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TEXTBOOK OF
GENERAL AND ORAL
SURGERY
Commissioning Editor: Michael Parkinson
Project Development Manager: Hannah Kenner
Project Manager: Nancy Arnott
Designer: Erik Bigland
TEXTBOOK OF
GENERAL AND ORAL
SURGERY
CHURCHILL
LIVINGSTONE
EDINBURGH LONDON NEW YORK PHILADELPHIA ST LOUIS SYDNEY TORONTO 2003
CHURCHILL LIVINGSTONE
An imprint of Elsevier Science Limited
© 2003, Elsevier Science Limited. All rights reserved.
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First published 2003
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Preface
The scope of dental practice has evolved enormously
since the era of the barber surgeon. Oral surgery remains,
however, not only a traditional skill in dentistry but also
a core skill for all dental surgeons regardless of their area
of specialism, and therefore it is an important part of the
undergraduate curriculum and general professional
training.
Over the years, as the medical status of the population
has become more complex and surgical expertise has
increased, oral surgery has evolved into identified subspecialties. These include maxillofacial surgery, which,
in the UK, is a specialty of medicine; oral surgery, which
embraces maxillofacial trauma and orthognathic surgery;
and dentoalveolar surgery, which is designated surgical
dentistry by the General Dental Council in the UK. The
first two - maxillofacial surgery and oral surgery - are
the remit of specialists, whereas all dentists are expected
to be competent in dentoalveolar surgery. A sound knowledge of basic surgical principles is a prerequisite to the
practice of any of these areas of surgery.
This text includes a consideration of general surgical
principles, specialist surgical areas and minor oral surgery.
The section on general surgical principles has been
written mainly by general surgeons and provides core
knowledge that informs the safe practice of surgery. It
will be of practical help to those working as senior house
officers in maxillofacial surgery wards. This section also
considers cross-infection control and provides an overview of both general anaesthesia and conscious sedation.
The second section includes chapters on individual
areas of specialist surgical practice of interest to oral and
maxillofacial operators, written by experts. These are
written to provide insight into these relevant areas of
surgical practice so that the dentist can be confident in
the information he or she provides to patients and can
also make appropriate referrals. This section is not intended
to inform practice in these areas and so it is short and
readable.
The third section - oral surgery - is a practical guide
to the practice of dentoalveolar surgery or surgical dentistry.
It provides core information required to complete the
undergraduate curriculum.
The integrated nature of this text, which includes
general and oral surgery, is a companion to the Textbook
of General and Oral Medicine, and is recommended for
students studying human disease earlier in the undergraduate curriculum and, subsequently, oral surgery in
the clinical years. Although intended primarily for undergraduate students, the book also provides a comprehensive range of information for those preparing for
membership examinations and will be a useful bench
book in a dental practice environment.
The authors have taken great pleasure and satisfaction
in compiling this text, which is unique in bringing together
succinct knowledge on the whole scope of surgical practice in dentistry. It is hoped that the reader will also be
pleased and satisfied.
Finally, I would sincerely like to thank Dr Declan
Millett, Senior Lecturer in Orthodontics, for providing
his expertise in the areas where there is an interface with
orthodontics. I would also like to record my thanks to
Mrs Grace Dobson and Mrs Betty Bulloch for the manuscript, and to Mrs Kay Shepherd and Mrs Gail Drake of
the Dental Illustration Department, in addition to those
who have contributed to this text.
D Wray
Glasgow, 2003
VII
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Contributors
Professor Jeremy Bagg, PHD, BDS, FDS RCS(Ed), FDS
RCPS(Glasg), FRC Path
Professor of Clinical Microbiology, University of
Glasgow
Honorary Consultant Microbiologist, North Glasgow
University Hospitals NHS Trust
Mr Philip Barlow, MPhii, BSC, MB ChB, FRCS(Ed)
Consultant Neurosurgeon, South Glasgow University
Hospitals NHS Trust
Honorary Senior Lecturer, University of Glasgow
Dr Andrew J E Clark, BSc(Hons), MB ChBMRCS(Ed)
Clinical Research Fellow in General Surgery
Western General Hospital, Edinburgh
and Arran Acute Hospitals NHS Trust
Honorary 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, Edinburgh
Member of Council, Royal College of Surgeons of
Edinburgh
Mr Jason A Leitch, BDS, FDS RCS(Eng)
Lecturer in Oral Surgery, University of Glasgow
Honorary Associate Specialist, North Glasgow
University Hospitals NHS Trust
Mr Gerald W McGarry, MD, MB ChB, FRCS(Ed),
Mr Howard A Critchlow, BDS, FDS RCS(Eng), FDS
FRCS(Glasg)
RCPS(Glasg)
Consultant Otolaryngologist, North Glasgow University
Hospitals NHS Trust
Honorary Senior Lecturer, University of Glasgow
Consultant Oral Surgeon, South Glasgow University
Hospitals NHS Trust
Honorary Senior Lecturer, University of Glasgow
Professor Khursheed F Moos, BDS, MB BS, FDS RCS(Eng),
Mr Hugh Harvie, BDS, FDS RCS(Ed), FDS RCPS(Glasg), Dip
FDS RCS(Ed), FDS RCPS(Glasg), FRCS(Ed)
For Med
Honorary Professor, University of Glasgow
Honorary Consultant in Oral Surgery, North Glasgow
University Hospitals NHS Trust
Head of Dental Division, Medical and Dental Defence
Union of Scotland
Honorary Senior Lecturer, University of Glasgow
Dr James R I R Dougall, MB ChB, FFA RCSI
Consultant in Anaesthesia and Intensive Care, North
Glasgow University Hospitals NHS Trust
Honorary 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
Mr Arup K Ray, MS, MB BS, FRCS(Ed), FRCS(Glasg)
Consultant Plastic and Reconstructive Surgeon, North
Glasgow University Hospitals NHS Trust
Honorary Senior Lecturer, University of Glasgow
Mr R J Sanderson, MB ChB, FRCS(Eng), FRCS(Ed)
Consultant Otolaryngologist and Head and Neck
Surgeon, West Lothian and Lothian University
Hospitals NHS Trust
IX
Mr David Soutar, ChM, MB ChB, FRCS RCPS(Glasg), FRCS(Ed)
Consultant Plastic Surgeon, North Glasgow University
Hospitals NHS Trust
Honorary Senior Lecturer, University of Glasgow
Mr David Stenhouse, DDS, BDS, FDS RCPS(Glasg)
Senior Lecturer in Oral Surgery, University of Glasgow
Honorary Consultant in Oral Surgery, North Glasgow
University Hospitals NHS Trust
Mr David Still, BDS, FDS RCPS(Glasg)
Lecturer in Oral Surgery
Honorary Consultant in Oral Surgery, North Glasgow
University Hospitals NHS Trust
X
Mr Graham A Wood, BDS, MB ChB, FDS RCPS(Glasg), FDS
RCS(Eng)
Consultant Oral and Maxillofacial Surgeon, South
Glasgow University Hospitals NHS Trust
Honorary Senior Lecturer, University of Glasgow
Professor David Wray, MD, FDS Rcs(Ed), FDS RCPS(Glasg), F
Med Sci
Dean of the Dental School and Professor of Oral
Medicine, University of Glasgow
Honorary Consultant in Oral Medicine, North Glasgow
University Hospitals NHS Trust
Contents
List of contributors
Section B
Specialist surgical principles
ix
PART I
GENERAL SURGERY
12 Fractures of the facial bones
Khursheed Moos
Section A
Basic principles
13 Orthognathic surgery
Khursheed Moos
1 Introduction 3
David Lee and David Wray
14 Salivary gland surgery
R J Sanderson
2 History taking 5
David Lee and David Wray
15 Plastic surgery
David Soutar
3 Wound healing and suture materials
David Lee and Andrew J E Clark
103
110
122
16 Clefts of the lip and palate
Arup Ray
7
89
131
17 Management of orofacial malignancy
William S Hislop and David Soutar
4 Complications of surgery 13
David Lee and Andrew J E Clark
5 Fluid balance, metabolism and nutrition
David Lee and Andrew J E Clark
6 Blood disorders and their management in
surgical practice 36
David Lee and Andrew J E Clark
7 Cross-infection 46
Jeremy Bagg
26
18 Otorhinolaryngology (ENT surgery)
Gerry McGarry
19 Neurosurgery
Philip Barlow
140
147
161
20 Temporomandibular joint investigation and
surgery 173
Graham Wood
8 Surgical sepsis 54
David Lee and Andrew J E Clark
9 Fractures 59
David Lee and Andrew J E Clark
10 General anaesthesia
James Dougall
PART II
ORAL SURGERY
69
11 Conscious sedation techniques
Jason Leitch
81
21 Introduction 180
David Stenhouse and David Wray
22 History and examination 181
David Wray and Hugh Harvie
XI
23 Basic oral surgical techniques
David Stenhouse
24 Local anaesthesia
David Stenhouse
200
25 Extraction techniques
Jason Leitch
208
31 Orthodontics and oral surgery
Harry Critchlow
250
32 Tissue sampling and soft tissue lesions
David Stenhouse
33 Pyogenic dental infection and its spread
David Stenhouse
26 Complications of extractions 212
David Still and David Stenhouse
34 Salivary gland diseases
David Stenhouse
27 Wisdom teeth 219
David Still and David Stenhouse
35 Oral surgery in the medically
compromised patient 274
David Stenhouse and David Wray
28 Cysts of the jaws
David Stenhouse
229
29 Periradicular surgery
David Stenhouse
30 Preprosthetic surgery
David Stenhouse
XII
189
270
36 Diseases of bone 279
David Stenhouse and David Wray
238
243
37 Dental implants 292
Harry Critchlow
38 Cryosurgery and laser surgery
Harry Critchlow
301
257
263
PART I
GENERAL
SURGERY
1
1
Section A
Basic Principles
2
1
Introduction
If they are to achieve an acceptably high standard of
clinical practice, it is essential that all surgeons including dentists and oral surgeons - have a background
knowledge of surgery in general. A specialised knowledge
of oral and dental disorders and their management is not
sufficient. An understanding of the basic principles of
surgery is essential for all surgeons to be able to apply
such knowledge to their specialty. Once they have
acquired such knowledge, surgeons can use it to form the
basis of their specialty knowledge and utilise it to achieve
the standard required and desired.
Such a knowledge of 'surgery in general' is essential
for dental/oral surgeons to ensure that they will be able
to:
• recognise disease by detecting key abnormalities in
the patient assessment
• recognise important disorders that might impinge on
their practice
• assess and balance the needs for treatment against the
risks of avoiding therapy in the patient with
coincidental 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 lifethreatening complications, which may arise in the
course of surgery and how to manage these
• understand the role of specialist colleagues in all
aspects of patient care.
Part I of this book - 'General surgery' - affords a good
basis, 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 by
a section on 'Specialist surgical principles', which has
been written by surgeons who specialise in the field. This
is followed by Part II - 'Oral surgery' - which is now able
to develop the practice of oral surgery within the context
of, and with the background knowledge of, surgery in
general. The text is produced at a level that is suitable
both for undergraduate and postgraduate students.
The chapters in the 'Basic principles' section have
been selected carefully to cover those topics that are of
immediate interest to oral and dental surgeons. These
basic principles are detailed to allow clear understanding
of the topic at undergraduate level. The detail is of more
practical relevance to the postgraduate with patient-care
responsibilities. A chapter on 'History taking' technique
is followed by chapters highlighting:
• Wound healing, incisions and suturing to achieve the
best surgical and cosmetic results.
• Complications of surgery and how to identify and
manage these.
• Fluid balance, together with the potential problems
and dangers of improper fluid and electrolyte
balance, and how to avoid or deal with these.
• Blood disorders, which have a major impact on
surgical practice. Many of the problems are avoidable
and this chapter highlights relevant areas.
• Infections related to surgery, either as a presenting
problem or as a consequence of surgery, which play a
large part in patient management. Cross-infection can
be a major problem and the principles of care and
how to avoid the problems are highlighted. The role
3
of antibiotics, both prophylactic and therapeutic, is
discussed.
• The basic principles of fracture management, which
are very important to the oral surgeon; a full chapter
covers this area.
• Anaesthesia and sedation, which form a major section
of the care of the surgical patient and are discussed in
detail.
The 'Specialist surgical principles' section provides a
succinct overview of those specialist areas of surgical
expertise that lie outside the remit of the dental surgeon,
but a sound understanding of these areas is essential
within the healthcare team to allow appropriate referral,
4
provide appropriate information to the patient and to
participate in the holistic care of the patient.
Part II - 'Oral surgery' - can then be studied based on
a robust understanding of basic surgical principles.
As a final comment, it is good practice that all
surgeons should document clearly each step of patientcare in writing, giving the reasoning behind each
decision made. This is especially the case when making
decisions that seem to lie outside the scope of normal
practice. It is hoped that this book will afford a support
for specialist oral or dental surgeons, to help them make
accurate and calculated decisions that can be justified by
the strength of a good background knowledge of basic
surgical principles applied to good oral surgical practice.
2
History taking
Introduction
History taking is a most important process and must be
rehearsed well. A patient who has not met the surgeon
before is coming to explain about his or her problem and
putting total trust in the surgeon's ability to sort this. The
patient will be very apprehensive. No matter how
efficient and skilled the surgeon is, he or she must make
the patient feel confident. The surgeon's appearance and
demeanor must exude professionalism. A hand-shake, a
smile, a pleasant introduction and a caring gesture will
make the remainder of contact with the patient much
easier and more pleasant.
One's initial approach might have to be modified
according to the patient, for example children, the very
elderly and infirm, patients who are poor of hearing and
patients who are mentally impaired all need different
approaches. The surgeon must also take account of any
accompanying relative or friend. It is very important,
however, to ensure that the accompanying relative does
not dominate the consultation.
The history should then be elicited in a rehearsed way
as 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 appropriate. Details relating to the specifics of history taking
are given in Chapter 22. The sections below highlight
certain basic points.
History of the presenting
complaint
This is the patient's opportunity to tell the surgeon about
the problem and it is important to avoid prompting with
leading questions. Some patients will give a really good
account of their problem but many will need guidance;
Table 2.1
History taking
History of present complaint
Relevant medical history
Family history
Social history
Drug and allergy history
many will also have difficulty in remembering the timescale of the illness. A good initial beginning with history
taking is to ask the patient to think back to the start of the
problem to ensure that he or she gives an account in
chronological order. It is also important, while the patient
is giving the history, to ensure that he or she gives a clear
account of what has happened, and does not discuss what
he or she thinks is the cause of the problem.
Relevant medical history
This is the surgeon's chance to take a history from the
patient. This part has two aspects: first, the opportunity to
elaborate on any points in the history that the surgeon felt
were unclear; second, to enquire from the patient any
aspect of his or her health that might otherwise influence
the treatment plan.
Family history
Two main items are worth enquiring regarding family
history: (1) is there a genetic family problem, especially
any blood-related problem such as haemophilia? (2)
has any member of the family had any problem with
anaesthetics, especially muscle relaxants? Prolonged
action of depolarising agents such as suxamethonium
runs in families and should be detected prior to any
general anaesthetic.
5
Eliciting the significant diseases in family members or
the cause of death of deceased members can give insight
into disease susceptibility such as cancer or cardiovascular disease.
Drug therapy
As outlined above, it is critical to know about certain
drugs prior to performing any surgery. Dosage of corticosteroids might need to be increased and anticoagulants
need to be controlled and monitored carefully. Possible
interactions between drugs need to be assessed.
Social history
The patient's occupation might be relevant to the
complaint or to the opportunity for recovery. The
6
patient's social circumstances and family support will
also dictate opportunities for convalescence.
Knowledge of tobacco smoking and alcohol consumption will not only inform the surgeon of the
potential risks for general anaesthesia and surgery but
also the patient's likelihood of smoking- and alcoholrelated diseases.
Allergies
A history of asthma and anaphylaxis is important. The
surgeon must know about drug allergies and any
idiosyncratic reaction that might have occurred at any
time in the past, no matter how long ago.
Skin allergies, especially reaction to prepping agents
such as iodine, must be discussed and these agents
avoided.
3
Wound healing and suture
materials
Introduction
Secondary intention
The main goal when trying to get a wound to heal is to
achieve anatomical integrity of the injured part and to
restore full function. As a secondary consideration, this
should be combined with an attempt to produce as perfect
a cosmetic result as possible.
A sound knowledge of the principles of wound
healing is necessary to achieve these aims and to allow
appropriate planning of incisions and their closure. An
understanding of the complications that can occur during
wound healing is vital to try to avoid these or to treat
them appropriately if they arise.
To achieve the best result during wound closure, every
surgeon should be aware of the wide selection of suture
materials available so as to be able to choose the most
appropriate for each situation.
Wound healing by secondary intention occurs when the
wound edges are separated and the gap between them
cannot be bridged directly. This occurs when there has
been extensive loss of epithelium, severe wound contamination or significant subepithelial tissue damage.
Healing occurs slowly from the bottom of the wound
towards the surface by the process of granulation. This
larger defect results in a greater mass of scar tissue than
healing by primary intention. In time, such scarring tends
to shrink, resulting in wound contracture.
Classification of wound
healing
A fundamental distinction in wound healing is between
clean, incised wound edges that are closely apposed to
each other, and wounds where the edges are separated.
The former undergo healing by 'primary intention', the
latter by 'secondary intention'.
Primary intention
Where the edges are clean and held together with
ligatures, there is little gap to bridge. Healing, when
uncomplicated, occurs quickly with rapid ingrowth of
wound healing cells (macrophages, fibroblasts, etc.) and
restoration of the gap by a small amount of scar tissue.
Such wounds are soundly united within 2 weeks and
dense scar tissue is laid down within 1 month.
Normal sequence of wound
healing
Despite the differences in time taken and amount of scar
tissue produced, the sequence of events in wound healing
by primary and secondary intention is similar:
• Skin trauma results in damage to superficial blood
vessels and haemorrhage. Blood clotting results in
fibrin clot formation, and this is stabilised by a
number of factors, including fibronectin.
• Within 24 h neutrophils have migrated to the area,
and epidermal cells have extended out in a single
layer from the wound edges in an attempt to cover
the defect.
• Between days 1 to 3 the neutrophils are replaced by
macrophages, which clear debris and play a role in
producing the environment that stimulates local and
recruited fibroblasts to produce collagen. This milieu,
along with new blood vessel formation
(neovascularisation), constitutes 'granulation tissue'.
• Towards the end of the first week neovascularisation
>n
is at its peak. In healing by primary intention at this
stage the incised gap is bridged by collagen. The full
7
thickness of epithelium is recons
tituted, including
surface keratinisation, a process that requires both
epithelial cell migration and proliferation.
• During the second week there is increased fibroblast
activity and collagen formation, with decreasing
vascularity and cellularity in the wound.
With primary intention by 1 month there is a cellular
connective tissue scar with normal overlying epidermis.
By 2 months the wound has regained approximately 80%
of its original strength. The redevelopment of strength in
the wound involves remodelling and orientation of
collagen fibres and continues for a number of months.
In healing by secondary intention there is more
necrotic debris, exudate and fibrin, and a more intense
inflammatory response results. There is a larger defect,
therefore, with more granulation tissue and a greater
mass of scar tissue. Wound coverage takes longer and
wound contraction occurs caused by myofibroblasts.
Regulation of the complex interactions involved in
wound healing is achieved by a number of local and
systemic factors. These are produced both at distant sites
(e.g. growth factor) and locally by the cells involved in
the healing process. Many factors are involved, important
examples including cytokines, platelet-derived growth
factor and epidermal growth factor.
Factors affecting healing
A number of local and systemic factors affect wound
healing (Table 3.1); these are discussed in turn.
Local factors
Wound sepsis
8
Removal of hair allows better visualisation of the wound.
It also facilitates application of adhesive dressings and
suture removal. However, evidence has shown that
shaving of skin at an early stage preoperatively increases
bacterial counts in the area, and shaving more than 12 h
before incision can significantly increase the rate of
wound infection. Hair removal should therefore be
performed where necessary just prior to surgery (see
Ch. 8).
Preparing the skin with antiseptic wash prior to surgery
is vitally important. Preparation should be thorough.
Chlorhexidine and povidone-iodine have been shown
to reduce the skin bacterial flora by up to 95%. Most
surgeons perform a double scrub of the area, preparing
Table 3.1
Factors affecting wound healing
Local
wound sepsis
poor blood supply
wound tension
foreign bodies
previous irradiation
poor technique
Systemic
nutritional deficiencies
systemic diseases
therapeutic agents
age
the skin well wide of the area of surgery. Careful hand
wash by the surgeon using these antiseptics is also very
important in reducing wound sepsis.
Poor blood supply
As described above, bleeding and neovascularisation
play fundamental roles in wound healing. Areas with
good vascularity, such as the scalp and face, heal well,
whereas those with poor blood supply, such as pretibial
skin, heal poorly. Surgical technique can also have a
significant effect on the blood supply to the area. Care
should be taken where possible to maintain the vascular
supply to the incised area. For example, creation of a
distally based skin flap is likely to disrupt the vessels to
the skin of the flap, and impair wound healing. Appropriate planning of incisions minimises vascular damage.
Wound tension
Tension across a healing wound serves to separate the
wound edges, impairs the blood supply to the area and
predisposes to complications of wound healing. Care
should be taken, therefore, when planning incisions to
avoid creating tension if possible.
Where the gap between the wound edges is large,
primary apposition of the edges might not be appropriate
or even possible. Bridging of such a gap can be achieved
by a number of plastic surgery techniques, including skin
grafting or tissue flaps (see Ch. 15).
Better cosmetic results from surgery tend to be
achieved if incisions are made along the lines of the
collagen bundles of the skin (Langer's lines). These
follow the natural skin creases on the face, transversely
at the joints and longitudinally on the long parts of the
limbs.
Foreign bodies
Nutritional deficiencies
The presence of extraneous material within the wound
predisposes to infection. It also results in a larger and
more prolonged inflammatory reaction, which can
predispose to excess scar tissue formation. Foreign
material can enter a traumatic wound at the time of injury
and should be removed at the onset of treatment with
adequate debridement.
With surgical wounds, however, complications can
result from endogenous material being inappropriately
present within the wound, such as devascularised pieces
of fat, necrotic tissue resulting from excess use of the
diathermy, or the patient's hair. Thorough wound cleaning
before closure helps to remove these materials.
Vitamins important in the process of wound healing
include A and C. Vitamin A is involved in epithelialisation
and collagen production; vitamin C has an important role
in the production and modification of collagen. This has
been recognised for centuries by virtue of the disease
scurvy caused by vitamin C deficiency.
Certain minerals are also essential in wound healing.
Zinc acts as an enzyme cofactor and has a role in cell
proliferation. It accelerates wound healing in experimental models. Deficiency may be encountered in
patients on long-term total parenteral nutrition.
Protein is the main building block in wound healing.
A malnourished, hypoproteinaemic patient has impaired
inflammatory and immune responses, vital for normal
wound healing and prevention of wound infection.
Protein amino acids are essential for collagen production,
which is itself a protein.
Previous irradiation
Areas that have undergone preoperative radiotherapy
suffer from a patchy vasculitis, impairing their blood
supply and hence healing potential. Radiation also
damages skin stem cells, resulting in poor reepithelialisation.
Systemic diseases
Several diseases are known to impair wound healing via
a number of mechanisms. Important examples include
diabetes, uraemia and jaundice.
Poor technique
Care should be taken when making an incision to create
a clean precise cut. The incision should be made
vertically through the skin. Gentle handling of tissues
throughout the operation is important. Rough handling
and damaging of tissues can result in tissue edge
necrosis, predisposing to poor healing and infection.
Careful haemostasis not only allows good visualisation
during surgery but also reduces tissue bruising and
haematoma formation.
Choice of appropriate suture material is important.
Suture placement should be precise and suture tension
sufficient to result in tissue apposition, but not too tight
to cause tissue necrosis. Skin closure should include the
strength-supplying dermis within the bite. Removal of
sutures at the correct time (variable between sites) helps
prevent scarring associated with the sutures themselves.
Systemic factors
Many systemic factors are necessary for wound healing
and deficiency of these impairs the process. Certain
diseases and therapies can also have detrimental effects
on the wound.
Therapeutic agents
Immunosuppressive drugs dampen the inflammatory and
immune responses, hence impairing wound healing.
These include chemotherapeutic agents for malignancy
and immunosuppressive and antiprostaglandin drugs
used for inflammatory conditions such as rheumatoid
disease. Probably the most important and widely used
example is corticosteroid therapy. Steroids have the
additional effect of increasing the fragility of small blood
vessels.
Age
Prior to puberty, the rate of wound healing is increased
compared to postpuberty.
Complications of wound
healing
A number of complications of wound healing can occur;
these are listed in Table 3.2.
9
Table 3.2
Complications of wound healing
Infection
Dehiscence
Incisional hernia
Hypertrophic scarring
Keloid scarring
Contractures
Infection
Wound infection is dealt with further in Chapter 8. As
outlined in Table 8.2 (p. 54), several local and systemic
factors predispose to wound sepsis.
Dehiscence
Total breakdown of all the layers of the surgical repair
of a wound is called 'dehiscence'. The mortality of
abdominal 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 meticulous
surgical technique to negate the technical factors that can
cause 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 include
layers with most strength within the bite of the suture.
Excess tension on the suture line also impairs wound
healing. Wounds should be sutured with only enough
tension to close the defect.
Incisional hernia
Dehiscence of the deeper layers of a wound in which the
skin layer remains intact will result in incisional hernia
formation with protrusion of underlying structures
through the deeper defect. This is of particular
importance for abdominal wounds, where viscera such as
small intestine can herniate, with the attendant risks of
irreducibility, obstruction and strangulation. Incisional
hernias in other areas can be unsightly and cause the
patient discomfort (e.g. herniation of underlying muscle
through a gap in fascia lata following hip replacement).
Hypertrophic scarring
Hypertrophic scarring is essentially excess collagen scar
tissue formation - almost an overhealing of a wound. It
is non-progressive after 6 months and does not extend
beyond the edges of the wound. It occurs most frequently
in specific areas, particularly around joints and where
Langer's lines of tension are crossed by the incision.
Poor skin suturing technique frequently results in hypertrophic scar formation, especially where the edges of the
skin are overlapping instead of being accurately apposed.
Treatment is difficult and further surgery should not
be attempted for at least 6 months. Excision of the scar
and resuturing often has disappointing results, resulting
in the same overhealing. Radiotherapy used to be used
but has now been abandoned. Some improvement can be
achieved with local injection of corticosteroids directly
into the scar, a process that might need repeating several
times.
Keloid scarring
Keloid scars are due to abnormal collagen metabolism.
The excess scar tissue extends out beyond the wound
edges and might continue to enlarge after 6 months.
Prevalence is higher in patients with dark skin, especially
those of African origin, in younger patients and in those
with burn wounds.
Areas prone to this type of scarring are the face,
dorsal surfaces of the body, sternum and deltopectoral
region.
Excision generally results in a larger recurrence,
although excision followed by compression bandaging
can have slightly better results. Corticosteroid injections
can give some improvement.
Contractures
Table 3.3
10
Factors causing wound dehiscence
Suture breakage
Knot slippage
'Cutting out' of sutures
Excess tension on the suture line
Wound Contractures can occur with any wounds but are
more commonly associated with wounds that experience
delayed healing (including infection), burns and those in
which the incision crosses Langer's lines.
Contracture of a scar across a joint can result in
marked limitation of movement. It is therefore essential
to avoid vertical incisions across a joint if possible. At a
joint, Langer's lines tend to run horizontally.
Surgical treatment of a scar contracture might be the
only treatment available and can include skin grafting,
local flaps or wound Z-plasty.
Suture materials
Classification
There is a wide variety of suture materials commercially
available. Although the selection for a specific surgical
repair will vary according to surgeon preference,
financial considerations must be borne in mind.
Suture materials are classified as those that are
absorbable and those that are non-absorbable (Table 3.4).
Each of these categories is subdivided into sutures made
from natural fibres, for example, silk, and those that are
man made. In addition, sutures can be made from single
strands (monofilament) or multiple strands (braided).
Most natural materials are now no longer used and
catgut, for example, is no longer commercially available.
These materials tended to have a variable suture strength,
which was not entirely consistent through the length of
the thread. Because of this, most surgeons now use
synthetic materials.
Each suture type is available in a variety of widths, the
larger the number, the finer the thread. For example, 1/0
suture is very thick whereas 6/0 suture is very fine.
Table 3.4
Classification of suture materials
Absorbable
synthetic, e.g. polydioxanone (PDS) (monofilament),
vicryl (braided)
natural, e.g. catgut
Non-absorbable
synthetic, e.g. Prolene (monofilament), nylon
(monofilament)
natural, e.g. silk (braided)
knowledge of the time taken for it to dissolve, and hence
lose its strength, is necessary.
The strength of the suture also varies with the arrangement of fibres, such that braided sutures are stronger than
monofilament sutures of the same material for the same
thickness.
Different materials possess different handling
properties, for example, Prolene has 'memory' (retains
the bends in the suture that result from its packaging),
and is more difficult to knot. With this in mind, the
number of throws in a knot should be altered according
to the suture material to prevent slippage and unravelling.
Tissue reactivity varies between sutures. Materials
with high tissue reactivity, such as silk, cause inflammation at the site of the suture and are more likely to
produce suture scarring. The different properties of
various suture materials are listed in Table 3.5.
Needles
Selection of materials
The first consideration when choosing a suture material
is whether an absorbable or non-absorbable suture is
required. Closing of the deep layers of a wound is usually
performed with an absorbable suture, whereas vascular
anastomoses are performed with fine-bore non-absorbable
materials. Where an absorbable suture is required, a
Table 3.5
Sutures are supplied attached to a number of different
needles and are swaged directly into the end of the needle
rather than through the eye of a needle; this avoids
having to pass a double thickness of suture.
Nowadays, most needles in common use are curved
and are used mounted on a needle-holding forceps.
Straight needles are available and used primarily for
Properties of different suture materials
Vicryl
Catgut
Polydioxanone (PDS)
Silk
Nylon
Polypropylene
Absorbable or non-absorbable
Tissue reactivity
Duration of strength
Absorbable
Absorbable
Absorbable
Non-absorbable
Non-absorbable
Non-absorbable
Mild
High
Mild
Moderate
Low
Low
60% at 2 weeks
Lost in 7-10 days
70% at 2 weeks
20% at 6 months
Loses 20% per year
Indefinite
11
subcuticular skin closure, but are associated with a higher
risk of needlestick injury to the surgeon. Other shapes are
available for specific tasks, such as the J-shaped needle
for femoral hernia repair.
Another variable is the shape of the needle in crosssection. Round-bodied needles are circular in crosssection and do not possess sharp edges. They are used for
suturing delicate structures, such as bowel anastomosis,
and are designed to push tissues to either side rather than
cut through them.
Blunt needles are also available, and are most
commonly used for closing the muscle layer of an
abdominal wound or for suturing liver. They are intended
to reduce the risk of needlestick injury to the operating
staff and damaging adjacent structures.
For use on tough tissues, such as skin and fascia, there
is 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 with
the use of skin clips. These come in a disposable sterile
stapler, are quick to use, cause minimal discomfort to the
patient, and are easily removed.
Qualities of a good incision
An incision must give good access to the structures being
explored. It should be positioned such that it can be
extended to give greater access if necessary. It should be
12
easy to perform and should be made with extreme care to
avoid skin and tissue damage, which can affect subsequent healing. Consideration should be given to the
final cosmetic result before deciding on the direction of
the incision, for example, Langer's lines (see Ch. 15).
Surgery should be carried out with care to avoid
tissue damage due to bad handling. Excess use of
diathermy should be avoided, especially at the skin edge.
Haemostasis should be meticulous and haematoma
formation should be avoided.
For good wound closure, the correct suture materials
and suture needles should be chosen. Where there is
likely to be a high degree of tissue tension on the deeper
layers of a wound, a strong suture is required and must
be placed accurately to grip the strongest layer of the
incision. Excess tension on this suture should be avoided
to prevent wound-edge necrosis and wound dehiscence.
Skin closure should be meticulous. This is the
surgeon's signature and poor suturing technique here can
cause permanent disfigurement that could have been
avoided. The skin edges should be apposed accurately
with no overlapping. Where there is tension on the skin
edges, for example, following excision of a skin lesion
such as a mole, fine interrupted sutures or clips are ideal
to support the skin tension until healing occurs. Where
there is no skin tension, subcuticular suturing with either
a braided absorbable suture such as Vicryl or a nonabsorbable monofilament suture such as Prolene, which
will be removed in a week, is ideal.
4
Complications of surgery
Introduction
All surgical procedures carry an innate degree of risk.
The benefits of any procedure being performed need to
be weighed against any potential complications so that
the clinician and the patient can make a balanced and
informed decision about whether the procedure should
be performed. It is therefore fundamental to have a sound
appreciation of adverse outcomes of surgery and to
define the population of patients that is most likely to
suffer from any such complications.
It is helpful to have a mental framework to categorise
complications. One such framework that is in common
use 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 complications
Surgery is a controlled insult to the patient, whose body
responds with a number of well-defined physiological
and pathophysiological responses that alter the body's
homeostatic mechanisms.
In addition, outside influences are often therapeutically
imposed, for example anaesthesia, intravenous fluids and
immobility.
Table 4.1
All of these factors have implications for the patient
and for the outcome of surgery.
Early-stage complications
Early-stage complications (Table 4.1) will be considered
in turn.
Anaesthesia-related complications
All but a few patients undergoing a surgical procedure
require some form of anaesthetic, be this local, regional
or general. The principles and adverse effects of general
anaesthesia are described in detail in Chapter 10 and
local anaesthetics are considered in Chapter 24. However, it is important to give some consideration to these
because a significant proportion of complications from
surgery are related to anaesthesia (Table 4.2). A patient's
ability to withstand anaesthesia will often dictate his or
her 'fitness' to undergo surgery or will have a bearing on
the surgical approach.
Nausea and vomiting
Temporary nausea is common after general anaesthesia
and might necessitate overnight admission for intended
daycase patients. Administration of an antiemetic and
a delay in restoration of oral intake usually suffice,
although pathological causes should be borne in mind.
Early-stage complications of surgery
Anaesthesia-related complications
Hypothermia
Nerve damage
Diathermy-related injuries
Hypotension
Metabolic complications
Pain
Table 4.2 Complications related to general
anaesthesia
Nausea and vomiting
Sore throat
Muscle pain
Damage to teeth
13
Sore throat
The use of airway adjuncts during anaesthesia, such as
an endotracheal tube or laryngeal mask, can cause
mechanical irritation of the pharynx. The symptom
resolves spontaneously and requires reassurance only.
Muscle pain
The use of depolarising muscle relaxants, such as
suxamethonium, causes initial muscle contraction and
might result in widespread postoperative muscle ache.
Damage to teeth
Teeth can be damaged during the process of intubation
and the anaesthetist must be careful when using a
laryngoscope.
Hypothermia
Surgical patients are relatively exposed to any drop in
temperature during the course of surgery, especially if
surgery is over a prolonged time period. Anaesthesia can
alter the patient's ability to control body temperature,
with many agents causing peripheral vasodilatation with
the consequent danger of hypothermia. It is important,
therefore, to maintain a suitable temperature and humidity
within the operating theatre. The use of warming blankets
and local hot-air circulating jackets can prevent a
significant 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 bony
prominences. Pressure over peripheral nerves should be
avoided where possible. Excessive movement of joints
can also result in nerve damage. For example, the
patient's arm should not be abducted more than 60
degrees (particularly in external rotation), to avoid
brachial plexus damage.
Diathermy can be monopolar or bipolar. The risk of
burn is less with bipolar diathermy, where the tissue
grasped between the forceps completes the circuit, with
current flowing from one tip of the forceps through this
tissue to the other limb of the forceps.
In monopolar diathermy the current travels in a circuit
from the diathermy machine, via a cable, to the forceps
that are holding the bleeding vessel, causing an electrocautery of the vessel. The current then returns, via the
path of least resistance, through the patient's tissues to
the return plate (which is attached to a remote part of the
body such as the thigh) and then to the diathermy
machine. The plate must have a certain surface area such
that the current is sufficiently dispersed so that the plate
does not burn the skin it is attached to. If the plate is
applied incorrectly, such that only part of it is touching
the patient, the full power of the current might be too
localised and a burn can occur in that area. Responsibility
for diathermy, including the plate, rests ultimately with
the surgeon. Metal objects touching other areas of the
patient provide an alternative route for the current to flow
and, again, burns will occur if there is a small surface
area at the exit site, for example, when there is contact
between skin and a drip stand.
The diathermy current can ignite flammable gases,
including bowel gas, certain anaesthetic agents, and
alcohol-based skin preparation solutions.
The presence of a cardiac pacemaker is not a
contraindication to the use of diathermy. The return plate
should be remote from the pacemaker and close to the
operative site. Short bursts of current should be used. The
anaesthetist should monitor pacemaker function by pulse
measurement and cardiac monitoring.
Hypotension
Low blood pressure is a common complication in the
postoperative period. The causes are numerous, of varying severity and can result in shock. Shock can be defined
as inadequate tissue perfusion and tissue oxygenation,
resulting in organ dysfunction. Postoperative hypotension
is not always pathological. It might not require treatment
and could even be the desired effect of therapy.
Diathermy-related injuries
14
The high-frequency alternating current of diathermy is a
versatile surgical tool used to produce haemostasis. The
main risk from diathermy is of burns because of incorrect
usage.
Therapeutic hypotension
Patients are often prescribed drugs that lower blood
pressure, such as beta-blockers or ACE inhibitors, to
reduce perioperative bleeding. For other medications,
hypotension is a side-effect, an important example being
morphine, which is often given postoperatively via
infusion. However, it is dangerous to assume that postoperative hypotension is secondary to medication and a
search for other causes should be performed.
Table 4.3
Types of shock
Obstructive shock
Hypovolaemic shock
Cardiogenic shock
Septic shock
Spinal/epidural anaesthesia
Local anaesthetic substances near the spinal nerves block
not only the fibres carrying pain signals but also the
sympathetic fibres that provide vasomotor tone to the
lower limbs. Blockade of these fibres results in vasodilatation and hence hypotension. A degree of increased
intravascular filling is required to compensate for this
increased potential intravascular volume. However, it is
important not to be overaggressive in fluid resuscitation
in an attempt to restore a blood pressure. Clinical signs
are the key and, if the patient is peripherally well perfused
and there is evidence of normal end-organ function (e.g.
good urine output), then the current status might be
acceptable.
Again it is essential that hypotension is not attributed
to regional anaesthesia until a search for other causes has
proved negative, and it is important to recognise that the
sympathetic blockade will decrease the patient's ability
to compensate for fluid loss.
Clinical assessment and close monitoring of blood
pressure 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 terms
of severity. The types of shock are listed in Table 4.3.
Obstructive shock
The obstructive form is a rare type of shock, where venous
return to the heart is impaired resulting in decreased atrial
and ventricular filling and therefore decreased cardiac
output. Important examples are massive pulmonary
embolus, tension pneumothorax and cardiac tamponade.
Pneumothorax is the presence of air within the pleural
space. Infrequently, the air can be trapped in this space
by a 'flutter valve' effect from the lung, such that more
air can get into the space but air cannot escape. This
results in increased pressure within the pleural space
with compression of thoracic and mediastinal structures
including the lungs, the heart and great vessels.
Any pneumothorax has the potential to become
a tension pneumothorax, especially under general
anaesthesia where the patient is being ventilated under
positive pressure. Urgent treatment is required.
Pneumothorax can be caused in the perioperative
period as a complication of positive pressure ventilation
or insertion of central venous access devices that
inadvertently breach the pleura.
Hypovolaemic shock
The most common cause of postoperative hypotension is
hypovolaemia, that is, insufficient intravascular volume.
Hypovolaemic shock is classified with regards to
severity and the clinical signs that accompany it
(Table 4.4). This classification is a broad outline and
represents a spectrum rather than distinct clinical entities.
