (could endanger airway)effects at the periphery (dysplastic changes can be

potentiated)whole lesion not available for pathologytumour growth may be acceleratednot effective for lymphangiomas

would be necessary to provide an adequate effect. Aliquid nitrogen spray would be preferable because itproduces a much faster and deeper freeze.

Care must be taken to retract and protect mucosalflaps and adjacent soft tissues, especially with liquidnitrogen machines.

It is also possible to freeze a resected portion ofmandibular bone after tumour ablation and replace it torestore continuity without the need to use a bone graft.The bone section is placed in a container of liquidnitrogen. This method is not often used because it ispossible that some cells from the original lesion couldsurvive. The most common reason for removal of fullthickness mandible is squamous cell carcinoma, and sucha risk would not be acceptable.

Advantages and disadvantages of cryosurgery

Cryosurgery is the preferred treatment for some con-ditions but it has certain drawbacks. The advantages anddisadvantages of cryosurgery are listed in Table 38.3.

Lasers'Laser' is an acronym for 'Light Amplification byStimulated Emission of Radiation'. The properties oflaser light depend on wavelength. A CO2 laser at 10.6 µmwavelength produces invisible light that is absorbed by

water and biological tissues and destroys them oncontact. An argon laser produces visible light at around0.5 µm; this passes through water but is absorbed bypigments such as melanin or haemoglobin. It may beused in eye surgery because it will not damage the lens oreye contents but acts on the retinal surface in treatingconditions such as diabetic retinopathy or a detachedretina. Surgical lasers are usually designed for cutting,coagulation and ablation of tissue. When a CO2 laserbeam meets the target tissue its energy is converted intoheat. Cell structure is destroyed by expansion as waterboils. Denaturation of proteins also occurs but the laserlesion deepens mainly as a result of cell disintegration atits surface. The result is a very narrow layer of tissuedamage below the treated area and better healing.

Light waves from a normal source do not produce apowerful cutting beam because they emerge randomly atvarious wavelengths. Laser light, however, is spatiallyand temporally coherent. This means that the waves areall of the same wavelength (monochromatic) and are inparallel, so that none of the energy from the light sourceis lost by interference. Compare a 60-watt light bulbproducing light and heat with a 60-watt laser beam thatwould cut through steel.

Laser light has many similar properties to ordinarylight. It is reflected by mirror surfaces. At some wave-lengths it will travel along an optic fibre or be refractedin a lens or prism. These effects are used to deliver thelight to the probe tip or operating microscope and tofocus it on the object. Alternatively, a fibre delivers theenergy by contact or proximity with the target. When thebeam is invisible, as with the CO2 laser, a red aiming beamis often provided.

Output may be in a continuous wave or pulsed. Pulsesare single or repeated typically with a duration of 0.1 s orless. Pulses of less than 1 µs are produced in Q-switchedlasers, which deliver very high energy without generatingexcessive heat.

Tissue effects may be photoablative (moleculardisruption), photothermal (cutting or coagulation),photomechanical (tissue disruption) or photochemical(photodynamic therapy). Low power lasers have beenused to enhance healing, promote blood clotting andrelieve pain, although these effects still require controlledclinical trials to exclude a placebo effect.

If a laser beam strikes a shiny surface it may bereflected and burn healthy tissue, the operator or othersnearby. Laser beams travel without loss of intensity, soeven if the beam is focused it may cause damage at a

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Table 38.4lasers

Precautions required when using

Non-reflective instruments (achieved by sand blasting)Protective gogglesWet swabs to protect tissuesRestricted access to laser area, warning lights and

noticesTraining and certification of usersArmoured or reflective endotraccheal tubes (+ inflation

of cuffs with water)Avoidance of inflammable skin prepping solutionsSmoke evacuation (+ face mask)

304

distance. Moreover, it will continue to cut deeper into thewound as long as it is applied An anaesthetic tube caneasily be pierced, resulting in ignition of anaestheticgases within the lungs, which is usually fatal.

There is also concern about the potential effects ofplume or surgical smoke produced by electrosurgery andlasers. Toxic chemicals are produced when tissue is burned.Blood aerosols and viruses such as human papillomavirus in the laser plume are thought to be capable oftransmitting disease. A surgeon's mask alone does notprovide adequate protection. High-volume aspiration(similar to that on dental units but with special filters) isrecommended.

In view of these hazards to patient and operator specialprecautions are needed and these are listed in Table 38.4.

Oral surgical applications

The CO2 laser is most useful and is readily available ingeneral hospitals. At present, the most frequent indi-cations are soft tissue lesions where the extent of theexcision prevents primary closure, and where skingrafting was previously required to prevent scarring.

White patches and premalignant lesions

Biopsy is essential to determine the diagnosis and degreeof epithelial dysplasia. Nutritional deficiencies such asiron or vitamin B12 should be treated. Patients must bestrongly advised to give up smoking. If lesions do notrespond and excision is required, the CO2 laser is a goodoption.

Erythroplakia and premalignant leukoplakia

These are treated similarly. Mildly dysplastic superficiallesions can be treated by ablation. Severely dysplastic

lesions need a deeper excision and it is then advisable touse the laser as a knife so that the whole lesion can besent for histopathology.

Erosive lichen planus

Erosive lichen planus that does not respond to any othertreatment is occasionally treated by laser with somesuccess, but this is best considered as a last resort kept forpatients with severe symptoms.

Denture-induced hyperplasia

This is a common condition that is very suitable for lasertreatment, especially if it is extensive. The denture shouldbe adjusted and left out as much as possible for severalweeks so that extent of surgery can be decided.

Squamous cell carcinoma

The CO2 laser is used in the resection of malignanttumours, such as squamous cell carcinoma. Smalltumours in the floor of mouth can be completely resectedwith a wide margin.

Other lesions

The submandibular ducts can be divided with littlechance of postoperative salivary obstruction. Smalltongue lesions can be excised with the laser alone, exceptthat larger blood vessels can be troublesome. Whenexcising large tumours the laser can be used selectivelyfor dividing tongue or treating areas of field changebeyond the excision margin.

Types of laser

Several types of laser are available (Table 38.5). Thesewill be discussed below.

Carbon dioxide

The CO2 laser has ideal properties for soft tissue surgery.It removes lesions with minimal damage to underlyingtissue. There is less inflammation and oedema and littlescarring, so that wide areas can be treated without theneed for skin or mucosal grafts. Small blood vessels(<0.5 mm) are coagulated so that haemostasis is rarely

Table 38.5 Therapeutic lasers

Type (and mode ) Wavelength and colour Uses

Excimer (pulsed) 0.190–0.351 µm invisible UV Skin lesions, corneal surgery, angioplasty,tooth surface conditioning

Argon (continuous wave) 0.488 µm blue and 0.515 µm green Vascular lesions, intraocular surgery, bloodcoagulation, middle ear lesions, compositecuring

KTP (pulsed) (fibreoptic delivery) 0.532 µm green Telangiectasia and coagulation of largervessels, tonsillectomy, urethral strictures,bladder surgery, salivary duct strictures

Tuneable dye laser (continuous wave 0.504 - 0.632 µm variable Vascular lesions, tattoo removal,or pulsed) photodynamic therapy, ?dentine sensitivity

and other dental usesHelium-neon (continuous wave) 0.633 µm red Aiming beams and pointers, laser Doppler

flowmetry, caries diagnosis, stimulation ofwound healing

Diode lasers (pulsed) 0.650-950 µm Pain relief, biostimulation, tooth whiteningNeodymiurrvYAG (continuous wave, 1.06 µm invisible infrared Tumour removal in oral surgery,pulsed or Q-switched) gynaecology, bleeding peptic ulcers,

fissure sealing, caries, dentinehypersensitivity, dentine, enamel and bonecutting, varicose veins (long pulse),analgesia (low power laser)

Holmium:YAG (pulsed) 2.100 µm invisible infrared Ureter and bladder surgery, lithotripsy,(fibreoptic delivery) myocardial revascularisation,

dacrocystorhinostomyErbium:YAG (pulsed) 2.94 µm invisible infrared Skin resurfacing, caries removal, enamel,

dentine and ?bone cuttingCarbon dioxide (continuous wave, 10.6 µm invisible infrared Tumour removal in gynaecology, ENT andpulsed or Q-switched ) oral surgery, denture-induced hyperplasia,

skin resurfacing, gingival surgery, implantexposure, fissure sealing, caries, scaling ofroot surfaces, ?dentine, enamel and bonecutting

required. Unlike cryosurgery, no potentiation of malig-nant change has been observed. Scanning technologyenables a focused beam to adopt a pattern for resurfacingprocedures such as wrinkle removal where it is claimedthat tissue is vaporised before any thermal damage orcarbonisation occurs.

The specific advantages of a CO2 laser are listed inTable 38.6.

Simple procedures can be quickly carried out underlocal anaesthesia. The lasered area is left raw and haemo-stasis is rarely needed. Carbonisation during treatmentleaves black particles on the surface. A greyish layerabout 2 mm thick forms on the surface due to coagulationof exudate. This eschar is lost as re-epithelialisation pro-ceeds beneath. The surface is restored after 1 or 2 weeksand further improvement continues in succeeding months.

Table 38.6laser

Advantages of the carbon dioxide

Excision of wide areas with minimal scarringHaemostasis, i.e. bloodless fieldNo significant swelling (airway not compromised)Moderate postoperative painSafe on malignant and pre-malignant lesionsExtent of excision visibleSkin graft not needed

Neodymium: YAG

The neodymium:YAG (or Nd:YAG) laser units are alsoused on soft tissue. 'YAG' is yttrium aluminium garnet,which is added to the neodymium lasing medium. Surface

305

lesions can be ablated as with the CO2 laser. Whendifferent settings are used, however, deeper penetration ispossible (e.g. in the treatment of endometriosis).