There are also a number of situations where the clinical
features are not reliable:
• Young children and fit young adults have a greater
cardiovascular reserve, and might therefore be able to
compensate for blood loss, maintaining their blood
pressure until the blood loss is so large that they
decompensate, resulting in a precipitous fall in blood
pressure.
• Elderly patients have decreased cardiovascular
reserve, such that relatively little blood loss can result
in shock.
• Pharmacological agents designed to alter pulse rate
and blood pressure naturally have an effect on the
clinical signs, a common example being beta-blockers
such as atenolol, which prevent a compensatory (and
diagnostic) tachycardia. Where confusing variables
are present, further monitoring modalities (e.g. such
as central venous pressure recording) might be
indicated to assess the patient's fluid status.
The causes of hypovolaemic shock are primary haemorrhage, transcellular loss and insensible loss. Primary
haemorrhage is defined as haemorrhage occurring within
24 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 pressure
Pulse pressure
Respiratory rate (breaths per min)
Urine output(mL/h)
Colour
Mental state
16
Class /
Class II
Class III
Class IV
<750
<15
< 100
Normal
Normal
12-20
>30
Normal
Normal
750-1500
15-30
100-120
Normal
Narrow
20-30
20-30
Pale
Mildly anxious
1500-2000
30-40
> 120
Decreased
Narrow
30-40
10-20
Pale
Anxious, confused
>2000
>40
> 120, thready
Decreased
Narrow
>40
Minimal
White
Confused, drowsy
haemostasis at the time of operation. It can be clinically
difficult to decide whether reoperation is required to halt
the bleeding and when. Initial non-operative techniques
can be tried (e.g. local pressure or reversal of
coagulopathy). However, if there is evidence of ongoing
bleeding causing shock, attempts should be made to
arrest the bleeding.
A key clinical indicator of whether the blood loss is
ongoing is the patient's response to fluid resuscitation.
Before administering fluid resuscitation, it is important
to consider cardiogenic causes of shock, which might be
aggravated by further fluid load (see below). Monitoring
of the response can be either by simple clinical means
such as pulse and blood pressure recording, or by
invasive monitoring techniques such as central venous
pressure measurements. Three categories of response are
classically described:
blood clotting, such as those on the anticoagulant
warfarin, and also those with fragile blood vessels, such
as the elderly and patients on long-term corticosteroid
therapy.
Transcellular loss can be considerable. An example is
loss of fluid into the gastrointestinal tract in cases of
bowel obstruction.
Insensible loss, such as fluid loss by sweating, can be
greater than usual for patients in the perioperative period.
Exposure of usually covered moist organs at surgery, for
example, intra-abdominal viscera, can greatly increase
fluid loss in this way. Postoperative pyrexia also increases
insensible fluid loss.
These losses must be considered when evaluating
the amount of fluid required to render the patient
normovolaemic.
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 a
loss of less than 20% of circulating volume, without
ongoing blood loss.
2. Transient response: Fluid bolus initially causes an
improvement of clinical measures, although the
improvement is not sustained. This indicates ongoing
blood loss or inadequate resuscitation. Blood transfusion should be considered, as should measures to
control haemorrhage.
3. Minimal response: Fluid bolus results in little or no
clinical improvement. Blood loss is ongoing at a rate
faster than the infusion of fluid. Blood transfusion and
measures to arrest bleeding are urgently indicated.
Cardiogenic shock
Certain patients are more prone to haemorrhagic
complications than others: patients with abnormalities of
Cardiogenic shock occurs when the heart fails to produce
sufficient cardiac output to maintain adequate tissue
oxygenation, despite normovolaemia and sufficient
venous return (Table 4.5).
Impaired contractile strength can be caused by
myocardial infarction (MI) or left ventricular failure
Table 4.5
Causes of cardiogenic shock
Impaired contractile strength
myocardial infarction
left ventricular failure
Disordered contraction, arrhythmia
atrial fibrillation
other arrhythmias
(LVF). MI is the death of an area of cardiac muscle. It is
differentiated from myocardial ischaemia in which there
is a severe reduction in myocardial perfusion but not
muscle death. Such ischaemia occurs, for example, when
a patient suffers from angina.
Surgical patients with established ischaemic heart
disease are at increased risk of undergoing perioperative
MI. This is significantly greater in patients who have had
an MI within the 6 months before surgery. As these
patients have an increased risk of mortality, elective
surgery is not recommended in this period if it can be
delayed without undue risk to the patient. Diagnosis of
perioperative MI can be difficult because pain is not
always a feature, but monitoring during anaesthesia can
detect changes in the electrocardiogram (ECG) pattern.
Clinical features include the onset of arrhythmias and the
symptoms and signs of heart failure.
Treatment of perioperative MI is a difficult clinical
problem and specialist cardiology advice should be
sought. Standard thrombolytic therapy is contraindicated
in the postoperative period because of haemorrhagic
problems.
Acute LVF can result from an acute MI or, more
commonly, simply in patients with ischaemic heart
disease. The diagnosis can be made clinically with
breathlessness, elevated jugular venous pulse in the neck,
and peripheral oedema. Simple investigations such as
chest radiography should be performed. In severe cases,
invasive monitoring techniques such as central venous
pressure monitoring might be necessary.
Treatment of heart failure includes reduction of fluid
load and administration of diuretics such as furosemide
(frusemide) and digoxin.
Cardiology advice should be sought in patients who
do not respond to standard therapy and further specialised
tests might be performed, such as ECHO cardiography or
cardiac catheterisation. Such patients probably require
care in a high dependency unit. Fluid input and output
charts should be kept, with the amount and rate of
infusion of intravenous fluids being regulated carefully
to prevent excess infusion and the development of
cardiac failure.
To function as an efficient pump, the myocardium
contracts in a synchronised order. Disorders of this
rhythm - dysrhythmias - result in ineffectivefillingand
emptying of the chambers of the heart and therefore in
reduced cardiac output. A fundamental distinction in
assessment of patients with dysrhythmias is whether
there is associated cardiovascular compromise, such as
hypotension and shock, or whether the patient is able to
compensate and maintain blood pressure.
Atrial fibrillation (AF) is perhaps the most common
perioperative dysrhythmia. The diagnosis of AF is divided
into those with and without cardiovascular compromise.
Most patients know if they have an irregular pulse but
are asymptomatic. AF is often detected on admission to
the unit when the pulse is noted to be irregular. Some
patients, however, are symptomatic, possibly with
palpitations, light headedness, syncope or cardiac failure.
These patients usually have a rapid, irregular pulse with
an uncontrolled ventricular response. As a result, the
ventricles do not have time to fill adequately before
contraction, causing decreased stroke volume and hence
a drop in cardiac output. An ECG is diagnostic and can
also show signs of myocardial ischaemia.
Urgency of treatment depends on the presence and
degree of complications such as cardiac failure. In
surgical wards, rate control is usually achieved by the use
of drugs such as digoxin, which can be administered
either orally or intravenously. Where digoxin fails to
control the heart rate, a number of other antiarrhythmic
drugs can be tried.
Many patients have chronic AF with a controlled
ventricular rate. Research has demonstrated an outcome
benefit of anticoagulation with warfarin for these
patients, with a reduction in the incidence of embolic
stroke. It is important in such patients to reduce or even
stop the warfarin before surgery (Ch. 6).
Many other types of arrhythmia can occur in the
postoperative period. Although a description of cardiac
arrhythmias is beyond the scope of this chapter, it is
important to note that many arrhythmias can result from
or be exacerbated by electrolyte imbalance, particularly
an abnormal potassium level. Electrolyte levels should
be checked regularly and abnormalities corrected (see
Ch. 5).
Septic shock
Septic shock is an intermediate-stage complication and is
discussed below.
Metabolic complications
The insult of surgery causes an alteration in a number of
metabolic processes (see Ch. 5). In particular, this can
cause problems in diabetic patients. Requirements for
insulin can change because patients have to fast. In
17
addition to this, however, the production of endogenous
insulin and its effectiveness (end-organ resistance) are
altered. As a result, blood glucose levels might be erratic.
It is vital that this is controlled accurately. In this
situation, for short-term control, diabetes is frequently
regulated by the intravenous use of glucose, insulin and
potassium.
Classically, the patient presents with symptoms of a deep
vein thrombosis (DVT) between postoperative days 5
and 7, although it can occur at any stage. A number of
factors predispose patients to DVT in the postoperative
period (Table 4.7). The degree of risk varies between
different operations, being very low in some but up to
40-50% in other operations, such as knee replacements.
Pain
Prophylaxis
One of the main reasons a patient might be reluctant to
consider surgery is the thought of postoperative pain. The
principles of pain control are dealt with in Chapter 23.
However, it is worth considering briefly here, as there are
some pathophysiological consequences of ineffective
pain control.
Pain results in increased sympathetic activity, causing
increased heart rate, vasoconstriction and hypertension.
This produces an increased demand for cardiac work and
the oxygen supply might not be sufficient to meet this
demand. Pain can therefore reduce cardiovascular reserve
and predispose to cardiovascular complications.
Surgery predisposes patients to thromboembolism and
prophylactic measures are essential. Most units will
have a protocol indicating prophylactic measures to be
employed for different operations. Patients will be
categorised into low, intermediate and high risk; depending on the patient, the surgery and other factors as listed
in Table 4.7. A suitable combination of measures will
then be employed. Prophylactic measures are either
mechanical or pharmacological.
Intermediate-stage
complications
Intermediate-stage complications are listed in Table 4.6
and are considered in turn.
Deep venous thrombosis (DVT)
Venous thromboembolism is a leading cause of preventable postoperative mortality. Clots form in the veins of
the lower leg or in the pelvic veins during surgery.
Mechanical
Thromboembolic deterrent stockings (TEDS) provide
graduated calf compression in an attempt to reduce
venous stasis in the lower leg. TEDS can be either calf or
full length.
AV boots are pneumatic devices attached to the
patient's feet that intermittently dorsiflex and plantarflex,
mimicking the venous pump action of the weight-bearing
foot. These can be used postoperatively in high-risk
patients.
Flotron boots are attached to the patient's calves
intraoperatively. Inflation compresses the calf, producing
Table 4.7 Factors predisposing to deep venous
thrombosis (DVT)
Table 4.6
surgery
18
Intermediate-stage complications of
Deep venous thrombosis (DVT)
Pulmonary embolism
Secondary bleeding
Respiratory complications
Line infection
Urinary retention and urinary tract infection (UTI)
Sepsis
Systemic inflammatory response syndrome (SIRS)
Anaemia
Gastrointestinal ileus
Pressure sores
Immobility
Blood viscosity
Local trauma
Intraoperative blood stasis
Malignancy
Infection
Oral contraceptive pill
Pregnancy
Air travel
Thrombophilia
Previous DVT/pulmonary embolus
Cardiac failure
Inflammatory bowel disease
venous flow in the leg, similar to that induced by calf
muscles in the process of walking.
Movement and early mobilisation are also important.
All patients should be actively encouraged to move
their feet and lower legs whilst still confined to bed.
Mobilisation is important as soon as the underlying
pathology and operation allow.
of the clot and hence appropriate treatment. Venography
is the gold standard, demonstrating all clots including
those below the knee. However, this technique is very
invasive and painful and there is evidence that it might
potentiate further clotting. Doppler ultrasound scan is
non-invasive and is good for detecting thigh thrombosis,
which are arguably the clinically significant ones.
Pharmacological
Treatment
Heparin is a mixture of polysaccharide substances with
varying molecular weights that inhibits thrombosis by
potentiating the action of antithrombin III. For DVT
prophylaxis, low-dose subcutaneous heparin (e.g. 5000
international units (IU) twice a day) can be used.
Monitoring of levels of anticoagulation is not necessary.
Low molecular weight heparin (LMWH) is thought to
be more effective than standard heparin and is gradually
replacing this. Standard heparin is enzymatically
degraded into smaller molecules, which have a different
anticoagulant effect. LMWH results in a reduced risk of
bleeding complications. Also beneficial is the longer
half-life, such that administration is only necessary once
a day.
Aspirin has an antiplatelet action and therefore antithrombotic activity. However, its effects must be balanced
against the adverse effects of gastrointestinal ulceration
and precipitation of renal failure, particularly in elderly
patients.
Treatment is instituted to prevent propagation and
embolism of the clot while the body's inherent
thrombolytic mechanisms dissolve the clot that has
already formed. The fact that DVTs situated solely below
the knee are at low risk of embolisation very much
influences the extent of treatment needed for these. In
this situation, the need for anticoagulation is debatable.
Where anticoagulation is required (especially with
thigh or pelvic vein thrombosis) this can be induced
rapidly by intravenous heparin administered by a infusion
pump. Longer-term anticoagulation is achieved by the
use of the oral anticoagulant warfarin. How long therapy
is continued depends on the patient's circumstances, but
3 months is a frequent length of time. Patients with recurrent DVT/PE might require life long anticoagulation.
Clinical features
The majority of patients with DVT are asymptomatic and
therefore might remain undiagnosed. Symptomatic DVT
causes swelling and pain in the affected leg. This can be
associated with engorged superficial veins and warmth
with a tense and tender calf.
Irrespective of whether symptomatic or asymptomatic,
a clot can be cast off from a DVT and float freely in the
circulation until it lodges in the pulmonary vessels. This
is known as a pulmonary embolus (PE) and can be the
cause of sudden collapse and unexpected postoperative
death.
Investigation
Clinical diagnosis is notoriously unreliable, with accuracy
figures of around 50% even for experienced clinicians.
Radiological imaging is essential to determine the extent
Pulmonary embolus (PE)
Aetiology
The majority of PE arise from thrombi in systemic veins
as described above, emboli passing through the right
heart chambers and lodging in the narrow calibre
pulmonary arterioles or capillaries. Rarely the embolus
can arise from the right chambers of the heart itself, for
example, 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 heart
causing cardiac arrest. Smaller emboli block blood flow
to the alveoli of the affected part of the lung. This area of
lung continues to be ventilated but is no longer perfused,
resulting in a block of gas transfer to and from the
bloodstream. With a larger embolus, blood pressure in
the pulmonary circulation increases (increased resistance)
and venous return to the left side of the heart is reduced
with a consequent drop in cardiac output.
19
Clinical features
Clinical features are variable and relate to the amount
and size of emboli. Small emboli can be asymptomatic,
might cause a shortness of breath, or might induce a
cardiac arrhythmia such as AF. Death of the affected area
of lung tissue is known as infarction and is generally
prevented in the case of small emboli by collateral supply
from the bronchial blood vessels. Clinical signs are
usually minimal.
However, moderate-sized emboli can cause lung
infarction with the accompanying symptoms of pain,
haemoptysis and more severe shortness of breath. Where
infarction has occurred a pleural rub may be present on
auscultation.
Large and massive PE constitutes a medical emergency and resuscitation might be required. Prevention of
blood reaching alveoli results in profound hypoxaemia,
and prevention of venous return to the left side of the
heart can give a precipitous fall in cardiac output, shock
and cardiac arrest. Signs are those suggesting outflow
obstruction from the right side of the heart.
perfusion (Q) and ventilation (V) of the lungs can then be
compared, a PE producing a mismatch where an area is
ventilated but not perfused. This picture is frequently
obscured because, after a period of decreased blood
supply, alveoli tend to collapse, resulting in reduced
ventilation as well as perfusion. As a result, the results of
V/Q scans can be indeterminate.
Angiography
Pulmonary artery angiography is the gold standard,
directly visualising emboli. It is, however, technically
difficult and invasive.
Computed tomographic (CT) pulmonary angiogram
The advent of spiral computerised tomography (CT),
used in conjunction with intravenous contrast, has led
to a widespread role for this non-invasive, sensitive test
for PE.
Treatment
Investigation
Electrocardiogram (ECG)
ECG changes are not diagnostic. Most frequently there is
sinus tachycardia. There might or might not be signs of
right 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 respiratory
drive 'blowing off' more carbon dioxide.
Radiology
A chest radiograph is rarely diagnostic. Most changes
seen are non-specific with opacification secondary to
atelectasis and possibly a pleural effusion. Larger emboli
can result in a visible cut-off in the pulmonary artery, and
lack of vascular pattern distal to this. Wedge-shaped
pulmonary infarcts might be visible.
Prevention of further clot/emboli
The patient requires immediate anticoagulation with
intravenous heparin. Low molecular weight heparin is
now licensed for use in PE. However, conventional
heparin infusion has some advantage in perioperative
patients: namely (1) its effect is easily monitored using
activated partial thromboplastin time (APTT); and (2) it
can be reversed rapidly with protamine, should the
patient develop life-threatening bleeding complications
of surgery.
Oral anticoagulation with warfarin is indicated for a
variable period. Patients who are unable to comply with
or tolerate warfarin anticoagulation, or those who
continue to have 'PEs despite a therapeutic dose of
warfarin as monitored by the international normalized
ratio (INR), might be suitable for a caval filter. This is a
mechanical filter placed percutaneously through a neck
vein into the inferior vena cava, which 'catches' emboli
from the leg veins en route to the right side of the heart.
Removal of clot
A ventilation/perfusion (V/Q) scan
20
Labelled isotopes are separately administered at the same
time by inspiration and by intravenous injection. The
Fibrinolytic therapy such as streptokinase (thrombolysis)
might be indicated for patients with large PE. This is
contraindicated in the postoperative period because of
haemorrhagic complications. Surgical embolectomy is
rarely required but is an alternative for life-threatening
PE where thrombolysis is contraindicated.
therapy, clear the mucus plugs. It is important to do this
because unresolved collapse and mucus clearance predispose to bacterial superinfection.
Secondary bleeding
Lower respiratory tract infection (LRTI)
Secondary bleeding is defined as bleeding occurring
more than 24 h after surgery. It has a number of causes,
including dissolution of a clot sealing a blood vessel and
erosion or unravelling of a haemostatic ligature.
Secondary bleeding is rarely as significant as primary
haemorrhage, but it can result in hypovolaemic shock
and occasionally requires reoperation.
Microbial colonisation of the lung parenchyma causes
inflammation, termed pneumonia or LRTI, where again a
wide spectrum of severity is encountered.
By far the most common pathogens are bacteria,
although other pathogens such as fungi can cause
problems particularly in the severely ill patient requiring
multiple system support. The bacteria implicated are
numerous. Oropharyngeal and particularly tracheal
instrumentation for anaesthesia introduce bacteria into
the 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 of
pneumonias is not in the scope of this chapter, but the
principles of diagnosis and treatment are essential to any
surgeon's practice. Pneumonia can be classified according to pathogen or anatomical site affected.
Respiratory complications
Respiratory complications are perhaps the most common
postoperative complication. Their severity is a spectrum
from an asymptomatic pyrexia to life-threatening pulmonary failure. The causes of respiratory complications
are listed in Table 4.8.
A patient's risk of undergoing a respiratory complication depends on the underlying condition of his or her
lungs and the circumstances they are exposed to. Smoking
has a significant impact because smokers are predisposed
to bronchitis and emphysema, ischaemic heart disease
and heart failure. The normal action of the mucociliary
apparatus in the tracheobronchial tree is to clear
secretions and this is significantly affected in smokers.
Atelectasis
Atelectasis describes a degree of alveolar collapse that
occurs after relative hypoventilation, inability to cough
and suppressed ciliary action during general anaesthesia.
Small mucus plugs block the alveoli causing them to
collapse. Postoperatively, patients may develop a cough
and a mild transient pyrexia. Deep breathing exercises,
which might require supplementation with chest physio-
Table 4.8
surgery
Clinical features
Patients develop a combination of symptoms of varying
severity, including cough, production of discoloured
sputum, pleuritic chest pain, shortness of breath,
tachypnoea and pyrexia. Chest examination might reveal
localised areas of decreased chest wall movement, dullness to percussion and auscultation reveals a combination
of decreased air entry, crepitations and bronchial
breathing.
Diagnosis
A radiograph can demonstrate areas of consolidation
or associated features such as pleural effusion. Radiographic changes might take some weeks to clear after the
pneumonia has clinically resolved.
Causes of respiratory complications of
Blood tests
Atelectasis
Lower respiratory tract infections
Aspiration
Adult respiratory distress syndrome (ARDS)
Pulmonary embolus
Pneumothorax
The white cell count is usually raised, although there are
exceptions, especially in elderly or immunosuppressed
patients. Arterial blood gas analysis reveals abnormalities, particularly of partial pressure of oxygen, which
will help direct supportive therapy.
21
Sputum culture
It is fundamental to try to isolate the infecting organism,
so that appropriate antibiotics can be given. This is
not always possible, and repeated cultures and multiple
changes in antibiotic treatment might be required.
Treatment
General supportive treatment should be instituted
quickly. Oxygen should be administered at a concentration guided by blood gas analysis. Saline nebulisers
and aggressive chest physiotherapy help to clear the
consolidation. The patient should be sat up in bed to
improve ventilation/perfusion matching. Bronchodilators
may be indicated where there is evidence of some
reversible airway narrowing such as a wheeze.
Antibiotic best-guess therapy should be started at the
time of diagnosis. At this stage, culture results are not
available and therapy should be directed at organisms
that are most likely to be involved. This might involve the
use of more than one antibiotic, and the combined
therapy has a broader spectrum of activity than a single
drug. Targeted therapy should be tailored accordingly
when results of sensitivities from sputum culture are
available. Where severe chest infection occurs, or in cases
that are failing to resolve, the input of chest physicians is
invaluable.
Aspiration
The protective airway reflexes that prevent inhalation of
substances from the gastrointestinal tract in the fully
conscious patient are depressed by general anaesthesia.
Inhalation of regurgitated gastric contents is known as
aspiration and results in a potentially virulent form of
pneumonia. Appropriate antibiotics should be given to
cover gastrointestinal bacteria. The acid and digestive
juices from the stomach also contribute in causing a
severe chemical pneumonitis.
Adult respiratory distress syndrome (ARDS)
22
ARDS is a syndrome resulting in lung failure. It is
characterised by respiratory distress, hypoxaemia that is
difficult to treat, decreased lung compliance and diffuse
pulmonary infiltrates. Its precise aetiology is not clear,
but is probably involved in a systemic inflammatory
response syndrome (SIRS). As such, it essentially
constitutes 'lung failure' and frequently precedes or is
part of a multiorgan failure syndrome (MOFS)
There are many known precipitants of ARDS, and
effective treatment of these in an attempt to prevent
ARDS occurring, is the best form of management.
Treatment other than that of the underlying cause is
supportive, with the administration of oxygen often
requiring mechanical ventilation, careful fluid balance
and monitoring of cardiovascular parameters to minimise
pulmonary oedema. The prognosis for established ARDS
is 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 inserted
perioperatively. Intravascular lines that are inserted
percutaneously have an inherent risk of becoming
infected, predominantly with skin flora. Certain bacteria
have an affinity for sticking to the synthetic material of
the cannulae. It is important that all lines are inserted
with an aseptic technique and adequately prepared skin.
Lines should be inspected regularly for signs of infection
and replaced where necessary. Lines should be removed
as soon as they are no longer required. Blood cultures,
taken from a line that is suspected as a source of sepsis
and also from a peripheral vein, can help elucidate if the
line is the cause.
Urinary retention and urinary tract infection
(UTI)
Both men and women are at increased risk of UTI postoperatively, predominantly due to urinary tract instrumentation. Males who have any prostatic symptoms
preoperatively are at risk of developing postoperative
urinary retention; preoperative bladder catheterisation
should be considered. Urinary catheters are commonly
inserted before major surgery to ensure accurate
measurement of postoperative urine output. This aids the
monitoring of fluid balance and makes nursing care of
the patient easier. Catheters should be inserted under an
aseptic technique.
Patients with catheters in situ are at risk of urinary
infections but might be asymptomatic because of the
catheter. Pyrexia and cloudy urine should alert the
clinician. A specimen of urine should be sent for culture
and sensitivity and an appropriate antibiotic started while
awaiting the results. Where metal implants have been
used, as in total hip replacement, prophylactic antibiotics
are commonly used while the patient has a urinary
catheter in situ, or, alternatively, individual doses are
given at insertion and removal of the catheter. This is in
an attempt to prevent blood-borne spread of the urinary
tract pathogens to the prosthesis, with potential implant
failure.
Sepsis
adequate intravascular volume and fluid resuscitation is
often necessary before these features are seen.
Septic shock has a high mortality rate (up to 50%) and
often requires the support afforded in an intensive care
unit. Septic shock often precedes, and can even be the
cause of, multiorgan failure, which in part explains its
high mortality.
Systemic inflammatory response syndrome
(SIRS)
The term SIRS has been coined to describe this common
pathophysiological state and its clinical features. The
complex mixture of chemicals produced by the host in
response to severe sepsis has been implicated as the
pathophysiological cause of septic shock and its complications. Similar host responses might occur as a result of
other, non-infective, insults to the patient such as major
trauma, burns and pancreatitis. Multiorgan failure can be
precipitated, with a high mortality.
Sources of postoperative infection are multiple, the most
common ones having been dealt with above, and are
discussed in detail in Chapter 8. Other causes are specific
to particular operations or types of surgery, such as intraabdominal sepsis due to a leaking intestinal anastomosis,
meningitis after breach of the meninges and deep-seated
prosthetic infection in arthroplasty surgery. Often, the
only overt symptom is pyrexia and a thorough, systematic
search for the cause is needed, bearing in mind that it
may not be infective (e.g. DVT). Failure to identify a
cause should be met by starting the process again,
reculturing specimens and widening the search to more
obscure causes. Early diagnosis and treatment of infective complications is necessary to prevent progression to
septicaemia and septic shock. Pathogens spread from the
site of initial infection to the bloodstream, where they
multiply, resulting in septicaemia and spread to any part
of the body.
Blood loss at operation results in a fall in haemoglobin
concentration. Unless the haemoglobin is replaced, the
blood has a decreased oxygen carrying capacity with
wide-ranging effects including decreased cardiovascular
reserve and impaired wound healing. Oral iron therapy is
given for mild to moderate postoperative anaemia. Lower
levels of haemoglobin, or cases where oxygen delivery
must be maximised (coexisting disease, or concurrent
complication), should be restored with blood transfusion.
Septic shock
Gastrointestinal ileus
The presence of bacteria in the bloodstream, particularly
those that possess endotoxin (Gram-negative bacteria),
has a profound effect on the cardiovascular system and
can induce septic shock. There is a complex interaction
between the pathogen and host via multiple mediator
systems. By a complex process, endotoxin induces
increased permeability and reduced vascular tone in
blood vessels by direct damage to the endothelial lining.
This results in a profound decrease in peripheral vascular
resistance, and hence hypotension. A greatly increased
cardiac output is required to maintain adequate tissue
oxygenation, and might not be achieved, causing shock.
Classically, therefore, the patient has warm peripheries
and a large cardiac output. This, however, assumes
The insult of abdominal surgery can result in temporary
intestinal dysfunction and lack of contraction and
peristalsis. Although this is particularly the case for intraabdominal surgery, it can occur in any severely ill patient
especially those with deranged blood electrolytes. When
this occurs, nutrition might need to be given by an
alternative route, and this is discussed in Chapter 5.
Anaemia
Pressure sores
Breakdown of the skin over an area where pressure has
been applied too long is a common postoperative problem.
Pressure sores can become infected and cause sepsis, or
grow to involve a significant area of skin. Prevention is
23
the key, as these lesions are notoriously difficult to treat
once established. Expert nursing care is required from an
early stage.
Patients with increased risk of pressure sores are those
with severe immobility, altered skin sensation, such as
those with spinal cord lesions, and those with poor skin
quality such as the elderly and those on corticosteroid
therapy.
Table 4.9 Specific complications of surgical
operations
Approach used
Surrounding structures might be damaged accidentally
or sacrificed by necessity
Hazards of repairs made, including complications of
wound closure
Risks associated with materials implanted
Effect of removal of diseased tissue
Late-stage complications
The main aim of surgery is to return the patient to his or
her previous good state of health. For numerous reasons
this might never be achieved. Apart from a failure to
'cure' a patient's illness, other patient factors can play a
role in the development of long-term disability
Psychological
A minority of patients has difficulty adjusting to illness
and the fact they have had to have an operation.
Naturally, this depends on the extent of surgery and the
disease process that has necessitated it. In extreme cases,
this attitude can result in adoption of the 'sick role', with
abnormal conceptions of health and healthcare-seeking
behaviour. Support groups and psychiatric services can
be beneficial.
Table 4.10
Local complications of surgery
Early
damage to surrounding structures
haematoma/bruising
Intermediate
wound infection
wound dehiscence
wound seroma
breakdown of repair
failure of implant
Late
abnormal wound healing
loss of function
psychological
Early complications
Damage to surrounding structures
Pain
Chronic pain syndromes can occur postoperatively for
complex reasons. Where simple measures are unsuccessful, referral to a pain team might be indicated.
Specific complications
Operation-specific complications are generally considered
when discussing that operation. It is helpful to maintain
a framework into which specific complications can fit.
These are listed in Table 4.9.
Local complications
24
Local complications related to the wound are listed in
Table 4.10 and are discussed in detail in Chapter 3. The
temporal classification of local complications of surgery
is also listed in Table 4.10.
A detailed knowledge of anatomy is necessary to avoid
unnecessary damage to nearby structures and plan suitable surgical approaches. Patients should be warned of
the side-effects of damage to structures liable to be
affected such as scrotal paraesthesia following damage to
the ilioinguinal nerve in revision inguinal herniorrhaphy.
Haematoma/bruising
Patients can be alarmed by bruising around the wound.
Bruising and haematoma formation cause pain and predispose to wound complications including infection.
Intermediate complications
Complications relating to the surgical wound itself are
discussed in Chapter 3. Other complications are discussed
below.
Surgical repairs made during the operation can fail
for a number of reasons, including patient factors (poor
healing), inadequate surgical technique and failure of
materials used to carry out the repair. The expected
results of repair breakdown should be considered and the
patient observed closely for these, followed by appropriate investigations. The action required once repair
failure has been ascertained varies widely between types
of repair and the extent of failure.
An enormous range of surgical implants is available,
all with their own idiosyncrasies. However, they can fail
for a number of common reasons, for example, incorrect
application results in forces being applied that the
implant is unable to cope with. Material defects occur
occasionally and design faults can take up to several
years to become apparent and be corrected. Synthetic
materials are prone to infection, which often leads to
failure, and prophylaxis might be required.
Loss of function
Where diseased tissue has been removed, the previous
function of that area is either compensated for by another
area, or the patient suffers effects of loss of function.
This is an expected side-effect of surgery, rather than a
complication per se, but often requires symptomatic
treatment.
Psychological complications
Psychological problems often relate to loss of function
and any disability that arises from this. Obviously, this
varies enormously between operations and should be
borne in mind preoperatively, especially for high-risk
operations such as limb amputations. The patient should
be directed to suitable support groups.
Late complications
Abnormal wound healing
Hypertrophic and keloid scarring are discussed in
Chapter 3.
25
5
Fluid balance, metabolism
and nutrition
Fluid and electrolyte balance
The fluid in the body is separated into different
'compartments' - the intracellular compartment (within
the cells) and the extracellular compartment, which is
further subdivided into interstitial (between the cells) and
intravascular (in the blood vessels) - and in each of these
areas the concentration of salts, or electrolytes, differs.
These variations are subject to highly complex control
mechanisms and this degree of tight control is essential to
maintain efficient cell function. Abnormalities of fluid and
electrolyte concentrations can induce life-threatening
cellular dysfunction, e.g. cardiac arrhythmias.
The body normally maintains excellent electrolyte
balance, better than any doctor could hope to achieve by
careful fluid and electrolyte infusions, and in this regard
the kidneys play a vital role. However, as with any body
system, diseases occur that prevent normal homeostasis.
In addition, during the perioperative period, patients are
subjected to a number of exogenous influences, for
example, fasting and intravenous fluid administration,
which can outstrip the body's normal homeostatic capabilities. As a result, great care needs to be taken at this
time with regard to fluid and electrolyte administration,
and careful monitoring of electrolyte levels in the body is
needed.
A consideration of the principles of electrolytes balance
will be followed by a discussion of normal homeostatic
mechanisms, abnormalities of body water and electrolytes and finally, a further discussion of fluid replacement
and acid-base balance as listed in Table 5.1.
Principles of electrolyte balance
26
Some common principles apply when considering
homeostasis of any electrolyte. These are based on a
number of factors:
Table 5.1
Fluid and electrolyte balance
Principles of electrolyte balance
Normal homeostasis
fluid compartments
barriers between compartments
homeostatic mechanisms
Abnormalities of body water
dehydration
fluid overload
Abnormalities of electrolytes
sodium
potassium
Fluid replacement
Acid-base balance
abnormalities
compensation
• Distribution and barriers: it is important to know the
normal concentration of an electrolyte in any given
fluid compartment. Fundamental to this is an
appreciation of how a concentration gradient between
compartments is maintained and can be manipulated.
• Output: it is necessary to know the amount of the
electrolyte that is consumed each day through normal
cellular and systemic functions, and also how much is
lost normally by excretion.
• Intake: the amount of the electrolyte that needs to be
acquired to maintain normal concentrations of the
electrolyte in the body should be balanced with the
amounts actually taken in. Any inefficiency in uptake,
either lack or excess from the method of
administration, needs to be noted and corrected.
Normal homeostasis
Fluid compartments
A patient's body water content depends on the constitution of that person's body. This varies according to
Table 5.2
Fluid compartments (70-kg man)
Intracellular fluid (ICF)
Extracellular fluid (ECF)
interstitial fluid
intravascular fluid
28 L
14L
10.5 L
3.5 L
age, sex and percentage of body fat, and can range from
50 to 75% of body weight. For simplicity an account of
an average 70 kg man is given.
A 70 kg man is 60% water, and therefore contains
70 kg x 0.6 = 42 L water (1 L weighs 1 kg). This is distributed between the two main compartments as shown in
Table 5.2.
There are a number of other small extracellular compartments, which are of less clinical relevance with regards
to salt and water homeostasis, namely transcellular water
(e.g. cerebrospinal fluid) and water associated with bone
and dense connective tissue.
Barriers between compartments, osmolality and
electrolyte concentrations
Osmolality (measured in milliOsmoles; mOsm) is
defined as the strength of a solution. It is derived from the
amount of active ions in that solution. Cations are
positively charged ions and anions are negatively
charged. In each body compartment, there is normally a
balance between cations and anions. The main extracellular cation is sodium (Na2+) and the main intracellular
cation is potassium (K+). The osmolality of plasma is
derived from the equation:
2 x sodium (Na) + urea + glucose
The normal range is 280-290 mOsm/L. This value allows
the clinician to estimate whether the patient has a relative
excess or lack of water in the body and can be measured
easily clinically.
The above equation is an approximation only because,
although sodium is the main extracellular cation, various
factors can affect plasma osmolality, causing inaccuracies
that must be noted clinically. The presence of an
exogenous, osmotically active molecule such as alcohol
in the blood is a good example, and the body will try to
maintain the correct osmolality of plasma by recruitment
of water from the intracellular compartment.
The intracellular and extracellular fluid are separated
by the cell membrane. This acts as a semipermeable
membrane, allowing free passage of water but not
electrolytes. Because of the difference in concentration
of electrolytes between the two compartments, water will
move from the compartment with lower osmolality to
that with higher osmolality, therefore diluting it. This is
known as an osmolality gradient
To maintain the differences in ions between intracellular and extracellular fluids, sodium ions are constantly driven from the intracellular compartment by a
pump mechanism, which actively drives them out in
exchange for potassium ions. The enzyme involved in
this active pumping mechanism is ATPase, and thus this
process is known as the ATPase exchange pump. As a
result sodium is the major extracellular cation and
potassium is the major intracellular cation. To maintain
the balance of electrical charge, chloride (Cl - ) is associated with sodium ions outside the cell and potassium is
balanced mainly by the anion phosphate (PO42-) and
anionic protein inside the cell.
In the extracellular compartment, intravascular and
interstitial fluid are separated by the endothelium or
blood vessel membrane, which, at capillary level, is one
cell thick. Fluid balance between these two compartments is determined by hydrostatic or blood pressure
forcing fluid out from the intravascular area, and oncotic
pressure sucking fluid in. The endothelium is freely
permeable to small molecules such as sodium and
potassium ions, and relatively impermeable to the larger
protein molecules in the plasma. As a result, there is a
protein concentration gradient across the endothelium,
caused mainly by the plasma protein albumin, which has
an appreciable effect on water movement between the
compartments. Again, fluid moves towards the area of
highest concentration and this is called oncotic or colloid
osmotic pressure.
Homeostatic mechanisms
Sodium regulation
The volume of extracellular fluid (ECF) relates directly
to the total amount of sodium in the body, the vast
majority of which is extracellular. The concentration of
sodium is maintained between narrow limits by free
transfer of water between the ECF and the intracellular
fluid (ICF). Hence, a large amount of total sodium,
held in the extracellular compartment, recruits water
from the ICF, increasing the volume of the ECF and
diluting the sodium such that it is maintained at a normal
concentration.
27
28
Control of total body sodium therefore relates directly
to control of ECF volume. This is subject to homeostatic
mechanisms that are both renal and extrarenal in origin,
but ultimately alter sodium excretion by the kidney.
Sodium is ultrafiltrated by the glomerulus of the
kidney; the rate of this process (the glomerular filtration
rate; GFR) relates directly to renal plasma flow (RPF) or
renal blood flow. Renal blood flow, like the flow of blood
to the brain, is autoregulated such that this is constant
within a range of systemic blood pressures. The majority
of the filtered sodium is resorbed in the renal tubules,
mainly in the proximal tubule with fine tuning occurring
in the distal tubule.
Renal mechanisms can involve blood flow or sodium
concentration. Changes in renal blood flow alter GFR
and hence the amount of sodium that is filtered.
Blood flow to the glomeruli of the kidney is monitored
via receptors in the afferent arterioles. Changes in perfusion activate messenger systems in the arterioles,
which alter the renal vascular tone and correct the
abnormality in blood flow. This process is known as
'autoregulation' and attempts to maintain the glomerular
perfusion as a constant.
One of the factors involved in autoregulation is local
production of prostaglandins, which alter arteriole wall
tone. This is an important precipitant of renal failure,
particularly in elderly surgical patients with decreased
renal reserve. The administration of non-steroidal antiinflammatory drugs (NSAIDs) impairs the patient's
ability to produce prostaglandins and hence regulate
renal blood flow.
Changes in renal blood flow also result in modulation
of the renin–angiotensin–aldosterone system. Renin is
produced in the juxtaglomerular apparatus in the kidney.
A drop in renal perfusion pressure results in release of
renin into the systemic circulation. This in turn results in
conversion of angiotensinogen to angiotensin I and then
to angiotensin II, which in turn results in release of
aldosterone by the adrenal glands.
Aldosterone causes increased permeability of the
distal renal tubules to sodium and, as a result, more
sodium is reabsorbed, with resultant increased loss of
potassium. The sodium pulls water with it back into the
circulation, causing salt and water retention and a consequent rise in blood pressure.
Extrarenal mechanisms can also occur via the
mechanisms of autoregulation of blood flow as described
above; the renal circulation is relatively detached from
the general vascular tone. However, volume receptors
present in the great vessels in the chest have an effect on
renal perfusion via the sympathetic nervous system.
Additionally, activation of stretch receptors in the right
atrium causes release of a hormone called atrial natriuretic factor. This peptide causes increased sodium
excretion by reducing sodium resorption in the distal
tubule. Hence, sodium and accompanying water is
excreted, resulting in a fall in the ECF volume.
Potassium regulation
Potassium excretion and secretion by the kidney is
intimately associated with sodium reabsorption. Nearly
all the potassium that is filtered in the glomerulus is
reabsorbed in conjunction with sodium (cotransporter) in
the proximal nephron. In the distal tubule the reabsorption of sodium causes an electrochemical gradient,
resulting in secretion of potassium (and hydrogen ions).
Therefore, the more sodium that is reabsorbed, under the
action of aldosterone, the more potassium is excreted.
Water regulation
As described above the main determinate of water reabsorption is the osmotic drive associated with sodium
reabsorption. There is capacity for fine-tuning of water
reabsorption, independent of sodium, which occurs in the
most distal part of the nephron, called the collecting duct.