Argon

The argon laser produces visible light that is absorbed bypigments such as melanin. It is suitable for retinal sur-gery and is particularly effective in diabetic retinopathy.It may also be used for vascular lesions such as port-winenaevus, and is effective in removing some tattoos.

Helium-neon

Helium-neon (He-Ne) lasers produce a low-power, red,aiming beam for some invisible lasers and are usefulpointers in the lecture theatre.

Dye lasers

Dye lasers can be tuned to selected wavelengths fortreatment of various types of vascular naevus accordingto their colour. They are used similarly in tattoo removal,

although removal of green pigment is not achieved bythis, or any other, laser. In photodynamic therapy theymay be used to switch on a cytotoxic drug at the site of amalignant tumour.

KTP lasers

KTP lasers produce a green light that is used for treatingtelangiectasia and pigmented lesions; they are used forbladder surgery and urethral strictures. In ENT surgery,KTP lasers are used for tonsillectomy, sinus surgery andtear-duct surgery. Their versatility is partly due to thedelivery system, which uses optic fibres of 1 mm or lessin diameter. KTP lasers have the potential for treatingparotid or submandibular duct strictures.

Other lasers

A laser may be set to produce a continuous wave or apulsed output. Very short pulses allow high energy levelsto be achieved without generation of excessive heat.Wider surgical applications are then possible. Carbondioxide and erbium:YAG lasers are being developed tocut enamel dentine and bone.

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Index

Page numbers in italics refer to figuresand tables. Entries are arranged in word-by-word alphabetical order.

abdominal woundsdehiscence 10, 57incisional hernia 10, 58

ABO blood groups 43mismatch 44

abscesses see brain abscess; dentalabscess; periodontal abscess

achondroplasia 279, 280acid-base balance 33

abnormalities 33vomiting 29compensation 33-34monitoring in anaesthesia 79

acidosis 33acinic cell tumour, salivary gland 118actinomycosis see cervicofacial

actinomyosisactivated partial thromboplastin time

(APTT) 40and heparin infusion 20

acute submandibular staphylococcallymphadenitis 269

adenocarcinoma, salivary gland 119adenoid cystic tumour, salivary gland

118-119adenoidal hypertrophy 150adenoidectomy 150adenoiditis 150adenolymphoma 118

parotid gland see Warthin's tumouradenomatoid odontogenic tumour 288ADH see antidiuretic hormoneadrenaline (epinephrine) 44

interactionshalothane 75potassium 275

in oral surgery 201, 202-203, 217, 239adult respiratory distress syndrome

(ARDS) 22aerocoeles, cranial 101aesthetic assessment 103-104AF see atrial fibrillationage factors

bone remodelling 63dental extraction 211

falls 89general anaesthesia 71hypovolaemic shock 15wound healing 9see also children; elderly patients

agitation, postoperative 80air-borne spread of infection 46–47air-filtering systems 56airway maintenance 74-75, 80

clefts of the lip and palate 134–135airway obstruction

emergency management 147–149inhalational induction 72

albumin 27, 30solution 44

alcoholdrug interactions 82, 86facial fractures 89history taking 6, 182-183laryngeal cancer 154oral cancer 141, 143sialadenosis 115withdrawal 70

alcoholic hand rubs 46aldehydes 49aldosterone 28

antagonists 32alfentanil 77alkalosis 33allergies

blood transfusion 44history taking 6, 70inferior dental blocks 205metal 90

alloplasts 177alveolar clefting 133

repair 137-138alveolar plate fracture 213alveolectomy/alveolotomy 247ameloblastomas 286-287

clinical features 286-287cystic 232, 287differential diagnosis 231, 232, 233treatment 287

American Society of Anesthetists (ASA)69, 70, 82

amnesia, conscious sedation 82amoxicillin 198, 267, 271–272amylase 112

anabolic state 34anaemia 23, 42–43

complication of blood transfusion 45oral surgery 274

anaesthesia see general anaesthesia; localanaesthesia; nerve damage

analgesiaagents 77-78fracture management 63postoperative 80

oral surgery 196-198stage of anaesthesia 73, 84, 85see also pain relief

anaphylaxiscomplication of blood transfusion 44history taking 6, 70

aneurysmsbone cyst 279, 280carotid 159-160subarachnoid haemorrhage 168-169

angiography 20, 166angiotensin I & II 28angulation, fractures 62ankylosis

dental 254implants see osseointegration

facial fractures 93-94, 102TMJ

trauma 175treatment 177, 178

anosmia 99, 162anthrography 174antibiotic prophylaxis

excessive use 56, 227mandibular fractures 92maxillary fractures 99open fractures 65oral surgery 198, 227, 275oroantral fistula (OAF) 213–214perioperative 52, 56, 57postoperative 58preoperative 71UTI 23

antibiotic resistance (MRSA) 48, 49, 198antibiotic therapy

acute sialadentitis 271–272cervicofacial actinomyosis 268–269dental abscess 266–267non-union of fractures 67

307

antibiotic therapy—(cont'd)respiratory tract infections 22tonsilitis 150

anticholinergics 71–72anticoagulants 6

contraindications 70intravenous see heparinoral see warfarin

anticonvulsants 76–77, 171, 277antidiuretic hormone (ADH) 28

increased secretion 34lack of response to 31

antiemetics 13premedication 72

antihistamines 44, 72antiseptic packs/dressings 58antithrombin III 37antrostomy 101anxiety

assessment 82control 71, 72, 81, 82, 84, 85

Apert syndrome 108, 170apicectomy see periradicular surgeryapnoea monitoring 134–135APTT see activated partial thromboplastin

timeaqueduct stenosis 171ARDS see adult respiratory distress

syndromeargon lasers 306Arnold–Chiari malformation 170arterial blood gas analysis 20, 21, 79artery forceps 266arthrocentesis 175arthroscopy 175ASA see American Society of

AnesthetistsAsche's forceps 98Ash pattern elevator 191aspiration

from pathological lesions 257-258see also fine-needle aspiration

of gastric contents 22, 72-73aspirin 19, 40, 274

see also non-steroidal anti-inflammatory drugs (NSAIDs)

assistance, oral surgery 190asthma

conscious sedation 84, 85history taking 6, 70, 82non-steroidal anti-inflammatory drugs

278oral surgery 278

astringents 222ataxia 171atelectasis 21ATPase exchange pump 27atracurium 78atrial fibrillation (AF) 17

embolus formation 19, 20atrial naturetic factor 28atropine71–72, 78, 80audit, sepsis rate 57

308 autoclaving 48–49autoimmune thrombocytopenic purpura 39

AV boots 18avascular necrosis 67azidothymidine (AZT) 51

bacteria see infection; skin flora; woundsepsis; specific organisms

bacterial meningitis 170Bacteroides 56barium swallow 151Battle's sign 167benzodiazepines

alcohol interaction 70conscious sedation 81–82, 83, 85-86.

87general anaesthesia 78

premedication 71respiratory depression 87reversal 78, 87

beta-blockers 15, 70, 275bicarbonate (HCOO 33

renal retention 33-34bile salts 41biliary disease 41biopsy 257

bone 286lymph nodes 145-146, 158-159oral premalignant lesions 142, 304salivary glands 113–114, 273techniques

excision 258incision 258punch 258

bleeding tendency, increased 39–42block anaesthesia, oral surgery 203-207blood clotting 36-39

abnormal 39-42disollution 37–38fracture healing 62, 63initiation 36–37limitation 37prevention 38-39stabilisation 37wound healing 7

blood cultures, intravascular lines 22blood disorders

increased bleeding tendency 39–42increased clotting tendency 42oral surgery 274-275

dental implants 296see also anaemia

blood gas analysis 20, 21, 79blood glucose monitoring 18, 70blood loss monitoring 79blood pressure

monitoring 72, 78, 86see also hypertension; hypotension

blood products 43–44blood samples 257blood serum 257blood supply, wound healing 8blood tests

donor screening 41, 45LRTI 21

blood transfusion 23, 43–45complications 44–45

massive 42products 43–44

blood warmers 45blood-borne viruses 48

see also specific virusesblunt dissection 266, 272, 273body osteotomy 106Bohr effect 43bone augmentation, dental implants

299-300bone cavities, cryosurgery 300, 302-303bone diseases

aetiology 280see also specific diseases

bone drilling, dental implants 294, 298bone grafts

alveolar 137chin deformities 107dental implants 299-300facial fractures 92, 93, 97, 102iliac crest 92, 93rib 93, 178TMJ 178

bone morphogenic protein 102bone necrosis 62bone plates 106

resorbable 102bone removal

oral surgery 192periradicular surgery 240wisdom tooth extraction 226

bone ronguers 192, 193bone surgery 247-249

alveolectomy/alveolotomy 247bony exostoses and bone undercuts

247genial tubercles 249ridge augmentation 249sharp bony ridges 247-248sharp mylohyoid ridge 249torus mandibularis 248–249torus palatinus 248vestibuloplasty 249

bone undercuts 247bonewax 216bony exostoses 247boots, DVT prevention 18–19bovine spongiform encephalopathy (BSE)

53bowel see abdominal wounds;

gastrointestinal systembrachial plexus 14brachy therapy 144brain abscess 170brain damage 167–168brainstem signs 162branchial cleft anomalies 120branchial cyst 120, 159Bristow elevator 96bronchodilator therapy 71Brown's syndrome 101bruising 24, 39

floor of the mouth 90fractures 60, 90mastoid process 167

BSE see bovine spongiformencephalopathy

buccal advancement flap 193–194, 214,218

buccal expansion 210buccal injection 204–205buccal retraction 191–192buccal sulcus

abscess 264, 265ecchymosis 96

bupivacaine 201, 206buprenorphine 77

calcifying epithelial odontogenic tumour287

calcium 37binding 42defective metabolism 291

calcium gluconate 31callus

hypertrophic/hypotrophic 67provisional 63

Candida 245canines 252

conservative management 252reimplantation 253surgical exposure 252–253

buccal 256palatal 255–256

surgical removal 253cannulae

arterial, monitoring 78insertion 86intravenous induction 70removal 86

capnography see carbon dioxide (CO2),expired

carbamazepine 171, 277carbon dioxide (CO2) 33, 34

expired (ETCO,) 72, 75, 79lasers 303, 304–305

carbonic acid 33carbonic anhydrase 33carcinoma expleomorphic, salivary gland

119cardiac arrhythmias

atrial fibrillation (AF) 17, 19, 20halothane 75potassium levels 31, 32

cardiac catheterisation 17cardiac disease see endocarditis;

ischaemic heart disease;myocardial infarction (MI);valvular disease

cardiac functiondysrhythmias 17LVF 17obstructive shock 15septic shock 23

cardiac pacemaker, and use of diathermy14

cardiogenic shock 16–17cardiorespiratory monitoring in

anaesthesia 78–79cardiorespiratory problems 42–43, 70

cardiovascular reserveage 15anaemia 23pain 18

caries, untreatable 220carotid aneurysms 159–160catabolic state 34caval filter 20cavernous sinus thrombosis 267cellulitis 55, 57, 58, 265cemento–ossifying dysplasia 280, 282cemento–ossifying fibroma 280, 282cementoma 288central giant–cell granuloma 279, 280Central Sterile Supply Unit (CSSU) 48central venous lines

pneumothorax 15pressure monitoring 15, 16, 17, 29, 79TPN 35

cephalograms 104–105ceramic dental implants 293cerebellar pontine angle tumours 172cerebellar signs 162cerebral function monitors (CFM) 79cerebral perfusion 163cerebrospinal fluid (CSF)

lumbar puncture (LP) 165obstructed flow 162, 163, 170. 171otorrhoea 100–101persistent leak 98, 101, 109, 167rhinorrhoea 97, 98, 101shunt 171

cervical facial flap 126cervical spine, imaging 60, 99, 100, 166cervicofacial actinomyosis 268–269

aetiology 268clinical features 268diagnosis 268management 268–269postextraction 218

CFM see cerebral function monitorschemical pneumonitis 22chemical sterilising agents 49cherubism 279, 280, 281–282chest examination 21chest physiotherapy 21, 22chest sepsis 54children

adenoiditis 150airway obstruction 148branchial cleft anomalies/cysts 120, 159conscious sedation 82, 84, 86consent 186–187epistaxis 158foreign bodies, nasal 156fractures

craniofacial 102mandibular 90, 91–92, 93–94

general anaesthesia 72, 74pyogenic dental infections 268, 269see also age factors

chin deformities 105, 107chisels 192

Coupland's 193, 227chlorhexidine

handwash 8, 56irrigation 222mouthwash 93, 198–199skin preparation 57

chloride (Cl~) 27cholinesterase abnormalities 70Christmas disease 41chronic subdural haematoma (CSDH) 168cirrhosis 30citrate 42, 43CJD see Creutzfeldt–Jakob disease (CJD)clean contaminated wounds 55, 56, 58clean wounds 55, 56cleaning instruments 48cleft team 134clefts of the lip and palate 131–139

classification 132embryology 131–132patient management 134–135

airways 134–135feeding 135philosophy 139

structural abnormalities 132–134surgical treatment 135–139

Le Fort III osteotomy 108, 109primary 136–138secondary 138–139

cleidocranial dysostosis 252, 280, 281coagulation disorders 40–41

acquired 41–42inherited 40–41investigations 40

coagulation factors 37, 40, 41concentrates 44transfused blood 42

coagulation pathway 37, 38common 37extrinsic 37intrinsic 37

codeine 198collagen 7, 8, 9

fracture healing 63platelet adhesion 37

colloid osmotic pressure 27colloid solution 32–33commensals 56communication, conscious sedation 84, 86compartment syndrome 66

plaster casts 64Volkmann's contractures 67

complications of surgery 13–25early–stage 13–18, 24general 13intermediate–stage 18–24late–stage 24, 25local 24–25specific 24see also specific procedures

composite grafts 126–127computerised tomography (CT)

dental implants 297–298fractures 61

mandibular condyle 91–92maxillary 99 309zygomatic (malar) 96

computerised tomography (CT)—(cont'd)neurological 166, 169, 170, 171oral cancer 143, 144pulmonary angiogram 20salivary glands 112–113, 117TMJ 174–175

condylectomy 177condylotomy 177confusion 168, 169

postoperative 80coning 163, 165conscious level, reduced

Glasgow Coma Scale 163–164, 765signs and symptoms 163

conscious sedation 81–87agents 81–82assessment 82definition 81methods 82–87

inhalational 83–85intravenous 85–86oral 83

monitoring 86–87treatment planning 82

consent 82, 84children 186–187competence to give 186mental capacity 187oral surgery 185–187

general anaesthesia 187, 189–190unconscious patients 187

contaminated wounds 55, 56, 58contour lines

facial 123see also Langer's lines

contractures 10–11surgical treatment 11

corticosteroids 6, 9, 24, 40, 70adverse effects 276–277complications of blood transfusion 44dental implants 297inhalers 278local injection

in scarring 10, 125TMJ 175

Coupland's chisels 193, 227cow–horn forceps 208, 210cranial nerve

palsy 162vascular compression syndromes

171–172craniofacial fractures 100–102

complications 101–102examination 100–101

craniosynostosis 170craniotomy 166crepitus, mandibular fractures 90Creutzfeldt–Jakob disease (CJD) 52–53

healthcare workers 51tonsillar tissue 151use of disposables 49

cricoid pressure 72–73cricopharyngeal spasm 151

310 cricothyroidotomy 149cross–infection

extent of the problem 46routes of transmission 46–47universal infection control 47—50see also infection

Crouzon's syndrome 108, 170crush syndrome 66Cryer's elevators 193cryoprobes 302cryosurgery 300–303

advantages and disadvantages 303techniques 302–303uses 262, 300–302

crystalloid solutions 32CSDH see chronic subdural haematomaCSF see cerebrospinal fluidCSSU see Central Sterile Supply UnitCT see computerised tomographycurrettage, periradicular surgery 240cyclosporin 252cystic ameloblastomas 232, 287cystic change, wisdom teeth extraction

220cystic lesions, aspiration 258cysts

branchial 120, 159dermoid 159extravasation 272, 273salivary gland 120thyroglossal 159tonsillar inclusion 152see also jaw cysts

Dautrey procedure 176debridement, oral surgery 193deep vein thrombosis (DVT) 18–19

clinical features 19investigation 19, 37predisposing factors 18, 42, 65prophylaxis 18–19, 65treatment 19

dehiscence 10, 57dehydration, causes and mechanisms

29–30deltopectoral flap 128dental abscess 263–267

apical 263clinical features 263–264complications 267management 265–267

antibiotic therapy 266–267drainage 265–266removal of source of infection

266periapical 263spread of infection 264–265tooth transplantation 251

dental castsdental implants 298feeding plates 135orthognathic surgery 104

dental complications of craniofacialfractures 101–102

dental extraction 208–211abscess management 265, 266complications 212–218

immediate 212–214postextraction 215–218

equipment 208marsupialisation of radicular cysts 232non–surgical 250–251preoperative assessment 211preprosthetic surgery 243–244supernumerary teeth 255technique 208–210

application 208–210consolidation 210displacement 210postdelivery 210

unerupted teeth 244, 251see also wisdom teeth

dental forceps 208, 209application 210complications of extraction 212, 213placement difficulties 211

dental implants 292–300bone augmentation 299–300

guided bone regeneration 299materials 299onlay grafts 299ridge expansion 300sinus lift procedure 299–300

bone quality and quantity 294–295complications 300healing phase 295indication for treatment 295–296materials 292–293patient selection 296–297

clinical history and examination296

medical history 296–297primary stability 294success rates 300surgical principles 293–294surgical technique 298–299

abutment connection 299bone drilling 298flap design 298insertion 298–299

systems 293, 294treatment planning 297–298

radiographic examination 297–298study casts 298

types 292wisdom teeth extraction 221see also preprosthetic surgery

dental infection see dental abscess;infection, dental

dental luxators 193, 208dental malocclusions 101–102dental tweezers 196dentigerous cysts 232–233

clinical features 232diagnosis 232radiolucencies 232treatment 233

dentistryguidelines on general anaesthesia 187intravenous sedation 85

dentofacial deformities see orthognathicsurgery

denture(s)design, wisdom teeth extraction 221–induced hyperplasia 244–245

laser therapy 304modified, fixation 92stomatitis 245

dermoid cysts 159desferrioxamine 45desflurane 76dexmedetomidine 78dextrose solution 32diabetes insipidus (DI) 31diabetes mellitus 17–18

delayed wound healing 9history taking 70and oral surgery 276postoperative status 80

diabetic ketoacidosis 33diabetic nephropathy 30diarrhoea 29diathermy 12

–related injuries 14operating technique 57

diazepam 83, 85see also benzodiazepines

DIC see disseminated intravascularcoagulation

diclofen 78diet see nutritiondiethyl ether 75diffusional hypoxia 85digoxin 15diplopia 95, 98, 100, 101, 108–109dirty wounds 55, 56disease susceptibility, history taking 6disposable instruments 49, 53disseminated intravascular coagulation

(DIC) 39, 42, 44distraction osteogenesis 102, 109diuresis/diuretics

cause of dehydration 30in heart failure 15potassium–losing 275

Down syndrome 252drills/drilling 192, 226, 294, 298drooling 120drug history 6, 70, 182drug interactions/precautions

DVT prophylaxis 19gingival overgrowth 252hyperkalaemia 32hypovolaemic shock 15impaired wound healing 9oral surgery 182, 274–275, 277, 278pregnancy 277

dry socket 216–217postextraction 228predisposing factors 216–217treatment 201, 217