The hormone antidiuretic hormone (ADH) is produced
by the posterior part of the pituitary gland. Its release
is influenced by numerous factors including plasma
osmolality, stress, surgery and thirst. ADH increases the
permeability of the collecting duct to water, increasing its
reabsorption. This results in water conservation by the
body 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 are
listed in Table 5.3. These losses are balanced by an intake
Table 5.3
Normal daily water losses (70-kg man)
Gastrointestinal (faeces)
Respiration
Insensible (latent
evaporation from skin)
Urine
Total
100mL
500 mL
700 mL
1700 mL (variable, depending
on fluid status)
3000 mL
Table 5.4
Normal daily water intake sources
Ingested fluids
Food
Metabolism
Total
1750 mL
900 mL
350 mL
3000 mL
of about 3 L water per day from the sources in Table 5.4.
These amounts can be drastically different in the conditions described below, where the correct amount of
fluid to be administered is guided by monitoring fluid
output and electrolyte concentrations in the blood.
Abnormalities of body water
Dehydration
In the case of water or electrolyte deficiency the kidney
is acted upon by numerous systems (as discussed briefly
above) to prevent further excess loss while maintaining
adequate waste product excretion. However, in extreme
circumstances these compensatory mechanisms are outstripped, causing shrinkage of the body fluid compartments. Insufficient fluid in the interstitial space results in
loss of skin turgor. Shrinkage of the intravascular volume
causes circulatory changes, which, in extreme cases, can
result in shock. Relative hypovolaemia can occur in
conditions affecting vascular tone, such as septic shock
(see Ch. 4).
Monitoring of the intravascular fluid is achieved by
clinical examination and particularly by measurement of
heart rate and blood pressure. Invasive monitoring of the
central venous pressure is helpful in severe cases or those
with confounding variables. The causes of dehydration
are listed in Table 5.5 and are now discussed in turn.
Insufficient intake
Failure to match fluid output with sufficient intake results
in dehydration. This is a common danger in surgical
practice, with patients undergoing periods of starvation
due to disease processes, preoperative preparation and
postoperative recovery. Examples are found in all
branches of surgery and include inability to swallow
(coma, oral disease) and enforced starvation (prior to
anaesthesia, postoperative resting of the gastrointestinal
tract). Adequate input is maintained with intravenous
fluids, guided by output monitoring and electrolyte
measurement, bearing in mind that a pre-existing deficit
must be compensated for.
Table 5.5
Causes of dehydration
Insufficient fluid intake
Excess loss of fluid
Haemorrhage
Diarrhoea, bowel obstruction, bowel preparation
Vomiting
Fistulae
Diuresis
Insensible losses
Respiratory
Excess loss
Common surgical procedures, diseases and complications cause an abnormally high fluid loss. The principles
for management of these are the same. Treatment should
be directed at the underlying cause, in an attempt to
decrease future losses. Supportive replacement therapy is
determined by measuring the amount and type of fluid
loss, with special note being made of its electrolyte
concentration so that appropriate loss can be corrected.
Direct analysis of the electrolyte concentration of the
fluid lost (by laboratory testing) can be helpful.
Haemorrhage
Bleeding can lead to a fluid deficit that requires replacement, the principles of which are considered in the
section on shock (see Ch. 4).
Diarrhoea, bowel obstruction and bowel preparation
Gastrointestinal secretions are rich in solutes and the
increased losses occurring in the above conditions can
need aggressive replacement. When the bowel is
obstructed, the fluids do not leave the body but
accumulate in the gut lumen, outside the extracellular
fluid compartment. This is known as a third-space loss.
Vomiting
Vomitus is also solute rich. In addition, it is highly acidic
and the loss of hydrogen ions has an important effect on
acid-base balance in the body.
Fistulae
Gastrointestinal fistulae bypass the capability of fluid
reabsorption further down the gastrointestinal tract.
29
Losses therefore, particularly from high fistulae and
particularly to the skin, can be large and solute rich.
patients, generalised oedema and acute heart failure can
be easily precipitated.
Diuresis: drugs and renal disease
Decreased loss
Diuretic drugs used for the treatment of fluid overload
(see below) can be overeffective and result in dehydration by losses into the urine. Similarly, a number of renal
diseases, including common disorders such as diabetic
nephropathy, result in production of excess amounts of
urine.
Several medical conditions result in pathophysiological
salt and water retention. They are of relevance to surgical
practice as these patients might require surgical intervention, where inappropriate fluid management can
exacerbate their condition. The altered cardiovascular
dynamics of cardiac failure results in pathophysiological
alterations in the renin-angiotensin-aldosterone axis,
causing salt and water retention and further increases in
venous pressure.
A low plasma albumin concentration - hypoalbuminaemia - results in a decreased colloid osmotic
pressure of the blood. This results in more fluid shifting
into the interstitial space, causing peripheral oedema.
This fluid is lost from the intravascular space and results
in activation of mechanisms effecting salt and water
retention.
Insensible losses
Losses through the skin can be significant. A common
example is pyrexia, whereby water evaporates from the
surface using latent heat of evaporation.
Massive amounts of plasma are lost from the surface of
burns, and one of the mainstays of burns management is
fluid resuscitation.
Respiratory losses
The tachypnoea and pyrexia of respiratory complications
of 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 compartment
in which the excess fluid is distributed (Table 5.6).
Excess intake
By far the most common cause of fluid overload in
surgical practice is excessive intravenous administration.
This is more likely to occur in patients with pre-existing
renal and cardiovascular disease, and such patients therefore require careful thought about their fluid regime and
may need close monitoring modalities. Maintenance
of accurate fluid balance charts is essential. In such
Table 5.6
30
Causes of fluid overload
Excess intake
Decreased loss
Renal disease
Liver disease
Renal disease
Diseases that reduce the glomerular filtration rate result
in an impaired ability to excrete sodium. Complex interactions are seen in many renal diseases that alter tubular
reabsorption of sodium and lead to retention of sodium
and its accompanying water.
Liver disease
Patients with cirrhosis have raised portal venous
pressure, causing similar changes to those seen in cardiac
failure and hence salt and water retention. Many of these
conditions require tight fluid restriction. In those patients
who become overloaded with fluid, reduction in body
water is achieved predominantly with diuretic drugs, of
which there are several different classes with different
mechanisms of action.
A commonly used class of drugs is loop diuretics, e.g.
furosemide (frusemide), the main effect of which is to
block the sodium-chloride cotransporter in the loop of
Henle. This results in an increased sodium load in the
distal tubules. The tubule attempts to reabsorb this extra
sodium, at the expense of excreting potassium and
hydrogen ions, but its capacity is not sufficient and more
salt and water is lost to the urine. As a result, the major
side-effects of furosemide (frusemide) therapy are
hypokalaemia, metabolic alkalosis and the effects of
overaction (i.e. salt and water depletion).
Abnormalities of electrolytes
Sodium
As discussed above, sodium and water homeostasis are
intimately related. The classic abnormalities described
below relate to plasma sodium concentrations. These can
occur in the presence of low, normal or high levels of
total body sodium. Daily requirements of sodium in a
normal 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 often
results from water deficiency. The raised plasma osmolality
results in activation of mechanisms to conserve water and
increase intake (e.g. stimulating thirst).
There are many causes of hypernatraemia and only
those 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 respiratory
complications.
• Administration of excess sodium, either with
intravenous sodium solutions or medications
containing large amounts of sodium.
• Diabetes insipidus (DI), which is either a failure of
production (pituitary DI) or lack of response to ADH
(nephrogenic DI).
Generally, these causes are easily prevented by consideration and monitoring the patient's fluid balance.
Correction of the water deficiency is effected with
administration of appropriate intravenous fluids. Sodium
concentration should be corrected gradually to minimise
the risk of inducing cerebral oedema (as water shifts
from the newly hypotonic or isotonic plasma). Treatment
of DI depends on the underlying cause.
Hyponatraemia
Low serum concentrations of sodium can occur in the
presence of high, normal or low total body sodium levels.
The clinical picture seen and treatment required depends
on which of these is present.
Most commonly seen in surgical practice is combined
salt and water depletion. The disease processes are the
same as those causing dehydration from excess fluid
losses (see above), particularly where the losses are
solute rich. The decreased extracellular fluid stimulates
water reabsorption under the influence of ADH. More
water is therefore preserved relative to sodium, diluting
sodium in the ECF, and hence resulting in hyponatraemia. The clinical signs are as for dehydration.
Treatment is by restoration of salt and water by
intravenous administration of normal saline.
The processes involved in fluid overload can also
result in hyponatraemia, with more water being retained
relative to sodium. The total body sodium is therefore
increased, but not as much as the total body water,
causing dilution and hyponatraemia. Treatment is as
described for fluid overload above.
Potassium
Daily requirements of potassium are between 60 and 140
mmol per day. This is dependent on the rate of excretion
and also the rate of liberation from the intracellular fluid
compartment (see below).
Hyperkalaemia
A significantly raised serum potassium concentration
(>7.0 mmol/L) can cause life-threatening cardiac
arrhythmias and urgent treatment is required to prevent
these. Symptoms are rare until complications have occurred,
so awareness and prevention are essential. Treatment is
resuscitative, performing life support manoeuvres where
required. If complications have not yet occurred, treatment is directed at preventing complications and reducing
serum potassium levels. Calcium gluconate (10 mL of
10%) protects the heart from arrhythmias.
Insulin drives potassium into the intracellular fluid.
There is some debate as to whether glucose should be
given simultaneously to prevent a fall in blood glucose
concentration. Treatment is then directed at the underlying cause, e.g. renal support may be required. Causes
include either increased release or administration, or
decreased excretion.
The vast majority of body potassium is intracellular.
Cell lysis, or inefficient functioning of the sodiumpotassium exchange pump in the cell membrane, results
in liberation of potassium into the circulation. As a
result, processes that cause cellular damage or cellular
31
dysfunction (e.g. surgery, trauma, acidosis) can increase
serum potassium levels.
Excessive administration of potassium is most frequently iatrogenic. Patients receiving supplementation
should receive this slowly, and close monitoring of blood
levels is required.
Renal insufficiency results in impairment of potassium
excretion and acute renal failure can result in a
precipitous rise in serum potassium levels. Severe chronic
renal failure can have a similar effect, particularly where
tubular function is affected.
Drugs that affect distal tubular function can cause
inefficient potassium excretion. An example is the class
of diuretics that antagonises the action of aldosterone
(e.g. spironolactone, which prevents the reabsorption of
sodium at the expense of potassium). Similarly, drugs
and diseases that affect the rennin-angiotensinaldosterone axis result in hyperkalaemia (e.g. ACE
inhibitors, Addison's disease).
Hypokalaemia
Low serum potassium levels result from insufficient
intake or excess loss of potassium. Again, symptoms are
rare, but the deficit is rarely life-threatening, unlike
hyperkalaemia. An exception is concomitant treatment
with digoxin, where hypokalaemia causes a dangerous
potentiation of the drug's action and can result in cardiac
arrhythmias. Treatment of hypokalaemia is based on
replacing the deficit either orally or in dilute intravenous
fluids (never as a potassium salt bolus), and treatment of
the underlying cause.
There are very many causes of hypokalaemia and
descriptions of all of these are beyond the scope of this
chapter. Examples of those most commonly encountered
in surgical practice are given in Table 5.7.
there being some evidence that use of colloids in critically
ill patients actually increases mortality. However, the
fundamentals of fluid replacement remain unchanged
and a knowledge of the constituents of the infused fluid
and its pattern of distribution within fluid compartments,
is important. Solutions available for fluid replacement
are 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 plasma
potassium levels.
Dextrose
Glucose solution is isotonic at 5%, and this is the
standard fluid infused. It is transferred freely between all
fluid compartments so that only 8% remains in the
intravascular space. Its energy content is negligible, the
glucose in each 500 mL bag producing only 100 calories
of energy.
Saline
Isotonic saline is 0.9%, and is called 'normal saline'.
Each 500 mL bag contains 75 mmol of sodium, balanced
with 75 mmol of chloride. Following intravenous
infusion, it is distributed freely within the ECF, with 25%
remaining intravascular.
Colloid
Colloid solutions contain large-molecular-weight substances that are designed not to cross the vascular
Fluid replacement
There is a long-standing debate over the relative value of
fluid replacement with crystalloid and colloid solutions,
Table 5.7
32
Common causes of hypokalaemia
Insufficient intake: inadequate intravenous replacement
Excess gastrointestinal losses: diarrhoea, fistulae, villous
adenomas
Excess renal losses: diuretic therapy
Table 5.8
Solutions for fluid replacement
Crystalloid
dextrose
saline
Ringer's lactate
Colloid
gelatines
dextrans
heta starch
human albumin solution
Blood
endothelium and thus remain within the intravascular
space. They are used to increase the colloid osmotic
pressure causing retention of fluid in the circulation.
However, some molecules do cross to the interstitial
space, and this proportion can be increased in disease
processes where vascular permeability is affected.
Blood
Where fluid loss is by way of significant haemorrhage,
replacement with blood is appropriate. The principles of
blood transfusion are discussed in Chapter 6.
haemoglobin reaches the tissues, where there is a higher
concentration of carbonic and other acids, it more readily
releases 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 by
imbalance at any point of the Henderson-Hasselbach
equation as a result of either respiratory or renal changes
in acid-base management.
Respiratory acidosis
Acid-base balance
For efficient cellular function to occur, the cellular and
plasma pH, or hydrogen ion concentration, must be
maintained between narrow limits (pH 7.36-7.44).
Values outside these parameters result in cellular and
system dysfunction, which become profound and can
ultimately result in cell death and system failure.
Hydrogen ions are generated by several metabolic
processes, and by equilibration of carbon dioxide (CO2 )
in solution. Maintenance of normal pH is achieved through
a number of different systems: namely, buffering, respiration and renal excretion of hydrogen ions and
bicarbonate.
The main determinant of pH is the equilibration of
CO2 in solution. CO2 is generated as a waste product in
normal aerobic respiration. It is excreted by the lungs
during respiration. Transport of CO2 from the tissues to
the lungs is performed by the blood, with the CO2 being
dissolved in solution. The enzyme carbonic anhydrase
forms carbonic acid according to the HendersonHasselbach equation:
This equation has to remain in equilibrium, and is therefore dependent on CO2 excretion by the lungs and the
bicarbonate (HCO 3 - ) concentration in plasma. Bicarbonate concentration is controlled by renal excretion.
Other forms of acid are produced by tissues, e.g. lactic
acid from anaerobic metabolism. These are buffered in
plasma by bicarbonate, phosphate, haemoglobin and
other plasma proteins. Renal excretion of hydrogen ions
is important in their elimination.
An important effect of the interaction between
hydrogen ions and haemoglobin (Hb) is the reduction in
the affinity of Hb for oxygen. As a result, when oxy-
Decreased CO2 excretion by the lungs results in
increased plasma carbonic acid and hence hydrogen ion
concentration. Causes include decreased respiratory
drive (e.g. opiate overdose) and diseases of lung
parenchyma that result in inefficient gas transfer.
Respiratory alkalosis
Overventilation increases CO2 excretion, decreasing
plasma carbonic acid and hence hydrogen ion concentration. Hyperventilation can be psychological, pathological
(e.g. tachypnoea of respiratory tract infection) or
iatrogenic (e.g. Overventilation of mechanically ventilated
patients).
Metabolic acidosis
Metabolic acidosis is an increase in plasma hydrogen ion
concentration derived from another source than CO2.
Examples include lactic acidosis and diabetic
ketoacidosis.
Metabolic alkalosis
This is a fall in plasma hydrogen ion concentration not
related to carbon dioxide. It can result from many
processes that cause either increased renal H+ excretion
or from excess plasma bicarbonate (e.g. iatrogenic
administration, renal conservation of bicarbonate).
Compensation
The clear-cut abnormalities described above are rarely
seen because the system not affected by the abnormal
process will act to compensate for the problem. Thus, in
33
respiratory acidosis the kidney will retain bicarbonate
and excrete H+. This in effect causes a partial metabolic
alkalosis and combats the fall in pH driven by CO2
retention. Similarly, in metabolic acidosis, respiration is
increased, blowing-off more CO2, causing a compensatory partial respiratory alkalosis.
Metabolic response to
surgery
The insult of trauma, including surgery, results in a
number of metabolic changes directed at containing and
repairing the damage. This response is complex and
involves many metabolic processes and body systems.
The effects are mediated by the sympathetic nervous
system, endocrine, inflammatory and endothelial
responses. Not only has the response been implicated in
healing but, more recently, has been suggested to play an
important pathophysiological role in the complications
of trauma, such as systemic inflammatory response
syndrome (SIRS) and multiorgan failure (MOF). A full
description of the changes observed is excessive for the
purpose of this chapter, but it is worth highlighting a
number of points that have bearing on everyday clinical
practice.
Sympathetic activity causes a rise in heart rate and
blood pressure, increasing cardiac work. Mobilisation of
energy stores occurs shortly after injury, causing relative
hyperglycaemia and insulin resistance. ADH secretion is
increased resulting in water retention and a fall in urine
output. Vascular permeability is increased, predisposing
to oedema formation. Inflammatory mediators (e.g.
prostaglandins and leucotrienes) are produced, causing
systemic effects such as pyrexia; they might also be implicated in trauma pathophysiology. The immune system
is impaired, predisposing to infective complications.
After the initial brief mobilisation of energy stores
(catabolic state) the body enters a more prolonged
reparative anabolic state with increased energy and
nitrogen demands. Activation of platelets leads to a
hypercoagulable state.
Postoperative feeding
34
For effective healing to occur after trauma or surgery, the
body must be supplied with the correct substrates in
sufficient amounts. Whereas these are normally supplied
via the gastrointestinal tract by a balanced diet, demand
for, and the ability to attain, the substrates can be dramatically altered perioperatively.
Patients' ability to ingest, digest, absorb and utilise
substrates is affected by any number of disease processes. In cases where the effects of these processes are
expected to be prolonged, or are superimposed on a
background of malnutrition, nutritional support may be
indicated. This support can be provided either to the gastrointestinal tract (enteral) or intravenously (parenteral).
Trauma and major surgery induce metabolic changes
such that energy and nitrogen demands are increased,
and this should be taken into account when deciding on
a feeding regime. Reasonable figures for normal daily
requirements of energy and nitrogen are 2000-2500 kcal
and 14-16 g, respectively.
Enteral feeding
Where possible, enteral dietary supplementation is
preferable. Stimulation of the gut mucosa with food has
been implicated in reducing sepsis in critically ill
patients. It is thought that continued mucosal activity
maintains 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 the
pathophysiology of multiorgan failure.
Enteral nutritional support can be given as oral
supplements, or where appropriate by intubation of the
gastrointestinal tract (e.g. nasogastric, feeding
jejunostomy). The feed needs to contain each food group
- carbohydrate, fat and protein. These can be given in
several different proportions and forms, particularly
relating to protein and its degree of predigestion prior to
administration. Disease-specific diets are also available.
Trace elements are also added (e.g. zinc and magnesium). Enteral feeding is appropriate in patients who
are comatose, those with oropharyngeal diseases that
prevent ingestion, mastication and swallowing, and some
patients with certain diseases further down the gastrointestinal tract.
In the presence of a poorly functioning gastrointestinal tract, enteral feeding can lead to further complications, including diarrhoea, vomiting and aspiration.
Complications relating to method of administration are
not uncommon, including incorrect positioning of the
feeding tube and bacterial growth in the excellent
medium that the feed provides.
Parenteral feeding
When patients with a non-functioning gastrointestinal
tract require nutritional support, and when it is not
practical to gain access for enteral feeding, feeding can
be given intravenously. The feed is designed to meet all
the body's requirements and is termed 'total parenteral
nutrition' or TPN.
Constituents
To meet the body's needs, TPN solutions contain fat,
amino acids and carbohydrate (mainly glucose). The
composition of a feed varies, is prepared for individual
patients and is tailored to their needs. There are a number
of standard feeds with different amounts of nitrogen, and
the majority of energy supplied by carbohydrates or fats.
These are further manipulated, for example, with the
addition of potassium, as guided by monitoring of serum
levels and markers of metabolic state.
Complications
The constituents of TPN solutions render them hyperosmolar, and hence irritant, and when given through
peripheral veins cause thrombophlebitis. They are there-
fore administered via a large-bore central venous
cannula. There is, however, an increasing role for peripherally sited 'long' feeding lines.
The hyperosmolality of TPN solutions can also cause
metabolic complications, most commonly hyperglycaemia. If this occurs, insulin might be required and,
in future feeds, more of the energy should be supplied as
fat. Rebound hypoglycaemia can occur on cessation of
feeding.
Patients on TPN are more prone to hepatobiliary
disease.
Trace element and vitamin deficiencies can occur,
more commonly in prolonged TPN administration, and
these should be replaced accordingly.
However, the majority of complications of TPN relate
to the feeding line. The majority of these lines are sited
centrally, and so are subject to the risks of central line
insertion (e.g. pneumothorax or arterial puncture). Infection is a common problem, as is secondary line
thrombosis and failure. Patients requiring long-term TPN
can benefit from the placement of a buried subcutaneous
feeding line to minimise these risks. All TPN should be
administered through a lumen dedicated solely to it and
not used for other purposes such as intravenous antibiotic
administration or blood transfusion.
35
6
Blood disorders and
their management in
surgical practice
Introduction
Poor haemostasis (control of bleeding) is one of the most
common surgical complications and can range from
catastrophic blood loss causing hypovolaemia and shock
to small wound haematomas that provide an excellent
growth medium for microorganisms. By virtue of the
coagulation or clotting cascade, blood and blood vessels
are a self-sealing system, and therefore have an inherent
ability to provide haemostasis. However, there is no
substitute for careful technique and meticulous surgical
haemostasis.
This chapter describes, under the headings shown in
Table 6.1 the normal sequence of events involved in blood
clotting and also those mechanisms that prevent clotting
in normal, undamaged vessels. Also described are conditions where abnormalities in clotting occur, their
recognition and treatment. The implications of anaemia
in surgery are considered, the principles of blood transfusion are described and a guideline for the recognition
and care of a patient with potential bleeding problems is
provided. The specific management of a dental postextraction haemorrhage is considered in Chapter 26.
Table 6.1 Blood disorders and their
management
Normal clotting
Abnormal clotting
increased bleeding tendency
increased clotting tendency
Patients with anaemia
Transfusion
Summary and guidelines
Table 6.2
Normal blood clotting
Initiation of clotting
platelet adhesion
platelet activation
platelet aggregation
Stabilisation
coagulation
intrinsic pathway
extrinsic pathway
common pathway
Limitation of clotting
Dissolution of clot
Prevention of inappropriate clotting
structural
chemical mediators
Normal clotting
36
The whole process of blood clotting, limitation of propagation of clot and ultimate dissolution of clot is a complex interactive system interdependent on, and subject to,
numerous feedback controls. Blood clotting will be considered under the headings listed in Table 6.2.
The immediate response to vessel damage is vasoconstriction, which reduces blood flow in the area thereby
reducing blood loss and preventing the fledgling blood
clot from being washed away. This is mediated both as a
local reflex and by a number of mediators that are released
mainly from activated platelets, such as thromboxane
(TxA2). Thus, although coagulation, as measured by
clotting time, takes around 8 min to occur, haemorrhage
is reduced and arrested much sooner.
Initiation of clotting
Circulating platelets play a central role in the initiation of
blood clotting by three main mechanisms:
1. Platelet adhesion: platelets possess membrane receptors to many proteins not encountered in normal blood
or endothelium. Disruption of endothelium exposes
platelets to 'foreign' proteins, for example, different
types of collagen, to which they have receptors and to
which they therefore stick.
2. Platelet activation: platelet adherence results in a
change in the shape of platelets. Within seconds, by
way of complex intracellular messaging, the platelet
becomes 'activated'. This results in synthesis and
release of mediators such as histamine and TxA2 from
intracellular stores (lysosomes).
3. Platelet aggregation: the conformational changes in
the platelets and the milieu of mediators released
attract other platelets and allow them to stick to one
another. This is known as aggregation.
Platelet adhesion, activation and aggregation result in the
formation of a platelet plug, which is an attempt to cover
the breach in the endothelium and acts as the starting point
from which the rest of the process of coagulation occurs.
Stabilisation
Coagulation
A mature blood clot is a combination of cross-linked
fibrin admixed with blood cells and plasma. Platelet
events described above stimulate a stepwise pathway that
results in the formation of cross-linked fibrin. This system is known as the 'coagulation cascade', which consists
of two routes that run in parallel - the intrinsic pathway
and the extrinsic pathway. Current thinking in coagulation research is that this might be oversimplified and
there are now thought to be multiple interactions between
the pathways, resulting in a more integrated system.
However, the sequences described here are accurate and
provide a good framework for understanding the process
of coagulation.
Ionised calcium is a crucial cofactor for many of the
clotting factors, and deficiency has an important effect on
coagulation.
Intrinsic pathway
This is the more intricate portion of the coagulation cascade, and there is debate over the relevance of different
aspects seen in vivo compared to results seen in vitro
experiments. Essentially, contact with injured tissue results
in activation of factor XII, which in turn activates factor
XI, which in turn cascades to the common pathway as
shown in Fig. 6.1.
Extrinsic pathway
This is coagulation initiated by tissue factor. Tissue factor
(TF) is expressed on the surface of the subendothelial
tissue that is exposed when endothelium is damaged.
Tissue factor activates factor VII, which, in turn, activates
factor X, the beginning of the common pathway.
Common pathway
This is the common endpoint of the intrinsic and extrinsic
pathways. It begins with activation of factor X and, via
the steps in Fig. 6.1, results in the formation of crosslinked fibrin.
Limitation of clotting
It is vital that clotting is limited to the local area of
damage to prevent propagation of clot throughout the
vascular system. Activated clotting factors are removed
from the propagating clot by blood flow. There is also a
form of negative feedback on clotting by naturally
occurring substances that inhibit coagulation, some of
which are activated by products of the coagulation
cascade itself. Examples of these are proteins C and S
and antithrombin III. Abnormalities of these factors can
cause 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 and
re-endothelialised, the adherent clot will be removed.
This is known as fibrinolysis. In this process, tissue
plasminogen activator (TPA), produced by vascular
endothelium in the presence of thrombin, acts on
circulating plasminogen to form plasmin; this action is
dependent on the presence of fibrin. Plasmin now acts in
turn on fibrin, which is degraded to soluble fibrin
degradation products (FDPs).
Fibrinolysis maintains vessel patency and helps to
prevent overpropagation of clot. Not surprisingly, there
are also inhibitors of plasmin and plasminogen activators.
Levels of fibrinogen and FDPs can be measured and
provide helpful diagnostic clues, for example elevated Ddimer FDP levels are indicative of the presence of blood
clot and can be used in the diagnosis of suspected deep
venous thrombosis (DVT).
This very intricate system of control prevents
excessive bleeding while at the same time preventing
37
Fig. 6.1 The coagulation cascade showing the numbered factors (a, activated
form). The factors involved in the intrinsic system, beginning with the activation of
factor XII and ending with the activation of factor X are all present in the circulating
plasma: 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 the
final steps, culminating in the conversion of fibrinogen to fibrin by thrombin.
excess intravascular coagulation once clotting has been
initiated: the body has developed a very finely balanced
feedback system.
Prevention of inappropriate clotting
To prevent inappropriate clotting in normal blood
vessels, physiological systems act to counteract those
38
that stimulate blood clotting. Interference with these
systems stimulate the initiation of blood clotting, as
described below. The mechanisms that prevent blood
from clotting in normal blood vessels can be divided into
structural and chemical:
• Structural prevention mechanisms: the smooth lining
of the blood vessel provided by endothelium does not
express surface proteins that stimulate platelet
adhesion as has been described above. Rough or
damaged endothelium (e.g. atherosclerotic plaques)
not only allows platelets to come into contact with
proteins that they adhere to but also results in
turbulent blood flow, which also predisposes to blood
clotting.
• Chemical mediators: normal vascular endothelium
produces the prostaglandin, prostacyclin (PGI2). This
opposes the actions of TxA2, causing vasodilatation
and opposing platelet activation and aggregation.
Abnormal clotting increased bleeding tendency
Careful history taking is fundamental in the diagnosis of
bleeding disorders and is essential before surgery. In
patients who express a past history of bleeding problems,
the site and type of bleeding (e.g. spontaneous Vs induced
by trauma) needs to be determined accurately. This can
give clues to the type of bleeding disorder. A history of
excess bleeding at the time of previous surgery is very
important to note. A detailed family history can suggest
if such a disorder is inherited or acquired.
Full physical examination can show further evidence
of a bleeding disorder, including bruising, petechiae
(subcutaneous red spots that do not blanch on pressure
and which represent areas of small capillary bleeding) or
previous bleeding into joints.
However, despite a careful history and examination,
excessive bleeding at the time of surgery might be a
patient's first presentation of a bleeding disorder, and it is
therefore important for a surgeon to be aware of the
concepts and how to control bleeding in this situation
should it occur. Close liaison with a haematologist will
be necessary at this time. The causes of an increased
bleeding tendency are listed in Table 6.3.
Platelets disorders
These can be either quantitative (number) or qualitative
(function). Disorders of platelets can result in bleeding
from small vessels in mucous membranes such as nose
bleeds (epistaxis), or in skin causing bruising or
petechiae.
Table 6.3
Causes of increased bleeding tendency
Platelet disorders
decreased numbers
idiopathic thrombocytopenic purpura (ITP)
hypersplenism
disseminated intravascular coagulation (DIC)
decreased function
Vessel disorders
Coagulation disorders
inherited
haemophilia A
haemophilia B
von Willebrand's disease
Acquired
liver and biliary disease
DIC
massive blood transfusion
value is 150-400 x 109 per litre. Bleeding is rarely a
problem when the platelet count is above 50. Severe or
spontaneous bleeding occurs with values below 20.
There are multiple causes of thrombocytopenia,
which can be broadly divided into those with excessive
loss or consumption of platelets and those with impaired
production. Either form can be congenital or acquired.
Important examples are discussed below.
Idiopathic thrombocytopenic purpura (ITP)
This condition is also known as autoimmune thrombocytopenic purpura and the platelet count might be
undetectable.
Treatment of thrombocytopenia is directed at the
underlying cause (e.g. ITP might respond to steroid
therapy or splenectomy). During surgery, if a patient is
actively bleeding with a low platelet count, platelet transfusion can provide a temporary solution. However, these
transfusions are prone to the same fate as the patient's
endogenous platelets (e.g. rapid consumption).
Hypersplenism
This occurs where platelets are sequestered in an enlarged
spleen.
Disseminated intravascular coagulation (DIC)
Decreased numbers
This is known as thrombocytopenia. Platelet count is
measured routinely as part of a full blood count. A normal
This occurs where platelets and coagulation factors are
consumed in widespread inappropriate coagulation
within normal blood vessels (see below).
39
Decreased function
These disorders can also be congenital or acquired.
Assessment of platelet function is difficult and reliance is
initially on the bleeding time, which is the time taken for
bleeding to stop under standard test conditions. However.
this is a difficult test to standardise and has a wide normal
range between 2 and 10 min.
An important acquired cause of decreased platelet
function is medication, the most common of which is
aspirin. This is now widely used in prophylaxis and
treatment of vascular disease because of its effect on
platelet function and its effects can last up to 10 days.
Aspirin should therefore be withheld for 10 days prior to
major procedures associated with a potential high risk of
bleeding complications.
Vessel disorders
These form a generally rare, heterogeneous group with a
clinical presentation similar to that of platelet disorders,
but where investigations of platelet number and function
are normal. Essentially, the capillaries are fragile and
bleeding occurs more easily. Again, there are congenital
and acquired forms. Corticosteroid therapy is a common
example of an acquired cause.
One of the interesting congenital causes is hereditary
haemorrhagic telangiectasia, characterised by recurrent
bleeds from mucous membranes. The lesions look like
small 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 condition
should be identified before surgery. This is of particular
relevance to dentists.
Coagulation disorders
40
Disorders of coagulation factors are characterised by a
more generalised bleeding tendency than platelet and
vascular disorders, including spontaneous bleeding from
larger vessels and into joints. The vast majority of coagulation factor defects encountered in surgical practice are
acquired. The most common cause is iatrogenic, related
to treatment with warfarin. Inherited disorders are
uncommon but require special consideration.
A number of laboratory investigations can help
elucidate the type of a coagulation defect. Although some
of these are specialised, an appreciation of standard
clotting tests is essential for surgeons:
• Prothrombin time (PT): this gives an indication of the
extrinsic and common pathways of the coagulation
cascade. Abnormalities in these portions of the
cascade result in a prolonged time. Times are related
to an international standardised sample designated
international normalised ratio (INR). An INR of 1.0
is normal, whereas an INR of 2.0 denotes that the
patient's blood takes twice as long as 'normal' to clot
under test conditions.
• Activated partial thromboplastin time (APTT): this
measures the efficiency of the intrinsic and common
pathways.
If abnormalities of INR or APTT are discovered then
normal plasma is added to the sample in the laboratory.
If this corrects the abnormality, then the problem must
relate to a factor deficiency or dysfunction (because the
factors present in the normal added plasma corrected the
problem). If the abnormality is not corrected then it is
likely to be due to the presence of a substance that
inhibits coagulation. This procedure is known as
'correction testing'.
Inherited coagulation disorders:
Inherited defects are specific genetic abnormalities that
generally affect only one clotting factor.
Haemophilia A
This is an X-linked recessive disorder that therefore
affects only males but which is transmitted by females.
The prevalence is about 1:10000. Statistically, all the
daughters of haemophiliacs will carry the gene and none
of the sons will inherit the disease or transmit it. However, in the second generation, only 50% of the sons of
female carriers will inherit the disorder and only 50%
of their daughters will inherit the gene.
Haemophilia A can be caused by a number of genetic
abnormalities, all of which result in decreased or absent
factor VIII:C. Deficiency of factor VIII:vWF results in
the closely related von Willebrand's disease (see below).
Different affected individuals have a different level of
VIII in the blood and there is therefore a spectrum of
disease. Factor VIII levels can be measured in the patient's
plasma and are expressed as a percentage of normal.
Bleeding into joints causing arthritis is common and
produces clinically obvious joint deformities in many
cases. Bleeding can also occur into body cavities and
intracranially.
Preoperative transfusion of factor VIII concentrate is
aimed at raising factor VIII levels to nearer normal, for
example, 60% for dental extraction, and as near 100% as
possible for major surgery. These levels need to be
maintained postoperatively.
Tragically, many haemophiliacs who received blood
transfusions prior to HIV blood donor screening introduction in the UK contracted HIV, and in these patients
high-risk precautions are indicated perioperatively.
Haemophilia B
This is also known as Christmas disease. It is similar to
haemophilia A but the disorder is related to deficiency
of factor IX. The incidence is less common, with a
prevalence of around 1:100 000 and the defect can be
corrected by the transfusion of fresh-frozen plasma
(FFP).
von Willebrand's disease
von Willebrand's disease is not sex-linked and can occur
via a number of genetic abnormalities. It is usually due to
autosomal dominant inheritance.
Surgery - elective or emergency - on any of the above
patients should only be performed in close consultation
with a haematologist (preferably the patient's own).
Acquired coagulation disorders
Bile salts are produced by the liver and enter the duodenum via the common bile duct to aid the absorption of
fats and fat-soluble vitamins such as vitamin K. The
presence of vitamin K is essential for the synthesis of
coagulation factors II, VII, IX and X (and also proteins C
and S). Disorders of bile production and of biliary
drainage will affect coagulation.
It should be noted that the majority of clotting factors
are produced by hepatocytes. Remembering this physiology
is 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 description 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 dysfunction is complex. The damaged liver produces too few
clotting factors. Bile salt synthesis, needed for vitamin K
absorption, is also impaired. Portal hypertension can
result in hypersplenism, and therefore thrombocytopenia.
Surgical jaundice secondary to obstruction of the
common bile duct due to gallstones or malignancy of the
pancreas prevents bile salts reaching the duodenal lumen.
Vitamin K malabsorption results, followed by deficiencies
of factors II, VII, IX and X. Other causes of vitamin K
deficiency, such as dietary deficiency, have the same
result. However, the effect of 'back pressure' on hepatocyte function also plays a role in the coagulopathy of
biliary obstruction.
Vitamin K deficiency can be corrected by parenteral
injection of a water-soluble vitamin K analogue before
elective surgery, but this will not be immediately
effective. It will be several days before the liver can
synthesise sufficient factors to correct the bleeding
tendency. Urgent or emergency surgery might therefore
require infusion with solutions containing the deficient
factors. The INR should be checked immediately before
surgery, with the aim of reducing it to 1.
Warfarin therapy
Warfarin, a coumarin drug, is a vitamin K antagonist (it
prevents conversion of vitamin K to an active form).
Warfarin therapy is indicated in a number of common
conditions including atrial fibrillation, pulmonary
embolus and prosthetic heart valve replacement. Normal
medical practice for most conditions dictates that
warfarin therapy should be administered to achieve an
INR of around 3. Excessive bleeding will occur where
the INR is greater than 2.
The effects of warfarin are slow to reverse because,
again, even if vitamin K is administered, the clotting
factors still have to be synthesised. When emergency
surgery is needed, vitamin-K-dependent factor concentrates can be administered intravenously, reducing the
INR quickly, as noted above in obstructive jaundice. This
must always be done with care. A balance needs to be
achieved between maintaining an acceptable level of
anticoagulation (e.g. to prevent thrombosis. of a
prosthetic heart valve) and not exposing the patient to the
risk of haemorrhage during surgery. It is vital, therefore,
that the administration of these concentrates is done in
consultation with a haematologist, and that the INR is
maintained well above 1. It is recommended that patients
undergoing elective surgical should have their warfarin
stopped for 2-3 days before surgery and, depending on
41
the procedure to be performed, are perhaps switched
perioperatively onto faster and more malleable anticoagulation therapy with heparin. Coagulation tests
should always be performed on the morning before
operation. In most cases, an INR of 2 is acceptable. In
dental procedures, an INR of less than 4 is acceptable
because local haemostatic measures can be used as an
adjunct (see Ch. 26).
Disseminated intravascular coagulation (DIC)
DIC is a major complication seen in seriously ill or
injured patients. The triggers to DIC are multiple and
include infections, malignancy and trauma. Inappropriate
extensive coagulation occurs, often in fundamentally
normal blood vessels. This process uses up clotting factors, fibrinogen and platelets, resulting in an increased
bleeding tendency.
Clinical features are paradoxically of both bleeding
and organ dysfunction from ischaemic damage caused by
microthrombi. Investigations show consumption of
fibrinogen and platelets, an increase in FDPs and
deranged clotting studies. Treatment is based on the
underlying cause, along with supportive therapy and
transfusion of clotting factors and platelets that have
been consumed. As can be appreciated, this is an
extremely serious condition.
Massive blood transfusions
42
Stored blood has relatively low concentrations of
platelets and clotting factors, particularly factors V and
VIII. This is not only because of the short lifespan of
these substances but also because platelets and clotting
factors are often removed from fresh blood for specific
infusions as described above. In addition to this, stored
blood must contain an anticoagulant to prevent it clotting
while in storage. Citrate, which binds ionised calcium, is
used for this purpose. As outlined above, calcium is an
important cofactor in the coagulation cascade. Although
this effect of citrate is essential for storage, it means that
transfused blood has poor clotting ability. This is not
usually a problem clinically, unless the patient has
received a 'massive transfusion' (defined as receiving a
transfusion volume greater than the patient's normal
blood volume, i.e. 4-5 L). If this happens, the recipient is
reliant on transfused factors, of which there are not
enough in stored blood. The recipient will therefore
require simultaneous transfusion with platelets and
clotting factors along with calcium. The management of
such patients is again done in close collaboration with a
haematologist.
Abnormal clotting increased clotting tendency
This group of diseases is actually more prevalent than
diseases with increased bleeding tendency. Their
relevance to surgical practice relates to an increased risk
of deep venous thrombosis (DVT). Thrombosis can be
recurrent or atypical, as in spontaneous axillary vein
thrombosis.
Patients with suggestive features require referral to
haematology for further investigation before surgery.
Patients already diagnosed with an increased clotting
tendency require prophylactic measures against DVT no
matter how minor the procedure (Ch. 4). Patients who
have previously been diagnosed with such a problem
might already be receiving treatment with warfarin,
which will alter operative preparation (see above).
Patients with anaemia
There are many different forms of anaemia, and multiple
causes for each type. A description of these is beyond the
scope of this chapter. However, the existence of anaemia
in surgical patients has implications that are worth brief
consideration.
Anaemia is defined as a haemoglobin concentration
below an arbitrary designated level, which is generally
accepted as 13 g/dL for men and 12 g/dL for women.
Anaemia has a number of pathophysiological consequences of surgical relevance (Table 6.4) as a consequence of the decreased oxygen-carrying capacity of
the blood.
Cardiorespiratory problems
The reduced oxygen-carrying capacity of the blood
results in an impaired ability to cope with the stresses of
Table 6.4
Consequences of anaemia
Cardiorespiratory problems
Impaired wound healing
Precipitation of haemolysis
anaesthesia and surgery. For example, myocardial
ischaemia is more easily induced and might result in an
increased incidence of myocardial infarction (MI).
Postoperative respiratory complications are less well
tolerated.
Wound healing
Relative hypoxia impairs tissue healing, and increases
the risk of infection (Chs 3 and 8).
possesses anti-B antibody. AB possesses no antibodies
and is therefore the 'universal recipient'; group O
individuals possess antibodies to both A and B.
The other major blood grouping is Rhesus factor, and
patients are either positive or negative.
Patients that are group O rhesus negative have no A or
B antigens and no rhesus factor, and can therefore be
transfused to other groups with minimal risk of reaction
('universal donors').
Blood products
Precipitation of haemolysis
The hypoxia of anaesthesia can induce haemolytic crises
in certain hereditary haemolytic anaemias such as sicklecell disease. Preoperative planning, with or without
transfusion, and careful anaesthesia aim to prevent this.
Operating on a background of anaemia will result in
the patient having fewer reserves to compensate for
operative blood loss. There might be associated depletion
of other blood cells, including white blood cells (which
increases susceptibility to infection) and platelets (which
increases the bleeding tendency).
As a result, the haemoglobin concentration should be
returned to near normal preoperatively, for example, with
iron therapy in elective patients (failure to respond could
indicate an alternative cause of anaemia), or transfusion
for emergency operations.
The oxygen-carrying capacity of transfused blood is
lowered by the presence of high concentrations of 2,3
diphosphoglycerate (DPG) and hydrogen ions, which
shift the oxygen-haemoglobin dissociation curve to the
right (this is known as the Bohr effect).
Replacement of blood loss:
transfusion
Whole blood is rarely given because the scarce resources
of donated blood are used more efficiently when given in
constituent parts. Blood is commonly fractionated into its
constituent parts, which are used for specific indications.
This ensures more efficient use of each unit of donated
blood.
It is essential that each patient is cross-matched
correctly before transfusion. Patients are grouped
according to antigens expressed on their red blood cells
as A, B, AB and O. Each group contains antibodies
against foreign antigen, for example, group A blood
The range of blood products available is listed in Table
6.5 and are discussed below.
Red cell concentrate (RCC)
Red cells are extracted and suspended in a near optimum
solution containing glucose, adenine, mannitol, sodium
chloride and citrate (the last prevents clotting). Cell lysis
during storage means that each unit contains a high
concentration of extracellular potassium. RCC has a
haematocrit of 65-70% and hence has poor flow characteristics. Simultaneous crystalloid infusion reduces the
haematocrit and provides volume repletion.
RCC is used for transfusion in patients with anaemia
and in those suffering acute blood loss, but it has a
reduced oxygen-carrying capacity (see above). It must be
blood group ABO- and Rhesus-factor-compatible (see
below).
One unit of RCC is derived from one donation. The
shelf-life is 35 days at 4°C. The volume varies by unit,
but is approximately 400 mL.
Platelets
Infused platelets are suspended in plasma (and therefore
infusions contain some clotting factors). Full crossmatch is not necessary before transfusion.
Table 6.5
Blood products
Red cell concentrate
Platelets
Fresh-frozen plasma
Cryoprecipitate
Factor concentrates
Albumin solution
Other
43
One unit is obtained from 4-6 blood donations. The
shelf-life is 5 days at room temperature and the volume
is 300 mL. No viral inactivation procedures are used in
processing. Platelets are used perioperatively in patients
with thrombocytopenia.
Fresh-frozen plasma (FFP)
This is pure plasma that is separated and frozen shortly
after donation. It contains all the plasma-derived clotting
factors, but has relatively low levels of factor VIII and
fibrinogen. The shelf-life is 1 year at -30°C and its
volume is 150-300 mL per unit. FFP is used for correcting factor deficiencies.
Cryoprecipitate
Contains high levels of factor VIII and fibrinogen. Again,
the shelf-life is 1 year at -30°C. Each unit is approximately 10-20 mL and the standard dose is 10 units.
Factor concentrates
Multiples are available and are either derived from
plasma or are manufactured using recombinant DNA
technology.
Albumin solution
This is derived from whole blood after removal of cells
and factors. Shelf-life is 3-5 years. It is used to expand
intravascular volume, although it has now been largely
superseded by synthetic gelatin solutions such as
gelofusin and haemacel. It is also used for fluid replacement after burns and during plasmapheresis
Other
There are multiple other blood products available for
treatment of more unusual conditions, including specific
immunoglobulins.
Complications
44
The complications of blood transfusion can be
immunological, infective or due to miscellaneous causes
(Table "6.6).
Table 6.6
Complications of blood transfusion
Immunological
immediate haemolytic
non-haemolytic
delayed haemolytic
Infective
Miscellaneous
fluid overload
hyperkalaemia
coagulation disorder
haemosiderosis
hypothermia
Immunological complications
Immediate haemolytic complications
This can result from mismatched blood-cell antigens
between donor and recipient. The most important
antigens are those of the ABO system. These reactions
are severe and sudden and most often result from human
error, for example if the wrong unit of blood is given to
the wrong patient because of a labelling, handling or
patient identification error. Activation of the complement
system occurs when the recipient possesses antibodies
to an antigen on the donated red blood cells, and
haemolysis (breakdown of the red blood cells) ensues.
Clinically, the patient rapidly becomes unwell with
fever, hypotension and difficulty breathing. Activation of
coagulation can occur, leading to DIC. The haemoglobin
released from the haemolysis, along with hypotension,
can cause acute renal failure.
Treatment involves preventing further reaction by
stopping the transfusion immediately. The patient might
require life-saving resuscitation, including measures to
maintain oxygenation and blood pressure. Intensive care
might be appropriate.
Where a reaction occurs, the unit of blood must be
returned to the laboratory, along with a cross-match
sample from the patient.
Non-haemolytic complications
Febrile, allergic and anaphylactic reactions can occur and
will necessitate immediate cessation of the transfusion
and possibly medical resuscitation, depending on the
severity. Allergic and anaphylactic reactions might require
immediate treatment with adrenaline (epinephrine), antihistamine or corticosteroids.
Delayed haemolytic complications
Coagulation disorder
These result from incompatibility of blood with regards
to less important antigens. They occur in patients who
have previously been sensitised to the antigens.
Examples include Rhesus antibodies and rarer antibodies
to minor antigens such as Kell and Duffy. Haemolysis
occurs several days after the transfusion. The patient is
not generally acutely unwell and might develop jaundice
and anaemia several days after the transfusion.
This was considered under massive transfusion, above.
Infective complications
Blood that is donated in the UK is routinely screened for
HIV, syphilis, hepatitis B and hepatitis C. However, a
number of these diseases have a latent period before their
detection is possible and so transmission of infection can
still occur. Before screening for certain diseases was
introduced, many blood recipients were infected with
hepatitis C and people with haemophilia contracted HIV.
The risk of transmission of infection is related to how
many donors the blood product was derived from and to
the pretransfusion treatment the product has received
(see above).
Miscellaneous complications
Fluid overload
The volume load of the transfusion might precipitate
heart failure in the elderly or those with a history of heart
disease, particularly as a unit of blood has to be
transfused in less than 4 h. Prophylactic diuretic therapy
is often given with a transfusion to prevent this. Central
venous pressure monitoring, in a surgical high dependency or intensive care unit, can help to prevent this.
Hyperkalaemia
As mentioned above, stored blood has a high concentration of potassium and when multiple units are
given the recipient's serum potassium level can rise to
dangerous levels. Electrolyte levels must therefore be
monitored.
Haemosiderosis
Patients who receive regular or multiple blood transfusions can suffer from iron overload. Excess iron is
deposited in vital organs such as the pancreas, myocardium or liver, causing them to dysfunction. This is
reduced by using an iron chelator such as
desferrioxamine.
Hypothermia
Blood is stored cooled to 4°C. If large volumes of
unwarmed blood are transfused the patient will suffer
hypothermia. The role of blood warmers is particularly
important in trauma cases.
Summary and guidelines
Bleeding is a potentially serious surgical complication
and a knowledge of the principles of coagulation and of
the disorders that can precipitate bleeding is essential for
all surgeons. Recognition and prevention of a problem is
obviously preferable to having to deal with a haemorrhaging patient, particularly if the problem could have
been recognised and avoided.
A careful history is essential. This should include a
history of any previous bleeding problem, especially if
related to surgery, a family history of any bleeding problem
and a drug history, especially to note if the patient is on
anticoagulants, aspirin or corticosteroids.
Examination should look for abnormal bruising or
petechiae, and telangiectasis around the mouth.
If there is any doubt, the advice of a physician or
haematologist should be sought before embarking on
even the most minor surgery.
Where a significant bleeding problem is encountered
at surgery, immediate control by compression should be
followed by urgent admission to hospital for investigation and correction of any coagulopathy.
45
w7
Cross-infection
Introduction
To a large extent, the heightened professional and public
awareness of the potential for cross-infection in surgical
and other medical settings has followed the discovery of
human immunodeficiency virus (HIV) as the cause of
AIDS. However, although transmission of blood-borne
viruses, especially hepatitis B, has been documented in
surgical practice, many other microorganisms also pose a
significant threat and most of them are far more
infectious than HIV. In surgery, bacteria are the major
cause of postoperative sepsis (see Ch. 8). These can be
acquired from a number of sources, including the patient's
own bacterial flora and by cross-infection from other
contacts including - importantly - healthcare workers
such as doctors and nurses.
The extent of the problem and other aspects important
in cross-infection will be considered as described in
Table 7.1.
The extent of the problem
Surgical-site infections account for 14-16% of all
nosocomial infections and are the third most frequently
reported nosocomial infection. A UK study published in
1993 of the excess costs attributable to nosocomial
infection in surgical patients reported a mean extra cost
Table 7.1
46
Aspects of infection control
Extent of the problem
Routes of transmission
Universal infection control
Occupationally acquired infection
Healthcare workers infected with blood-borne viruses
Antimicrobial prophylaxis in surgery
Creutzfeldt-Jakob disease
per patient of £1041 and an increased length of hospital
stay of 8.2 days. A more recent study has calculated that
hospital-acquired infections (HAI) cost the NHS in
England £1000 million per annum, and it is believed that
5000 patients die of HAI in the UK every year. Similarly
large figures are available from the USA where, in 1992,
the cost of treating nosocomial infections was estimated
at $4.5 billion, of which $1.6 billion was allotted to
surgical-site infections (SSI). These data highlight the
enormous problem posed by infection for the health
services and indicate the importance of measures to
improve infection control.
Routes of transmission
The possible routes for cross-infection in surgery are
summarised in Fig. 7.1. Direct contact is an important
mechanism of transmission for hospital-acquired
infections, particularly in surgical units. The best
example is the fundamental role played by hands as
vectors for spread of microorganisms. Many infections
acquired in hospitals are transmitted on the hands of
healthcare workers and it is known that regular handwashing between the examination or treatment of
individual patients results in a significant reduction in the
carriage of potential pathogens on the hands. Handwashing has, therefore, been stressed as a simple, cheap
and highly effective infection control intervention.
Unfortunately, both European and US studies have
shown repeatedly that handwashing compliance rates in
hospitals are lower than 50%. The use of alcoholic hand
rubs, rather than handwashing, is now recommended by
some authorities as a convenient means of improving
compliance with hand hygiene protocols.
It has been recognised for many years that healthcare
workers can acquire occupational infections, for example
hepatitis B, from patients they are treating. Transmission
Fig. 7.1
Routes of cross-infection in surgery.
of these infections can occur by direct contact with the
patient or indirectly through contact with contaminated
instruments or surfaces. More recently, there has been
considerable professional and media interest in the
possible risk of patients becoming infected from healthcare workers who are themselves carriers of blood-borne
viruses (see below).
Some microorganisms are transmitted by droplet
spread and aerosols are, therefore, another important
potential mode of spread of infection in surgery. Airborne spread of infection is a major hazard, for example,
in total joint replacement surgery, and use of 'hypersterile' (laminar airflow) operating theatres can play an
important role in preventing infection.
Finally, there is a risk that patients might become
infected from instruments or other items contaminated
during treatment of a previous patient. Effective sterilisation of instruments, which is central to all infection
control policies, will prevent this route of transmission.
The importance of thorough decontamination and
sterilisation of used surgical instruments cannot be overstressed. However, the emergence of prion diseases, in
particular variant Creutzfeldt-Jakob disease (vCJD), is
now proving a major challenge, because these agents are
resistant to standard sterilisation procedures (see below).
Universal infection control
In the light of the multiple routes of transmission noted
above, the key principles that underpin modern infection
control procedures are shown in Table 7.2. These apply
in all healthcare settings, including dental surgery.
47
Table 7.2
Principles of universal infection control
Many different pathogenic microorganisms pose a
problem
There are many sources of infection
Any patient might be a carrier of pathogenic
microorganisms
Routine procedures must be effective in preventing
cross-infection
All blood, regardless of source, is potentially infectious
The same cross-infection control procedures must be
used for all patients
First, although there is widespread concern about
blood-borne viruses such as HIV, a wide range of pathogenic microorganisms is encountered in clinical practice.
Thus, attention must be given to preventing the spread of
all infections, both rare and common.
Second, there are many potential sources of infection,
most of them unrecognised. For example, carriers of
hepatitis B virus frequently appear clinically well and are
unaware of their carrier status. Similarly, patients could
be colonised by antibiotic resistant bacteria, such as
methicillin resistant Staphylococcus aureus (MRSA),
with no outward clinical signs or symptoms. Thus any
patient, regardless of background or medical history,
must be considered to pose an infection risk.
The logical conclusion to these concepts is the
adoption of universal infection control, whereby every
patient is treated as a potential carrier. The infection
control protocol adopted must be sufficiently stringent to
reduce the risk of contamination of patients or staff to a
level that is highly unlikely to cause infection. It also
follows that patients who are known carriers of pathogens,
including blood-borne viruses, will pose no additional
risk and can be treated safely under the same operating
conditions.
Table 7.3
control
Key elements of universal infection
Medical history
Cleaning instruments
Sterilising instruments
Use of disposables
Decontamination of operatory surfaces
Protective workwear
Avoiding needlestick injuries
Immunising staff
Safe waste disposal
Effective training of staff
of previous infectious diseases the clinician must be
aware that it does not allow for the categorisation of
patients into 'high risk' and 'low risk' from the point of
view of infectivity to staff and other patients. One current
exception to this concept relates to patients who fall into
the risk groups for CJD (see below).
Cleaning instruments
The cleaning of used surgical instruments to remove
visible deposits is an essential step prior to their
sterilisation. In hospitals, both the cleaning and the subsequent sterilisation procedures are usually performed
in a Central Sterile Supply Unit (CSSU). However,
increasing amounts of minor surgery are performed in
primary care and, under these circumstances, the
decontamination of used instruments might be performed
in a medical or dental practice. In such cases, instrument
cleaning may be achieved by hand scrubbing in soap or
detergent, but ultrasonic baths and washer disinfectors
are very useful and more effective for many items. Heavyduty protective gloves should be worn during instrument
cleaning, and care taken to avoid sharps injuries.
Sterilising instruments
Key elements of universal infection control
The key elements of universal infection control are listed
in Table 7.3 and will be discussed in turn.
Medical history
48
The collection of an accurate medical history is part of
good clinical practice and is helpful in the identification
of immunocompromised patients. However, although a
medical history can provide useful information in respect
After clinical use, all surgical instruments must be
sterilised before they are used to treat a subsequent
patient. The sterilisation method of choice for heat-stable
instruments is the autoclave. It is critical that the steam
makes physical contact with the surfaces of all the
instruments and care must be therefore be taken not to
overload the autoclave and impede steam penetration.
Effective monitoring of autoclave efficacy is important.
Physical, chemical and biological tests of efficacy are
available; for example, a chemical indicator strip can
be placed in the centre of the load as a check on the
effectiveness of each cycle of a bench-top autoclave.
Hot air ovens are microbiologically acceptable as a
sterilisation measure and are used for specific purposes,
such as the sterilisation of greases. However, the higher
temperature and longer cycle time (160°C for 60 min)
make them more damaging to instruments and they are
not ideal for routine sterilisation procedures.
Chemical agents such as aldehydes are not
appropriate for routine sterilisation of surgical items and
equipment. They are unreliable and some are toxic or
corrosive. However, for certain expensive, heat-sensitive
items such as endoscopes, high level disinfection with
chemicals, under strictly controlled conditions, is
employed.
In the light of concerns over the resitance of prions to
sterilisation procedures, there are now calls for the
'tagging' (e.g. by bar coding) of all individual surgical
instruments. This would permit the recording, in a
patient's notes, of exactly which instruments were used
and so introduce 'traceability' of instruments into the
recycling process. It would, however, be a massive
logistical exercise with major cost implications.
example the pens used by healthcare workers, many of
which have been shown to be contaminated with
pathogens such as MRSA.
In the event of an overt spillage of blood or other body
fluid, it should be soaked into an absorbent cloth and a
disinfectant such as hypochlorite (l0 000 ppm available
chlorine) applied. Alternatively, commercially available
spillage granules could be used.
Protective workwear
All staff should wear protective coats on wards to protect
their outdoor clothing from contamination. However,
white coats themselves become contaminated with
microorganisms, especially at points of frequent contact,
such as the sleeve and pocket. Indeed, the uniforms worn
by healthcare workers have been shown to play a role in
transmitting bacteria in the hospital setting and the
importance of hygiene, with regular laundering of
uniforms, should again be stressed. Appropriate theatre
dress, including operating gown, gloves and eye
protection must be worn routinely when undertaking
surgical procedures, together with a well-fitting surgical
facemask.
Use of disposables
Disposable items are generally recommended, although
there is a cost implication. Disposable items must always
be used once only and then discarded. The routine use of
disposable instruments for surgery involving tissues that
pose a risk from vCJD, for example tonsillectomies, has
been recommended in the UK.
As needles cannot be reliably cleaned and sterilised,
they must always be discarded into a sharps bin after use
on a single patient. Similarly, a local anaesthetic
cartridge must never be used for the treatment of more
than one patient.
Decontamination of operatory surfaces
Good hygiene in healthcare facilities is an important and
underrated element of infection control, with particular
relevance to surgical sepsis. In addition to general
environmental contamination, surfaces in clinical areas
can become contaminated with microorganisms following contact with tissues and body fluids of patients.
Regular cleaning of surfaces with detergent, together
with application of disinfectants in appropriate sites, are
essential. Other 'surfaces' can also pose a problem, for
Avoiding needlestick injuries
Sharps injuries are common among staff performing
surgical procedures and many go unreported to
occupational health departments and so are not followed
up. However, occupationally acquired infections with
hepatitis B and C viruses, and with HIV, have been
recorded following needlestick injuries and related
sharps accidents. It is, therefore, essential that healthcare
workers are encouraged to seek appropriate management
following such incidents. The principles of management
of needlestick and related injuries are discussed below.
Although some of these injuries are unavoidable, many
are essentially preventable and great care must be taken
when handling and disposing of all sharps.
Needles should never be resheathed after use, unless a
safe resheathing device is used. Care must also be taken
not to injure other staff, for example when sharp
instruments are being passed between surgeons and
nurses. Unsheathed needles must never be left exposed
where others might injure themselves. All contaminated
sharp items must be discarded into a sharps box (see
below) and staff must never put their hands into the
opening of the box.
49
Immunising staff
Vaccination against hepatitis B virus is now a requirement in the UK for all healthcare workers undertaking
exposure-prone procedures. This vaccine, which contains
hepatitis B surface antigen (HBsAg), provides protection
from one of the most important and serious occupational
infections of healthcare workers. The course of three
doses of vaccine must be followed by a blood test to
ensure that the recipient has developed a protective level
of antibody.
For healthcare workers who are non-responders to the
vaccine, further serological tests are required to ensure
that they are not high-risk carriers of hepatitis B. Highrisk carriers are those who are HBeAg positive or who
are HBeAg negative but with a viral load exceeding 103
genome equivalents per mL. Such individuals pose a
potential risk of infection to patients and would not be
permitted to undertake exposure-prone procedures,
which clearly include all forms of surgical practice.
Immunisation against other infectious diseases such
as tuberculosis (in the UK), tetanus and poliomyelitis is
also recommended and non-pregnant female personnel
of child-bearing age should be protected against rubella.
Safe waste disposal
Hospitals have a responsibility to ensure the safe disposal
of all contaminated waste generated during surgery.
Arrangements must be made with a local authority or
private contractor for final collection and disposal.
Regulated waste includes contaminated sharps, liquid
blood and other body fluids, tissues, and non-sharp solid
waste that is saturated or caked with body fluid.
All sharp items must be consigned to rigid, punctureresistant containers, which should never be filled to more
than two-thirds of their capacity. The containers should
be securely closed and fastened before uplift for
incineration. Soft waste contaminated with blood must
be placed into sturdy, impervious, sealed bags and
clearly labelled as infective waste.
Effective training for staff
50
Good training of all staff engaged in patient care is an
important element of infection control. Good infection
control procedures should become an automatic part
of clinical practice for all healthcare workers but,
unfortunately, they are often not afforded the priority
they deserve. A written infection control policy must be
available in all healthcare facilities and procedures
reviewed on a regular basis. The overseeing of all aspects
of infection control in hospitals, including training, is the
responsibility of the Infection Control Committee, which
is usually chaired by a Consultant Medical Microbiologist.
This committee will also include one or more specially
trained Infection Control Nurses, who play an important
role in dealing with day-to-day cross-infection issues in
hospitals.
Occupationally acquired
infections
The main concern of healthcare workers relates to the
risk of infection with blood-borne viruses, notably HIV.
Hepatitis B remains the major infectious occupational
hazard for surgeons and other healthcare workers who,
prior to the availability of a vaccine, were up to ten times
more likely to become infected than members of the
general population. Table 7.4 summarises the relative
risks of infection with HIV and hepatitis B virus.
Hepatitis B virus is far more infectious than HIV and it is
fortunate that most healthcare workers respond to the
hepatitis B vaccine, thereby gaining protection.
According to the most recent figures available, the
totals of 'definite' and 'possible' occupationally acquired
HIV infections have amounted to 319 cases worldwide.
These have comprised 102 definite (5 in UK) and 217
possible (8 in UK), most of which followed sharps
accidents with large-bore needles.
The occupational risk of infection with hepatitis C
virus is not yet clear but several recent studies suggest
that the overall risk is low. However, well-documented
Table 7.4 The relative risks of occupational
infection with HIV and hepatitis B virus (HBV)
Minimum volume of blood
to transmit infection
Risk of infection following
needlestick injury from a
seropositive patient
HIV
HBV
0.1 mL
0.00004 mL
0.3%
7-30%*
*The risk of infection with hepatitis B virus depends on
whether the source patient is a high-risk carrier
seroconversions following needlestick accidents have
been reported and emphasise the importance of avoiding
such injuries.
Other infections can be occupationally acquired by
surgeons: there is a documented occupational risk for
healthcare workers of infection with Mycobacterium
tuberculosis. There is no evidence of an occupational risk
for healthcare workers from prion diseases such as CJD.
Management of sharps injuries
Prevention of sharps injuries is extremely important but
it is recognised that, within healthcare facilities, and
particularly during surgical procedures, such incidents
are still fairly common. A significant proportion are
essentially preventable if staff follow guidelines on
handling sharps and, in addition, many commercial
companies are now developing new 'needle-less'
devices. However, it is impossible to eliminate the risks
completely. The effective management of sharps injuries
is, therefore, an important issue in the prevention of
occupationally acquired infections with blood-borne
viruses; it also has medicolegal implications.
Every hospital should have a policy and procedure
for managing sharps injuries, and this should be well
publicised and readily available to all staff. The
principles of management are summarised in Fig. 7.2. All
such events should be officially recorded in an accident
book. Immediate first aid involves cleaning the wound
under running water, without scrubbing or manipulation,
and the application of a waterproof dressing. Expert
medical advice should then be sought.
Ideally, blood should be taken at the time of the
accident from the healthcare worker and the titre of antiHBs antibody measured. Residual serum is stored so that
it is available in the future for HIV and hepatitis C virus
antibody testing, if necessary.
Although the concept of approaching the source
patient is controversial, ideally blood should also be
collected from this individual. Appropriate discussion
and counselling are obviously essential but, if consent is
given, the blood can be screened for hepatitis markers
and HIV antibody, which in most cases will be negative.
Such information can be very reassuring to a healthcare
worker who has sustained an injury, but no pressure
should be exerted on the source patient to donate the
appropriate sample.
Immediate treatment for the healthcare worker might
include passive immunisation for a hepatitis B vaccine
Fig. 7.2
Management of sharps injuries.
non-responder, or a vaccine booster for those whose antiHBs antibody titre has waned. The administration of
prophylactic azidothymidine (AZT) for those who have
sustained an injury from a known HIV-positive patient
has been controversial but recent evidence suggests that,
in combination with other antiretroviral drugs, it can
further reduce the risk of infection. Such prophylaxis is
now officially recommended for significant injuries and
should be administered promptly, ideally within 1 h of
the injury. However, the treatment is not without sideeffects and the risk assessment of the injury should be
made in conjunction with a physician who is experienced
in this area.
Healthcare workers infected
with blood-borne viruses
There is strong epidemiological evidence that healthcare
workers who are high-risk carriers of hepatitis B virus, as
defined earlier, can transmit hepatitis B to patients if they
51
undertake
osure-exp
prone
edures.
proc
prone
E-
procedures are those in which there is a risk that injury to
the worker could result in the exposure of the patient's
open tissues to the blood of the healthcare worker. Those
who are HBsAg positive but not HBeAg positive, and
whose viral load does not exceed 103 genome equivalents
per mL, are permitted to continue with exposure-prone
procedures, providing they have not been associated with
spread of infection to patients.
Apart from the case in which a Florida dentist with
AIDS apparently transmitted HIV to several patients,
there is only one other report of an HIV-infected healthcare worker transmitting the virus to a patient. This
involved an HIV-seropositive orthopaedic surgeon in
France, who apparently transmitted HIV to a patient
during hip surgery in 1992. At the time, the surgeon was
asymptomatic and unaware of his infection. Thus,
currently available data suggest that the risk of transmission of HIV to patients from HIV-infected healthcare
workers is extremely low. Nevertheless, healthcare
workers who are known to be HIV seropositive are not
permitted to undertake exposure-prone procedures in
the UK.
There is increasing epidemiological evidence that
hepatitis C virus can be transmitted from seropositive
healthcare workers to patients during exposure-prone
procedures. UK guidelines published in 2002 place
restrictions on the clinical activities of healthcare workers
who are infected with hepatitis C (HCV RNA positive).
Antimicrobial prophylaxis
during surgery
A number of factors can increase the risk of surgical site
infection and these are considered in detail in Chapter 8;
they can be patient-related or procedure-related (see
Table 8.2). The risk of surgical site infection also depends
on whether the surgical procedure is a clean, cleancontaminated, contaminated, or dirty-infected procedure
(see Table 8.3).
Improvements in operating room ventilation, sterilisation methods, barriers and surgical techniques have all
helped to reduce the incidence of surgical site infections,
but the use of topical, oral and intravenous antimicrobial
prophylaxis has also played an important role. However,
in the current climate of increasing antimicrobial
resistance, it is important that prophylaxis is not
52
overused but is reserved for well-defined indications.
Table 7.5
Goals of surgical prophylaxis
Prevent postoperative infection of the surgical site
Prevent postoperative infectious morbidity and mortality
Reduce the duration and cost of health care
Produce no adverse effects
Have no adverse effects for the microbial flora of the
patient or hospital
Perioperative antimicrobial surgical prophylaxis is
recommended for operative procedures that have a high
rate of postoperative wound infection, when foreign
materials are to be implanted, or when the wound
infection rate is low but the development of a wound
infection results in a disastrous event. It is beyond the
scope of this chapter to provide details of all those
surgical procedures for which prophylaxis is indicated
but examples include colorectal surgery and joint replacement surgery. The goals of an anti-infective drug used
for surgical prophylaxis are summarised in Table 7.5. To
achieve these goals, an ideal prophylactic antimicrobial
agent should be bactericidal, non-toxic, inexpensive and
have in vitro activity against the common organisms that
cause postoperative wound infection after a specific
surgical procedure.
There is no benefit in commencing intravenous
antimicrobial therapy before the perioperative period.
Normally, prophylactic antimicrobial agents should be
administered no more than 30-60 min before surgery.
A common practice is to administer the intravenous
prophylactic agent at the time of induction of
anaesthesia. Therapeutic concentrations of antimicrobial
agents in tissues should be present throughout the period
that the wound is open. For prolonged procedures, or
antimicrobial agents with short half-lives, an additional
dose may need to be administered intraoperatively. The
duration of antimicrobial prophylaxis for most procedures is controversial, but expert opinion recommends at
most one or two postoperative doses. Prolonged prophylaxis should be discouraged because of the possibility
of added antimicrobial toxicity, selection of resistant
organisms and unnecessary expense.
Creutzfeldt-Jakob disease
The transmissible, spongiform encephalopathies (TSEs)
comprise a group of neurodegenerative disorders caused
by infection with agents called prions. This group of
diseases includes sporadic, familial and iatrogenic forms
of Creutzfeldt-Jakob disease (CJD). The description of
a new form of CJD, now called variant CJD (vCJD),
together with evidence that it is caused by the same agent
as bovine spongiform encephalopathy (BSE), has
significantly raised the profile of the TSEs.
The relevance of TSEs to this chapter is that these
diseases are causing serious concerns in relation to infection control procedures. Prion proteins are remarkably
stable and resistant to most conventional sterilisation
measures. Iatrogenic transmission of human prion
diseases via neurosurgical instruments has been reported
and there is some evidence that transmission via other
surgical procedures can also occur. For the sporadic,
familial and iatrogenic forms of CJD, the tissues in
which there is a high level of infectivity are the brain,
spinal cord and eye. However, the position is further
complicated because vCJD differs from the sporadic,
iatrogenic and familial forms in that the lymphoreticular
tissues of vCJD cases are also consistently infected with
prion proteins.
Current guidelines are that all the instruments used in
a surgical procedure on a patient suffering from a TSE
must be disposable and destroyed by incineration. In
addition, current recommendations from the Spongiform
Encephalopathy Advisory Committee suggest using the
medical history form to identify patients who may be at
risk of (although not clinically suffering from) iatrogenic
or familial forms of CJD. Questions enquire about
previous brain surgery (to identify possible recipients of
dura mater grafts), growth hormone use before the mid1980s (after which artificially synthesised growth
hormone came into use), and close family members who
might have had CJD (to identify those at risk of familial
CJD). For patients who are identified as being at risk, any
surgery involving the brain, spinal cord or eye should be
undertaken using disposable instruments that are' subsequently incinerated. Surgery involving other tissues in
such patients is ideally also undertaken with disposable
instruments and, if non-disposable instruments are used,
they must pass through a stringent decontamination
process, separately from other instruments. This involves
two washing cycles and a total of 18 min in a porous load
(vacuum) autoclave.
However, no questions in the medical history will
identify those patients at risk of sporadic or vCJD. The
latter is a major concern because of the infectivity in
lymphoreticular tissues. The number of cases of vCJD in
the UK is still low (122 confirmed cases to 3 February
2003), and a preliminary screening study of vCJD reactivity
in approximately 3000 archived tonsils and appendix
specimens revealed no positive results. However, there is
still concern among many experts that an epidemic,
linked to consumption of meat from BSE-infected herds,
could develop. The routine use of disposable instruments
for all patients undergoing certain surgical procedures
that involve high-risk tissues is now being given serious
consideration and, where practicable, implemented.
53
8
Surgical sepsis
Introduction
The principles of the control of cross-infection were
discussed in Chapter 7. Sepsis as a specific complication
of surgery is considered in this chapter (Table 8.1).
The body possesses a complex system of mechanisms
to protect itself from infection. These include:
• methods to prevent entry of bacteria into the body,
such as skin and mucous membranes, which act as a
barrier 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 they
manage to invade the body tissues, for example, the
local inflammatory reaction resulting in cellulitis and
abscess formation
• methods to deal with organisms if they start to invade
tissues, including lymph node reaction and systemic
lymphocyte response.
54
Surgery predisposes to infection by affecting the body
defences at all levels. It also causes a breach in the
protective barrier, allowing organisms a portal of entry.
However, tissue damage will also inhibit the inflammatory response locally by causing tissue ischaemia or
by formation of haematoma. Surgery also affects the
systemic response of the body to trauma.
Thus, postoperative sepsis may be local - affecting
the wound itself - or sepsis may occur at a remote site.
Chest sepsis is the most common remote site infection
but other sites may be involved. For example, patients
may be predisposed to chest sepsis if they have a preexisting upper respiratory tract infection, if they smoke
or if they have chronic lung disease such as asthma or
bronchiectasis. An example of sepsis at another site is
urinary tract infection resulting from a poor catherisation
technique. Factors that may increase the risk of wound
Table 8.1
Wound infection following surgery
Classification of wounds
Infecting organisms
Prevention of wound infections
Clinical features of wound sepsis
Diagnosis of wound sepsis
Treatment
Table 8.2 Factors that may increase the risk of
surgical site infection
Patient-related
age
nutritional status
diabetes mellitus
cancer
uraemia
jaundice
smoking status
obesity
coexisting infection at a remote site
colonisation with microorganisms
altered immune response, e.g. HIV
drugs, e.g. corticosteroids, anti-inflammatories,
chemotherapy
length of preoperative stay
Procedure-related
duration of surgical scrub
skin antisepsis
preoperative shaving
duration of operation
operating room ventilation
inadequate sterilisation of instruments
foreign material at the surgical site
surgical drains
surgical technique
haematoma
poor blood supply
sepsis are listed in Table 8.2. These may be patientrelated 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 a
wound. In the initial phase of bacterial penetration of the
tissues, the body will host an inflammatory response
against the invading organisms to try to contain them in
the area and to destroy them. This inflammation will be
apparent clinically as cellulitis, which is a tender redness
of the tissues. However, a similar response may result
from inflammation from other causes (e.g. haematoma,
excess tissue handling or trauma during surgery). Because
of this, the presence of cellulitis alone may not always
indicate infection.
One can only be sure that a wound is infected when
pus forms, hence the above definition. Studies comparing
methods to control wound infection only discuss wounds
where pus is confirmed to be present.
For a wound infection to occur, there must be a
sufficient number of organisms inoculated into the
wound (>107 viable cocci must be injected into a wound
in a normal person to cause an abscess) and conditions
within the wound area must be suitable for growth of the
organisms. The presence of necrotic tissue, haematoma,
seroma and foreign bodies all predispose to sepsis.
Classification of wounds
Certain wounds are more prone to infection than others.
Surgeons therefore divide wounds into different types
according to the level of risk of sepsis (Table 8.3).
Table 8.3
Classification of wounds
Clean wounds
Clean contaminated wounds
Contaminated wounds
Dirty wounds
Contaminated wounds
This is surgery where there is gross spillage of
organisms, where there is infection already present but
without pus formation, where there is a major break in
aseptic technique or where there is an open wound that
has been exposed for less than 4 h (e.g. following major
trauma). In this type of wound, sepsis frequently exceeds
30%.
Dirty wounds
This is an operation through an infected area (e.g.
perforated viscus, abscess or traumatic wound) that has
been exposed for over 4 h. By definition, all these wounds
are infected.
This classification of wounds allows comparative studies
to be conducted between centres and of varying
techniques to try to control wound sepsis. It also allows
surgeons to monitor their own data to ensure that they are
achieving acceptable standards of surgery with regard to
sepsis.
Infecting organisms
Clean wounds
These are wounds in which no viscus has been entered,
no septic area has been encountered and there has been
no break in aseptic technique. Such wounds should never
become infected; infection rates with such wounds
should be less than 3%.
Clean contaminated wounds
In this situation, the operation enters a non-infected area
but may encounter bacteria. Careful control of the area
should result in minimal spillage of organisms. Examples
of this include surgery on the upper gastrointestinal tract,
biliary tree or respiratory tract. Infection rates for this
type of surgery should be less than 10%.
Infecting organisms can be subdivided into two types.
Exogenous organisms
Exogenous organisms are organisms introduced into a
wound from an external source. The two main exogenous
organisms responsible for wound sepsis are Staphylococcus aureus and Streptococcus pyogenes. These are
encountered 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 wound
sepsis occurs with these bacteria, it usually indicates a
breakdown of sterile surgical technique. The longer an
operative procedure, the more likely the procedure is to
become infected by an exogenous organism.
55
Endogenous organisms
Endogenous organisms are bacteria that are usually
present in the body but are non-infective under normal
circumstances. Such organisms are known as commensals.
These organisms are encountered in clean-contaminated,
contaminated and dirty wounds. Such organisms are
common in gastrointestinal surgery, for example,
Escherichia coli, enteroccocci and Bacteroides species.
In clean-contaminated and contaminated wounds, where
it is expected that a significant number of organisms may
be encountered, the use of prophylactic antibiotics given
from the time of surgery has been shown in many cases
to significantly reduce the risk of wound infection. Such
use of antibiotics, however, must not be seen to be an
alternative to meticulous and careful atraumatic surgical
technique.
Excessive use of prophylactic antibiotics is not
without problems, for example, allergic side-effects to
the drug, development of bacterial resistance to specific
antibiotics and cross-transfer of these resistant strains
within the hospital environment (see Ch. 7).
Prevention of wound
infections
'Clean wounds' lend themselves to studies of techniques
of control of infection. When the wound sepsis rate of
clean wounds is unacceptably high, it suggests that a
problem within the unit is allowing the introduction of
large numbers of exogenous organisms into the operation
field.
The infection rate due to exogenous organisms has
reduced dramatically because of aseptic techniques. It is
impossible to sterilise the atmosphere in an operating
theatre, to sterilise the skin of a patient completely and to
avoid the carrying of microorganisms into the operating
area by theatre personnel. However, equipment and
drapes can be sterilised and much can be done to reduce
Table 8.4
56
Prevention of wound infection
Environment
Theatre personnel
Patient preparation
Operating technique
Prophylactic antibiotics
the transport of organisms to the patient's wound. Key
elements of universal infection control were discussed in
detail in Chapter 7 but factors relating specifically to
prevention of wound infection (Table 8.4) are discussed
here.
Environment
The design of a modern operating theatre with laminar
air-flow and air-filtering systems has significantly
reduced the number of organisms in the atmosphere. In
recent years, however, further advances have made little
effect on wound sepsis rates because most infections are
now endogenous in nature.
The longer the duration of surgery and the greater the
number of personnel in theatre, the higher the wound
sepsis rate.
Theatre personnel
Contamination of a wound occurs easily from theatre
staff.
The surgeon, theatre assistant(s) and nursing staff
should wash/scrub their hands and forearms with an
antimicrobial agent such as chlorhexidine or povidoneiodine to reduce bacterial load on the skin. The initial
scrub of the day is the most important and should include
a careful nail scrub and a wash lasting at least 5 min.