DVT see deep vein thrombosisdye lasers 306dysmorphophobia 103dysphagia

hypopharyngeal conditions 151, 153mandibular fractures 90

dysphasia 162dysphonia 154

facial fractures 89'glue ear' 150mandibular fractures 90, 93pain referred to 151

ear lobe, postoperative numbness 120early mobilisation 19, 64–65early–stage complications

of dental extraction 212–214of fractures 65of surgery 13–18, 24

EBA see ethoxy benzoic acid cementecchymosis

buccal 96circumorbital 95, 98postextraction 217

ECF see extracellular fluidECG see electrocardiogramECHO cardiography 17edentulous patients

dental implant 295raising a flap 191torus mandibularis 249

elderly patientsadverse effects of aspirin 19blood tests 21lateral neck swellings 159–160pressure sores 24see also age factors

elective patients, preoperative assessment71

electrocardiogram (ECG) 17, 20induction/monitoring of anaesthesia

72, 78electrolytes

abnormalities 31–32cardiac arrhythmias 17gastrointestinal ileus 23

fluid compartments and osmolarity 27homeostatic mechanisms 26, 27–28intravenous replacement 29monitoring, blood transfusion 45

electromyography 165elevators

oral surgery 191, 193, 208, 213wisdom tooth extraction 226, 227zygomatic (malar) bone fracture 96

embolectomy 21emergency management

airway obstruction 147–149rapid sequence induction 72–73

eminectomy 176end tidal carbon dioxide concentration

(ETCO2) 72, 79end tidal volatile anaesthetic

concentrations 79endocarditis 71, 218, 275, 276, 296endocrine disorders 275–277endoscopy 147

bronchus 143hypopharyngeal 153laryngeal 154, 155

nasal 151, 157oesophageal 143

endotracheal intubation 74assessment 70–71complication 14extubation 75induction 72

enflurane 75enophthalmos

complication of Le Fort III osteotomy109

orbital blow–out fractures 95, 100, 101ENT, examination techniques 147enteral feeding 34enterocococci 56enucleation, jaw cysts 231, 235–236'envelope' flap, oral surgery 191, 226EORTC see European Organisation for

Recognition and Treatment ofCancer

epinephrine see adrenaline (epinephrine)epistaxis 155, 157–158

adult 158childhood 158fractures

maxillary 98nasal 97zygomatic (malar) 95

epithelial cell migration and proliferation7–8

erythroplakia, laser therapy 304Escherichia coli 56escorts, post–sedation 82, 85ethmoid carcinoma 157ethoxy benzoic acid cement (EBA) 240etomidate 77European Organisation for Recognition

and Treatment of Cancer(EORTC) 146

Eustachian tubesmiddle–ear effusions 150obstruction 152

Eve's sign 86examination 70–71, 183–185

chest 21ENT techniques 147neurological 161–163oral cavity 184–185, 211

excisionof mucocoele 273of scarring 10

excision biopsy 258external fixation 64, 65extracellular fluid (ECF) 26, 27–28, 31extradural haematoma 168extraoral abscess, incision of 266extravasation cysts 272, 273extubation 75eye

closure, dental abscess 264examination 184see also ophthalmic injury; orbital

blow–out fractures; visualdisturbances

eyelid reconstruction 126, 127311

ear

facial examination 184facial expression 110, 122, 123facial fractures 89–102

aetiology 89current developments 102general examination 89mandibular 89–94middle third 94–102

facial incisions 123–124facial lacerations 124facial muscles 123facial nerve

anatomical relationshipsparotid gland 110, 114, 116, 117,

119SMAS 123submandibular gland 111, 119

function 119mobilisation/removal 117, 118monitor and stimulator 119operating microscope 124

facial paralysis/palsy 119, 184free skin flaps 128inferior dental block 205

facial reconstructionwound closure 125–130, 146see also orthognathic surgery

facial scars, management 124—125factor(s) see coagulation factorsfainting, inferior dental blocks 205falls 89family history 5–6, 70

oral surgery 182fasciotomy 66fasting, perioperative

conscious sedation 82diabetes mellitus 276fluid/electrolyte balance 29, 31postponement of surgery 71

fat embolism 65–66feeding see nutritionfelypressin 202, 277fenanyl 77FESS see functional endoscopic sinus

surgeryFFP see fresh–frozen plasmafibrin degradation products (FDP) 37, 42fibrinogen 37, 44fibrinolysis 37–38fibrinolytic therapy 20–21fibro–osseous lesions 280, 281–282fibroblasts 7, 8, 63fibrocartilage 63fibronectin 7fibrous dysplasia 280, 281

clinical appearance 281diagnosis 281management 281

fibrous epulis 259fibrous overgrowth/tuberosities 246,

259–260Fickling's forceps 193fine–needle aspiration 258

312 neck lumps 143, 158–159salivary glands 113, 117

fissural cysts 235fistulae

branchial 120cause of dehydration 29–30cleft deformities 138oroantral (OAF) 213–214, 218salivary 120

'flabby' ridges 246–247flaps

oral surgery 191–192buccal advancement 193–194, 214,

218dental implants 298'envelope' 191, 226labial 255lingual 249mucoperiosteal 191, 243–244, 247,

298osteoplastic 244palatal gingival margin 256periradicular surgery 240

skin see skin flapsflotron boots 18–19fluid compartments 26–27

distribution of crystalloid solutions 32osmolarity and electrolyte

concentrations 27fluid and electrolyte balance 26–34fluid monitoring 30, 31fluid overload 30–31

complication of blood transfusion 45fluid replacement

categories of response 16in dehydration 29, 30solutions 32–33

flumazenil 78, 87fluorosis 280, 281follow–up, oral surgery 199forceps

artery 266Asche's 98Fickling's 193tissue 194Walsham's 98see also dental forceps

foreign bodies 9airway obstruction 148–149facial lacerations 124nasal 156

fractures 59–68aetiology 59–60classification 61–62

angulation 62configuration 61displacement 62extent 61impaction 62joint involvement 62overlying skin integrity 61–62rotation 62site 61stability 62

closed 60, 61–62management 63–66

complications 65–68

delayed union 67diagnosis 60–61

clinical examination 60investigations 60–61

early physiological loading/movement64–65

healing 62–63inflammatory phase 62–63remodelling phase 63reparative phase 63

immobilisation 64open 60, 61–62

management 65principles of management 63–65, 65reduction 63tooth extraction

alveolar plate 213crown 212mandible 213root 212

see also facial fracturesfraenal attachments 244, 251fraenectomy 251free end saddles, dental implant 296free skin flaps 128–129fresh–frozen plasma (FFP) 41, 44Prey's syndrome 120frusemide 15, 30–31full thickness skin grafts 125–126functional endoscopic sinus surgery

(FESS) 157

gamma–amino butyric acid (GABA) 81gap arthroplasty, TMJ 177, 178gastrointestinal system

endogenous organisms 56fluid losses 29history, oral surgery 182ileus 23

gelofusin 44gender

dry socket 217haemoglobin (Hb) levels 42haemophilia 40

general anaesthesia 69–80agents 75–77

inhalational 75–76intravenous 76–77supplementary drugs 77–78

airway maintenance 74–75complications of surgery 13–14induction 72–73

emergency/rapid sequence72–73

inhalational 72intravenous 72

maintenance 73monitoring 78–79oral surgery 187–188, 189

consent 187, 189–190dislocation of TMJ 215

postoperative care 79–80postponement of surgery 71premedication 71–72preoperative assessment 69–72

preoperative assessment—(cont'd)elective patients 71history and examination 70–71

preoperative therapy 71preparation 72risk

aspiration of gastric contents 22,72–73

assessment 69ischaemic heart disease 275

signs and stages 73General Dental Council

definition, conscious sedation 81guidelines, general anaesthesia 187

genial tuberclesaetiology and clinical appearance 249management 249

GFR see glomerular filtration rategiant cell

epulis 260granuloma 279, 280

giantism 280, 282Gigli saw 177Gillies temporal approach 96gingival overgrowth 252gingivitis 222gingivoperiosteoplasty 137Glasgow Coma Scale 163–164, 165gliomas 169globus pharyngeus syndrome 151glomerular filtration rate (GFR) 28

reduced 30glossopharyngeal neuralgia (GPN) 172glossoptosis 134gloves 56glucose test

rhinorrhoea 97see also blood glucose

'glue ear' 150glyceryl trinitrate (GTN) 275glycine 81glycopyrronium 71, 78gold chain attachment 255, 256Gorlin–Goltz syndrome 234GPN see glossopharyngeal neuralgiagranulation tissue 7, 8, 58

fracture healing 63granuloma

central giant–cell 279, 280pyogenic 261

greater auricular nerve 120GTN see glyceryl trinitrateGuedel airway 74Guedel, signs and stage of anaesthesia 73,

83–84guided bone regeneration, dental implants

299gun shot wounds 102Gunning splints 92Gustillo and Anderson, classification of

open fractures 61–62gutta percha 245

haemacel 44haemangioma 260–261

haematological disease see blooddisorders

haematologists 39, 41, 42haematoma 24

intracranial 167, 168periorbital 166–167surgical technique 57

haemoglobin (Hb) 23hydrogen ion interaction 33normal levels 42

haemolysiscomplication of blood transfusion 44,

45perioperative precipitation 43

haemophilia A 40–41haemophilia B 41haemorrhage

dehydration 29intracranial 168–169postoperative

dental extraction 216oral surgery 199, 210

primary 15–16, 199secondary 21, 199subconjuctival 95, 98, 166–167

haemorrhagic vesicles 57haemosiderosis 45haemostasis

surgical technique 9, 12see also blood clotting

hair–bearing skinpreoperative preparation 8, 57scalp reconstruction 127

halitosis 151, 222halothane 75hamartoma 260–261hammer, oral surgery 192hand examination 184hand washing 8, 46, 56Hb see haemoglobinhead injuries 166–167headaches 163, 168, 169, 171

postconcussional 101healthcare workers

immunisation 50infection risk 46–47, 49, 50–52theatre personnel 56training in infection control 50

Heimlich manoeuvre 148–149helium–neon lasers 306hemifacial spasm 172Henderson—Hasselbach equation 33heparin 19

infusion pump 19perioperative 41–42potentiation of antithrombin III 37prevention of clot/emboli extension

20hepatitis B

blood donor screening 45carriers 46–47, 48, 51–52HBeAg 50, 52HBsAg 50, 52healthcare workers 46–47, 49, 50,

51–52

vaccination 50, 51non–responders 50, 51

hepatitis Cblood donor screening 45healthcare workers 49, 50–51, 52patients 52

hepatocytes 41hereditary haemorrhagic telangiectasis 40Hilton–type forceps 266histamine 37history 5–6, 70

allergies 6, 70drug 6, 70, 182family 5–6, 70, 182medical 5, 48, 70, 82, 181–182, 183neurosurgery 161–163oral surgery 181–183of presenting complaint 5, 181social 6, 70, 182–183

HIVblood donor screening 41, 45family history 70healthcare workers 50, 51, 52

homeostasis, fluid and electrolyte balance26–29

hormone–replacement therapy (HRT) 290hospital–acquired infections (HAI) see

cross–infectionhot air ovens 49Howarth elevator 191hydrocephalus 162, 163, 170, 171active 171hydrogen ions

concentration 33–34loss of 29transfused blood 43

hydroxyapatite 107, 293hyoscine 71, 80hypercoagulable state 34hyperglycaemia 34, 35hyperkalaemia 31–32, 45hypernatraemia 31hyperparathyroidism 280, 282

clinical features 282diagnosis 282management 282

hypersplenism 39, 41hypertension 71, 275hypertrophic scarring 10hyperventilation 33hypoalbuminaemia 30hypochlorite 49hypoglossal nerve 111, 119–120hypokalaemia 32

diuretic therapy 30–31, 70hyponatraemia 31hypopharynx

anatomy and physiology 149benign conditions 151tumours 153, 160

hypophosphatasia 280, 282–283hypotension 14–15

secondary brain damage 168spinal/epidural anaesthetic–induced 15therapeutic 14–15

313

314

hypothermia 14, 45hypovolaemia, in dehydration 29hypovolaemic shock 15–16

classification 16secondary bleeding 21

hypoxiaof anaesthesia 43, 79diffusional 85secondary brain damage 168

ICF see intracellular fluidICP see raised intracranial pressureidiopathic thrombocytopenic purpura

(ITP) 39iliac crest bone grafts 92, 93immobilisation, fractures 64immunisation

healthcare workers 50, 51open fracture management 65

immunocompromised patients 48bone infection 283

immunological complicationsblood transfusion 44–45dental implants 297

incision biopsy 258incisional hernia 10, 58incisions 9, 12

abscess 265–266facial 123–124oral surgery 190–191

incisorsankylosis 254orthodontic management 251–252surgical exposure 255

indomethacin 78induction, general anaesthesia 72–73infection

agents 55–56bone 283–285

see also jaw, cystscomplication of blood transfusion 45dental 268–269

dry socket 216periradicular 238, 239wisdom teeth 220, 221–222see also dental abscess

fractures 66internal/external fixation 64mandibular 93open 65

intracranial 163, 169–170intravascular lines 22, 35oroantral fistula (OAF) 213–214, 218oropharynx 150postoperative 23prevention, oral surgery 198–199respiratory tract

laryngitis 154LRTI21–22nasopharyngeal 150

salivary gland 115–116sinusitis 157urinary tract 22–23, 54see also cross–infection; wound sepsis

Infection Control Committee 50

Infection Control Nurses 50infection control policy 50inferior dental nerve

block 201,203–205buccal injection 204–205complications 205determination of adequate

anaesthesia 204fractured mandible 213technique 203–204

damage, postextraction 225, 228infiltration technique, local anaesthesia

202–203infraorbital nerve block 201, 206–207

technique 206–207infratentorial pathology 162inhalation pneumonitis 22inhalational agents 75–76inhalational induction 72inhalational sedation

clinical application 83–84disadvantage 84history 83procedure 84–85

insensible fluid loss 16, 30insulin 17–18, 31, 70

TPN solutions 35insulin resistance 34internal fixation 62, 64, 65International Normalised Ratio (INR) 20,

41, 42, 296intra–articular fractures 62, 63, 67intracellular fluid (ICF) 26, 27, 31intracranial haematoma 167, 168intracranial haemorrhage 168–169intracranial infection 163, 169–170intracranial tumours 169intradural haematoma 168intraosseous injection 207intrapulpal injection 207intravenous agents 76–77intravenous induction 72intravenous sedation

assessment 82clinical application 85–86contraindications 85–86history 83, 85procedure 86

introduction to the patient 181intubation see endotracheal intubationinverted L osteotomy 107iron overload 45iron therapy 23, 43ischaemic heart disease 16–17

oral surgery 275isoflurane 75–76ITP see idiopathic thrombocytopenic

purpura

jaundice 184complication of blood transfusion 45delayed wound healing 9surgical 41

jawassessment 104

central giant–cell granuloma 279, 280cysts 229–237

aneurysmal bone 279, 280dentigerous 232–233features 229keratocysts 233–234nasolabial 236nasopalatine 235–236radicular 230–232, 239solitary bone 236Staphne's idiopathic bone 236–237

tumours 285–286see also mandible; mandibular;

maxilla; maxillaryjoint(s)

deformity 40, 60intra–articular fractures 62, 63, 67movement

complications of surgery 14in examination 60scar contractures 10–11

see also temporomandibular joint(TMJ)

Jorgensen technique 85juvenile nasopharyngeal angiofibroma

(JNA) 151

Kell and Duffy antigens 45keloid scarring 10keratinisation 7–8keratocysts 233–234

aspiration 258clinical features 233diagnosis 233Gorlin–Goltz syndrome 234radiolucency 233treatment 233–234

ketamine hydrochloride 77kidney see entries beginning renalKTP lasers 306Kufner osteotomy 108

labial flap 255labial fraenectomy 251

upper 254–255lactic acidosis 33laminar airflow system 47, 56Langer's lines 8

contractures 10–11hypertrophic scarring 10see also contour lines; wrinkle lines

laryngeal mask airway (LMA) 72, 74propofol 77

laryngeal obstruction, emergencymanagement 148–149

laryngeal spasm 75, 76laryngectomy 155laryngitis

acute 154chronic 154

laryngoscopes 74, 75laryngotomy 149larynx

anatomy and physiology 153–154benign conditions 154

larynx—(cont'd)examination techniques 147, 154malignant tumours 154–155

lasers 303–306applications 146, 304precautions 304types 304–306

late–stage complicationsof fractures 66, 67–68of surgery 24, 25

Le Fort fractures 94classification 94–95, 98I 94, 98, 99II 94–95, 98, 99III 95, 98, 99late deformity 102

Le Fort osteotomiesI 105, 107–108, 109

complications 108II 105, 108

complications 108III 105, 108–109

complications 109leaf fibroma 245–246

aetiology and clinical appearance245–246

management 246left ventricular failure (LVF) 17leukoplakia, laser therapy 304lichen planus 184

laser therapy 304lidocaine (lignocaine) 201–202, 277line infection 22

TNP 35lines of election 123, 124lingual flap 249lingual fraenectomy 251lingual nerve 1 1 1 , 119–120

block 272damage 225–226, 228

lingual thyroid tumours 152lip

incisions 124lower, nerve supply 110, 111primary closure 146

lip adhesion 136–137lip deformities 133lip repair 136–137

at 3 months 137at 6 months or later 137

lipoma 261Little's area 158liver disease

coagulation disorders 41fluid overload 30oral surgery 277

LMA see laryngeal mask airwayLMWH see low molecular weight heparinlocal anaesthesia 197–198, 200–207

and adrenaline (epinephrine) 201,202–203, 217

agents 201–202action 201–202maximum safe dose 202

cannula insertion 86

difficulty in obtaining 207and inhalational sedation 85in ischaemic heart disease 275non–surgical extractions 250–251techniques 202–207

block 203–207deposition 203infiltration 202–203needle insertion 203other 207

uses 200–201diagnostic 200perioperative 201postoperative 201therapeutic 201

local complicationsof fractures 66–67of surgery 24–25

local skin flaps 726, 127long bridge spans, dental implant 295–296loss of function 25, 67low molecular weight heparin (LMWH)

19, 20lower respiratory tract infection (LRTI)

21–22clinical features 21diagnosis 21investigation 21–22treatment 22

Ludwig's angina 265, 267lumbar puncture (LP) 165lung infarction 20LVF see left ventricular failurelymph node biopsy 145–146, 158–159lymph node tumours

metastatic 158–159, 160nasopharyngeal cancer 152oral cancer 143, 144, 145

parotid tumour, differential diagnosis116, 117

lymphadentitis, acute submandibularstaphylococcal 269

lymphangioma 260–261lymphomas 116, 152, 153, 159lymphoscintigraphy 144, 146lysosomes 37