Thereafter, scrubbing for further operations requires only
a 1 min careful wash and nail scrubbing is no longer
necessary. This reduces the numbers of skin organisms
but, after 30 min, the bacterial count on the skin starts to
rise again and may exceed the prescrub levels after 2 h.
Staff in intimate contact with an operation should
therefore wear suitable sterile protective clothing with
sterile gowns and gloves. As there can be a glove
puncture rate of up to 10% by the end of an operation,
many surgeons now double-glove. This may also protect
the surgeon from organisms that might be acquired from
a patient.
The use of theatre masks is controversial, with
evidence to suggest that they are ineffective within a
relatively short period of time.
The number of personnel in theatre should be reduced
to the minimum, with little movement of staff through
theatre while surgery is being undertaken.
Staff with a severe upper respiratory infection or sore
throat should be excluded from the theatre area.
Patient preparation
Prophylactic antibiotics
Patients who have been inpatients in hospital for a
significant period prior to surgery tend to develop a skin
contamination of 'hospital-acquired' organisms. These
bacteria tend to be highly resistant to commonly used
antibiotics. In such patients, bacterial scrub the night
before surgery may be beneficial, although this is
unproven.
Any patient harbouring an infection at a site distant to
the operation wound has a significantly increased risk of
wound sepsis, perhaps doubling the incidence. Therefore
any patient with an infected lesion should have this
treated before surgery is contemplated.
Shaving the skin in the area of the operation on the
night before surgery has now been shown to increase
wound sepsis rates. Tiny nicks in the skin acquire
bacterial contamination, which is at a much higher level
than in the unshaven skin. Hair removal by clipper is
advised, or it should not be done at all. Certainly, if
shaving is to be performed, this should be done in the
anaesthetic area immediately before surgery is about to
take place.
Various skin preparation agents for 'sterilising' the
skin in the operation field are available, the most
commonly used being chlorhexidine and povidoneiodine. A double wash is traditionally performed and the
operation area is covered with sterile drapes leaving only
a window for surgery. However, it is not possible to
sterilise skin completely by the use of such agents.
As discussed in Chapter 7, antibiotics have been shown
to reduce wound sepsis in clean/contaminated and
contaminated wounds only. The use of antibiotics in
clean wounds is of no value in reducing wound sepsis but
they should always be given if there is insertion of
foreign material or if the patient has cardiac valvular
disease. This is especially important during dental
procedures.
Operating technique
Surgical technique is most important in control of wound
sepsis. Wound sepsis rates vary between surgeons and are
almost certainly related to individual technique such as
careful handling of tissues, removal of all foreign bodies
or dead tissue, avoiding the use of excess diathermy and
sutures, avoiding excessive suture tension, accurate
placement of sutures, and avoiding the formation of
haematoma. Monofilament sutures are probably associated with less wound sepsis than braided suture
materials.
A careful audit comparing one surgeon's infection
rates with those of another surgeon usually results in a
steady reduction in infection, and this is certainly related
to increased careful technique. Surgeons should therefore
keep a close audit of their own sepsis rates and, if they
are unacceptably high compared with other surgeons,
must address the reasons for this.
Clinical features of wound
sepsis
Classically, wound sepsis produces a tachycardia and
pyrexia approximately 2–4 days postsurgery. The patient
usually complains of increasing pain in the wound,
perhaps exceeding that noted immediately after surgery.
The features of an infected wound usually develop
very rapidly. The wound develops a cellulitis, perhaps
with some purulent material oozing from the surface of
the incision or from the suture sites. The wound then
becomes oedematous and bronzed in appearance with
marked swelling. Attempted palpation reveals a marked
local increase in temperature and exquisite tenderness.
At this point, removal of some or all of the sutures
results in release of pus and the wound margins will then
be 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 should
always be aware of the fact that the sepsis may be arising
from the peritoneal cavity and not just be superficial
under the skin. Severe wound sepsis may result in
complete breakdown or dehiscence of the wound,
necessitating wound resuture.
Diagnosis of wound sepsis
This is usually made on clinical grounds alone.
Bacteriology culture swabs may allow confirmation of
the infecting organism(s) and their antibiotic sensitivity.
This is especially useful if the patient does not seem to be
responding satisfactorily to apparently adequate therapy
and knowledge of the infecting organisms now obtained
by such swabs will allow a more accurate choice of
antibiotic to be made.
57
Treatment
Initial treatment of a suspected wound infection is
usually by antibiotics. The choice depends on the type of
wound and the nature of the surgery. In contaminated and
clean/contaminated wounds, antibiotic therapy may
merely consist of continuing the prophylactic antibiotic
originally used. Certainly, if there is severe or spreading
cellulitis, antibiotic usage is essential and may be more
effective if given intravenously.
Where there is obvious pus formation, sutures should
be removed from the skin and the wound allowed to gape
or, if necessary, probed. Any pus obtained should be
forwarded to the bacteriologist for culture. If there is no
significant cellulitis, lymphangitis or lymphadenopathy,
simple release of pus may be all that is indicated and
antibiotics may not be necessary.
58
After release of pus, the wound should be left open. It
may be filled with antiseptic packs. There are many
different techniques and agents available for dressing
such wounds and each unit tends to have its own
preferences. Normally, an infected wound is left to heal
by granulation from below, with the packs being changed
regularly to keep the wound as clean as possible and to
allow the granulation to fill the cavity. When the wound
is clean and granulating, if it is large, it may be
secondarily resutured. In many instances, however, these
wounds reheal rapidly without the need for resuturing
and, as soon as the wound has healed by granulation, it
will rapidly re-epithelialise.
Abdominal wounds that have been badly infected and
allowed to heal by this method are commonly weakened,
with the subsequent formation of incisional hernia.
9
Fractures
Introduction
A fracture is a break in the continuity of bone; it can be
complete or incomplete. Fractures are the cause of a
considerable degree of morbidity and even mortality
across all age groups. Patients suffer both in the short
term from pain and in the long term from disability and
deformity. These effects are, in the main, largely preventable. A sound appreciation of the principles of fractures
and their management has a profound effect on patients'
quality of life, not only in orthopaedics but in many other
specialties including maxillofacial and oral surgery,
neurosurgery and accident and emergency surgery.
A discussion of the aetiology of fractures is followed
by their diagnosis and classification. The process of
fracture healing will also be discussed, followed by
consideration of the management of fractures and the
complications that can occur (Table 9.1).
This chapter deals with the general principles of
fracture management and gives specific examples as
appropriate. The detailed management of maxillofacial
fractures and its variance from general principles is
considered in Chapter 12.
Aetiology of fractures
Fractures can be caused by a number of different
mechanisms (Table 9.2) and this leads to a variation in
the pattern of fractures. The vast majority of fractures are
caused by an excessive force applied to that bone,
causing it to break. Biomechanics are the key in relation
to bony injury, both in terms of the injury sustained and
its appropriate management. A direct force applied to a
bone will cause a fracture at the site of impact. Indirect
forces cause fractures distant to where the force is
applied, such as spiral long-bone fractures.
Table 9.1 Important considerations in the
management of fractures
Aetiology of fractures
Diagnosis of fractures
Classification of fractures
Fracture healing
Principles of management
treatment of closed fractures
treatment of open fractures
Complications
Table 9.2
Mechanisms of bony fracture
Direct force
Indirect force
Stress fractures
Pathological fractures
The pattern of fractures also differs with age, relating
to the nature of the patient's skeleton and bone stock.
Different types of bone tend to show different types of
fracture. For example, cancellous bone, when put under
sufficient stress, generally undergoes crush fracture,
which can be comminuted.
The history will indicate which injuries are likely to
be present and will help to direct investigation. For
example, in the driver of car involved in a road traffic
accident, the presence of a broken windscreen will alert
to the probability of head and facial injuries.
Stress fractures are caused by repeated relatively
minor injury. Their exact aetiology is not known but
again, a detailed history alerts to their possibility as, for
example, in a runner with painful metatarsals.
Pathological fractures occur in abnormal bone. The
force applied would not normally be enough to cause a
break if the bone was normal. The weakness of the bone
59
can be caused by very many disease processes. The most
common underlying pathologies for pathological fractures
include osteoporosis and malignant infiltration of the
bone, either secondaries or rarely primaries. Naturally,
the diagnosis of a pathological fracture, and the underlying pathology, have a bearing on appropriate subsequent
management.
injury minimal movement is possible. Often patients
feel that they are unable to move any of the joints in a
large surrounding area such as a whole limb. Careful
'passive' movements can be carried out, always
gently and never forcing the movement.
Other tests
Diagnosis of fractures
Clinical examination
Injuries to bone are often present in combination with
other injuries, and initial consideration should be directed
to the patient as a whole and particularly if there is need
for resuscitation.
The fundamentals for diagnosis are based on history
and examination. History has been alluded to above. A
detailed clinical examination, with emphasis directed by
the history not only indicates which investigations are
required for definitive diagnosis but also alerts to injury
of underlying or surrounding structures.
Look, feel, move is a good way to approach the
examination of bony injury:
60
• Look: for signs of injury; swelling is often the most
useful sign. Fractures are associated with a greater
degree of swelling than soft tissue injuries. The
distribution of the swelling can also be enlightening.
For example, if confined to the joint, swelling can
indicate excess fluid or blood in that joint. Deformity
generally leaves little doubt about the existence of
underlying bony injury. Bruising might be present if
there is delay in presentation. It is important to look
for and document the integrity of the skin overlying
the injury, as this will allow classification into open
(compound) or closed fractures, and will affect
management. Colour - particularly distal to the injury
- will give clues to vascular status.
• Feel: palpation needs to be done carefully, but
sufficiently firmly to give the answers. Often large
areas around the site of injury are tender, but it is
important to elicit the area or areas of maximum
tenderness to direct subsequent investigations, and
focus analysis of those investigations. Temperature
of the injured area should be noted and may indicate
infection, for example, if presentation is delayed.
• Move: initially, patients should be asked to perform
relevant movements themselves. If there is significant
The important structures most commonly affected by
limb fractures are either blood vessels or nerves and it is
essential to document neurovascular status around, and
particularly distal to, all fractures. Vascular compromise
in particular will alter immediate management, in an
attempt to restore blood flow.
Vascular
Pulses and capillary refill distal to the site of injury
should be assessed. Although this is performed at this
stage in a systematic examination, an early assessment of
vascular status should be carried out, for example during
preliminary history taking.
Neurological
Sensory and motor function should be tested in the
distribution of nerves that may have been affected by the
injury.
Other
Surrounding structures can be affected and are often
fracture specific. Tendons might be disrupted by the
sharp edges of the fracture, for example in the hand. Any
structure lying in proximity to the fracture is at risk and
careful examination should be carried to assess for
damage to underlying structure, such as orbital blow-out
fractures (where the inferior rectus can be tethered) or
pelvic fractures (where there might be urethral injury);
rib fractures can cause lung injury or pneumothorax.
Radiographic examination
There is no place for blanket radiographs. Clinical
suspicion is of paramount importance. Radiographs are
sometimes indicated where bony tenderness cannot be
excluded. For example, unconscious trauma patients must
have cervical spine films.
Radiographs of at least two views at 90° to each other
are essential. A fracture cannot be excluded without these
views and accurate classification and description of an
obvious fracture cannot be complete without them.
Obvious signs of bony injury show as disruption of
the cortex. However, cortical breaks can be difficult to
see and clinicians should develop a systematic routine for
reviewing radiographs that involves tracing around the
cortical lines. It is useful to stand back from the radiograph to assess if its overall appearance is normal, and
also whether the general state of the bone looks normal.
Once a fracture is seen, it is important to look for
other fractures associated with it. Rings of bone rarely
break in only one place and a second fracture should be
suspected, for example, in the pelvis or mandible. It might
be 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 subtle
evidence that is visible radiographically. The only clue to
a bony injury might be surrounding soft tissue swelling
or blood visible within usually empty spaces, such as in
maxillary sinuses.
Table 9.3
Classification of fractures
Site
Extent
Configuration
Overlying skin integrity
Pathological
Displacement
Angulation, rotation, impaction and distraction
Joint involvement
Stability
The following classifications are the most common
and most helpful with regards to treatment and referring
the patient to a surgeon who will undertake treatment
(Table 9.3).
Site
The most important consideration is which bone is
fractured and which part of that bone is fractured, clearly
documenting the side, for example, fractured right distal
third of radius.
Further imaging
When used appropriately, plain radiographs have both
high sensitivity and specificity. However, they can be
fallible and, in the presence of a negative radiograph,
reliance is on clinical suspicion. If either the mechanism
of injury or the clinical examination suggests a particular
injury then further imaging is necessary.
Further plain radiographs might be indicated, either
different views or films taken with a joint in a particular
position or under stress (for example, flexion/extension
views).
More sophisticated forms of imaging might be
necessary and computerised tomography (CT) scanning
is particularly good at showing bony detail. Magnetic
resonance imaging (MRI) is excellent at showing soft
tissue detail. Radioisotope-uptake bone scans also have a
role in advanced investigation.
Classification of fractures
Fractures are classified in many different ways, and often
the same fracture is classified simultaneously a number
of different ways. For example, a single fracture can be
open, pathological, displaced, oblique, intra-articular and
unstable.
Extent
This differentiates between a complete disruption of
cortex and a partial disruption of cortex or a crack.
Incomplete fractures are more common in children and
are known as greenstick fractures.
Configuration
This is essentially the shape or direction of the fracture
line. Transverse fractures extend at right-angles to the
cortical surface. Oblique fractures are as their name
suggests, as are compression fractures. Spiral fractures
tend to occur in long bones and are the result of twisting
forces 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 fracture
open or compound and changes the subsequent management required, the principles of which are considered
later in this chapter.
Open fractures can be further classified with regards
to how 'open' they are (the Gustillo and Anderson
61
Table 9.4
Classification of open fractures
Grade I : less than 1 cm wound
Grade II: greater than 1 cm wound
Grade III: extensive skin and soft tissue damage
IIIA: wound can be covered with remaining
soft tissue
IIIB: wound cannot be covered with soft
tissue, periosteal stripping
IIIC: associated arterial injury
classification), which has bearing on how likely it is that
the wound will become infected (Table 9.4).
Pathological fractures
Pathological fractures were considered on page 59, under
the heading 'Aetiology of fractures'.
Displacement (apposition)
A fracture is displaced if the two ends are not in exact
anatomical apposition. This is caused by the force of the
injury and/or the action of muscles around the fracture
site. The degree of displacement or shift is often described
subjectively (e.g. 'moderately' displaced). However,
perhaps a more useful description is a measurement of
the displacement, for example with respect to the width
of the fractured bone. Correcting displacement has an
important impact on fracture healing, deformity and
function.
Angulation, rotation, impaction and distraction
These are other forms of deformity relating the fracture
ends to each other. Angulation can be thought of as tilt
between the ends, and rotation is the degree of twist.
Impaction is where the ends are forced into each other
and distraction where there is a gap between the ends in
the axis of the fractured bone. All of these can also result
in healing and functional problems and they might
require close clinical and radiological examination to
detect them.
Joint involvement
62
If the fracture line extends into the joint it disrupts the
articular surface and can be regarded as intra-articular.
This predisposes to long-term sequelae, mainly osteo-
arthritis. This type of fracture therefore requires an
accurate degree of reduction.
Stability
Unstable fractures are those whose positions are prone to
change. This is often the case even after initial reduction.
These injuries therefore require more immobilisation, for
example, with internal fixation. Unstable fractures of the
mandible are specifically discussed in Chapter 12.
Fracture healing
The process of fracture healing can be conveniently
divided into stages (Table 9.5). It is important to realise
that these stages are not discrete entities, but rather
overlap and blend into one another. Mediators and factors
affecting fracture healing are broadly similar to those
involved in wound healing (described above).
Inflammatory phase
• Bleeding and clot formation: bleeding occurs from
the fracture ends, predominantly from periosteal and
endosteal vessels. A clot forms between the ends of
the fracture.
• Acute inflammatory reaction and swelling: an
inflammatory infiltrate of white blood cells invades
the clot and fracture site. Resultant swelling causes
loosening of the periosteum.
• Bone necrosis: blood vessel disruption deprives
osteocytes at the fracture end of oxygen and they
undergo necrosis.
• Macrophage infiltration: macrophages and osteoclasts
are recruited to the area and remove dead material
including bone.
Table 9.5
Stages of fracture healing
Inflammatory phase
bleeding and clot formation
acute inflammatory reaction
bone necrosis
granulation tissue
Reparative phase
provisional callus
healing across fracture gap
Remodelling phase
• Granulation tissue: the blood clot is organised by
around day 3–4 and osteoblasts are generated within
it. Simultaneously, locally released factors stimulate
angiogenesis, revascularising the area.
Reparative phase
• Provisional callus: the organised clot contains
fibroblasts producing collagen, chondroblasts and
osteoblasts laying down matrix. The initial result is a
mixture of cartilage and connective tissue called
fibrocartilage. This material matures, over the course
of 2-6 weeks, into bone, and is described as callus.
• Healing across fracture gap: ossification begins at the
fracture ends, starting subperiosteally. Initially
relatively immature and less stable woven bone is
produced. Over 6-12 weeks, ossification occurs
throughout the provisional callus, bridging the
fracture gap. At the same time, maturation to more
structurally robust lamellar bone occurs and the
fracture is united.
Remodelling phase
The healing fracture site continues to adapt to its
environment and particularly the forces applied to it for
up to 2 years. Different bones have different capacities to
remodel and children have a marked ability to remodel
compared to adults, particularly the elderly.
Principles of management
The patient must be considered as a whole, not as
isolated injured parts. As always, the priority is to treat
life-threatening injuries by way of resuscitation. Bony
injury can indeed be life threatening in itself and hence
require early treatment, as in the case of maxillofacial
fractures such as Le Fort III, which can displace and
obstruct the patient's airway, and pelvic fractures, blood
loss from which can cause haemorrhagic shock.
With regards to orthopaedic injuries the priority is to
treat limb-threatening injuries such as displaced fractures
causing vascular compromise.
Analgesia is an important early consideration for the
obvious reason of patient comfort but also to combat the
pathophysiological effects of pain and distress.
Definitive fracture management is determined by the
type of fracture. A fundamental distinction is management of open compared to closed fractures.
Table 9.6
Treatment of closed fractures
Reduction
Immobilisation
plaster
traction
external fixation
internal 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 if
vascular compromise is present, and should take
precedence over investigation including radiographs.
Provided the blood supply is unaffected reduction can be
carried out under more considered circumstances.
Reduction is often not required. This is the case with
minimally displaced fractures where the process of
remodelling will compensate in the long term.
Where reduction is required, it is ideally effected by
closed manipulation, thereby minimising the risk of
introducing infection to the fracture site. It is important
to provide adequate analgesia for reduction and this
can involve regional or general anaesthesia, with their
attendant risks. These risks of reduction might outweigh
the benefits where the displacement or deformity will
result in no loss of function.
Different fractures require differing accuracy of
reduction. In general, alignment is more important than
apposition, which the process of fracture healing is good
at compensating.
Intra-articular fractures are a group that require
reduction to as close to the anatomical normal as possible.
This is mainly due to the risk of osteoarthritis. Often, this
can be achieved by closed manipulation. More precise
reduction can be achieved by operative open reduction,
and this is indicated when closed reduction has not
produced a satisfactory result including if there are soft
tissues interposed between fracture ends. This is also the
case for extra-articular fractures. Fractures that require
internal fixation are reduced operatively to the position
that they are to be held in, during the same operation.
Open reduction requires a form of anaesthesia and importantly - breaches the protection against infection
that the skin provides.
63
Immobilisation
A degree of movement at the fracture site is beneficial
for fracture healing, by providing a stimulus to callus
formation.
Splintage can be thought of as artificial callus put in
place early on. It prevents excessive movement at the
fracture site, relieving pain and keeping the fracture ends
in close proximity to undergo healing and union, and
therefore also minimising deformity.
There are several methods available for providing
immobilisation; the indications, risks and benefits are
described below.
Plaster
Plaster casts are easy, cheap and safe. Modern plaster
materials are light, waterproof and easy for the patient to
manage. They allow patients to mobilise and go home
early and maintain the fracture in good position. However, they allow little movement, particularly of the joints
surrounding the fracture, and therefore predispose to
stiffness.
Plaster casts are most suitable for fractures that are
minimally displaced, or those that have been adequately
reduced and whose new position is stable.
The main dangers of casts are if they are applied
incorrectly. A tight cast can act as a constraint and hence
cause a kind of iatrogenic compartment syndrome. This
is particularly the case shortly after injury, or manipulation, and often a 'backslab' (i.e. a plaster that does not
go around the whole circumference of the injured part) is
applied.
Pressure sores can occur within the plaster and skin
breaks can be induced by the patient trying to relieve
the itch in the plaster, for example with a knitting needle.
These predispose to infection.
Internal fixation
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 bandaging on the injured body part.
This form of immobilisation is achieved by open,
operative reduction of the fracture, which is then held in
place 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 and
includes pins, plates and screws, the particular indications for which are generally fracture specific. These
are considered further in Chapter 12.
The main advantage of this form of treatment is the
accuracy of reduction that can be achieved and indeed
maintained by the firm immobilisation provided.
This high degree of rigidity at the fracture site is not
completely beneficial, however, as it does not induce
callus, as previously mentioned. However, the main
disadvantage of internal fixation is the higher risk of
infection. Not only is the skin's barrier to infection
breached at operation but microorganisms also tend to
stick to prosthetic materials, including metal. Infection
on metal implants is hard to clear, as little systemic
antibiotic gets to the site, as do few of the body's natural
defences. Other complications include fracture of the
internal fixation device, particularly if it takes too great a
proportion of the load rather than the healing bone.
External fixation
Stress and movement
Pins or screws are inserted proximal and distal to the
fracture site, and these 'anchors' are attached to a rigid
Physiological loading of the fracture site not only allows
early return of function but also aids healing in the short
Traction
64
external device. This allows unique manipulation and can
also act as a form of localised traction device, or even
provide a force compressing the fracture ends together,
helping to bridge a fracture gap. Wounds can be left open
to 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 fixation
are those that would benefit from the above features,
particularly fractures at risk of infection or with significant soft tissue damage, such as open fractures. External
fixators are unsightly but, more important, they prevent
normal force loading of the fractured bone, slowing
healing. Although the force applied through the device
might be excessive, for example resulting in over
distraction of the fracture ends, the same device can be
manipulated to compensate this. However, external
fixators are not devoid of the risk of infection and pintrack infection is a considerable problem that can result
in chronic osteomyelitis.
term by stimulating callus formation, and in the long
term by providing the basis of remodelling. Early movement and physiotherapy of areas and joints around the
fracture site help prevent stiffness and deformity in the
longer term.
The caveat is inducing excessive movement at the
fracture site, which can also delay healing. This is a
delicate balance and the degree and duration of
immobilisation is fracture specific, and often even patient
specific. Therefore regular clinical review is essential, as
is close communication with paramedical specialties
such as physiotherapy.
Treatment of open fractures
The main risk of an open fracture per se is that of
infection. This risk is the result of breach of the barrier
provided by skin, the presence of foreign material and
dead tissue in the wound, and impaired blood supply
preventing the body's innate defences getting to the area
as normal.
One of the main principles of treatment is therefore
prevention of infection. This cannot be instituted too
early and the wound should be covered with a nonadherent sterile dressing as part of first aid management.
Ideally, this dressing should be left in place. Antibiotic
prophylaxis should be given early, as there is inevitably
some delay in definitive management. Intravenous broadspectrum antibiotics are indicated to cover Gramnegative, Gram-positive and anaerobic organisms.
Tetanus immunisation status should be considered early
and a booster given if indicated. Operative treatment is
based on the principles of debridement and fixation.
Current thinking is to aggressive debridement,
removing all foreign material and dead tissue. Thorough
washing of the wound should be followed by excision of
appropriate tissue. Several visits to theatre might be
required as it becomes apparent postoperatively that
further tissue is not viable. Although this can result in a
significant defect, a clean wound is amenable to later
closure and reconstruction, whereas an infected wound is
ultimately likely to produce more of a defect. A common
dilemma at initial operation is whether to close the wound.
In general, only small, clean wounds with minimal soft
tissue damage should be closed at the initial operation.
The fracture ends need to be washed and reduced to an
acceptable position. Holding the fracture in the reduced
position is most often achieved with external fixation,
which allows best drainage of the wound. Occasionally,
fixation is achieved with plaster or traction. Internal
fixation is relatively rare because of the risk of infection
of the implants; however, in experienced hands, and in
particular fractures, it can produce the best results (see
Ch. 12).
A postoperative course of antibiotics should be
continued irrespective of the method of fixation.
Complications of fractures
and fracture healing
As discussed in Chapter 4 'Complications of surgery',
it is helpful to divide complications into general and
specific (or local), and to subdivide with regards the
timeframe they occur in - early, intermediate and late
(see Table 4.10).
General
Early
As alluded to earlier, attention must be paid initially to
associated injuries, most often to other systems, that
might require life-saving resuscitation treatment.
Injuries to bones, particularly the pelvis and long
bones, can result in significant blood loss into the pelvic
cavity or soft tissues that can cause shock in their own
right, or exacerbate shock of other causes.
Intermediate
Some patients require treatment in hospital and are
subjected to a degree of immobility. This predisposes
them to a number of conditions, perhaps most importantly deep venous thrombosis (DVT) and pulmonary
embolism (PE). Prophylaxis for DVT is an important
consideration in inpatients with bony injury, and most
centres will have a form of protocol for this. Other risks
of immobility include pneumonia, constipation and
pressure sores, for which careful nursing prevention is
the best form of treatment. Patients requiring operative
treatment are exposed to the general risk of anaesthetic,
as discussed in Chapter 10.
Fat embolism syndrome is a phenomenon seen 3 to 10
days postinjury, and is most often seen following long
bone or pelvic fractures. Clinically, it is characterised by
an unwell patient with respiratory distress, who might
have visible petechial haemorrhages, particularly on the
trunk. Other clinical indicators are tachycardia and
pyrexia. Treatment is supportive. Crush syndrome is the
consequence of major trauma whereby muscle crushing
causes significant muscle destruction, with release of
proteins from the damaged muscle. These substances
prevent normal renal tubular function, and acute renal
failure and shock supervene. Treatment is again largely
supportive, with careful fluid and protein balance.
Prevention is also important and includes radical
measures including removal of severally damaged
tissues, e.g. amputation.
Late
Patients might be left with disability, deformity and
handicap. These factors can result in significant social,
occupational and psychological sequelae.
Local
Early
The important local early complications have already
been dealt with, being injuries to surrounding structures
including blood vessels and nerves.
non-compliant fascia) results in compression of the soft
structures within that compartment. Both blood vessels
and nerves are squashed, reducing their blood supply and
impairing their function. Tissue ischaemia results in tissue
damage and oedema, and therefore further swelling,
causing a vicious circle. This pathophysiology explains
the symptoms, signs, sequelae and treatment of compartment syndrome.
The earliest symptom is of pain in the injured area.
This might not seem terribly helpful but the pain of
compartment syndrome is disproportionately great
compared to the underlying injury and has a less-thanexpected response to analgesics.
The area is exquisitely tender and pain is experienced
on stretching (passively) any muscles that are also being
squashed within the compartment, or whose blood
supply is impaired. From these early features there is a
spectrum to the late features of compartment syndrome
that should not be seen (as treatment will have been
instituted). The late features are classically described as
the five Ps (Table 9.8).
A high level of suspicion allows monitoring and
prevents occurrence. If compartment syndrome is
developing, constricting dressings and traction should be
removed and the area elevated to try to reduce oedema. If
unresolving, it might be necessary to surgically decompress the compartment, for example by fasciotomy.
Intermediate
Local problems occurring at an intermediate stage are
listed in Table 9.7.
Compartment syndrome
This phenomenon generally occurs within hours of
injury and is associated with injuries in certain areas.
Whereas compartment syndrome is most commonly
associated with fractures, this is not always the case, as it
relates to soft tissue swelling. Swelling within a
relatively fixed compartment (e.g. enclosed by bone and
Table 9.7 Local intermediate problems
complicating fractures
66
Compartment syndrome
Infection
Delayed union
Non-union
Infection
Infection can seriously impair the physiological process
of fracture healing described above, and is one of the
more common causes of malunion and non-union
described below. Infection is much more common in
open fractures and this is one of the main reasons they
are treated differently.
Another risk factor for the development of infection is
the insertion of foreign bodies. This is particularly
important when considering the insertion of metal such
as plates and screws.
Table 9.8
Pale
Pulseless
Paraesthesia
Painful
Paralysed
The five Ps of compartment syndrome
Delayed union
Loss of function
In delayed union, fracture healing takes longer than
expected. This is predominantly a clinical diagnosis with
persistent pain and excessive mobility at the fracture site.
Even under normal circumstances, radiological union
takes longer than clinical union.
There are numerous causes of delayed union and it is
less common in cancellous bone than cortical bone.
Infection is a common cause and the presence or absence
of infection has an influence on management. Other
important causes include poor alignment of the fracture
(inadequate reduction), poor blood supply to the fracture
site and excessive mobility at the fracture site.
Uncorrected deformity can result in loss of function, as
relationships are no longer anatomical. Similarly, prolonged immobilisation can result in soft tissue fibrosis,
resulting in contractures, for example, fixed flexion
deformity. Other causes of dysfunction include muscle
weakness and loose ligament complexes.
Non-union
Causes are similar to those of delayed union, with the
addition of interposition of soft tissues. A gap remains
between the ends of the fracture, which is radiographically
visible, and it might also be possible to see that the
medullary cavities have sealed off. Clinically, the patient
has persistent pain and mobility, with or without crepitus,
on stressing the fracture site. The diagnosis is therefore
both clinical and radiological.
Treatment of abnormal fracture union depends on
whether there is infection present. Healing in the
presence of pus and dead bone (sequestrum) is unlikely,
and surgical debridement with antibiotic therapy is often
required.
Delayed union is classified into fractures with
hypertrophic callus and hypotrophic callus. Where there
is excess callus, normal healing is the rule with a prolonged period of immobilisation. Where there is minimal
or no callus, healing is likely to remain inadequate and
operative treatment, for example with bone grafting may
be indicated.
Osteoarthritis
Intra-articular fractures that are not correctly aligned
result in abnormal wear of the articular surface,
Osteoarthritis. Altered biomechanics from a fracture, for
example, gait, can result in abnormal loads through joints
not involved in the original injury, also leading to
premature wear and tear.
Post-traumatic ossification
This is the laying down of bony elements within soft
tissues around the site of injury. Its aetiology is not
known. Clinically patients have pain and may have a
tender palpable mass. Treatment is with rest, and can be
followed up by elective excision of the affected tissues.
Nerve, tendon and muscle complications
Callus or irregularly healed fracture edges can impinge
on adjacent tendons or nerves, with either rupture or
dysfunction ensuing. These features are often fracture
specific, and seen in classic patterns. Muscles that have
been involved in compartment syndrome die and contract,
producing so-called Volkmann's contractures.
Avascular necrosis
Late
The late local complications are listed in Table 9.9.
Table 9.9
Late local complications of fractures
Loss of function
Osteoarthritis
Post-traumatic ossification
Nerve tendon and muscle complications
Avascular necrosis
Suedeck's atrophy
Where the fracture disrupts the blood supply to a piece of
bone, it can undergo necrosis. An example is the femoral
head that derives some of its blood supply through the
femoral 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, often
precipitated by trauma that might be thought to have
67
been relatively insignificant. Clinically, it is characterised
by persistent, burning pain. Joints are red and swollen,
and later the skin becomes shiny and atrophic. Radiographs show patchy reduction in bone density.
68
Treatment is by having an index of clinical suspicion,
and early institution of physiotherapy and elevation. If
these measures are unsuccessful then treatments blocking sympathetic innervation to the area can be of benefit.
10
General anaesthesia
Introduction
Anaesthesia means absence of all sensation; analgesia
means absence of pain. General anaesthesia is a state
where all sensation is lost and the patient is rendered
unconscious by drugs. Some anaesthetic agents have
little analgesic effect whereas some analgesics produce
little sleep. Combinations of drugs are, thus, commonly
used in modern practice although, historically, an
inhalational agent, such as ether or chloroform, was all
that was available and was used as a single agent.
The administration of general anaesthesia used to
be performed in a variety of settings, such as dental
practices. Increased standards have now precluded this
practice and general anaesthesia should be performed
only by qualified anaesthetists in a hospital setting with
access to appropriate medical support.
Some operations, such as cardiac surgery, are
performed only under general anaesthesia. Other
procedures, such as dental extraction, can often be
performed under local anaesthesia with or without
concurrent sedation, even in small children.
It is important, because of the risks of general
anaesthesia alluded to below, that all methods of
Table 10.1
Aspects of general anaesthesia
Assessment of risk
Preoperative assessment and premedication
Induction of anaesthesia
Maintenance of anaesthesia
Maintenance of the airway
Inhalational anaesthetic agents
Anaesthetic gases
Intravenous agents
Drugs used to supplement anaesthesia
Monitoring during anaesthesia
Postoperative care
providing pain-free surgery are explained and the patient
or guardian allowed to give informed consent to the
methods of analgesia or anaesthesia to be employed (see
Ch. 22).
The surgeon and the anaesthetist have a shared
responsibility for the patient's wellbeing, and so an
understanding of general anaesthesia is important for all
surgeons. General anaesthesia will be considered here, as
described in Table 10.1. Local anaesthesia for dental
procedures is considered in Chapter 24.
Assessment of risk
The patient should first be made as fit as possible for
operation in the time available. Second, the anticipated
benefits of surgery should outweigh the anaesthetic and
surgical risks involved. The overall mortality rate
attributable to anaesthesia itself is approximately 1 in
100 000, whereas a broad average of surgical mortality is
more than 1 in 1000. Factors that have been shown to
contribute to this mortality include poor preoperative
assessment, inadequate supervision and monitoring in the
intraoperative period and inadequate postoperative care.
Audits of operative mortality commonly use the
American Society of Anesthetists' (ASA) physical status
scale (Table 10.2). Fitness for operation is always relative
to the urgency of the proposed procedure.
Preoperative assessment
and premedication
The anaesthetist must see and assess the patient preoperatively; failure to do so can be regarded as negligent.
Many patients will be seen the night before surgery. With
increasing economic pressures to admit patients on the
69
Table 10.2 The American Society of
Anesthetists' physical status scale
Class I A normally healthy individual
Class II A patient with mild systemic disease
Class III A patient with severe systemic disease that is
not incapacitating
Class IV A patient with incapacitating systemic disease
that is a constant threat to life
Class V A moribund patient who is not expected to
survive 24 h with or without operation
Class E Added as a suffix for emergency operation
Table 10.3
Aspects of the preoperative visit
Evaluation of history and physical examination
Ordering of special investigations
Institution of preoperative management
Risk assessment
Discussion regarding anaesthetic management which
will involve patient consent
Prescription of premedication
day of operation, a screening process must be used to
identify suitable patients. Preassessment clinics with a
combination of nursing and medical input are increasingly
being developed to improve efficiency and streamline
'the patient journey'. They must run to carefully designed
protocols.
After a preoperative visit there should be no surprises
for either patient or anaesthetist. The visit should
establish rapport with the patient and should allow time
for the various factors listed in Table 10.3.
History
A comprehensive history is important. It can reveal
diseases, particularly of the cardiovascular and respiratory systems (for which breathlessness and chest pain
are especially relevant). The identification of pregnancy
is important because it is a contraindication to elective
surgery in the first trimester due to the risk of
teratogenicity. Later in pregnancy the patient faces the
risks of regurgitation and aspiration of gastric contents.
70
A past history of HIV infection or other infective
agents can affect both patients and their carers. A history
of previous anaesthesia can highlight problems of drug
allergy, deep venous thrombosis or postoperative nausea
and vomiting. Anaphylaxis is the most serious of these.
Drug history
Many interactions can be potentially dangerous, for
example, anticoagulants might be a contraindication to
spinal, epidural or other regional techniques; anticonvulsants might increase the requirements for
anaesthetic agents and enflurane, a volatile anaesthetic
agent, should be avoided as it might precipitate seizures.
Beta-blockers have negative inotropic effects and can
cause hypotension. They can also mask a compensatory
tachycardia, concealing evidence of blood loss. Plasma
potassium concentration should be checked in all
patients taking diuretics because they might have
hypokalaemia and careful monitoring of plasma glucose
can be important in patients receiving insulin. Such
measures may require a special perioperative regime.
Corticosteroids have many well-known complications
and extra corticosteroid cover to compensate for a
relative lack might be needed.
Social history
Ceasing smoking 12 h before surgery can improve
the oxygen-carrying capacity of the blood, although
abstinence for a longer period is required to reduce the
incidence of postoperative respiratory morbidity.
Excessive alcohol can result in both hepatic and cardiac
damage. Acute withdrawal in alcoholics can result in
delirium tremens, which will require both a sedative such
as a benzodiazepine agent and thiamine (vitamin B1).
Family history
The anaesthetist must be aware of hereditary traits such
as haemophilia and porphyria. Cholinesterase abnormalities can lead to prolongation of muscle relaxants
such as suxamethonium.
Past medical history
Physical examination
This should elicit evidence of asthma, diabetes,
tuberculosis, seizures or any chronic major organ
dysfunction.
A full physical examination is important to complement
the history but the anaesthetist will also pay particular
attention to the upper airway with a view to assessing the
ease of tracheal intubation. This will involve assessment
of the teeth and extent of mouth opening and flexibility
of the neck.
Preoperative investigation of elective patients
Healthy patients less than 40 years old do not generally
require any preanaesthetic investigation. Only relevant
tests should be ordered and these will reflect age,
comorbidity and complexity of the surgery. Circumstances where investigation would be important are listed
in Table 10.4.
Other investigations, such as radiography of the
cervical spine or lung function tests, will be undertaken
for specific indications.
Table 10.4 Indications of preoperative
investigations
Full blood count
anaemia
females post menarche
cardiopulmonary disease
possible haematological pathology, e.g.
haemoglobinopathies
likelihood of significant intraoperative blood loss
history of anticoagulants
chronic diseases such as rheumatoid disease
Clotting screen
liver disease
anticoagulant drugs or a history of bleeding or
bruising
kidney disease
major surgery
Urea and electrolyte concentrations
major surgery >40 years
kidney disease
diabetes mellitis
digoxin, diuretics, corticosteroids, lithium
history of diarrhoea and vomiting
Liver function tests: these will be carried out when there
is any suspicion of liver disease
ECG
>40 years asymptomatic male or >50 years
asymptomatic female
history of myocardial infarction or other heart or
vascular disease
<40 years with risk factors e.g. hyperlipidaemia,
diabetes mellitis, smoking, obesity, hypertension
and cardiac medication
Chest radiography
breathlessness on mild exertion
suspected malignancy, tuberculosis or chest infection
thoracic surgery
Preoperative therapy
Patients with respiratory disease can be improved by
physiotherapy or bronchodilator therapy. Prophylactic
antibiotics are required in those at risk of subacute
bacterial endocarditis. Hypertensive patients can sometimes require adjustment of their drug therapy to obtain
optimal control, but it is usually reasonable to proceed
with surgery if their diastolic pressure is below
110 mmHg.
Postponement of surgery
If time allows, it is not sensible to anaesthetise a patient
with an acute upper respiratory tract infection and
operation might also have to be delayed for patients with
cardiac or endocrine diseases that are not yet under
optimal control. Likewise, resuscitation and restoration
of circulating blood volume can require delay in
anaesthesia. Elective surgery should not be undertaken
unless the patient has fasted for 6 h for solid food, infant
formula or other milk, 4 h for breast milk or 2 h for clear
non-particulate and non-carbonated fluids
Premedication
Whereas reassurance and explanation remain the most
important components of the preoperative visit, drugs
can be used to obtain one or a combination of the effects
listed in Table 10.5.
Anxiolysis is most commonly achieved with the use
of benzodiazepines such as diazapem or lorazepam, and
these drugs also cause a degree of anterograde amnesia.