McGill laryngoscope 74Mclntosh laryngoscope 74macrophages 7, 62magnetic resonance imaging (MRI)

fractures 61maxillary 99zygomatic (malar) 96

neurological 166oral cancer 143, 144salivary gland 113TMJ 175

malar bone fracture see zygomatic (malar)bone fracture

mandibleatrophic 220–221cleft deformities 133dental implant 294, 295, 296osteomyelitis 217

spread of infection 264torus mandibularis 248–249

mandibular fractures 89–94angular 90, 91, 92–93clinical features 90–91complications 93–94condylar 90, 91–92, 93–94dental extraction

complication 213, 228criteria 220

displacement 91radiography 91 –92treatment 92–93

mandibular processes, embryology 131mandibular prognathism 105–106

body osteotomy 106vertical subsigmoid osteotomy

105–106mandibular retrusion 106–107

inverted L osteotomy 107saggital split osteotomy 106segmental osteotomy 107

MAOIs see monoamine oxidase inhibitorsmarsupialisation

jaw cysts 231–232, 233, 234mucocoele 273

masksanaesthetic 72, 74oxygen 70surgical 56

masseter muscles 95, 123, 174, 177mattress sutures 195maxilla

cleft deformities 133complications of dental extraction

213–215dental implants 294–295spread of infection 264

maxillary fractures 98–100clinical features 98–99radiography 99soft tissue management 100surgical access 99–100treatment 99–100tuberosity 214–215

maxillary processes, embryology 131maxillary sinus tumours 124, 157maxillary surgery see Le Fort

osteotomiesmedical history 5, 70

oral surgery 181–182, 183universal infection control 48

meningiomas 169meningism 163meningitis 169–170meniscal plication 175meniscectomy 175–176meniscus replacement 177mental abscess 264mental capacity, consent issues 187mental nerve 191

blocks 201, 205–206metabolic acidosis 33

compensation 34metabolic alkalosis 33

315

316

metabolic bone diseases 280metabolic complications of surgery 17–18,

34metal allergy, intermaxiliary fixation 90metastatic nodal disease 158–159, 160methicillin resistant Staphylococcus

aureus (MRSA) 48, 49, 198metoclopramide 72metronidazole 198, 267microcysts (satellite cysts) 234microplate fixation, orbital rim fractures

97, 100microvascular anastomosis 128, 129midazolam 83, 85–86, 87

see also benzodiazepinesmigratory abscess 222Mitchell's osteotrimmer 191mobilisation, early 19, 64–65MOFS see multiorgan failure syndromemolars

ankylosis and submerged deciduous254

complications of extraction 213, 214,217

first and second permanent 253third see wisdom teeth

monoamine oxidase inhibitors (MAOIs) 77monomorphic adenoma, parotid gland see

Warthin's tumourmorphine 77mortality

general anaesthesia 69septic shock 23

motor neuron lesions 162motor response, testing 164mouthwashes

chlorhexidine 93, 198–199saline 199, 210, 222

MRI see magnetic resonance imagingmucocoele/ranula 121, 272–273

aetiology 272clinical features 272–273diagnosis 273management 273

mucoepidermoid tumour, salivary gland118

mucoperiosteal flap 191, 243–244, 247,298

multiorgan failure syndrome (MOFS) 22,23

musclecomplications of anaesthesia 14, 78complications of fractures 67

muscle relaxants 78depolarising 78

suxamethonium 5, 14, 70, 72, 78non–depolarising 78

myeloneuropathy, nitrous oxide exposure76

myocardial infarction (MI) 16–17perioperative 17, 43recent 296

nails, examination 184naloxone 78

nasal complications of craniofacialfractures 101

nasal deformity 133nasal intubation 75nasal masks 74nasal obstruction 155–156, 157nasal polyps 156nasal reconstruction 126, 127, 137nasal septum displacement 97, 98, 156nasal/nasoethmoidal fractures 97–98

clinical features 97radiographs 97treatment 98

nasogastric feeding 135nasolabial cysts 236nasolacrimal damage 97, 98, 101, 109nasopalatine cysts 235–236

clinical features 235diagnosis 235radiographic appearance 235treatment 235–236

nasopharynxanatomy and physiology 149benign conditions 150examination techniques 147tumours 151–152

benign 151malignant 152

nausea see vomitingneck

anatomy 158examination 184lateral swellings 159–160midline swellings 159reconstruction 146treatment 145–146

necrosisbone 62osteoradionecrosis 284–285soft tissue 57

necrotising fasciitis 267needle holders 11, 194needle insertion, local anaesthesia 203needlestick injuries

avoiding 49, 51management 51

neodymium:YAG laser 305–306neoplasms see tumoursneostigmine 78neovascularisation see granulation tissuenerve conduction studies 165nerve damage

complications of surgery 14oral 189, 197–198

dental extraction 215, 225, 228facial fractures 101

mandibular 90, 94maxillary fractures 98, 99, 100zygomatic (malar) 96

fractures 67salivary gland 119–120

neurogenic sialadenosis 115neurological assessment, fractures 60

craniofacial 100neurological conditions 166–172, 277

acquired 166–170congenital 170–171non–localising symptoms 163see also Creutzfeldt–Jakob disease

(CJD)neurological deficit see nerve damageneurosurgery

conscious level 163–164, 165history taking and examination

161–163anatomic localisation 162, 163general pathology 162–163special pathology 163

investigations and procedures 165–166nitrogen, daily requirement 34nitrous oxide 72, 76, 81

cryosurgery 302see also inhalational sedation

non–Hodgkin's lymphoma 116, 152, 153non–sterile dressings 65non–steroidal anti–inflammatory drugs

(NSAIDs) 28, 78, 80caution in asthma 278caution in diabetes mellitus 276oral surgery 198see also aspirin

non–surgical extractions 250–251non–union of fractures 67nose

anatomy and physiology 155see also entries beginning nasal

nose–blowing, avoidance 213–214nutrition

clefts of the lip and palate 135deficiencies 9postoperative 34–35semifluid diet 93

OAF see oroantral fistulaobstructive shock 15obstructive sialadenitis 271–273

major gland 271–272aetiology 271clinical features 271diagnosis 271management 271–272

mucocoeles 272–273Obwegeser osteotomy 106occupational diseases

carpenters 157healthcare workers 46–47, 49, 50–52

odontogenic myxoma 288odontogenic tumours 286–288odontotomes 288–289

complex 288–289compound 289germinated 289invaginated 288

oedemafluid overload 30–31Reinke's 154wound sepsis 57

oncotic osmotic pressure see colloidosmotic pressure

ondansetron 72

onlay grafts, dental implants 299operating microscope 124, 128operating theatre, prevention of infection

49, 56operator dentist 187ophthalmic injury

facial fracture 89, 101Le Fort HI osteotomy 108–109maxillary fracture 98zygomatic bone fracture 95–96see also orbital blow–out fractures

opioid(s) 77, 80antagonists 78post–oral surgery 198

OPT see orthopantomographoral cancer 140

aetiology 140–141'field change' 143index primary 143, 144investigation 143–144

clinical 143imaging 143–144

morbidity 141–142premalignant lesions 142quality of life issues 146signs and symptoms 142staging 142–143synchronous primary 143treatment

multidisciplinary approach 144planning 144–145

tumour thickness 144–145oral cavity

examination 184–185surgical access 124

oral hygiene 93oral surgery 189–199

consent 185–187equipment 190examination 183–185, 211follow–up 199history taking 181–183medically compromised patients

274–278postoperative care 196–199preoperative considerations 189–190techniques 190–196

see also cryosurgery; lasersorbital blow–out fractures 60, 95

enophthalmos 95, 100, 101imaging 96, 99, 100treatment 100see also ophthalmic injury

orbital floor defects 97orbital rim fractures 97, 100orbital wall defects 100oroantral fistula (OAF) 213–214

chronic 218orofacial sinus 267oropharyngeal airway 74oropharynx

anatomy and physiology 149benign conditions 150–151tumours 152–153

benign 152

malignant 143, 144, 152–153orthodontic assessment 104orthodontic problems

causes 250surgical management 251–254surgical procedures 254–256treatment options 250–251

orthodontic wire 214orthognathic surgery 103–109, 139

assessment 103–105dental casts 104distraction osteogenesis 109mandibular 105–107maxillary (Le Fort osteotomies) 105,

107–109orthodontic preparation 105preoperative preparation 105splint construction 105treatment planning 104

orthopantomograph (OPT) 90, 91, 297osmolarity 27osseointegration, dental implants 292–295ossification

fracture healing 63post–traumatic 67

osteitis see dry socketosteoarthritis 62, 63, 67osteoclasts 62osteogenesis imperfecta 280, 290osteoma 285osteomyelitis 64

acute 283–284clinical features 283management 283–284radiographic features 283, 284

chronic 284chronic sclerosing 284dental abscess 267mandibular 217subperiosteal 284

osteopetrosis 280, 290osteoplastic flaps 244osteoporosis 280, 290

dental implants 297fractures 60risk factors 290

osteoradionecrosis 284–285osteosarcoma 285–286

clinical appearance 285–286diagnosis 286management 286

osteotomiesbody 106inverted L 107saggital split 106segmental 107vertical subsigmoid 105–106see also Le Fort osteotomies

otitis media 150oxygen (O2)

dangers 76extubation 75induction of anaesthesia 70monitoring in anaesthesia 79

see also pulse oximetry

postoperative 80, 85, 87see also inhalational sedation

oxygen saturation alarm 87oxygen therapy

ischaemic heart disease 275respiratory conditions 22, 278

oxygen–carrying capacity 42–43smoking 70transfused blood 43

Paget's disease 280, 290–291clinical appearance 290–291diagnosis 291management 291osteosarcoma 285

pain 18abscess

dental 263periodontal 268

chronic pain syndromes 24deep vein thrombosis (DVT) 19fractures

compartment syndrome 66facial 90

muscle, anaesthetic–related 14, 78oral surgery

diagnosis, local anaesthetics 200presenting complaint 181, 182

pleuritic 21postextraction 217pulmonary embolism (PE) 20referred to the ear 151TMJ 173, 174

pain reliefcryosurgery 300see also analgesia

palatal anaesthesia 203palatal gingival margin flap 256palatal hyperplasia 245palatal splint 248palatal swellings 264, 266palate clefts 132

primary 133, 138secondary 133, 138soft 133–134, 138surgical treatment 135–136

palpation of fractures 60facial 89

Pancoast's tumour 160pancuronium 78paracetamol 198paranasal sinuses 156–157

inflammatory conditions 156–157malignant tumours 157

parasinal tumours 157parenteral feeding see total parenteral

nutrition (TPN)parotid duct 270

cysts 120parotid gland

anatomy 110saliva production 112sialadenosis 114–115sialolithiasis 114, 271tumours

317

parotid gland—(cont'd)differential diagnosis 116, 117pleomorphic adenoma 113,

117–118Warthin's 113, 118, 120

parotidectomy 115, 116, 117–118branchial cleft anomalies 120complications 119, 120incision 114

paroxysmal trigeminal neuralgia (PTN)see trigeminal neuralgia

patchy vasculitis 9pathological fractures 59–60patient discharge 86

escorts 82, 85patient preparation 8, 57patient–operator position 210PE see pulmonary embolismpectoralis major myocutaneous flap 128pelvic fractures 60, 63, 65

fat embolism 65–66penicillin 267, 269, 275periapical pathology 220pericoronitis 221–222

spread of infection from 222treatment 222wisdom teeth extraction 220

periodontal ligament injection 207periodontal abscess 263, 268

clinical features 268management 268

perioperative fasting see fasting,perioperative

periorbital haematoma 166–167periradicular surgery 238–242, 266

indications 238–239endodontic failure 238pathology 239, 266post–crowned teeth 239

post perforation 239, 241–242post perforations

diagnosis 242management 242

reasons for failure 241technique 239–241

anaesthesia 239apex removal 240bone removal 240currettage 240flap design 240follow–up 241retrograde root filling 240wound closure 241

PET see positron emission tomographypetechiae 39, 65–66pethidine 77pharyngeal pouch 151, 752pharyngitis 150pharyngoplasties 138pharynx 149–153

anatomy and physiology 149benign conditions 150–151endoscopic examination 147

318 tumours 151–153phenytoin 252, 277

phosphate (PO42-) 27

photocephalometric assessment 104—105physical examination 70–71, 183–185physical violence 89physiotherapy

fracture management 64–65jaw 175, 178preoperative 71

Pierre Robin sequence 134Pindborg tumour 287piriform fossa tumours 153plasmin 37plaster casts 64plate fixation 106platelet activation 37, 38–39platelet adhesion 36–37platelet aggregation 37platelet count, normal 39platelet disorders 39–40

decreased function 40decreased numbers 39

platelet plug 37platelet transfusion 39, 42, 43–44plates

bone 102, 106miniplates 91, 92, 93titanium 90, 92, 101

pleomorphic adenoma 113, 117–118pleural effusion 21pneumonia see lower respiratory tract

infection (LRTI)pneumothorax 15

rib fractures 60poliomyelitis immunisation 50porphyria 70, 76–77positron emission tomography (PET)

143–144post perforation 239, 241–242post–crowned teeth, periradicular surgery

239post–traumatic ossification 67postcricoid tumours 153posterior superior alveolar block 206postoperative care

general anaesthesia 79–80oral surgery 196–199see also under specific

conditions/procedurespostponement of surgery 71potassium (K+)

daily requirement 31interactions

adrenaline (epinephrine) 275suxamethonium 78

intracellular concentration 27red cell concentrate (RCC) 43, 45regulation 28

abnormalities 31–32, 45diuretic therapy 30–31, 70

supplementation 32TPN 35

povidone—iodine 8, 56, 57preauricular incision 175, 776prefabrication, flap reconstruction 130pregnancy

history taking 70oral surgery 277–278sialadenosis 115

pregnancy epulis 261premalignant lesions, oral 142, 304premedication, general anaesthesia 71–72premolars

orthodontic management 253second, extraction 256

preoperative careoral surgery 189–190see also specific conditions/

procedurespreprosthetic surgery 243–249

bone 247–249extraction 243–244soft tissue 244–247

presenting complainthistory 5oral surgery 181

pressure sores 23–24plaster casts 64

prilocaine hydrochloride 201–202, 207,277

prions see Creutzfeldt–Jacob disease(CJD)

Prolene 11, 12propofol 77proptosis 101prostaglandins 28, 39protamine 20protective workwear see theatre dressprothrombin time (PT) 40psychological assessment 103psychological support 134psychological complications 24, 25, 66ptergoid muscles 91, 174, 177ptergoid plates 95, 174ptergoid venous plexus 206pterygomandibular raphe 204pulmonary artery catheterisation 79pulmonary embolism (PE) 19–21

aetiology 19clinical features 20investigation 20pathophysiology 19

fractures 65treatment 20–21

pulp pathology 220pulp testing 235, 268pulse

drugs altering 15recording 16

pulse oximetry (SpO2) 72, 79, 80, 86, 87punch biopsy 258pus

aspiration 257–258dental abscess drainage 265–266formation 55, 57, 58

pyogenic granuloma 261pyrexia 21, 23, 34

fat embolism 65–66insensible fluid loss 16, 30UTI 23wound sepsis 57

Quantiflex MDM machine 84

radiation sialadenitis 116radicular cysts 230–232, 239

clinical features 230diagnosis 230–231radiolucencies 230, 231treatment 231–232

enucleation 231marsupialisation 231–232

radiographic viewing screens 190radiography

bone diseasesmetabolic 281, 282neoplasms 285, 286–287odontomes 288–289osteomyelitis 283Paget's disease 291

deep vein thrombosis (DVT) 19dental extraction 211, 213, 214–215

wisdom teeth 222–225dental implants 297–298dental, parallax methods 252–253, 255fractures 60–61

mandibular 91–92maxillary 99nasal/nasoethmoidal 97zygomatic (malar) bone 96

head and spine 165–166jaw cysts 230, 231, 232, 233, 235,

236–237, 279lower respiratory tract infection

(LRTI) 21obstructive sialadenitis 271oral cancer 143orthognathic surgery 104in pregnancy 277pulmonary embolism (PE) 20TMJ 174

radioisotope scanningbone 61salivary gland 113

radiotherapycomplications 9, 129, 217, 294, 297laryngeal cancer 155nasopharyngeal cancer 152oral/oropharyngeal cancer 144, 145salivary gland tumours 118, 119tonsillar carcinoma 153

raised intracranial pressure (ICP)in 'active hydrocephalus' 171signs and symptoms 163

raising a flap 191–192ranula see mucocoele/ranularapid sequence induction 72–73red cell concentrate (RCC) 43, 45red patches, oral premaligant lesions 142referring dentist 187Reinke's oedema 154remifentalin 77renal blood flow 28renal disease

dehydration 30fluid overload 30and oral surgery 278

renal excretion of hydrogen ions 33–34renal failure

complication of blood transfusion 44fat embolism 66hyperkalaemia 32

renin 28renin–angiotensin–aldosterone system 28

alterations 30, 32respiratory acidosis 33

compensation 33–34respiratory alkalosis 33respiratory complications of surgery

21–22respiratory depression 81–82, 87respiratory disease

intravenous sedation contraindicated86

and oral surgery 278preoperative preparation 71theatre staff 56

respiratory fluid losses 30, 31respiratory system

history 182monitoring in anaesthesia 79

resuscitation'ABC' 168fracture management 63preoperative 71see also fluid replacement

retrobulbar haemorrhage 95Rhesus factor 43, 45rhinitis 155–156rhinoplasty 138–139rhinorrhoea

CSF 97, 98foul–smelling 156

rib bone grafts 93, 178rib fractures 60rickets 280, 291ridge augmentation/expansion 249, 300root canal

drainage 265filling 240

root forceps 208root resorption, incisors 252, 253, 254rotation

dental extraction 210fractures 62

Rowe's elevator 96

saggital split osteotomy 106SAH see subarachnoid haemorrhagesalbutamol inhalers 278saline irrigation 241saline mouthwashes 199, 210, 222saline solution 32saliva

drooling 120production 111–112

salivary duct cysts 120salivary fistula 120salivary gland 110–121

anatomy 110–111,270–271branchial cleft anomalies 120complications of surgery 119–120

investigation 112–114biopsy 113–114fine–needle aspiration 113, 117radiological 112–113

minor 270–271biopsy 273

mucocoele/ranula 121, 272–273obstructive sialadenitis 271–273physiology 111–112swellings 114–116tumours 116–119

benign 117–118malignant 118–119

sarcoidosis 116scalp injuries 166scalp reconstruction 127scar(s)

delayed eruption of teeth 251, 252formation 7, 8hypertrophic 10keloid 10management 124–125neck 184

scavenging systems 72, 84scrubbing see hand washingscurvy 280, 291sealants 240secondary bleeding 21, 199sedative agents 81–82segmental osteotomy 107seizures/epilepsy 162, 167, 169

enflurane contraindicated 75inhalational sedation 84intravenous sedation 85post–infective 109post–traumatic 101

sentinel node biopsy 145–146sepsis see cross–infection; infection;

wound sepsisseptic shock 23septicaemia 23sequestra, postextraction 218sevoflurane 76sharp bony ridges 247–248

aetiology and clinical appearance 247management 248

sharp mylohyoid ridgeaetiology and clinical appearance 249management 249

sharps bins 49, 50sharps injuries see needlestick injuriesshaving, preoperative 8, 57shock 15–17

cardiogenic 16–17hypovolaemic 15–16obstructive 15pulmonary embolism (PE) 20septic 23

shortness of breath 20history 70

sialadenitis 115–116acute 115chronic 115–116

sialadenosis 114–115sialography 112

319

sialolithiasis 114, 271removal of stones 272

'sick role' 24sickle–cell disease 43sinus lift procedure, dental implants

299–300sinusitis 156–157

acute 157chronic 156–157

SIRS see systemic inflammatory responsesyndrome

Sjogren's syndrome 116, 273skin

head and neck 122integrity see fractures, openpreoperative preparation 8, 57

skin allergies 6skin clips 12skin flaps

blood supply 8distant 128free 128–129local 726, 127

tissue expansion 127novel methods 130wound tension 8

skin flora 8inpatients 57line infection 22

skin grafts 125–126, 130, 146skin rashes 184skull

fracture 166–167radiography 165–166sutures, premature fusion 170

SMAS see superficial muscular andaponeurotic system

smokingdental implants 297dry socket 217history taking 6, 182–183laryngeal conditions 154oral cancer 140–141, 143oxygen–carrying capacity 70respiratory complications of surgery