Excessive secretions in the airway are less of a problem
with modern anaesthetic agents but can be reduced with
anticholinergic drugs either given before or at operation.
Three drugs commonly used in this circumstance are
the anticholinergic agents atropine, hyoscine and glycopyrronium. Vagal bradycardia, such as occurs with the
Table 10.5
Effect of premedication
Reduction in anxiety and fear
Amnesia
Reduction in secretions
Potentiation of the effects of general anaesthetics
Reduction in the volume and acidity of gastric contents
Reduction in postoperative nausea and vomiting
Attenuation of both the sympathetic and vagal reflexes
71
oculocardiac reflex, can be severe and atropine is protective of all the above. Antiemetics such as metoclopramide,
ondansetron or antihistamines are administered preoperatively from time to time; metoclopramide also
enhances gastric emptying. If it is desired to reduce
gastric 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 with
information from the previous section and after
discussion between surgeon and anaesthetist, a plan of
action should be formed that will include the assembly of
the necessary staff, equipment for airway care and
monitoring, intravenous fluids and arrangements for
proper postoperative and recovery facilities. The
'preflight' check of the anaesthetic machine must be
carried out and the nature of the operation to be
performed and consent checked with the patient. The
patient must be on a tilting bed or trolley. Trained and
dedicated anaesthetic assistance is essential.
Induction of anaesthesia
Anaesthesia can be induced by inhalational agents or by
drugs administered intravenously.
72
concentration (ETCO2) can be monitored; this is
mandatory in intubated patients. As consciousness is lost,
the airway will require increasing support, which will
usually involve pulling up the patient's chin. It can also
require insertion of an artificial airway. This might be an
oral or nasopharyngeal airway. A laryngeal mask airway
(LMA) or an endotracheal tube can be inserted if
required. For endotracheal intubation without muscle
relaxants the patient must be at a much deeper level of
anaesthesia. Airway obstruction is the most commonly
encountered difficulty. Scavenging systems are usually
employed to reduce environmental pollution from
expired gases.
Intravenous induction
Induction of anaesthesia with an intravenous agent is
used for most routine purposes and is the most appropriate technique for most patients undergoing emergency
surgery. A cannula should be sited in a vein in the back
of the hand or forearm to avoid the structures in the
antecubital fossa or risk of intra-arterial injection of the
brachial artery. Sterility should be maintained and local
anaesthesia used if a large cannula is required for
infusion of fluids. Prior to induction, the patient should
breathe 100% oxygen with a tight-fitting mask for 3 min
or, alternatively, be asked to take four deep breaths to
vital capacity.
Inhalational induction
Emergency/rapid sequence induction
Inhalational induction is more commonly proposed for
either young children or those with an obstruction somewhere in their airway (e.g. epiglottitis or a foreign body).
Rapport and patient confidence are important to ensure
the patient's cooperation, and a gentle and gradual
approach should be used. An anaesthetic mask should be
held gently on or very near the face and the patient
should be talked to calmly and reassuringly while being
encouraged to breathe normally. It is common for nitrous
oxide 70% in oxygen to be used; anaesthesia is gradually
deepened as the anaesthetist introduces a volatile
anaesthetic agent by increments. Patient monitoring will
have been attached before induction and the patient is
observed carefully for skin colour; the pattern and rate
of ventilation and the patient's pulse, blood pressure
ECG and arterial oxygen saturation by pulse oximetry
(SpO2) should all be observed. End tidal carbon dioxide
This is most commonly employed for patients with a full
stomach and a risk of regurgitation and aspiration of
gastric contents, provided preoperative evaluation
indicates no major difficulty with airway or intubation.
With all preparations made, intravenous access secured
and suitable assistance, the patient breathes 100%
oxygen for 3 min on a tilting trolley. The assistant on the
right of the patient applies firm pressure over the cricoid
cartilage with thumb and index finger. This posterior
pressure compresses the oesophagus between the cricoid
cartilage and the vertebral column. It is applied either
just before administration of the intravenous induction
agent or as soon as consciousness is lost. A predetermined
sleep dose of induction agent is followed immediately by
a paralysing dose of suxamethonium. As soon as the jaw
begins to relax, laryngoscopy is performed and the
endotracheal tube placed. Cricoid pressure is maintained
until the cuff of the tube is inflated and correct placement
is confirmed. This is intended to prevent regurgitation
and aspiration. Further muscle relaxants are not normally
given until control of the airway is secured, but this
technique balances the greater risk of aspiration against
the risk of losing control of the airway. Although this
technique is commonly used for general surgical
emergencies, it should not be used where there is any
obstruction to the upper airway from trauma or inflammation and, in these circumstances, an inhalational
technique or awake intubation is more appropriate.
Positioning of the patient for surgery
Patient safety is paramount and the patient should be
positioned carefully, taking into account requirement for
both surgical and anaesthetic access. The anaesthetist
must be aware of the varying effects of different
positions. Local pressure effects on nerves can result in
postoperative morbidity. Intraoperatively, the head-down
or prone positions will make abdominal breathing
difficult. The sitting position requires careful support of
the head and can result in cardiovascular instability from
pooling of blood in the leg veins. The supine position is
used for the majority of surgery. Aortocaval compression
in pregnant patients or those with large abdominal
masses can result in hypotension.
Maintenance of anaesthesia
Several options are available to maintain anaesthesia.
Inhalational agents, intravenous anaesthetic agents or
intravenous opioids can be used, either alone or in
combination. Muscle relaxants are commonly used to
facilitate tracheal intubation and subsequent ventilation
of the lungs. Regional anaesthesia can be used to
supplement any of these techniques.
Inhalational anaesthesia with spontaneous ventilation
is appropriate for superficial operations where profound
muscle relaxation is not required. The patient is allowed
to breathe spontaneously and a volatile anaesthetic agent
such as halothane, enflurane, isoflurane or sevoflurane is
used with carrier gases nitrous oxide and oxygen. Most
anaesthetic 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 deliver
a constant percentage of agent irrespective of the gas
flow through them, temperature or pressure. Analgesia
as determined by the patient's response might also be
required.
Minimal alveolar concentration (MAC) is the minimal
alveolar concentration of an inhaled anaesthetic agent
that prevents reflex movement in response to surgical
incision in 50% of subjects. This value is commonly used
as an index of relative potency and may be affected by
the patient's age and concomitant use of other drugs.
Signs of anaesthesia
The signs and stages of anaesthesia were originally
described by Guedel in patients premedicated with
morphine and atropine and breathing ether and air. With
newer agents the stages are less clearly differentiated but
they remain a useful general guide.
Stage 1 - analgesia
This can be attained using nitrous oxide 50% in oxygen
and provides 'relative analgesia'.
Stage 2 - excitement
This is seen with inhalational induction but with
intravenous induction it is commonly bypassed. The
eyelash reflex is often lost at this stage. Breathing is
irregular and laryngeal and pharyngeal reflexes are still
active. Patients might hold their breath and any instrumentation of the airway can produce laryngeal spasm.
Stage 3 - surgical anaesthesia
The patient develops rhythmic regular breathing and as
they descend through the four plains from light to deep,
respiratory reflexes are progressively abolished. Patients
can no longer protect their own airway. The pupils
become central and are classically large, although, with
the newer agents, they are often much smaller than with
the older agents.
Stage 4 - stage of impending respiratory and
circulatory failure
In this stage, anaesthesia is too deep and brainstem
reflexes are depressed by high anaesthetic concentrations.
Anaesthetic agents should be withdrawn and oxygen
administered.
73
Maintenance of the airway
Maintenance of the airway and of oxygenation is the
cornerstone of safe anaesthesia. Inhalational agents can
be administered with a face mask, a laryngeal mask
airway (LMA) or an endotracheal tube.
Face mask
Face masks come in various shapes and sizes and should
be chosen for the individual patient to provide an
adequate seal. Nasal masks are used during dental
anaesthesia. The mask is held against the patient's face
and the mandible is held forwards because pressure on
the submental soft tissues can exacerbate airway
obstruction by pushing the tongue backwards. The
reservoir bag on the anaesthetic circuit should be seen to
be moving in and out with the respiratory movement of
the patient. There should be no indrawing of the
suprasternal and supraclavicular areas - this indicates
obstruction. Breathing should be quiet; noisy ventilation
or stridor provides further evidence of obstruction. It
should be always remembered that total obstruction is
silent as there is no movement of air. An oropharyngeal
or Guedel airway can be used to assist in maintenance of
the airway (Fig. 10.1).
Endotracheal intubation
Laryngeal mask airways (LMAs) can be considered a
halfway house between a face mask and an endotracheal
An endotracheal tube provides the most secure airway
short of tracheostomy. It is passed via the mouth or nose
and between the vocal cords into the larynx. The cuff on
the tube lies below the cords and when it is inflated with
air protects the respiratory tract from blood, secretions or
inhalation of gastric contents. Likewise, the cuff prevents
leakage of air travelling upwards during controlled
ventilation. The tube also allows access for suction of the
respiratory tract. Cuffed tubes are used in adults, whereas
uncuffed tubes provide an acceptable seal in children.
There are a multitude of designs for laryngoscopes.
The McGill laryngoscope is favoured for children
because their epiglottis is floppy. It has a straight blade
and is designed to lift the epiglottis anteriorly, exposing
the larynx. The Mclntosh laryngoscope, which has a
curved blade, is designed so the tip lies anterior to the
epiglottis in the vallecula and pulls the epiglottis
anteriorly to expose the vocal cords.
Fig. 10.1
Fig. 10.2
Laryngeal mask airway covering the glottis but
not occluding the opening to the oesophagus.
Laryngeal mask airway
74
tube (Fig. 10.2). They avoid the need for tracheal
intubation during spontaneous ventilation while at the
same time providing a clear airway without the need to
hold on a mask. They can also occasionally be used to
assist with difficult intubation.
They should not be used in patients who are at risk of
regurgitation of gastric contents because an endotracheal
tube is required to provide secure protection and there
will be occasions when surgical access could be
obstructed by the bulk of the cuff on the LMA.
Guedel airway in place.
Laryngoscopy
The position of the patient's head and neck is important
and was classically described as 'scenting the morning
air'. The neck is flexed by raising the patient's head on
a pillow and the head is extended. The laryngoscope,
which is a left-handed instrument, is inserted into the
right side of the mouth and pulls the tongue to the left as
it is advanced slowly downwards. With the patient on his
or her back, the laryngoscope is thus pulled upwards and
away from the anaesthetist, avoiding levering against the
upper teeth. This should reveal the dark, almost
triangular orifice of the glottis. External pressure on the
thyroid cartilage can allow better visualisation. The tube
is placed through the glottis and its position within
the airway should be confirmed by auscultation and
monitoring of expired CO2.
For nasal intubation, slightly smaller tubes are used
after the introduction of vasoconstrictor into the nostrils
to reduce bleeding.
Tracheal intubation can be undertaken under general
anaesthesia but, where difficulties are anticipated, a tube
can be inserted over a fibreoptic endoscope under local
anaesthesia.
Table 10.6
Inhalational anaesthetic agents
Diethyl ether
Halothane
Enflurane
Isoflurane
Sevoflurane
Desflurane
administration and it should be neither flammable nor
explosive.
Diethyl ether
Diethyl ether has been abandoned in the West because of
its flammability, but it remains in widespread use in less
developed countries. As it has a higher therapeutic ratio
than more modern agents, it is relatively safe for
administration in the hands of unskilled individuals. Its
use is limited because it is highly irritant to the respiratory tract and can cause coughing, breath holding and
profuse secretions. However, at deeper levels it was at
one time a recommended treatment for bronchospasm.
Halothane
Extubation
Patients can be extubated supine if there is no risk of
regurgitation but it is often safer to remove the
endotracheal tube with the patient in the lateral recovery
position. Prior to extubation the patient is given 100%
oxygen and suction is performed to remove secretions
from the endotracheal tube and from the mouth. After
extubation the patient's clear airway, ability to breath,
cough and clear secretions are carefully assessed while
oxygen is continued by face mask. Laryngeal spasm
occurs if the vocal cords come together as a result of
irritation. A 'crowing' sound is heard and the patient will
show signs of airway obstruction. This is treated by
clearing secretions and applying positive airway pressure
with oxygen. Occasionally, reintubation might be required.
Inhalational anaesthetic agents
The range of inhalational anaesthetic agents is listed in
Table 10.6.
An ideal inhalational agent should be pleasant and
non-irritant to breathe. It should also be potent and yet
produce minimum depression of cardiovascular and
respiratory systems. It should be safe for repeat
Halothane is again less commonly used, having been in
widespread use for over 30 years. There has been concern because of the rare occurrence of hepatic toxicity
after repeated administrations and it is also a depressant
of myocardial contractility. Arrhythmias are also very
common during halothane anaesthesia. Myocardial
excitability is seen, particularly in the presence of
hypercapnoea, hypoxia and with increased circulating
catecholamines. Halothane should not be used in
combination with local infiltration of adrenaline.
Enflurane
This is a clear, relatively pleasant-smelling agent. In
common with the other agents it produces a dosedependent depression in ventilation and tidal volume. It
produces less depression of the cardiovascular system
and is associated with fewer arrhythmias than halothane.
It should be avoided in people with epilepsy.
Isoflurane
Isoflurane produces less myocardial depression than
halothane or enflurane. It is rather pungent and less
75
suitable for inhalational inductions. A large multicentre
study in North America showed no significant outcome
differences between these three agents.
occasion, toxicity of the central nervous system can be
seen. Hyperbaric pressures result in convulsions.
Retrolental fibroplasia is retinal damage with new vessel
formation seen in infants exposed to high concentrations.
Sevoflurane
Sevoflurane, popular for some time in Japan, was only
introduced to the west in the 1990s. It is now the most
commonly used agent for inhalational induction as it is
pleasant and non-irritant, and might have a less
depressant effect on breathing. Solubility characteristics
allow a more rapid induction of anaesthesia. Recovery is
also usually rapid.
Desflurane
Another new agent, desflurane, is the most recent addition
to the volatile agents. It has to be given via a heated
vaporiser and allows very rapid alterations in the depth of
anaesthesia with recovery being faster than with any of
the other agents.
Intravenous agents
Induction of anaesthesia with intravenous agents is
usually more rapid and smoother than with inhalation
agents (Table 10.7). The ideal agent should have a rapid
onset and recovery time with little hangover effect. It
should be free of side-effects such as nausea, vomiting,
cardiovascular and respiratory depression or toxicity to
any major organs and it should also, if possible, be
analgesic in low doses.
After intravenous administration, plasma concentrations rise rapidly and the drugs diffuse across the
blood-brain barrier into the brain producing their effect.
Reduced plasma concentrations and drug effects occur
predominantly as they are distributed to other tissues.
Metabolism occurs mostly in the liver but contributes
relatively little to the recovery of consciousness.
Anaesthetic gases
Nitrous oxide
Nitrous oxide delivered via a pipeline or from blue
cylinders is used with oxygen as a carrier gas for these
potent volatile agents. As the MAC value for nitrous
oxide is over 100%, it cannot be used with oxygen as an
anaesthetic agent without the addition of a potent volatile
agent, but it has proved safe over a long period in use. It
is important that a high inspired oxygen concentration is
given when nitrous oxide administration is discontinued.
Nitrous oxide has also been incriminated in altering
vitamin B12 synthesis by inhibiting the enzyme methianine
synthetase, and excessive occupational exposure can
result in myeloneuropathy. This condition is similar to
subacute combined degeneration of the spinal cord and
has been reported in individuals addicted to nitrous
oxide.
Thiopentone sodium
Thiopentone sodium is one of a group of barbiturate
agents and has proved safe in practice for over 50 years.
It is important as a hypnotic but has an antianalgesic
effect that can result in a reduction of pain threshold and
restlessness in the postoperative period. On induction,
consciousness is rapidly lost and in the absence of other
agents is not regained for 5 to 10 min. As it does not
depress airway reflexes to the same extent as other agents,
laryngeal spasm can be precipitated by stimulation of the
airway. There is usually a moderate tachycardia and
reduction in blood pressure. It is a relatively long-acting
drug and a hangover effect is common. This length of
action makes it unsuitable as a drug for use by infusion
in total intravenous anaesthesia (TIVA). It is an anti-
Table 10.7
Intravenous induction agents
Oxygen
76
Although oxygen is life-giving, there are some dangers
associated with its use. It is flammable, it can cause a rise
in the partial pressure of CO2 (Paco2) in patients with
chronic obstructive airways disease and, in high concentrations, it can lead to loss of pulmonary surfactant. On
-1
Agent
Induction dose (mg.kg )
Thiopentone
Etomidate
Propofol
Ketamine
3-5
0.3
1.5–2.5
2
convulsant and can be used in the treatment of status
epilepticus but must never be given to patients with
porphyria, who might show severe cardiovascular collapse
or neurological sequelae.
Etomidate
This is a rapidly acting general anaesthetic agent with a
duration of action of 2–3 min. It produces less cardiovascular depression or vasodilatation than other agents
and is most commonly used in patients with a compromised cardiovascular system. It causes more excitatory
phenomenon on induction, which, on occasion, can be
troublesome. Etomidate depresses the synthesis of
cortisol by the adrenal gland even as a single bolus dose.
Its use in intensive care has been abandoned as infusions
resulted in increased infection and mortality probably
related to reduced immunological competence.
Propofol
Propofol has become a very popular agent. It has rapid
recovery characteristics and gives rise to a lower instance
of postoperative nausea and vomiting than most other
agents. It is formulated as a white aqueous emulsion,
which contains soya bean oil. Loss of consciousness is
rapid but blood pressure tends to decrease to a greater
degree than with other agents. Respiratory reflexes are
suppressed quite markedly and there is a low incidence
of coughing and laryngospasm. Many regard propofol as
the agent of choice where a laryngeal mask airway is to
be inserted. Recovery is rapid, with little hangover effect.
The drug is redistributed rapidly and probably metabolised
not in the liver but in extrahepatic sites. The elimination
remains constant, even after infusions lasting for several
days, and it is thus the most suitable current agent for
total intravenous anaesthesia (TIVA). It is also used by
infusion for sedation in intensive care and is increasingly
used as a form of relative analgesia and sedation during
surgical procedures. Computer-operated infusion pumps
are available, which aim to deliver a target plasma
concentration based on patient's weight and age.
depression. It is used in high-risk shocked patients and
has, therefore, a place in anaesthesia and analgesia in
times of war and at the scene of accidents. It can be given
intramuscularly in low doses to produce analgesia. It has
also been used in less developed countries, where equipment and staff are not readily available. Its use, however,
is limited by the occurrence of restlessness, disorientation
and often unpleasant nightmares or hallucinations, which
can recur for up to 24 h.
Drugs used to supplement
anaesthesia
Analgesics
Morphine
Morphine, produced from the poppy Papaver somniferum,
and codeine are naturally occurring opium alkaloids.
Morphine is the gold standard of analgesics affecting both
the pain threshold and the psychological components of
pain. Although it has little effect on the cardiovascular
system, depression of ventilation is common; the cough
reflex is also depressed. However, administration can be
limited by distressing nausea and vomiting and it greatly
reduces gut motility.
Pethidine
Pethidine is a synthetic opioid that, as it tends to relax
the 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 taking
monoamine oxidase inhibitors (MAOI).
Buprenorphine
This can be useful on occasions as it can be administered
sublingually. However, nausea and vomiting may be
troublesome and subsequent use of other opioids, for
example, morphine may be compromised as the drugs
antagonise at opioid receptors.
Ketamine hydrochloride
This differs from the other agents in producing a
dissociative state rather than generalised depression of
the central nervous system. Blood pressure might, in fact,
increase with this agent and there is little respiratory
Other opioids
Progressively shorter-acting synthetic agents are fentanyl,
alfentanil and remifentanil. Remifentanil is sufficiently
short acting to be useful administered by infusion.
77
Opioid antagonists
Naloxone is the drug of choice for reversing opioidinduced ventilatory depression. It should be titrated
slowly because convulsions can occur occasionally and it
reverses not only respiratory depression but also the
analgesia.
Other analgesics
Non-steroidal anti-inflammatory drugs such as diclofenac,
ketorolac and indomethacin can be used as analgesia
in a balanced anaesthetic technique. The new alpha2
adrenergic agonist dexmedetomidine is currently proving
promising because it results in profound analgesia with
less sedation.
Benzodiazepines
Benzodiazepines such as diazepam and midazolam can
also be used as anaesthetic agents, but they have a longer
duration of action than other agents. These drugs can
be reversed with flumazenil, which is a competitive
antagonist and again should be given in small titrated
increments.
Neuromuscular blockade
Muscle relaxation is the third of the triad of anaesthesia
that includes narcosis and analgesia. Neuromuscular
blocking agents are classified into depolarising (or noncompetitive) and non-depolarising (or competitive)
agents.
Depolarising agents
78
The only depolarising agent now available in clinical
practice is suxamethonium. After administration it results
in an initial depolarisation of muscle cells. Muscular
contractions can be seen and are known as fasciculation.
Repolarisation does not occur and the muscle becomes
flaccid. It produces a profound neuromuscular block
within a minute and is useful to achieve rapid tracheal
intubation in a patient who may have a full stomach.
Recovery usually begins to occur within 3 min. It is
metabolised by the enzyme cholinesterase and recovery
can be delayed if this enzyme is either structurally
abnormal or reduced in quantity. This is usually genetically determined and might require the patient to be
ventilated until muscle function returns. Suxamethonium
can give rise to muscle pains after operation. A rise in the
plasma potassium can occur, which can be dangerous
particularly in patients with burns or in those with
neuromuscular disease.
Non-depolarising neuromuscular blocking agents
These compete with the neurotransmitter acetylcholine at
the postsynaptic junction to prevent the threshold for an
action potential being reached, and so the muscle does
not contract. Tubocurarine (curare) was used for centuries
by native South Americans as an arrow poison and was
the first agent to be used in humans. It has, however, been
superseded. Atracurium degrades spontaneously in
plasma and is therefore very safe for patients with liver
or renal dysfunction. Such drugs have a longer duration
of action of around 30 min. Vercuronium is also used
and, because it releases less histamine, many consider it
to be the drug of choice in asthmatics. Pancuronium, and
more recently rocuronium, are aminosteroids. The
advantage of rocuronium is its very rapid onset, which
provides good intubating conditions within 90 s.
Neuromuscular blockade can be monitored with a nerve
stimulator intraoperatively and at the end of operation
this block can be reversed by the administration of the
anticholinesterase neostigmine in combination with either
atropine or glycopyrronium. The addition of atropine
or glycopurronium reduces respiratory secretions and
prevents bradycardia.
Monitoring during
anaesthesia
The word monitor is derived from the Latin verb monere
'to warn'. No device can replace the requirement for
these warnings to be observed, interpreted and acted
upon.
Monitoring the circulation
Monitoring of the circulation is necessary to maintain
perfusion of vital organs (Table 10.8).
The pulse can be palpated and blood pressure
measured either indirectly or, if necessary, directly from
an arterial cannula. Electrocardiography gives information regarding heart rate, rhythm and ST changes
produced by left ventricular ischaemia. It should be
remembered that it is an index of electrical activity only
and does not measure the mechanical activity that
sustains life.
Table 10.8
Monitoring of the circulation
Heart rate and pulse
Blood pressure
Arterial oxygen saturation
ECG
Peripheral perfusion
Urine production
Pulse oximetry assesses the integrity of the components of the oxygen-delivery system to the tissues (see
Ch. 11). It therefore assesses the oxygen supply to the
patient, the oxygen uptake by the lungs and oxygen
delivery to the tissues by the heart and circulation.
Pulse oximeters provide a non-invasive measurement
of the arterial oxygen saturation (SpO2). The principle
involves the proportion of light absorbed by blood. This
depends on the wavelength of the light and the ratio of
oxyhaemoglobin to deoxyhaemoglobin. The wavelength
of light known as the isobestic point is where absorption
is the same for oxyhaemoglobin and deoxyhaemoglobin.
At other wavelengths the absorption differs. The proportion of haemoglobin that is saturated with oxygen
can, therefore, be calculated by measuring the absorption
of light at two different wavelengths. As the electronics
are capable of detecting a pulsatile component only the
saturation of arterial blood is recorded. Because of the
sigmoid shape of the oxyhaemoglobin dissociation curve
arterial oxygen tension falls rapidly with saturations
below 90%. The lower alarm limit is usually set at this
level.
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 hypoxia
than cyanosis. More intense monitoring of the cardiovascular system may involve insertion of a central venous
pressure line. Pulmonary artery catheterisation will allow
both measurement of filling pressure which reflects
volume status and measurement of cardiac output. Newer
Doppler systems also allow monitoring of these last two
variables. Blood loss should also be monitored.
Monitoring the respiratory system
Clinical monitoring is most important. The patient should
be observed for colour, respiratory rate, adequacy of
respiratory movement and the movement of the reservoir
bag or ventilator. Auscultation can detect intubation of a
bronchus, the presence of secretions or the occurrence of
a pneumothorax. It is important to detect respiratory
obstruction, which can be revealed by tracheal tug or
paradoxical abdominal movement with the absence of
movement in the reservoir bag. The inspired oxygen
concentration should always be monitored. When patients
are ventilated there should also be capacity to measure
airway pressures, volumes and both the inspiratory and
end tidal concentrations of oxygen, carbon dioxide and
volatile anaesthetic agents. Ventilator systems should
also be fitted with a disconnection alarm. Capnography
measures the end tidal carbon dioxide tension (ETCO2)
and provides the most reliable evidence of correct
placement of an endotracheal tube. ETCO2 will rise with
rebreathing or underventilation and can fall rapidly with
pulmonary embolism arising from air, fat or thrombos.
Monitoring the central nervous system
At the present time this is done clinically. The signs of
sympathetic overactivity such as lacrimation, sweating,
increasing pupil size or increase in heart rate or arterial
pressure indicate that anaesthesia is too light. These signs
are, however, not reliable but cerebral function monitors
(CFM) are not at present in widespread practice. The
depth of anaesthesia is often assumed from the measurement of end tidal volatile anaesthetic concentrations. It is
only since the advent of neuromuscular blockers and the
abolition of patient movement that undetected awareness
has become a potential complication.
Other monitoring
Peripheral and central temperature measurement, neuromuscular blockade, together with haematological and
biochemical variables may all be measured. Blood gas
and acid-base status can be measured accurately from a
sample of arterial blood and the patient's coagulation
status may also require to be assessed.
There is strong evidence that there has been a
reduction in intraoperative critical incidents and patient
morbidity as a result of the adoption of higher routine
standards of patient monitoring.
Postoperative care
The patient must be supervised and monitored closely at
all times and should not be discharged from the recovery
ward to the surgical ward until they are fully awake and
79
maintaining their own airway, ventilation is adequate, the
cardiovascular system is stable and they are not bleeding
excessively.
Central nervous system - conscious level
The patient's airway must be carefully maintained until
they are awake. If the patient is not awake in a reasonable
time then other factors should be considered. Hypo- or
hyperlgycaemia may occur particularly in diabetics and
intracranial pathology may occur. The following, most
particularly, should be excluded: hypoxaemia, hypercapnoea, hypotension and hypothermia.
Confusion and agitation may occur at this time
particularly in the elderly. This may be associated with
anticholinergic drugs such as atropine or hyoscine but
pain may also be a contributory factor. Bladder distension
may be covert. If neuromuscular blockade has not been
adequately reversed the patient may appear agitated and
distressed with uncoordinated movements.
Oxygen
Particular care should be given to the patient's requirements for oxygen which should be monitored by oximetry.
All patients should be given oxygen postoperatively.
80
Intravenous fluids
They may also require fluids as a result of either intraoperative blood loss or preoperative fluid depletion.
Analgesia
Good pain control starting in the intraoperative period
should be established in the recovery ward before return
to the ward. This may be achieved with opioids which if
the patient is sufficiently awake can be administered by a
patient-controlled infusion device. Non-steroidal antiinflammatory drugs and local and regional techniques
may also be very valuable.
The recovery ward should have the staff, equipment
and monitoring to deal with the full range of complications. Problems are as liable to arise there as in the
anaesthetic room or operating theatre.
Patients should be closely watched for a number of
surgical complications which may include haemorrhage
and blockage of drains or catheters. This high intensity
environment should allow the patient to return to the
appropriate level of ongoing care in the optimum
condition.
11
Conscious sedation
techniques
Introduction
Nitrous oxide
The use of conscious sedation has risen dramatically in
recent years. There are many circumstances responsible
for this change including reduced general anaesthetic
numbers as a result of its potential morbidity (see Ch. 10),
regulation by the General Dental Council and increased
patient education and expectations. The General Dental
Council's definition of conscious sedation is:
At room temperature, nitrous oxide is a colourless gas
with, arguably, a sweet smell. It is contained in blue
cylinders as a mixture of gas and liquid.
Nitrous oxide is a weak anaesthetic with a minimum
alveolar concentration (MAC) of 110% (see Ch. 10).
This represents the concentration of gas required to
anaesthetise 50% of subjects and is clearly impossible
unless the gas is given in a hyperbaric atmosphere.
Nitrous oxide has a blood gas solubility of 0.47, which
makes it highly soluble in blood. This allows rapid onset
of sedation and equally rapid recovery.
A technique in which the use of a drug or drugs
produces a state of depression of the central
nervous system enabling treatment to be carried
out, but during which communication can be
maintained and the modification of the patient's
state of mind is such that the patient will
respond throughout the period of sedation.
Techniques should carry a margin of safety wide
enough to render unintended loss of consciousness unlikely.
This definition gives some flexibility regarding drugs
used and specific procedures chosen yet it emphasises
the guiding principle of sedation: the patient is, by
definition, conscious. Sedation as described here is an
inherently safe method of anxiety control.
Sedative agents
Several currently available drugs are useful in sedation.
In practice, however, conscious sedation usually involves
the use of inhalational nitrous oxide or the newer
anxiolytics, the benzodiazepines.
Benzodiazepines
Benzodiazepines were discovered by accident in the
1950s in Switzerland by researchers at HoffmanLaRoche. They were first marketed in 1960 with the
introduction of Librium. Benzodiazepines have a number
of clinical effects: anxiolysis, sedation, amnesia, muscle
relaxation and eventually anaesthesia. They produce this
action by two main routes.
• First, and principally, benzodiazepines act in the
central nervous system (CNS) via the gamma-amino
butyric acid (GABA) network. GABA is an inhibitory
neurotransmitter found in the brain and spinal cord.
Benzodiazepines act by attaching to specific receptors
close to the GABA receptors, prolonging the time the
GABA is attached and producing a sedative effect.
• Second, benzodiazepines can attach directly to
receptors for glycine (another inhibitory
neurotransmitter) in the brainstem and spinal cord,
producing anxiolysis and relaxation.
All benzodiazepines produce respiratory depression to
some degree by a combination of CNS depression and
81
thoracic muscle relaxation. They also produce mild
hypotension as a result of muscle relaxation decreasing
vascular resistance. As a result, the heart rate often rises
as the body compensates for the reduction in blood
pressure.
Assessment
Case selection is important when considering conscious
sedation. An assessment visit prior to sedation is
imperative. This visit is used to explain the procedure
fully, to assess the patient's level of anxiety and to select
an appropriate sedation method. It should be done in an
environment that is pleasant and unthreatening. The
assessment includes the history, examination and
treatment planning.
History
82
An assessment of the patient's anxiety levels and
discussion of specific phobias will inform the practitioner
about the patient's likely behaviour and cooperation
during the operative procedure.
A comprehensive medical history is required, with
specific enquiry regarding previous general anaesthetics
and sedation.
A number of drugs interact with particular intravenous
sedation agents and can prolong sedation considerably.
These include alcohol, opioids, antidepressants, other
benzodiazepines and recreation drugs.
All intravenous sedation agents cause some level of
respiratory depression and therefore patients with
chronic obstructive airways disease are at risk. Upper
respiratory tract infections are relative contraindications
to both inhalational and intravenous sedation and if the
treatment can be put off it should be to allow the patient
time to recover. Asthma is often worsened by stress and
anxiety and patients who can be treated without anxiety
often display better control of their asthma throughout
the procedure.
In general, patients in classes I and II of the American
Society of Anesthetists (ASA) physical status scale (see
Table 10.2) can be treated safely in the primary care
sector, but ASA class III patients require management in
a hospital environment.
Patients will require an escort to take them home if
they are having intravenous sedation and will not be able
to 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 and
employment circumstances.
At the assessment visit, it is important to record vital
signs as baseline readings prior to treatment; these should
include blood pressure and heart rate. Some practitioners
advocate taking the patient's weight, although the dose of
most intravenous sedation agents does not relate in any
reliable way to weight.
Treatment planning
Conscious sedation offers a spectrum of anxiety control
and the appropriate method for each patient can be
decided only after a full history and examination is
undertaken. Consent should be obtained from the patient
or the patient's guardian. This should be written,
witnessed and understandable.
Written instructions telling the patient what he or she
can and cannot do before and after the operation should
be given at this visit. These should include the following:
• You must be accompanied by a responsible adult
who must remain in the waiting room throughout
your appointment, escort you home afterwards and
arrange for you to be looked after for the following
12 hours.
• You must not eat or drink anything for 2 hours prior
to your appointment time; before this you should
have a light meal e.g. toast and tea.
• If you are taking any medicines these should be taken
at the usual times and should also be brought with you.
• You must not drive any vehicle, operate any
machinery or use any domestic appliance for
12 hours after sedation.
• You must not drink alcohol, return to work, make any
important decisions or sign any legal documents for
12 hours after sedation.
There should also be a discussion of the amnesia that
often occurs in intravenous sedation.
Table 11.1
Ideal properties of a sedative agent
Anxiolytic
Easy to administer
Cheap
No side effects
Quick onset and recovery
No respiratory depression
Sedation methodsh
The ideal properties of a sedative agent are listed in
Table 11.1. No single sedative agent possesses ideal
properties and each of the following methods has distinct
advantages and disadvantages.
Oral sedation
Oral sedation is the least specialised of the sedation
methods. It presents a relatively simple way of providing
mild preoperative sedation. It is often described as
premedication and can be used alone or in conjunction
with another sedation method. It is used principally to
alleviate fear and anxiety, allowing the patient to tolerate
either deeper sedation or further procedures. Oral sedation
is almost universally acceptable because it requires very
little patient cooperation.
The main disadvantage of oral sedation is the
considerable individual variation in response. This is
due to different absorption and metabolism of the drugs
by individual patients. Benzodiazepines are the most
commonly used drug for oral sedation. These are
considered below.
Diazepam
Diazepam has been the most commonly used oral
sedative for many years. The response to the drug varies;
a suitable adult regime may be 5 mg the night before
the treatment, 5 mg on waking and 5 mg 1 h before the
procedure. This will not produce profound sedation but
will allow the patient to approach the procedure with
more confidence and less anxiety. Diazepam does have a
relatively long half-life and therefore patients should not
drive or operate machinery for 24 h after the operation,
and there is even a risk of some remaining sedation after
2-3 days, due to the production of active metabolites.
Patients taking diazepam, or other benzodiazepines long
term, become tolerant to the drugs and therefore sedating
these individuals with further benzodiazepines is very
difficult.
can vary between 10 and 40 mg, according to the patient's
weight, age, medical history and level of anxiety.
Temazepam is a class 2 restricted drug.
Midazolam
Midazolam is the principal drug used in the UK for
intravenous sedation, however it can be used orally and
experimental results are very encouraging, particularly in
children and special needs patients. The drug, however, is
not licensed for oral use in the UK. It is used at an oral
dose of 0.5 mg/kg.
A number of other drugs besides the benzodiazapines
give varying degrees of sedation when given orally; however, most are unsuitable for general use. They include
opiates and antihistamines, which are used particularly in
children.
Inhalational sedation
The use of inhalational sedation has increased in recent
years as a result of the reduced number of general
anaesthetics and its usefulness when treating anxious
children. It is often said that inhalational sedation is 50%
drug and 50% behaviour management.
History
In 1884 the American Horace Wells attended a local fair
and received what was known at the time as 'laughing
gas'. He was intrigued by its effects and later had his third
molar removed with 100% nitrous oxide anaesthesia.
Later in the nineteenth century, this method was used by
the American anaesthetist and inventor Gardner Colton,
who gave over 121 000 100% nitrous oxide anaesthetics
and reported no deaths. The first anaesthetic machine for
nitrous oxide was introduced in 1887 but, by 1945, after
local anaesthetic was introduced into dentistry, general
anaesthesia was no longer necessary for dental extraction.
A mixture of nitrous oxide and oxygen was first taught
in the undergraduate curriculum in the United States in
the 1960s.
Temazepam
Temazepam has advantages over diazepam because of
its much shorter half-life of approximately 4 h. The dose
for a normal, healthy 70-kg patient should be 20 mg
approximately 30 min before the procedure. This dose
Clinical application
The clinical effects of sedation with nitrous oxide can
be described within the stages of anaesthesia first used
by Guedel (see Ch. 10). The first stage in Guedel's
83
classification is called analgesia, and this is split into
three planes, the first two of which can be obtained by
concentrations of 5-25% nitrous oxide and 25-55%
nitrous oxide, respectively, and represent the so-called
relative analgesia phases. It is in these planes that the
most useful sedation is found. Going beyond these planes
produces increased dissociation, which most patients
find unpleasant. There is, however, considerable variation
from patient to patient and therefore, the dose of the drug
is given incrementally.
Inhalational sedation has a number of indications. As
well as simple anxiolysis it is also useful in patients who
have a hyperactive gagging reflex because it can often
reduce this sufficiently to allow dental treatment that was
previously impossible to be carried out. It is also useful
in patients with physical and mental special needs,
although there does have to be some level of understanding and communication because it must be possible
to undertake the behaviour management required to
allow the agent to fulfil its potential. It is also useful
in patients with mild medical problems worsened by
anxiety, such as well-controlled asthma and epilepsy.
The relative contraindications to the use of inhalational
sedation include upper respiratory tract infections that
make nasal breathing difficult. The procedure should, if
possible, be postponed in these circumstances. Particularly
in children, it can be a problem when the tonsils and
adenoids are enlarged, again making nasal breathing
difficult. Difficulty communicating or understanding the
nasal breathing required makes inhalational sedation
very difficult in children, certainly under the age of three
and in patients with severe special needs.
Inhalational sedation has a number of distinct
advantages 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 of
intramuscular 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.
84
The principal disadvantage is pollution. The nitrous oxide
that is expired into the atmosphere and consequently
breathed 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 recommendations
based around the Health and Safety Executive's 1996
decision to set a maximum dose of nitrous oxide of
100 parts per million in a time-waited 8-h period. These
safety recommendations include active scavenging,
which removes the expired gas as opposed to passive
scavenging resulting from open windows and fans, the
use of closed circuits so that the expired gas is exhausted
away from the clinical environment rather than into the
room and the monitoring of pollution levels.
Procedure
The importance of behaviour management to the
technique cannot be overemphasised. Written consent
is mandatory, as is a second appropriate person as a
chaperone. The Quantiflex MDM machine is the standard
machine used in the UK and it allows a variable mixture
of nitrous oxide and oxygen to be given to the patient via
a nasal mask. The machine is marked in 10% increments
allowing a minimum of 30% oxygen. The manufacturers
report a 5% error in either direction and therefore the
absolute maximum is 75% nitrous oxide, which is rarely
necessary. This still provides more oxygen than in
standard room air.
Gas leaves the two active cylinders at the front of the
machine (there are two full reserve cylinders on the back
of the machine) and is mixed in the flow control head.
The facemask is introduced and the patient is allowed to
breathe 100% oxygen at approximately 5–6L/min for
2 or 3 min. The flow rate can be adjusted according to the
reservoir bag, which is on the machine. The flow rate
will vary according to the size of the patient and the
frequency of respiration. Nitrous oxide concentration is
then slowly increased in 10% increments, approximately
every 60 s, until the patient begins to report signs of
sedation. It is important at this stage to ensure nasal
breathing only, and the patient should be encouraged to
speak only when absolutely necessary.