21snoring 151social history 6

oral surgery 182–183sodium

daily requirement 31extracellular concentration 27regulation 27–28

abnormalities 31sodium citrate 72soft palate deformities 133–134soft tissue

inflammatory response 263, 265oral lesions 259–262preprosthetic surgery 244–247trauma, tooth extraction complication

213soft tissue retractor 194

320 solitary bone cysts 236sore throat

anaesthetic–related complications 14theatre staff 56

special needs patients, sedation techniques83, 85

speech 109cleft deformities 138following total laryngectomy 155

spillagesblood/body fluids 49of organisms 55

spina bifida 170spinal lesions 162spinal/epidural anaesthetic–induced

hypotension 15spine radiography 165–166splint(s)

constructionfractured tuberosity 214orthognathic surgery 105

Gunning 92palatal 248

split bone technique 226split thickness skin grafts 125, 146sputum culture 22squamous cell carcinoma

larynx 154lymph node 159oral 140, 142parasinus 157salivary gland 119

squamous cell papilloma 261–262staff see healthcare workersStaphne's idiopathic bone cysts 236–237Staphylococcus aureiis 55, 269

methicillin resistant (MRSA) 48, 49,198

Stenson's duct see parotid ductsterilisation of instruments 47, 48–49Steristrips 98Streptococcus

beta–haemolytic 150pyogenes 55

streptokinase 20–21stress fractures 59stretch receptors 28subarachnoid haemorrhage (SAH)

168–169subconjuctival haemorrhage 95, 98,

166–167subdural empyema 170sublingual abscess 265, 266sublingual ducts 270sublingual gland, anatomy 111submandibular abscess 264–265, 266submandibular duct 270

laser therapy 304surgery 120

submandibular glandanatomy 111complications of surgery 119–120obstructive sialadenitis 271sialolithiasis 114, 271

submandibular staphylococcallymphadenitis, acute 269

submental abscess 264, 265, 266

subperiosteal implants 292suction, oral surgery 190Suedeck's atrophy 67–68superficial muscular and aponeurotic

system (SMAS) 123superior orbital fissure syndrome 96supernumerary teeth

extraction 255incisors 251, 252

supratentorial pathology 162surgical embolectomy 21surgical emphysema 95surgical exposure of teeth 251surgical implants 25surgical instruments 190

cleaning 48contaminated 21, 46–47disposable 49, 53sterilisation 47, 48–49'tagging' 49see also specific types

surgical techniquedehiscence 10prevention of wound infection 57wound healing 9

Surgicel 216suture breakage 10suture knot

oral surgery 195, 796slippage 10

prevention 11suture materials

classification 11oral surgery 195properties 77selection 11, 57

suture needles 11–12oral surgery 194

suture removal 9oral surgery 196wound sepsis 57, 58

suture techniqueoral surgery 193–194, 195–196wound healing 9

suxamethonium 5, 14, 70, 72, 78Swann–Morton blades 190–191sweating, complication of parotidectomy

120swelling

cervicofacial actinomyosis 268compartment syndrome 66dental abscess 263–264fractures 60, 62

facial 89, 90neck 159–160periodontal abscess 268postextraction 217salivary gland 114–116

sympathetic activity 34sympathetic block 68sympathetic monitoring 79synostosis 170syphilis, blood donor screening 45systemic inflammatory response syndrome

(SIRS) 22, 23

tachycardiacompensatory 15, 70, 82fat embolism 65–66wound sepsis 57

Talbot's iodine 222taste, altered perception 228TEDS see thromboembolic deterrent

stockingsteeth/tooth

anaesthetic–related complications 14crowding/impaction see orthodontic

problemsdivision 192mandibular fractures 90, 91, 92–93maxillary fractures 98, 99mobility, periodontal abscess 268post perforation 239, 241–242replacement 296transplantation 220, 251vertical fracture 241see also entries beginning dental;

specific typestemazepam 83temperature

local, fractures 60monitoring 79

temporalis muscle 123flap 177, 178

temporomandibular dysfunction 173temporomandibular joint (TMJ) 173–178

anatomy 173–174clicking 173, 174conditions 173dislocation 176

complication of tooth extraction215

examination 174history 174reconstruction 177–178special investigations 174–175treatment 173, 175–178

tendernessfractures 60, 63, 67wound sepsis 57

tendonscomplications 67examination 60

tetanus immunisationhealthcare workers 50open fracture management 65

TF see tissue factortheatre dress 49, 56theatre personnel 56therapeutic hypotension 14–15thiopentone sodium 76–77thrombocytopenia 39, 41

platelet transfusion 39, 44thromboembolic deterrent stockings

(TEDS) 18thromboxane (xA2) 37, 39thyroglossal cyst 159tissue damage 24tissue engineering 130tissue factor (TF) 37tissue forceps 194

tissue plasminogen activator (TPA) 37tissue sampling 257–259

disposition 258–259frozen section 259

titanium dental implants 293titanium plates 90, 92, 101TIVA see total intravenous anaesthesiaTMJ see temporomandibular jointTNM staging, oral cancer 142–143tobacco see smokingtongue see entries beginning lingualtonsillitis 150tonsillar carcinoma 152–153tonsillar inclusion cysts 152tonsillectomy 150–151

indications for 151tooth see teeth/tooth; entries beginning

dental; orthodontictorus mandibularis 248–249torus palatinus 248total intravenous anaesthesia (TIVA) 77total parenteral nutrition (TPN) 35

complications 35constituents 35zinc deficiency 9

TPA see tissue plasminogen activatortracheopharyngeal speaking valve 155traction 64trauma

metabolic responses to 34neurological 166–167

Treacher–Collins syndrome 109trichloracetic acid 222trigeminal nerve 123

block 172, 201, 206trigeminal neuralgia 171–172

cryosurgery 300trismus 102

dental abscess 266–267fractures

mandibular 90, 93maxillary 98zygomatic (malar) 96

inferior dental block 205oral cancer 142osteomyelitis 283postextraction 218tonsillitis 150

tuberculosishistory taking 70immunisation 50occupational risk 51sialadenitis 116

tuberculous meningitis 170tubocurarine 78tumours

cryosurgery 301, 303endoscopy 124neurological imaging 166wisdom tooth extraction 220see also specific types/regions

tympanic neurectomy 120

ulceration, oral cancer 142ultrasound

DVT 19salivary gland 112

unconscious patientscervical spine radiography 60consent 187mandibular fractures 91, 92

universal extraction forceps 209universal infection control 47–50

key elements 48–50principles 48

University of Washington Quality of LifeQuestionnaire (UW–QOL) 146

unstable fractures 62uraemia, delayed wound healing 9urinary catheters 22–23, 80urinary retention 22–23urinary tract infection (UTI) 22–23, 54urine specimen 23uvulopalatopharyngoplasty (UPPP) 151

vaccination see immunisationvagal bradycardia 71–72valvular disease 275

see also endocarditisvascular compression syndromes 171–172vascular damage, tooth extraction 215vascular disorders 40vascular endothelium 37, 38–39vascular examination, fractures 60vascular permeability 33, 34Vaseline 98vasoconstriction 36vCJD see Creutzfeldt–Jakob disease (CJD)velopharyngeal incompetence 138venography 19ventilation/perfusion (V/Q) scan 20, 22vercuronium 78Verrill's sign 86vertical subsigmoid osteotomy 105–106vessel see entries beginning vascularvestibular denture–induced hyperplasia

244–245vestibuloplasty 249Vicryl 12viral meningitis 169–170viral papilloma 152, 154viral warts 262

cryosurgery 300Virchow node 160visual disturbances 84–85

diplopia 95, 98, 100, 101, 108–109inferior dental block 205loss of vision 95, 96, 101, 109

vitamin A 9vitamin B1 70vitamin BI2 76vitamin C 9, 291vitamin D 297vitamin deficiencies 41, 291

TPN 35vitamin K 41vocal cord(s) 153–154

nodules 154palsy 154papilloma 154

321

Volkmann's contractures 67volume receptors 28vomiting

cause of dehydration 29complication of anaesthesia 13neurological disorders 163, 168

von Willebrand's disease 40, 41

Walsham's forceps 98war injuries 89warfarin 41–42

in chronic AF 17contraindication 296in DVT 19INR 20, 41, 42, 296in PE 20

Warthin's tumour 773, 118, 120Warwick James'elevators 191, 193,

227waste disposal 50water regulation 28–29

abnormalities 29–31Weber Fergusson incision, modified

124weight 82, 83Wharton's duct see submandibular ductwhite cell count 21white patches

laser therapy 304oral premalignant lesions 142tonsils 151

Whitehead's varnish pack 217, 232,254–255, 256, 259, 260, 285

wisdom teeth 219–228clinical assessment 222clinical management 225–227criteria for removal 219, 220–222,

253–254curve of Spee 223, 224extraction techniques 225–227

lower 225–227upper 227

perioperative complications 227–228postextraction complications 228

dry socket 217patient information 225

postoperative care 227radiographic assessment 222–225

wound classification 55wound closure 12

head and neck surgery 125–130, 146periradicular surgery 241

wound healingclassification 7complications 9–11factors affecting 8–9

local 8–9systemic 9

normal sequence 7–8rate 7, 8

age 9regulation 8

wound sepsis 8, 54–55causative organisms 55–56clinical features 57definition 55diagnosis 57prevention 56–57risk factors 54treatment 58

wound swabs 57, 58wound tension 8, 10, 12wrinkle lines

facial 123see also Langer's lines

written informationconsciousness sedation 82, 86oral surgery 189postoperative 196, 797preoperative 225

Z–plasty 254facial scars 125

zinc, role in wound healing 9zinc oxide pack 217, 240, 244, 245zygomatic arch 123, 128, 176zygomatic (malar) bone fracture 95–97

clinical features 95–96displacement 96radiography 96treatment 96–97

322