It requires considerable skill on the part of the
operator to maintain a calm and pleasant environment. As
the dose increases, the patient will report sensory
changes including paraesthesia in the extremities,
tinnitus and a general feeling of warmth. This is a result
of peripheral vasodilation and can be seen in the flushing
of the facial features. As the sedation level increases,
patients often begin to report visual disturbance and a
feeling of remoteness or disassociation. This is the stage
at which maximum useful anxiolysis and analgesia has
been obtained; beyond this level patients begin to feel
light-headed and then restless and even nauseous. It is
important to stop before reaching this stage, particularly
in children because they will become uncooperative and
it will be very difficult to persuade them that bringing the
concentration down will make them feel better again.
With increased use of the technique, the operator
becomes very adept at assessing the level of sedation
from the sensory changes and from the reaction of the
patient. The procedure can then be carried out, including
the local anaesthetic, which will be significantly easier to
administer because of the analgesia obtained from the
nitrous oxide. It is possible to increase and decrease the
concentration according to the procedure that is taking
place, for instance it might be necessary to increase the
concentration for the local anaesthetic injection and
reduce it then for the procedure itself. At the end of the
procedure it is important to let the patient breathe 100%
oxygen for 2–3 min, to prevent the theoretical risk of
diffusion hypoxia as nitrous oxide moves in significant
quantities from the blood back into the alveoli and is
rebreathed, therefore diluting the oxygen available for
respiration producing hypoxia. In reality this is rarely a
problem. The patient should be recovered until they feel
fit enough to leave. Approximately 20 min after the
procedure adults can leave unescorted; children require
the same escort arrangements as they would after local
anaesthetic.
Intravenous sedation
Intravenous sedation is, at present, the best method for
conscious sedation and is the technique of choice for
most adult patients. It requires considerable training and
experience but rewards this with excellent operating
conditions in a calm and relaxed environment even when
dealing with severely phobic patients.
History
The first time intravenous drugs were used for sedation,
rather than full anaesthesia, was in 1945 when the
so-called 'Jorgensen technique' was introduced. This
consisted of the intravenous injection of a barbiturate, an
opioid and scopolamine. By most standards nowadays
this would be considered deep sedation at best and
dangerous at worst. In the 1960s, however, the discovery
of benzodiazepines revolutionised the practice of
intravenous sedation. Initially in dentistry, intravenous
conscious sedation was done using diazepam but this had
a number of disadvantages, most importantly its
elimination half-life of 43 h and the production of active
metabolites. Patients were therefore sedated to some
extent for up to 2 days and there was a risk of rebound
sedation. Diazepam is insoluble in water, which means it
has to be either given as a solute dissolved in propylene
glycol, which is painful on injection, or emulsified in
soya bean oil, which is the most common formulation.
The next generation benzodiazepine, midazolam
solves many of the problems presented by diazepam. It is
a water-soluble imadazobenzodiazepine. Usefully, it is
water-soluble at a pH of less than 4 and lipid-soluble at
physiological pH, making it painless on injection. It is
available in two preparations: 10 mg in 2 mL of fluid or
10 mg in 5 mL of fluid. The latter is used for intravenous
sedation because it is easier to control the incremental
dosage. It acts more rapidly than diazepam and has a
much more reliable patient response. It has an elimination
half-life of between 90 and 150 min – considerably
shorter than that of diazepam – and is metabolised in the
liver.
Clinical application
There are a number of indications for intravenous
sedation with midazolam. Psychosocial indications are
often the most common reason for a patient to present for
intravenous sedation. This group of patients includes
those with anxieties and phobias related to dentistry
including needles and drills. There is a specific group of
patients who have considerable difficulty with vasovagal
attacks prior to and during dentistry and intravenous
sedation can often help.
There are a number of medical indications for
intravenous sedation, particularly if the patient has a
condition that is aggravated by stress. This group
includes those with asthma, epilepsy, hypertension and
those with mild ischaemic heart disease. Intravenous
sedation can also be useful in those with mental and
physical special needs.
Other indications for intravenous sedation include
difficult, long or unpleasant procedures and patient
preference.
There are a number of relative contraindications to
intravenous sedation. Social contraindications include
those who are unwilling to consider this mode of treatment or are extremely uncooperative. It is not possible
85
to provide intravenous sedation for an unaccompanied
patient and it is also difficult with extremes of age. The
use of intravenous midazolam is controversial in children
under 16 years.
Medical contraindications include severe systemic
disease, particularly respiratory disease such as severe
chronic obstructive airways disease, and severe mental or
physical special needs. A number of drug interactions
contraindicate the use of intravenous benzodiazepines,
particularly if a patient has a history of psychiatric treatment or has been prescribed benzodiazepines over a long
period of time, thereby making the patient very tolerant
to the drug. Intravenous sedation should be avoided
wherever possible in patients who are either pregnant or
breast-feeding.
The topping-up of midazolam sedation is not
recommended except in very skilled hands and, therefore, any procedure lasting longer than an hour is really
unsuitable for this treatment method.
Procedure
86
An indwelling cannula is mandatory for all forms of
intravenous sedation. It is useful to provide topical
anaesthetic. This can be either Emla® or Ametop®, which
are readily available and allow the painless insertion of
intravenous cannulae.
As with inhalational sedation, it is essential that there
is a second competent person in the room at all times
during intravenous sedation. This person should be trained
in both monitoring the sedated patient and assisting in
the event of an emergency.
The patient should have blood pressure monitored and
a pulse oximeter attached (Fig. 11.1). Midazolam is given
routinely as a 2 mg bolus and then 1 mg increments every
60 s to a standard endpoint. Patients become gradually
more comfortable with their surroundings, their speech
begins to slow and slur, they respond to commands in a
sluggish fashion and - most importantly - they become
willing to accept treatment that they previously would
have found unacceptable.
Verrill's sign occurs when the upper eyelid covers the
upper half of the patient's pupil. This sign is not reliable
with intravenous midazolam and often indicates oversedation. Eve's sign occurs when the patient is asked to
touch his or her nose with the forefinger and is unable to
do so, invariably touching the upper lip instead. This is
a more reliable sign for the endpoint for midazolam
sedation.
Fig. 11.1
Pulse oximeter showing digital display and
finger probe.
It is important not to lose verbal communication
with the patient at any point and, although response to
commands will be slower than normal, this should still
be possible. The total dose required varies considerably
as a result of many factors, including anxiety, sleep
deprivation, alcohol consumption in the previous 24 h
and other drugs, both prescription and recreational. It is
difficult to be prescriptive about a maximum dose but
considerable thought should be given before increasing
the dose above 10 mg.
Intravenous midazolam gives approximately 45–60
min of useful sedation, during which most procedures
can be carried out. When the procedure is finished the
patient should be given time to recover, either in the same
room or in a designated recovery area, and should be
monitored continuously. The patient's escort can be
invited to sit with the patient during this period. The
patient can be discharged approximately 1 h after the last
increment of drug is given, but this varies from individual
to individual and requires assessment of each case. It is
important to remove the cannula before discharge.
Postoperative instructions should be given to the escort,
although they should already have been given to the
patient at the assessment visit. The escort should be
provided with a telephone number in case any problems
arise.
Monitoring
Patients who are sedated have a reduced perception of
their surroundings and of their own body. The staff
around them, therefore, assume responsibility for their
vital signs. Monitoring allows early intervention before
injury takes place and is used to minimise risk to
the patient. Clinical monitoring is most important and
requires observation of the colour of the patient and their
respiration. Electronic monitoring via a pulse oximeter is
mandatory for intravenous sedation.
In normal, healthy patients the oxygen saturation of
arterial blood will be between 96 and 100%. The oxygen
saturation alarm should be set at 90% to allow remedial
action to be taken prior to any injury. The oximeter also
provides a constant reading of the patient's heart rate (see
Ch. 10).
The principal side-effect of intravenous benzodiazepines is respiratory depression. If this occurs, as indicated
by a reducing oxygen saturation, the first step is to talk to
the patient and perhaps to shake him or her gently, asking
them to take deep breaths. This will usually wake the
patient from the light sleep he or she has drifted into and
allow them to take a number of deep breaths, thereby,
increasing the oxygen saturation to normal. A patient
who is unable to carry this action out unaided is oversedated and the operator must assist the process of
respiration by lifting the patient's chin upwards, thrusting
the jaw forwards and tilting the head backwards. This
allows the airway to be straightened and makes respiration
considerably easier. The next stage, if necessary, is to
give oxygen via a mask, or more commonly via a nasal
cannula. Oxygen should be given at approximately 2 to
3 L per minute via a nasal cannula or at 5 to 6 L per
minute via a mask. If these measures are unsuccessful,
the next step is reversal of the sedation agent.
Flumazenil is a benzodiazepine antagonist. It was
discovered in 1978 and, although some practitioners
have advocated its routine use, it should be used for
emergencies only. It belongs to the benzodiazepine group
of drugs but lacks the active benzene ring that makes
benzodiazepines sedatives. Because it has a higher affinity
for receptors than midazolam, flumazenil reverses the
action of midazolam without having any sedative action
of its own. It is available in vials of 500 µg in 5 ml
of fluid and the standard dose is 200 µg (2 ml) initially
then 100 µg increments every 60 s until recovery. It has a
shorter half-life (50 min) than midazolam and should
therefore be used with care because there is a theoretical
risk of resedation once the flumazenil wears off and the
midazolam reattaches to the receptors.
87
Section B
Specialist Surgical Principles
88
12
Fractures of the facial bones
Introduction
Fractures of the facial bones are common and present in
Accident and Emergency departments and to medical or
dental practitioners. Physical violence tends to be the
most common aetiology in the UK, followed by road
traffic accidents and falls; sports and industrial injuries
are relatively uncommon. Most assaults result in lowenergy injuries and are associated with excess alcohol
consumption, most frequently in young males. They can
be accompanied by soft tissue injuries. The majority are
caused by fists and boots, glass bottles and knives and, in
recent years, baseball bats. When associated with drug
addiction, gunshot wounds are an increasingly common
factor.
Most high-energy injuries are traffic related. Despite
the increased use of safety belts and drink driving
regulations, severe injuries are still regularly seen; highspeed accidents often result in fatal or very severe
injuries, although improved car design has lessened the
risks to the front-seat passenger and driver. Other less
common causes of isolated fractures are industrial and
sports injuries, which mostly affect the upper and mid
face. War injuries tend to be high velocity injuries caused
by a mixture of exploding bombs, shells and gunshots,
often leading to extensive damage to the soft tissues and
facial skeleton.
Falls commonly cause injury to the nose or the malar
complex, but less so the mandible. They tend to occur
under 10 years of age and in the elderly infirm patient
with brittle bones.
The general examination
The general examination of the patient should take
account of the presence of alcohol and drugs before
examination of the facial injuries. Inspection and
palpation of the various parts of the face will pick up
Table 12.1
Fractures of the facial bones
Mandibular
Middle third
lateral
zygomatic (malar)
central
nasal
nasoethmoidal
maxillary
obvious asymmetry, often masked when there is swelling
present. This examination should be gentle but organised
and precise.
The ears and eyes need to be fully examined and,
where an ophthalmic injury is suspected, early ophthalmic
consultation is advisable. At least 12% of all orbital
injuries are associated with severe ocular injury, which is
often unrecognised. The injuries should be recorded and
further information sought from accompanying persons
at the incident. Other life-threatening injuries must be
excluded. Although conventional radiography is helpful
in identifying fracture sites, obtaining good films
requires a cooperative patient, and where this is in doubt,
radiography should be postponed.
Fractures of the facial bones affect either the mandible
or the middle third of the face, or both (Table 12.1).
These will be discussed in turn.
Mandibular fractures
The mandible is essentially a bone with three joints, both
condyles and the dental occlusion, and it is important that
the condyles remain in their fossae and that the occlusion
is correctly maintained. Simple approximation of fractures with intermaxillary fixation can lead to respiratory
and masticatory difficulties and is being superseded by
89
open reduction and plating. The intraoperative use of
intermaxillary fixation to fix the occlusion is valuable
but, after plating mandibular fractures, this can usually
be released. Semirigid fixation with miniplates is widely
employed and although titanium is probably the metal of
choice, other alloys and stainless steel are also used. The
last is likely to require removal and they are an
occasional cause of metal allergy.
Clinical features
There is usually swelling and pain at the fracture site.
Where there is significant displacement, malocclusion
is likely with an inability to bring the teeth correctly
together. Loosening of teeth commonly occurs at the
fracture site, often accompanied by partial avulsion of
teeth and root fractures. Early recognition is essential as
delay 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 may
be retained. All fractures where the teeth are involved are
compound into the mouth and there is some risk of
infection.
There will usually be some asymmetry of the mandible
with unilateral fractures. With condylar neck fractures
there is likely to be shortening of the mandibular ramus
and an anterior open bite (Fig. 12.1). Where there is gross
displacement at a fracture site there is often another
fracture elsewhere (Table 12.2).
Whenever a fracture arises in the tooth bearing area,
such as in the mandibular body between the lingula and
mental foramen, disruption of the inferior dental nerve is
likely, and with wide separation of fragments the nerve
may be torn and require repair. The accurate repositioning,
stabilisation of fragments and reconstitution of the canal
Table 12.2
90
often results in some recovery of lower lip and chin
sensation. Pain and crepitus may be present at the
fracture site but should not be elicited, although there
should be a check for mobility. Trismus is common,
irrespective of the site of the fracture, as mouth opening
will increase discomfort. Similarly, dysphagia and lack
of control of saliva (which may be blood stained) may be
due to discomfort when approximating the teeth on
swallowing.
Bruising in the floor of the mouth is a pathognomonic
sign of a mandibular fracture in the edentulous patient.
Almost the only other way this can occur is with a penetrating injury. More rarely, the fractured or intact condyle,
with severe force applied to the chin area, may pass
backwards tearing the external auditory meatus. This tear
tends to occur through the anterior or inferior part of the
ear canal, often accompanied by leakage of clear synovial
fluid or bleeding. If there is a tear on the superior or
posterior wall or tympanic membrane it is highly likely
that there is a fracture of the petrous temporal bone
accompanied by hearing loss and a CSF leak.
Fig.12.1 Orthopantomogram showing fractures of the
mandibular condyles.
Possible clinical features of common mandibular fractures with displacement
Pain, swelling bruising
Sublingual haematoma
Trismus
Mental anaesthesia
Occlusal disharmony
'Step' palpable
Bleeding from ear
Condyle palpable in fossa
Intraoral bleeding
Compound
Angle
Subcondyle
At angle of jaw
Yes
Yes
Yes
If fracture through or adjacent to standing tooth
Yes: at lower border
No
Yes
Possible
Commonly
Preauricular
No
Yes
No
Premature contact on affected side
Difficult to palpate
Possible
No: if fracture and dislocation
No
Very rarely
Displacement of the mandibular fracture is very much
related to its site. Extensive fractures of the mandibular
ramus often remain undisplaced because they are
splinted by the masseter and pterygoid muscles.
Fractures in the angle region of the mandible, however,
are subject to pull from the elevators, pterygoid and
suprahyoid muscles and displacement may well occur,
especially when the fracture is bilateral leading to
posterior displacement of the distal segment and an
anterior open bite with loss of chin prominence. A careful
note needs to be taken of these in the semiconscious
or unconscious patient, because airway obstruction can
occur. If plating techniques are not available it is
important to identify the direction of the fracture in the
angle region. If, on the orthopantomogram (OPT), it runs
obliquely from the external angle to the third molar
tooth, the proximal fragment tends to displace superiorly.
If, on the posteroanterior view, the fracture runs obliquely
from the angle region forwards, the proximal fragment
will again tend to displace but in this case medially as a
result of pterygoid muscle action (Fig. 12.2). The doubly
unfavourable fracture will need stabilisation with a wire
at the lower border of the mandible or plate or it will tend
to torque apart when in intermaxillary fixation. These
considerations tend to disappear with good plating
techniques that encourage accurate fragment interdigitation to take place (e.g. with a strong upper border
plate placed along the external oblique ridge). Accurate
Fig. 12.2
stable repositioning avoids the necessity for postoperative
intermaxillary fixation.
Radiography
Imaging of the mandible is largely through plain
radiographs taken in two planes. The orthopantomogram
(OPT) is essentially a lateral view of the whole mandible,
which visualises clearly body and ramus fractures but
is less effective in the parasymphyseal region (Fig. 12.3).
Both condylar heads and necks must be included. A
posteroanterior (PA) view at right angles to this is
essential. A reverse Towne's view will often show
anteromedial displacement or dislocation of the condyle
when not seen on a standard PA view. Dental and
occlusal intraoral views are particularly valuable and
should be taken routinely for suspected dental injuries
and alveolar fractures in the tooth-bearing area. They
demonstrate the relationship of the teeth to the fractures
and their involvement in the fracture line. Lower occlusal
views are helpful in picking up sagittal fractures in the
anterior mandible.
Imaging of the mandibular condyle is sometimes
difficult in young children, especially those under five
years where there is comminution of the condylar head in
intracapsular fractures, and also where there is suspected
condylar displacement through the glenoid fossa. Here,
computerised tomography (CT) scanning is particularly
Unfavourable fractures at the angle of the mandible and the direction of displacement.
91
Fig. 12.3 Orthopantomogram showing a fracture at the
angle of the mandible.
helpful in identifying the nature of the injury and the
extent of comminution present. This is important in the
young child where there is always a risk of disturbance
of growth and possibly ankylosis. If the patient is unconscious or has sustained injuries such as severe neck or
skull fractures or other spinal injuries then CT scanning
is essential. Good views of the temporomandibular joints
should be obtained and are best seen on coronal views.
Treatment
92
Preliminary treatment includes maintenance of the airway
by clearance of foreign bodies from the area. Local
bleeding needs to be stopped by suturing or pressure.
Temporary support at the fracture site is given when there
is any delay in treatment using a wire around adjacent
teeth at the fracture site to hold the fragments together or
by supporting the jaws in occlusion with a head bandage.
In the unconscious patient the passage of a suture through
the tongue to hold this forward with any symphyseal
bone fragments may also be necessary. All compound
fractures require early antibiotic therapy.
The general principles of fracture treatment are
reduction, fixation, immobilisation, prevention of
infection, and restoration of function. These need to be
considered in the management of mandibular fractures.
Manual reduction of the fracture by repositioning the
fragments can be carried out under either local or general
anaesthesia. For late-presenting fractures the application
of arch bars to the teeth both upper and lower will allow
elastic traction to be applied bringing the fragments into
occlusion.
Fixation, in the dentate patient, can be by a variety of
attachments made to the teeth. These include arch bars or
eyelet wiring around individual teeth, cast silver cap
Fig. 12.4
Radiograph showing bilateral fractures of the
mandible fixed with titanium plates.
splints and when teeth are missing the use of modified
dentures or Gunning splints.
With the establishment of rigid fixation as the method
of choice for stabilising facial fractures the principle of
intermaxillary fixation for a significant period after
reduction of the fractures has become less important.
Whereas in the past fractures were fixed with intermaxillary fixation and interosseous wiring, or various
combinations of special wiring techniques, nowadays
the majority of fractures are fixed with titanium or
occasionally steel alloy plates (Fig. 12.4). Various forms
of miniplates are available; usually a 2 mm thickness
plate, with appropriate screws, is required. Most fractures
can be fixed with a single plate provided at least two
monocortical screws are placed on each side of the
fracture. In certain areas of the mandible additional
fixation is required, principally in the symphyseal region
where two plates are advantageous in preventing torquing
of the bone fragments at the lower border. Bone plates
are normally inserted through an intraoral approach.
Where there is gross comminution of bone or there are
missing bone fragments then the use of a heavier, thicker
reconstruction plate should be considered. These heavy
plates are more difficult to mould to the bone and are
usually inserted through a skin incision just below the
lower border of the mandible. Additional corticocancellous
iliac crest bone graft is needed when there is bone loss.
The angle region is a common fracture site and here a
single plate along the external oblique ridge is normally
adequate. Teeth in the fracture line can be left if they are
undisplaced and intact. If the blood supply at the apex
has been destroyed, if infection is present or if the
fracture is treated late, consideration should be given to
early extraction. Teeth not requiring to be retained, such
as an impacted third molar, can be removed at the same
time unless this tends to disrupt the fracture line when
they should be temporarily retained (see Ch. 27).
The condylar segment in severe trauma may displace
posteriorly, leading to rupture of the external auditory
meatus; only occasionally is it fractured in this situation.
Certain fractures require special treatment: the
grossly infected fracture and the fracture where there is
significant bone loss can be stabilised by the insertion of
pins into the major fragments joined together with a bar
holding the fragments as far as possible in their correct
position. Following this, the infection will usually settle
and any bone loss can be replaced with iliac crest bone
graft.
For the atrophic mandible, especially in the elderly
where perhaps the main body of the mandible is less than
6-8 mm in height, primary bone grafting of the fractured
mandible with split ribs is often the best solution. The
ribs are split lengthwise and shaped to the mandible on
the lingual and buccal sides and held in place with at
least two circumferential wires on each side of the
fracture line. Additional small screws can be helpful for
stabilisation.
The condylar neck is commonly fractured and is
difficult to treat. Low condylar neck fractures, especially
bilateral and displaced or dislocated tend to develop an
anterior open bite. Open reduction and fixation with one
or two miniplates is often the treatment of choice. For
simple single condylar neck fractures, the use of arch
bars and light elastic traction may be all that is required
but, when accompanied by fractures elsewhere (e.g. in
the parasymphyseal region, body or angle), or by midface fractures, it is safer to reduce and fix the condyle.
Fractures in young children should be managed conservatively under the age of 12. No condylar fracture
requires operative treatment as they will all remodel and
reform. Comminuted condylar fractures in the young
child are usually intracapsular and can lead to ankylosis;
they require early but gentle mobilisation and generally
should not be explored. Minor degrees of irregularity in
the occlusion may be acceptable because remodelling
occurs and malocclusions tend to resolve. Simple splinting
devices for pain relief may be required.
Certain general principles need to be mentioned, such
as the provision of adequate analgesia. The semifluid diet
given should be high in protein and calories. Good oral
hygiene should be maintained using chlorhexidine and
saline mouthwashes and a toothbrush.
Good healing requires stabilisation for an adequate
length of time. Indirect reduction of fractures with inter-
maxillary fixation alone, although successful, often takes
6 weeks to unite. For most fractures, callus provides an
osteoid mass of tissue around the fracture site giving it
some stability. Conventional miniplates allow for excellent
repositioning of the fractures provided they are correctly
adapted to the surface of the mandible and they provide
the necessary immobilisation across the fracture.
Care needs to be taken to avoid the insertion of
miniplate screws into the inferior dental canal or the
roots of the teeth. With accurate reduction of the fracture,
any sensation lost due to separation of the fracture
usually recovers, but this may be incomplete when there
has been extensive damage to the inferior dental nerve or
considerable delay in treating the fracture.
Complications
Complications associated with mandibular fractures are
not uncommon and, although they can be related to the
fixation used (e.g. plates), are often due to infection or
exposure of the plate into the mouth. It does not
necessarily follow that a plate has to be removed
immediately if there is infection, only if infection persists
and there is a lack of bony union will this be necessary.
Minor infections do not necessarily prevent union when
there is adequate drainage and the fractures are well
fixed. Delayed union may result from infection arising
from the teeth, bone or a breakdown of the soft tissues. It
might also be caused by a poor reduction of the fracture,
interposition of soft tissue into the fracture line and
mobility of fragments. These problems run a high risk of
delayed or non-union. Complicating local pathology such
as a cyst or tumour may be present but even then most
fractures unite. Malunion is the result of poor reduction
of fragments, rarely seen with modern open techniques.
It can occur with late-treated or untreated fractures.
Osteotomy of that malunion may be required to achieve
a normal occlusion and symmetry of the mandible.
There is some argument about the retention of teeth in
the fracture line. If very loose or displaced, they may
well be lost at the time of injury, shortly afterwards or
later if there is extensive exposure of the root surface. A
very mobile tooth in the fracture line is likely to be nonvital and is best removed to prevent delayed union even
though there is plate fixation at the fracture site.
In fractures around the condyle, angle region and
ramus there may be late onset trismus after much trauma
to both muscle and bone or comminution in that area.
More rarely, ankylosis will result, or bony hyperplasia of
93
either the coronoid or condylar processes, typically in
young children. Early mobilisation of fractures in young
children is essential as union occurs quickly, often within
3–4 weeks. It is essential to keep the condyle moving with
comminuted condylar head fractures and haemarthroses.
Condylar remodelling occurhs over a period of months
and symmetry usually returns in childhood fractures.
Persistent mental anaesthesia can occur as a result
of damage to the inferior dental or mental nerves or
occasionally at the site of the lingula. Severe damage or
section of the nerve in the body of the mandible may
require nerve repair and consideration should be given
to this. Anatomical reduction of the fracture must be
obtained so that the inferior dental canal is maintained.
Middle third fractures
The middle third of the face consists of nasoethmoidal
complex, the maxillae and smaller bones attached to it
together with the malar complexes. It lies between the
mandible and the cranial cavity and calvarium, in
particular the frontal and sphenoid bones. Fractures,
when of some severity, are likely to involve the cranial
cavity especially following high-velocity or high-energy
injuries associated with road traffic trauma or gunshot
wounds. Cranial involvement should be excluded at an
early stage as this may require neurosurgical intervention
or a combined approach.
Classically, middle third fractures are divided into
central and lateral middle third fractures, the lateral
middle third being essentially the malar or zygomaticomaxillary complex. Central middle third fractures
include nasal, nasoethmoidal and maxillary fractures.
The original descriptions of Le Fort in 1901 divided
maxillary fractures into the Le Fort I fracture, which is
a subzygomatic fracture separating the dentoalveolar
complex from the nasal and antral cavities passing
through the pterygoid plates (Fig. 12.5).
The Le Fort II fracture is a pyramidal fracture, again
subzygomatic, which may involve the cranial cavity in
the 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 ligaments
often associated with blowout fractures of the orbits. The
Le Fort II fracture passes across the bridge of the nose,
not always at the frontonasal junction but through the
nasoethmoid and lacrimal bones, then usually between
the nasolacrimal duct and infraorbital nerves and around
the zygomatic buttress to the pterygoid plate area, where
there may also be fractures (Fig. 12.5). The nasal septum
will be separated.
The Le Fort III fracture is a craniofacial dysjunction
separating the whole of the midface structures from the
cranial bones. This extends from the frontozygomatic
sutures across the sphenoid bone into the inferior orbital
fissure and through the ethmoid, lacrimal bones, nasal
septum and frontonasal junction and then across to the
other side often with some comminution. The zygomatic
arches will be fractured and there will be separation or
fractures of the pterygoid plates (Fig. 12.5).
Displacement of all midface fractures tends to be
downwards and backwards, thus creating an anterior
open bite appearance, with lengthening of the midface as
the solid structure of the basisphenoid prevents upward
displacement.
Zygomatic (malar) bone fracture
The malar complex or zygomatic bone constitutes the
lateral middle third of the face and it is commonly
fractured in isolation. Fractures occur close to the suture
lines often with comminution of the anterolateral wall of
the maxilla and sometimes at the zygomatic arch or
infraorbital margin. The masseter muscle exerts some
pull on the malar and there is a tendency for it to displace
if not adequately fixed.
Clinical features
These include swelling, circumorbital ecchymosis and
sometimes surgical emphysema, as a result of blowing
the nose often after an epistaxis (Table 12.3). Infection
may spread from the nasal cavity into the sinus and soft
tissues. Unilateral epistaxis commonly occurs except in
zygomatic arch fractures.
Subconjunctival haemorrhages are common and tend
to be in the inferior and lateral aspect in malar fractures.
Diplopia is not uncommon. In the initial phase it
may be due to swelling or bleeding around the inferior
extra ocular muscles causing restriction of upward gaze.
Table 12.3
Possible clinical features of
zygomatic (malar) fracture
Swelling: periorbital and over prominence of cheek
Haematoma
periorbital (black eye)
in buccal sulcus
subconjunctival
epistaxis (via blood in air sinus)
Anaesthesia
infraorbital + anterior and middle superior
dental
zygomaticofacial, zygomaticotemporal - these are rare
Eye problems
loss of acuity/blindness (rarely)
diplopia
enophthalmos
drop in interpupillary line level
exophthalmos (proptosios) – rare after injury but
possible on reduction
Trismus: obstruction of coronoid process
Step palpable: possible at: frontozygomatic suture,
infraorbital margin, zygomatic arch
Occasionally, the inferior rectus or inferior oblique
muscles are damaged by bone fragments and, more
rarely, their nerve supply is damaged. True trapping of
the muscle can sometimes occur between bone fragments.
Much more commonly there is displacement of the orbital
contents with prolapse of orbital fat into the antrum. This
is known as a blowout fracture. Within the orbital fat
there are fine fibrous tissue bands attached to the muscle
sheaths which catch on bone fragments and restrict
normal eye movements. Where there is a very large
defect, gross displacement of the orbital contents can
occur into the antral cavity. This may be accompanied by
a medial wall blowout, which must be identified and
treated.
Whenever there is a floor blowout enophthalmos
(retraction of the eyeball within the orbital cavity) is
likely to be present usually with a drop in pupillary level.
This must be identified because it might not be
immediately evident because of intraorbital bleeding and
oedema. It is crucial that the bony orbit is fully restored
and the walls rendered intact, otherwise enophthalmos
will persist.
Occasionally, the malar is grossly displaced medially
with severe proptosis of the eye, which can need early
release, there being a risk of damage to the cornea from
exposure 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 ophthalmic
opinion, is mandatory when eye injury itself is suspected.
Rarely, with severe lateral middle third injuries there
is crushing of the superior orbital fissure resulting in a
superior orbital fissure syndrome with ophthalmoplegia,
a dilated pupil, ptosis, supraorbital anaesthesia and
proptosis; when there is associated blindness from
damage to the optic nerve or optic foramen this is called
the orbital apex syndrome. Vision is rarely recoverable
when the optic nerve is damaged but pressure can be
relieved where there is gross proptosis by drainage of any
retrobulbar haemorrhage reducing the risk of visual loss.
A strict protocol should be adopted for the management
of orbital injuries, with frequent reassessment of the at
risk patient. In most cases the superior orbital fissure
syndrome recovers spontaneously. Structures in the
narrowest upper part of the fissure recover most slowly,
the abducent and the lower branch of the oculomotor
nerve recover more quickly; surgical intervention is not
normally required.
Asymmetry from displacement of the malar complex
may not be apparent immediately because of the
swelling. An examination of the patient from above and
below, palpating the cheek prominences and orbital
margins, will usually show any flattening or asymmetry.
If there is any doubt about this, waiting up to 10 days will
clarify the position and any aesthetic need for treatment.
Separation of the frontozygomatic suture can lead to
inferior displacement of the malar complex and globe but
an intact periosteum will prevent this. Infraorbital margin
displacement is usually posterior and inferior or a
combination of both, when the arch is displaced. The
pupillary and canthal position should be noted and the
zygomatic arch checked for any step deformity.
Infraorbital anaesthesia is common with malar fractures, because the fracture line passes close to or through
the infraorbital foramen or canal. The anterior superior
dental nerve branch may also be damaged, causing
numbness of the incisor and canine teeth. If the nerve is
crushed or severely damaged, full recovery is unlikely. In
severe injuries damage to the zygomaticofrontal and
zygomaticotemporal nerves will result in numbness over
the cheek prominence and temporal region. Accurate
reduction of the malar assists recovery of infraorbital
sensation.
Trismus is common with malar fractures often due to
the impingement of the malar complex on the coronoid
process 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 the
fracture site is frequently seen.
Radiography
Imaging of the malar has become contentious in recent
years. The 10° and 30° occipitomental views show displacement of the malar complex and the submentovertex
view, the zygomatic arch and malar prominence (Fig.
12.6). Other views have been abandoned as a result of CT
scanning. It also provides clear information on soft tissue
changes in suspected blowout fractures. For simple
displaced fractures of the malar with no obvious orbital
floor damage, a single 15° occipitomental radiograph is
acceptable. MRI scanning has a small place in the
diagnosis of blowout fractures. B scan ultrasonography
can be used for detecting the medial wall blowout when
CT scanning or MRI are not available.
Treatment
If there is gross swelling it is usually worth waiting up to
10 days for it to reduce for a better assessment of the
orbit, its contents and its position. If, however, there are
compelling reasons for early treatment then often the
earlier the treatment the simpler the fixation can be.
In the UK, the Gillies temporal approach is widely
used for reduction. A Rowe's or Bristow elevator is
passed under the temporal fascia from a hairline incision
and is used to lift the malar forward and slightly laterally.
Occasionally, the malar remains stable but more
commonly additional fixation is required.
Fig. 12.6 30° occipitomental view showing displacement
of the malar complex (fracture lines arrowed).
It is possible - under local anaesthesia - to elevate a
simple malar fracture with a hook through a small cheek
incision, lifting it anterolaterally into a stable position.
However, for most unstable fractures additional fixation
is required. Usually, fixation with one or two miniplates
for low-energy injuries at the zygomatic buttress or
frontozygomatic suture where there is separation, is
required. At the infraorbital margin a microplate provides
the most aesthetic fixation.
Following malar repositioning, the orbital floor needs
to be checked and any significant defect needs to be
repaired. Calvarial bone graft is best for large defects but
for small defects silicone sheeting with dacron mesh has
been widely used. It works well, but there is a complication rate and around 12% are eventually lost or require
removal; a medial wall defect can be similarly repaired.
Microplate fixation is used for simple orbital rim fractures. For comminuted complex fractures, fixation at the
frontozygomatic suture and – intraorally - the buttress,
are the minimum requirements. Additional plates may be
required at the infraorbital margin, across a main body
fracture and along the zygomatic arch (Fig. 12.7).
Nasal and nasoethmoidal fractures
Nasal bone fractures are the most common facial bone
fracture caused by direct violence. They may be laterally
displaced or anteriorly depressed. Many are simple
requiring minimal treatment but where there is bony
displacement then reduction is required with straightening of the septum.
Clinical features
The clinical features depend on the extent of violence
and displacement of the nasoethmoid and adjacent
structures. Typically, there will be bilateral periorbital
haematomata, oedema and nasal obstruction with a
tendency to mouth breathe accompanied by epistaxis.
Nasal obstruction can be caused by septal displacement,
which needs to be identified. Lateral displacement is
common and may be associated with damage or separation of the cartilages and fractures of the nasal bridge.
With more severe trauma, the nose becomes saddle
shaped, shortened and broadened. With upwards force
there may be telescoping of the nasoethmoidal complex
into the frontal sinus and then intracranially through the
cribriform plate. There is likely to be telecanthus and
separation of the medial canthal attachments. Damage to
the nasolacrimal apparatus can occur and penetrating
injuries can tear the nasolacrimal duct. Obstruction of the
canaliculae and duct stenosis at the lacrimal sac can lead
later to drainage problems. Damage to the cribriform
plate area may result in persistent cerebrospinal fluid
(CSF) rhinorrhoea. This needs to be recognised early and
managed appropriately. It is sometimes difficult to
ascertain whether the clear discharge from the nose is
CSF or mucus. Once bleeding has stopped it is possible
to identify this by testing the fluid for glucose or
transferrin, which will not be present in mucus. Other
tests, such as radioisotope studies, can be used to identify
difficult and intermittent CSF leaks.
Radiographs
Fig. 12.7 Radiograph showing a reduced malar fracture
fixed using microplate (A) and miniplate (B).
Radiographs of the nasal bones or nasoethmoidal
complex are usually unsatisfactory, with around 50% of
the fractures not adequately shown. Marked
displacements can be seen on 10° and 30° occipitomental
views where there is displacement of the septum, but this
is usually clinically obvious. Nasal bone fractures can
often be seen on a soft tissue lateral view. The detail of a
nasoethmoidal injury can only be ascertained from good
CT scans. MRI can also be helpful where there is a CSF
leak, as this is likely to show rather better than on CT
scans. Medial wall blowout fractures, comminution of
the nasoethmoidal complex and involvement of the
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frontal sinus will be well demonstrated on CT scans
taken in the coronal and axial planes.
Treatment
Simple nasal bone fractures can be repositioned with
Walsham's forceps. In addition, the nasal septum needs
to be straightened with Asche's forceps and the lower
portion of the septum relocated in its groove on the nasal
floor. Where there is doubt about the support for the nasal
bones and the septal position, gentle packing with
Vaseline® gauze is usually all that is required. The use of
an external splint is controversial; some feel it helps to
hold the complex in place, others use Steri-strips® to
support and maintain the position.
In the past, when there has been a degree of
telecanthus present, various forms of external fixation
using transnasal wires with lead plates or acrylic buttons
have been used to bring the canthal attachments into
position. This has sometimes proved successful but it
depends on the size of the bone fragments. In most cases
where there is significant telecanthus, exploration and
open reduction is necessary. Any damage to the
nasolacrimal system needs to be repaired before closure
of the soft tissues. Additional support of the soft tissues
in the medial canthal area is valuable. A nasal plaster
may be applied and sometimes a small nasal pack. Early
treatment 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 lowlevel fracture; Le Fort II and III fractures frequently can
involve the cranial cavity. Some symptoms of each
fracture are common but others are individual. It is not
unusual to see combinations of Le Fort fractures, with
perhaps a Le Fort I or Le Fort II on one side and a Le Fort
III on the other, depending on the force applied to the
midface. There may be a midline split of the palate,
which, if wide, will require repair.
Clinical features
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Bilateral periorbital ecchymosis and oedema are typically
seen with Le Fort II and III fractures, and sometimes
with Le Fort I fractures. Subconjunctival haemorrhages
are usually seen with Le Fort II and III fractures but
where there is good drainage of blood into the antrum
they may be absent; they are limited by the corneal
attachment and extend into the fornix and tend to be
segmental rather than complete. There is a flattened dish
face appearance to the face and often an increase in the
midface height with extensively mobile fractures.
The midface may be foreshortened and impacted upwards and posteriorly with an accompanying telecanthus
but in general there is an anterior open bite with gagging
of the bite posteriorly and trismus. A check should be
made for a split of the palate by gently springing the
molar teeth apart on their palatal surface. Sometimes this
split is obvious but there may be just bruising in the midline. A check on the mobility of the teeth and fragments
should be undertaken.
In the Le Fort II fracture, typically, there is dense
bilateral infraorbital anaesthesia. A mild degree of
anaesthesia may be present in the Le Fort I and also in
the 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 fractures
and diplopia and restriction of eye movements may be
evident. There may be marked proptosis of the eyes due
to intraorbital bleeding and oedema. The eyes must be
examined carefully to exclude any serious globe damage;
the incidence of which varies in different case series
but around 20% is a likely figure, with around 10%
permanent visual loss. In craniofacial injuries there may
be visual field changes. Retinal detachments and other
intraocular injuries must be excluded to avoid their
deterioration during mobilisation of the midface or
intraorbital surgical intervention. Usually, if 7-10 days
are allowed to elapse it becomes safe to operate on the
orbit. Careful examination of the lids and surface of the
eye will identify lacerations and other injuries; an early
ophthalmic assessment is advisable.
CSF rhinorrhoea and bleeding from the nose are
commonplace in Le Fort II and III fractures. Patients
should be questioned for any discharge or a salty taste at
the back of the throat. They should be sat up and leant
forwards, placing a filter paper strip under the external
nares. If after 15 min there is no staining then it is unlikely
that leakage is present. The CSF leak usually stops after
fixation of the midface. In the absence of any intracranial
injury, early reduction of the facial bone fractures is
advised. A persistent CSF leak beyond 10 days after jaw
fixation is an indication for dural repair. Neurosurgical
views are mixed on the repair of dural leaks: some insist
on repair of all, others feel that only persistent leaks
beyond 10 days need repair. Small defects will be plugged
by brain tissue and fibrosis and the defect seals off in the
cribriform plate area, however CSF leaks elsewhere may
persist, especially in the frontal sinus area.
Where there is insignificant displacement of the
midface then the dental occlusion can be maintained. A
check on the mobility of the midface by supporting the
head and feeling with a finger in the palate will indicate
any movement there. Tapping of the teeth of a fractured
maxilla will give a hollow percussion note. With significant displacements and an anterior open bite usually the
midface is easily repositioned but in late fractures there
may be a degree of impaction and mobility may be
difficult to ascertain.
With major midface injuries the rest of the craniofacial skeleton should be examined fully to exclude
mandibular condylar and skull fractures. Intracranial
involvement in major Le Fort II and III fractures often
gives rise to anosmia. Early anosmia may be due to
oedematous thick nasal mucosa, which settles over a few
weeks. Disruption of the olfactory nerves can lead to
permanent anosmia.
Radiography
Imaging in the midface has radically changed in recent
years with the availability of excellent CT imaging,
however certain basic radiographs may be taken in
Accident 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 is
taken with the patient horizontal, any intracranial air will
become obvious. Posterior maxillary displacement will
be seen, as will damage to the pterygoid plates. In major
injuries, mandibular and skull imaging should be undertaken with appropriate intraoral views. Neck injuries
must be excluded and the cervical spine should be appropriately imaged. Coronal and axial CT scans are taken
for nasoethmoidal injuries. MRI has only a limited place
in midface injuries. However some blowout fractures are
rather better seen on MRI and for all forms of brain
injury this form of imaging is superior. To avoid repeat
scans, patients with cranial injuries should if possible
have their midface imaged at the same time.
Treatment
Emergency treatment of severe injuries is primarily that
of 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). Careful
examination will ascertain the reason for this. Relief of
pain is not usually a major issue with midface injuries.
Narcotics should be avoided as they can confuse neurological examinations and interfere with the conscious
level.
It is usual to give antibiotic prophylaxis for potential
craniofacial communications, aerocoeles and CSF leaks,
although recent guidelines suggest this is unnecessary
(see Ch. 19). In the past, penicillin and sulphonamides
were given; more recently, cephalosporins have replaced
them. If antibiotics are given they should cross the
blood-brain barrier, but in the presence of injury this
presents no problem. Extensively compound dirty fractures
may require additional antistaphylococcal antibiotics.
Reduction and fixation of fractures is normally carried
out under general anaesthesia. Care should be taken to
ensure an intact airway in the pre-, peri- and postoperative
periods.
High-energy injuries should be differentiated from
low-energy injuries. The latter usually have a simpler
fracture pattern with less displacement and often minor
soft tissue injuries. The essence of reconstruction is to
ensure that the facial projection is correct, that the facial
width is not increased and that the facial height is
correctly maintained.
With low-energy injuries, relatively simple forms of
fixation for Le Fort I and Le Fort II fractures are often
effective. When there is minimal displacement, sandwiching techniques can be used with external pins into
the supraorbital ridge, attached by bars to the dentition of
the maxilla or mandible with intermaxillary fixation.
Additional malar complex fractures can be individually
explored and fixed after the central midface.
A greater degree of surgical intervention is required
for high-energy midface injuries. In recent years the
concepts of treatment and protocols have radically
changed. Vertical strutting may be identified in the
anatomy of the midface with three principal buttresses
on each side – nasomaxillary, zygomaticomaxillary and
pterygomaxillary (at the junction of the maxillary
tuberosities and pterygoid plates) - extending up to the
skull base. Comminution in those areas is uncommon
and it is usually possible to plate those sites.
Access to the upper midface is obtained through the
coronal scalp flap and to the inferior orbit through a
lower eyelid or transconjunctival incision. The subciliary
approach tends to yield more complications than a midlower lid incision made through a skin crease. The
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transconjunctival approach is also widely used, with a
crow's foot extension at the lateral canthus. This gives
good access to the inferior orbit but is limited for the
medial and lateral orbit the latter being better approached
bicoronally. A buccal vestibular incision is used to give
good access to the buttress areas. Reconstitution of the
zygomatic arch requires a bicoronal incision, taken well
down and extended around the tragus or in a preauricular
skin crease.
The general principles for management are to expose
all fracture sites or at least have good access to them and
to apply fixation with miniplates. Where there are small
fragments (e.g. at the infraorbital margin), the use of
microplates is advantageous. Where there are sizeable
missing fragments, primary bone grafting with calvarial
bone graft is the best solution. All bone fragments should
be preserved and used. Projection of the midface is
obtained by reconstruction and fixation of the zygomatic
arches, frontozygomatic sutures and by nasoethmoid
reconstruction to complete the orbit. The maxillary
dentoalveolar segment is realigned at an occlusal level
and plated at the malar buttress. The junction of the
greater wing of sphenoid and malar complex intraorbitally needs no fixation but should be checked for any
malpositioning. The dental occlusion, intact mandibular
dental arch and rest of mandible are critical for accurate
three-dimensional fixation of the middle third.
The principles are to obtain first projection of the
face, 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 rendered
intact. Facial width is corrected by plating the zygomatic
arches and frontozygomatic sutures and by reconstruction
of the nasoethmoidal complex and infraorbital margin.
Finally the height of the face is settled with buttress
plating.
There is always some conflict over management of
the soft tissues. If they are completely stripped off the
bone they tend to sag, not only as a result of their own
weight but because of oedema and haematoma present. It
may be possible to leave portions attached to large bony
fragments. This should be done if it is without detriment
to repositioning bone fragments, otherwise reattachment
of the soft tissue by suturing periosteum at various sites
is essential to avoid displacement of, for example, the
malar fat pads. Finally, orbital wall defects especially in
the floor and medial wall are repaired and when necessary
the superior and lateral walls. After medial canthai reconstruction the lateral canthi are checked and if necessary
stabilised with light wires to the supraorbital ridges.
Incision lines should be closed in layers with appropriate
attention to suturing the galea prior to skin closure with
clips or sutures. Large scalp areas should have suction
drainage for at least 24 h. Small facial incisions are
closed in layers with subcuticular or small interrupted
sutures. The intraoral vestibular incision is sutured with a
resorbable material.
Blowout fractures
Certain classic signs present notably diplopia, a lowering
of pupillary level and enophthalmos, which are pathognomonic of this injury. There is often accompanying
infraorbital anaesthesia. The diagnosis is confirmed by
CT scanning. Treatment is based on persistence of
diplopia and enophthalmos greater than 3 mm or a marked
loss of orbital contents out of the orbit. Surgery should
ideally be done within 10 days to achieve a good result.
Access for the pure blowout with no significant orbital
rim fracture is best through a transconjunctival approach.
If there are other fractures, a lower lid blepharoplasty
incision is effective but in the elderly an infraorbital skin
crease incision is safer. For reconstruction, cranial bone
or cartilage grafts or an alloplastic material such as a
silicone rubber with dacron mesh are widely used.
Craniofacial fractures
Serious craniofacial injuries require early recognition
and joint management with a neurosurgeon. The head
injury takes precedence in the management of the patient
and with a deteriorating conscious level early evacuation
of a blood clot can be lifesaving. Facial injuries and their
investigation take second place. Major high-energy
injuries should be treated relatively early, preferably
7–10 days from time of injury to obtain a good result. CT
scanning and an ophthalmic assessment of cranio-orbital
injuries will be needed.
With injuries of this severity, cervical spine injuries
and their management must be considered. Fractures of
the odontoid peg may be seen in association with craniofacial injuries. When presenting to the maxillofacial
surgeon, regular checks on eye opening, best verbal
response and best motor response (Glasgow Coma Scale)
are necessary; any deterioration requires neurosurgical
assessment. A careful visual check on acuity, eye movements and visual fields is needed. Sensory changes need
to be identified and the cranial nerves should be fully
tested. The external auditory meati should be inspected for
any sign of a petrous temporal fracture, noting any CSF
otorrhoea or haemotympanum. CSF rhinorrhoea needs to
be identified. Isolated cranial nerve injuries (e.g. to the
abducent nerve) are not uncommon. Fractures passing
through the frontal sinus area may involve the trochlea and
lead to a superior oblique paresis (Brown's syndrome).
Gross periorbital swelling can make the assessment of
telecanthus or traumatic hypertelorism difficult and CT
scanning is essential to distinguish these.
Whenever there is displacement of the cranial components in craniofacial injuries a combined neurosurgical
approach is required, and frequently when a CSF leak
persists (see Ch. 19).
Complications
Cranial
The most common cranial complication is a persistent
CSF leak. Failure to recognise this can lead to late onset
meningitis. This should be searched for pre- and postoperatively.
Frontal aerocoeles are not uncommon and arise as a
result of air being forced into the extradural or subdural
spaces at the time of injury, often when there are airway
difficulties. They can usually be managed expectantly
provided the airway is well maintained with oral
endotracheal intubation or a tracheostomy. Intracerebral
aerocoeles are an acute emergency and require immediate neurosurgical intervention.
Occasionally, there is infection postsurgically, with
loss of the frontal bone flap necessitating late aesthetic
reconstruction with a titanium plate.
Postconcussional headaches are common following
craniofacial injuries and may be persistent. Post-traumatic
epilepsy from local brain injury or surgical repair requires
anticonvulsant therapy.
Ophthalmic
Blindness can occur with severe pressure on the optic
nerve or from its avulsion in major trauma. Fundal
examination is essential, to detect this and injuries such
as retinal detachments, choroidal tears and lens dislocations. Persistent diplopia can result from damage to
muscles or persistent trapping and failure to reposition
prolapsed orbital contents. Enophthalmos persists following loss of orbital contents or an increase in orbital size
following poor surgery.
Proptosis is much less common; it can be due to an
inward repositioning of one of the orbital walls. Corneal
exposure is a risk when there is marked proptosis. It can
occur following operative treatment of orbital injuries.
The eye should be lubricated with chloramphenicol drops
and ointment.
Nasolacrimal
Nasolacrimal damage occurs with severe midface
injuries, often from penetrating objects or gross comminution. Early assessment after the injury is worthwhile
and immediate reconstruction of the ducts and sac should
be carried out if at all possible. The nasolacrimal duct
and sac is kept patent with a drainage tube. Initial
epiphora occurs but usually settles with adequate
drainage. Poor drainage will lead to infection and
dacryocystitis and recurrent infections will require
treatment and dacryocystorhinostomy. Careful evaluation
with appropriate imaging can be helpful in identifying
the site of the obstruction.
Neurological
Neurological deficit is not uncommon with midface
injuries. In the orbit, damage can occur to the optic nerve.
Total or partial loss of sight is not so uncommon (around
10-12%). Persistent ophthalmoplegia occurs most often
in relation to the abducent nerve with a lateral rectus
palsy, less commonly from oculomotor or trochlear nerve
damage. There may be sensory loss from supraorbital,
supratrochlear or infraorbital nerve damage. Most
commonly there is numbness of the upper lip, cheek
and side of nose. Damage to the zygomaticofrontal and
zygomaticotemporal nerves may lead to persistent pain
in their distribution but this is uncommon.
Nasal
Oroantral and oronasal fistulae occasionally occur and
these are easily treated by appropriate flap closure.
Persistent antral infection when there is an obstruction to
the orifice in the lateral nasal wall may necessitate some
form of antrostomy, but modern endoscopic surgery is
often effective.
Dental
Malocclusions may result from failure to reduce the
maxillae they usually present with an anterior open bite
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or retropositioned maxilla. Only osteotomy can
satisfactorily correct this (e.g. a Le Fort I osteotomy).
Occasionally, there is trismus and ankylosis from fusion
of malar to the coronoid process. This requires operative
intervention with separation of the fragments, best
carried out via a bicoronal and intraoral approach.
Late deformity
Severe craniofacial injuries in children can lead to a lack
of development of the midface, especially the frontonasal
area with a resulting saddle nose. Reconstruction with a
cantilever bone graft may be helpful but it is difficult
to achieve adequate nasal lengthening. There may be a
pseudohyperteloric appearance with canthal drifting.
Late correction is difficult but if there is adequate nasal
projection a slight increase in width of the nasal bridge
may be acceptable. Much scarring around the medial
canthus makes later surgery difficult. A failure to reduce
the midface at the Le Fort II and III levels will result in
major dishing of the face. At the Le Fort III level there is
an increased breadth of the face and vertical shortening
only correctable with a major osteotomy. Hollowing in the
temporal regions, usually following repeated bicoronal
flaps being taken down, can be corrected by inserting an
alloplastic material in the temporal fossa. Irregularities of
the frontal bone and supraorbital ridges can be corrected
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by onlaying cold-curing acrylic. A major displacement of
a segment requires osteotomy surgery with or without
bone grafting; minor degrees of deformity require
onlaying or masking procedures using cranial bone graft
or alloplastic materials. High quality early corrective
surgery almost always produces a better result.
Current developments
The development of resorbable bone plates may well
result in their replacing metal plates. This would avoid the
doubtful necessity for metal plate removal, considered
essential in some countries. Polylactide and other similar
materials are being used for this purpose.
Where there has been non-union the use of substances
such as bone morphogenic protein with its insertion at
that site might well prove valuable and where there has
been extensive bone loss again it may be possible to use
bone morphogenic protein at the site of interpositional
fibrous tissue or muscle.
There is also the possibility of using distraction osteogenesis in the mandible to create missing bone following
gun shot wounds. These techniques are now available
and should be considered for more complex fracture
situations.
13
13Orthognathic surgery
Introduction
Orthognathic surgery is widely carried out for the
correction of dentofacial deformities. Until the early
1970s there were relatively few techniques available for
this correction but since that time great advances have
been made, with regard to assessment, preparation for
surgery (which is often accompanied by orthodontic
treatment) and surgical technique.
A proper assessment of the patient must be carried out
in the first instance. The reason for the request for
elective surgery needs to be ascertained. In most cases
there is a concern about appearance. However, other
factors, such as mastication, speech, temporomandibular
joint symptoms and occasionally other features (e.g.
ocular problems) in relation to craniofacial deformity
may need to be considered. Proper patient selection is
mandatory for a successful outcome.
Preoperative assessment
As part of the preparation for Orthognathic surgery, the
patient must undergo assessment and treatment planning
(Table 13.1).
Assessment
Psychological
A psychological and social assessment is required for
patients with unreal expectations and dysmorphophobia.
The patient's personality may be affected by the facial
deformity and they sometimes present in an aggressive
way, or they may be withdrawn. However, the majority
are able to give a clear indication of their concerns.
Patients with significant deformity may be improved by
relatively simple surgery that allows them to be accepted
Table 13.1 Preoperative assessment, treatment
planning and preparation in Orthognathic surgery
Assessment
psychological
aesthetic
orthodontic
clinical
radiographic
Treatment planning
cephalometric
dental casts
photographic
Preparation
photocephalometric
orthodontic
splint construction
in society. The type of job that the patient has, and his or
her home background and social position may have an
effect on the type and extent of surgery; the expectations
from surgery for those in the public eye, who often
demand a perfect dentition and occlusion, is often greater
than for others, for whom the simple correction of major
jaw deformity and a minor discrepancy in the occlusion
will be acceptable.
It is important to have an assessment of the family
situation during the planning process and time should
be taken for identifying and prioritising a problem list,
discussing the issues not only with the patient but also
the 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 acceptable profile, they do not necessarily make one.
103
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 upper
incisors in association with gross mandibular retrusion.
The latter needs to be corrected and the former does not
need to be changed.
Orthodontic
It is essential to have a good orthodontic assessment and
preparation prior to surgery to obtain a sound interlocking postoperative occlusion. To prevent relapse, presurgical orthodontic treatment is, in most cases, required
and a refusal to participate in this needs to be taken very
seriously when deciding upon surgery. It is important to
recognise that orthodontic treatment alone can rarely
correct a significant discrepancy in jaw size. Pressures to
correct discrepancy in jaw size early in childhood need to
be resisted. Although severe retrusion of the mandible
and maxilla may be an indication for this, when extreme
protrusion is corrected early in adolescence, growth is
likely to continue and further surgery will be required at
the end of the growth period.
In the next decade it is likely that many severe
deficiencies in jaw size will be corrected by distraction
techniques, with osteotomy surgery being largely reserved
for the end of the growth period (see p. 102).
Clinical
The first step in treatment planning must be the correct
diagnosis of the deformities present and the associated
dental problems. Measurements of the face need to be
taken from both full face and profile views followed by
an oral examination and assessment of nasal and temporomandibular joint function. This will need to be evaluated
radiographically, photographically and with dental casts.
Additional investigations such as computerised tomography (CT) scanning, full speech assessment and in some
cases a full ophthalmic and neurological assessment will
be needed where changes to the jaws also involve the
upper midface.
Radiographic
104
There are two basic aspects of appropriate imaging
for orthognathic surgery. Conventional radiographs are
required for the diagnosis of pathology and to show
detail of the jaws and teeth. These will include panoramic
radiographs, intra-oral views, occipitomental views to
exclude infection in the midface and views of the
temporomandibular joints where there is a likelihood of
changes occurring there. Radiographs are also required
which are used essentially for planning purposes. These
include the lateral and posteroanterior (PA) cephalogram
and sometimes the submentovertex view to show
asymmetry.
The lateral and PA cephalograms need to be taken in
a standard position with the head in the natural position
and the Frankfort plane horizontal. The soft tissues need
to be imaged and it is therefore necessary to use appropriate intensifying screens for the lateral cephalogram.
Treatment planning
The basis of planning for the correction of jaw deformity
is through cephalometry. The skeletal, soft tissue and
dentoalveolar relationships are taken into consideration
in the three dimensions of anteroposterior, vertical and
transverse, and various analyses can be used for the
identification of the discrepancy in jaw size.
Cephalometric
To assess the projection of the maxilla and the mandible
in the anteroposterior dimension, SNA, SNB and Pogonion
points and angles are measured on a cephalogram. The
vertical dimension is assessed, not only in relation to the
maxilla but also the mandible. The occlusal plane and the
upper and lower incisal angulations and the relationship
of the lips and soft tissues to the dentition and to the jaw
bones are measured.
Dental casts
A clinical study of the patient's occlusion is helpful but a
proper analysis of the dental occlusion can only be
obtained by assessment of the study casts and these
should normally be placed on an anatomical articulator.
Photographic
Although it is customary to take photographs for record
purposes, a lateral profile photograph may also be
produced life size on an acetate sheet and superimposed
on the cephalogram. If they are matched carefully to the
soft tissues on the cephalogram, 'surgery' can be carried
out on the photograph. This form of photocephalometric
planning has provided a reliable way of demonstrating to
the patient the changes that can occur following surgery
and predictions using this method are helpful when
making a decision as to precisely what changes should be
made and whether these are acceptable to the patient. It
is essential that the photographs are taken in the natural
head position and that there is no posturing. Colour
transparencies of the head and neck, both lateral profile
positions, full face and with close-ups of the dental
occlusion and in a smiling position are desirable. Various
tracing methods are used for the photocephalometric
planning and the exact method chosen and the
cephalometric points used will depend on the orthodontist
and surgeon.
Preoperative preparation
Photocephalometric
In the process of photocephalometric planning the
osteotomies are carried out on the lateral profile as they
would be at the time of surgery. That is, the lines drawn
should be as for the osteotomy cuts. For bimaxillary
surgery, especially when height changes are involved, it
is usual to move the maxilla first so that the upper
anterior teeth are placed in their optimal position. The
mandible can then be rotated appropriately to achieve a
satisfactory interincisal relationship. The posterior part
of the maxilla can then be adjusted to complete the
occlusion.
It is essential to remember that the soft tissues do
not move the same amount as the hard tissues. When the
maxilla is advanced using a Le Fort I osteotomy the
upper lip is likely to move forwards only half of that
distance and the tip of the nose by one third. For Le Fort
II osteotomies, this changes to two-thirds movement, and
for the middle third at the Le Fort III level the movement
is approximately 1:1, whereas an advancement genioplasty
will move the soft tissues approximately 85-90% of the
bony advancement. Vertical changes of the chin as they
affect the soft tissues are close to 1:1. These changes are
estimated and recorded photocephalometrically.
Orthodontic
Orthodontic treatment can take 18 months or more to
obtain the optimal position for surgery. It is generally
better to complete orthodontic treatment prior to surgery;
only minor realignment should be left until after surgery
as any need to open the occlusion postoperatively may
lead to a degree of relapse.
Splint construction
Following completion of photocephalometric planning,
the precise movements need to be transferred to the
appropriately articulated casts so that a good occlusion is
obtained. The precise jaw movements need to be defined
when an ideal occlusion has been found.
Once the casts are set up on an articulator, and
following the measurements from photocephalometric
planning, each jaw movement is carried out. From this
optimal position, thin acrylic occlusal splints can be
made to record each movement. Each splint needs to be
checked individually in the mouth with the upper teeth
and lower teeth after any occlusal equilibration has been
carried out. They should be made within 1-2 days of
surgery because minor changes in the occlusion in the
postorthodontic period are not uncommon. The positional
changes of the casts are transferred to the jaws at the time
of surgery and appropriate markings made on the upper
and lower portions of the maxilla.
Mandibular surgery
Mandibular surgery can be divided into several sections:
1. surgery in which the jaw is moved in an anteroposterior direction by an osteotomy either in the
ramus or body of the mandible
2. surgery to the dentoalveolar area, such as segmental
surgery to shift teeth and alveolus but maintaining the
integrity of the lower part of the mandible
3. surgery to the chin, moving it in a superior, inferior,
posterior or anterior direction sometimes accompanied
by levelling and reshaping.
The best operation should be chosen for the patient by a
surgeon proficient in all forms of jaw surgery.
Mandibular prognathism
Mandibular prognathism is probably the most common
deformity that requires surgical treatment. It may be
corrected in several ways.
Vertical subsigmoid
The vertical subsigmoid osteotomy, (vertical ramus
osteotomy) is currently done through an intraoral
approach sectioning the ramus from sigmoid notch to
mandibular lower border. The coronoid processes may
105
Fig. 13.1 Vertical subsigmoid osteotomy. The ramus is
sectioned from the sigmoid notch to the lower border of the
mandible and the fragments are overlapped.
Fig. 13.2 Diagram showing body osteotomy of the
mandible with the segment of bone to be removed along
with the first premolar (hatched).
Fig. 13.3
Diagram showing a sagittal split osteotomy.
be removed (e.g. in the premolar region; Fig. 13.2). This
is often helpful in correcting vertical changes in the
mandible and can produce a very good occlusion. Surgery
tends to be carried out in front of the mental nerve, if at
all possible, by removing the first premolar and adjacent
bone, although it is acceptable to take the inferior dental
and mental nerves out of the canal and foramen and
reposition them if this produces a better occlusion. This
allows both height changes and some tipping of the
distal segment. It does, however, require careful planning
and some expertise. Fixation will be with bone plates
accompanied by light intermaxillary fixation with elastics
in the first instance.
Mandibular retrusion
also be sectioned (Fig. 13.1). This is followed by overlapping the proximal fragment and shaping it to lie flat
against the posteriorly repositioned ramus and mandibular
body in its optimal position. Usually this particular
operation is stabilised by keeping the teeth in occlusion
with intermaxillary fixation for at least 4-6 weeks.
If intermaxillary fixation has to be avoided then it is
possible to use the sagittal split osteotomy (see below),
taking the distal fragment posteriorly with removal of
bone followed by screw or plate fixation.
Body osteotomy
106
It is also possible to carry out a body osteotomy when
there is spacing in the lower jaw or a single tooth can
Sagittal split osteotomy
Mandibular retrusion is most commonly corrected with
an Obwegeser sagittal split osteotomy. The Obwegeser
dal Pont osteotomy splits the ramus and angle region of
the mandible sagittally and then slides the segments apart
maintaining the integrity of the inferior dental bundle
(Fig. 13.3). Fixation is usually by means of three screws
or a plate sometimes accompanied in the early stage by
light intermaxillary fixation. The sagittal split osteotomy
has been modified to produce better contact with less risk
of fragmentation and an improved blood supply reducing
the risk of aseptic necrosis at the angle of the mandible.
Most surgeons now fix the mandible with semirigid
fixation. This reduces the relapse rate, ensures bone
contact and a correctly aligned occlusion.
Fig. 13.4
Inverted L osteotomy (hatched area bone
grafted).
Inverted L osteotomy
The inverted L osteotomy is used for lengthening the
ramus of the mandible and is particularly helpful in
syndrome and congenital deformity patients (Fig. 13.4).
This can be done either through an intraoral or extraoral
approach but if a considerable amount of bone graft is
required then it is usually easier to do this through an
extraoral submandibular approach. Rigid fixation with
plates can be used to stabilise the segments.
Fig. 13.5
Segmental osteotomy. The first premolar and a
wedge of bone have been removed (red arrow) to allow the
segment to be repositioned back (black arrow).
usually with wires or alternatively screws and plates.
Vertical augmentation of the anterior mandible requires a
bone graft into the space created and care needs to be
taken to avoid retropositioning the chin point when this
procedure is carried out.
Segmental osteotomy
Maxillary surgery
Segmental procedures are largely carried out in the
anterior mandible. It is essential that the blood supply is
maintained through the genial muscles on the lingual
side and these must not be detached from the bone or
necrosis of the whole segment will occur. The approach
to the lower anterior segment is with a mucosal lip
incision (Fig. 13.5). If the segment has to be significantly
raised then some form of interpositional material such as
bone or hydroxyapatite may need to be placed in the
space accompanied by good plate fixation.
Maxillary osteotomies can be divided up into three
principal types. The first involves the dentoalveolar
component of the maxilla at a low level, the Le Fort I
osteotomy. This parallels the low level fracture of the
maxilla that occurs in association with trauma. The Le
Fort II and III osteotomies involved are at a higher level
and involve the nasoethmoidal complex and, for the Le
Fort III, the whole midface. Essentially, this becomes a
craniofacial dysjunction (see Ch. 12).
Le Fort I osteotomy
Chin deformities
The chin deformities of retrogenia and progenia are
corrected by advancing or retruding the lower border
segment of the mandible at the chin. Fixation is normally
by means of wires or screws or occasionally plates.
Changes in the chin for vertical reduction, require a piece
of mandible to be removed 5 mm below the level of the
teeth. Fixation is applied to the upper and lower segments
By far the commonest procedure carried out in the
midface is the Le Fort I osteotomy, which corrects
discrepancies in jaw size involving the lower half of the
maxilla and the dentoalveolar component. Thus the Le
Fort I osteotomy is used for advancement of the lower
midface and for inferior and superior repositioning. Any
form of setback of the maxilla involves removal of a
portion of the dentoalveolar segment because it is not
107
possible simply to set back the maxilla in its entirety
because it impinges on the pterygoid plates. It is often
difficult to obtain a satisfactory occlusion, usually due to
narrowness of the maxilla, especially in secondary cleft
deformities where there is scarring and collapse and in
this situation the maxilla should be expanded prior to
surgery. Small degrees of expansion can be carried out
orthodontically and in children rapid expansion is often
a way of separating the two halves of the maxilla through
the midline palatal suture. In the older age group
segmental surgery or alternatively surgical expansion of
the maxilla is required. Presurgical planning is essential
to detect any discrepancy in the arch size and any
problems with the occlusion following repositioning of
the maxilla.
Any verticomaxillary excess in the lower face height
can be corrected by raising the maxilla through removal
of a segment of bone on both sides, which includes the
lateral nasal walls and nasal septum. In the reverse situation where there is shortness of lower face height, this
can be corrected by an inferior repositioning Le Fort I
osteotomy, with bone grafting of the space created.
Superior repositioning tends to be a stable procedure,
whereas inferior repositioning has a reputation for some
degree of relapse and therefore appropriate compensations
might be needed. The tooth position must be related
accurately to the upper lip at rest. Any shortness of the
upper lip will not allow for major inferior repositioning
nd likewise raising the maxilla excessively with a short
upper lip can similarly give an ugly appearance.
Complications
Complications with this surgery include haemorrhage, a
failure to reposition the segments, damage to the teeth
(especially the roots) and loss or damage to the blood
supply of the segments; all of these are avoidable. The
patient needs to be warned of the potential risks of this
type of surgery. Residual oronasal or antral fistulae can
occur but these are uncommon. Fortunately, complete
necrosis of the segment occurs only rarely, usually when
the soft tissue flaps have been damaged extensively.
Hyperbaric oxygen therapy is sometimes helpful in this
situation.
Le Fort II osteotomy
108
The Le Fort II osteotomy has a unique place for patients
with central midface hypoplasia extending into the
nasoethmoidal area. It allows a certain amount of
lengthening of the midface, especially of the nose with a
complete advancement of the central midface.
Various modifications of the Le Fort II osteotomy
have been carried out in the past, simply advancing
the infraorbital margins, leaving the nose behind or
advancing the malars and infraorbital margin leaving the
nose behind (Kufner osteotomy). These have a small but
useful place in the armamentarium of osteotomies. With
rigid plate fixation intermaxillary fixation postoperatively
is not required.
Complications
The complications associated with Le Fort II osteotomy
are similar to those associated with a Le Fort I; occasional
orbital complications or damage to the infraorbital nerve
or nasolacrimal duct can occur, but this is unusual. There
is a slight tendency to vertical relapse anteriorly and this
is important when maxillary inferior repositioning is
being carried out and account needs to be taken of this
when planning. If onlaying of the maxilla especially over
the malar prominence is required then cranial outer plate
bone graft is best, fixing this to the anterior maxilla and
malar bones with small screws.
Le Fort III osteotomy
The subcranial Le Fort III osteotomy and its variants are
used primarily for correction of total midface hypoplasia,
usually of craniosynostotic origin, typically in the Apert
and Crouzon's syndromes. In this situation there is
usually significant proptosis of the eyes, severe malar and
maxillary hypoplasia and a class III malocclusion with a
short midface height. This can be accompanied by other
problems such as sleep apnoea, postnasal choanal atresia
and sometimes a cleft deformity. There is often a skull
deformity that may require correction either at the same
time or at a later date. It may be necessary to carry out
bimaxillary surgery in this situation, with the advancement of the midface as well as its vertical repositioning.
A Le Fort I osteotomy may be needed at the same time
for vertical repositioning and to achieve a good
occlusion.
Careful preoperative assessment is essential,
particularly with CT scanning to exclude any prolapse of
cranial contents into the naso-orbital areas. Preoperative
ophthalmic assessment is also important because changes
will occur within the orbits themselves and it is not
uncommon to see some diplopia following surgery, which
usually settles spontaneously but sometimes requires
extraocular muscle surgery. The approach to the upper
midface is through a coronal flap, which is extended
down into the preauricular areas on both sides, together
with an intraoral approach through vestibular incisions.
The latter allows for a Le Fort I osteotomy to be carried
out at the same time. Sometimes it is possible to do all the
surgery through these two incisions, but in other cases it
is preferable to use the transconjunctival approach to the
orbital floors, which allows accurate cutting and
repositioning in that area. Fixation with multiple
miniplates is required and orbital floor repair.
The Le Fort III osteotomy is occasionally used for
post-traumatic cases and rarely for secondary clefts. It
can also be used in Treacher-Collins syndrome and other
conditions. There is an increasing tendency to think that
this type of osteotomy surgery is becoming outmoded
and advancement through distraction may well be the
answer because this avoids the extensive bone grafting.
Complications
A number of complications can arise from this complex
surgery. Immediate complications associated with the
surgery are a cerebrospinal fluid leak if an inadvertent
communication with the cranial cavity has occurred.
Troublesome bleeding can occur probably from damage
to the maxillary vessels or from the pterygoid veins.
There can be airway problems and iatrogenic damage to
the endotracheal tube; rarely, blindness has been reported
and occasionally postoperative infections associated
with the bone grafting procedure. Later problems are
meningitis and postinfective epilepsy. In addition to
blindness, diplopia, residual exophthalmos or the
development of enophthalmos, ptosis of the lids or
corneal ulceration can complicate the orbital surgery.
There may be an inferior and lateral medial canthal drift.
Nasolacrimal damage has been reported, including
dacryocystitis and epiphora, the latter normally recovers
spontaneously. Nasal obstruction and paranasal sinus
infections rarely occur. There may be damage to the supra
and infraorbital nerves and rarely to the oculomotor
nerves and muscles, or facial nerve and occasionally
anosmia. Dental malocclusion with an anterior open bite
deformity is occasionally seen, as well as trismus.
Residual deformity can result from relapse or
asymmetric correction and temporal hollowing. Speech
is occasionally affected, with the development of
hypernasality.
Distraction osteogenesis
Distraction osteogenesis is now being widely practised as
an alternative approach to osteotomy surgery. Whereas
most mandibular and midface osteotomies are carried out
towards the end of the growth period, distraction therapy
is possible from infancy. An osteotomy is carried out,
gently mobilised and then gradually separated with a
distraction apparatus at a rate of 1 mm a day. This can be
carried out in the mandible for vertical repositioning, for
horizontal advancement and for transverse changes. It is
used in the maxilla, principally for advancement and
inferior repositioning and this can be at Le Fort I, II and
III levels. It avoids the necessity for bone grafting and
seems to be a stable process. There are a significant
number of reports on the various osteotomies and their
distraction but there have been no long-term comparisons
between conventional osteotomy surgery and distraction
osteogenesis.
109
14
Salivary gland surgery
Saliva is produced by the three pairs of major salivary
glands - the parotid, submandibular and sublingual glands
- as well as the many hundreds of small salivary glands
scattered throughout the buccal and pharyngeal mucosa.
The majority of surgical pathology affects the parotid or
submandibular gland, with the sublingual and minor
salivary glands being less frequently affected. Both the
anatomy and physiology of salivary gland function is
important in surgical pathology and these will be
discussed first.
Anatomy
Parotid gland
110
The parotid gland is the largest of the salivary glands. It
lies just in front of the ear extending from the zygomatic
arch downwards to between the angle of the mandible
and the mastoid process. This inferior portion is also
known as the tail of the parotid gland. The anterior border
corresponds approximately to the ascending ramus of the
mandible (Fig. 14.1). It is important to appreciate that
the tail of the parotid gland extends into the neck and
that lesions in this area can affect the parotid gland and
are sometimes mistaken for lymph nodes in the neck.
Swellings in this area should be assumed to be arising
from the parotid until proven otherwise (see below).
The facial nerve is intimately associated with the
parotid gland and runs through the gland, dividing it into
a 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 plane
exists between the superficial and the deep lobe. A
normal parotid gland consists of 80% superficial lobe
and 20% deep lobe. The facial nerve enters the parotid
Fig. 14.1
Anatomy of the parotid gland.
gland from the stylomastoid foramen and, shortly after
entry, divides into an upper and lower division. The
upper division gives off a temporal branch that supplies
the muscles of the forehead and eye, a zygomatic branch
that supplies the muscles of the eye, and occasionally a
buccal branch that supplies the muscles of the nostril and
upper lip. The lower division gives off a mandibular
branch that supplies the muscles of the lower lip and a
cervical branch that supplies platysma in the neck. The
lower division often also gives off the buccal branch.
(Fig. 14.2). The facial nerve controls the muscles of
facial expression.
The parotid gland is drained by the parotid duct,
which opens into the mouth opposite the second upper
molar tooth.
superficial and deep part, the superficial being the largest.
The superficial lobe lies superficial to the mylohyoid
muscle, whereas the deep lobe lies deep to the mylohyoid
muscle and is drained by a duct that drains forwards and
upwards to open close to the frenulum in the floor of the
mouth (Fig. 14.3). Three nerves are closely linked to the
submandibular gland - the marginal mandibular branch
of the facial nerve, the lingual nerve and the hypoglossal
nerve. As mentioned above, the marginal mandibular
nerve supplies the muscles of the lower lip and damage
to this nerve will leave the patient with deformity. The
lingual nerve supplies sensation to the anterior two-thirds
of the tongue whereas the hypoglossal nerve supplies
motor function to the tongue muscles.
Sublingual gland
Fig. 14.2
Branches of the facial nerve.
The sublingual gland is the smallest of the major glands
and lies beneath the mucosa of the floor of the mouth
near the midline. It drains into the mouth by small ducts,
as well as by ducts that open directly into the submandibular gland duct. It is closely associated with the
lingual nerve.
Submandibular gland
The submandibular gland lies in the submandibular
triangle bordered anteriorly by the digastric muscle,
posteriorly by the stylomandibular ligament and
superiorly by the mandible. This gland also has a
Fig. 14.3
Physiology
Between 1 and 1.5 L saliva are produced a day. In the
resting state, the submandibular gland produces most
Anatomy of the submandibular gland.
111
saliva but on stimulation most saliva is produced by the
parotid gland. The parotid gland produces a serous
secretion whereas the sublingual and submandibular
gland produce two-thirds mucous and one-third serous
secretion. Serous secretion contains amylase for digestion,
whereas the mucous secretion contains mucin for
lubricating purposes. Removing a major salivary gland
has a negligible clinical effect upon saliva production.
Investigation of salivary
gland disease
Radiological investigations
Plain radiography
Plain radiographs are usually only of use in diagnosing
the presence of stones in the submandibular gland as
the majority in this gland are radiopaque (Fig. 14.4).
Plain radiography is of little value if parotid duct stones
are thought to be present because the vast majority are
radiolucent; sialography is of more use.
Fig. 14.4
A lower occlusal radiograph showing a sialolith
in the submandibular duct.
Sialography
Sialography consists of injecting radio-opaque contrast
medium into the submandibular duct orifice or the
parotid duct orifice, depending upon which gland is
being investigated, and radiographs being taken. It is
useful in the diagnosis of radiolucent stones and duct
strictures. Sialography is of some value in sialadenitis
where a 'tree in leaf' or 'snowstorm' appearance is often
seen (Fig. 14.5). Sialography can also show tumours of
the parotid gland indirectly by showing duct displacement but computerised tomography (CT) and magnetic
resonance imaging (MRI) are much more useful for this.
It should be noted that sialography is contraindicated in
the presence of an acute infection as it may worsen the
condition.
Ultrasound
112
Ultrasound is a relatively quick and easy way of
identifying localised swellings of the salivary glands:
usually tumours but also abscesses. It has the advantage
of no radiation and can be easily combined with fineneedle aspiration cytology. Its disadvantage is that it is
not always easy to define deep lobe involvement of the
parotid gland and is also operator dependent.
Fig. 14.5
A parotid sialogram showing the 'snowstorm'
appearance of punctate sialectasis in a patient with
Sjogren's syndrome.
CT scanning
CT scanning is useful in defining tumours of the salivary
glands as it usually locates the tumour well and defines
extension outside the gland. It also shows lymph-
adenopathy in the neck, which is useful in assessing
malignant tumours as well as possible bone invasion
(Fig. 14.6). Its disadvantage is that it involves a substantial dose of radiation to the patient and it does not
always detect tumours in the deep lobe of the gland if
they have the same radiological density as the gland.
MRI scanning
MRI scanning is probably the best investigation of
salivary gland tumours as it gives excellent detail of size
and position and there is no radiation (Fig. 14.7). Its
disadvantages include availability, and some patients
can't tolerate it because of claustrophobia especially as it
takes a lot longer to perform than CT, and bony detail is
not as well seen.
Radioisotope scanning
At one time, radioisotope scans were used to help
differentiate different types of tumours in, especially, the
parotid gland. The procedure was unreliable and now
with the advent of fine-needle aspiration is no longer
performed to investigate salivary gland tumours, although
it is still occasionally used in assessing function of the
salivary glands.
Fig. 14.6 Computerised tomography (CT) scan of a
parotid Warthin's tumour.
Fine-needle aspiration
Fine-needle aspiration is a very valuable tool in the
diagnosis of salivary gland tumours. It is an easy
procedure and can be performed in the outpatient clinic.
With the aid of an experienced cytologist its yield is
good. However, it is sometimes not always possible to
differentiate one type of tumour from another. The
diagnostic success rate for malignant tumours is about
70% whereas for benign tumours it is about 90%. The
risk of tumour seeding following fine-needle aspiration
is more hypothetical than real and, if it does occur, is
exceedingly rare. Its use in non-neoplastic swellings is
less well defined as interpretation of these specimens
is difficult even for experienced cytologists.
Salivary gland biopsy
Open biopsy of a parotid swelling should be performed
only if it is certain that the lesion being biopsied is not
Fig. 14.7 Magnetic resonance imaging (MRI) scan of a
parotid pleomorphic adenoma.
a tumour, as biopsy of a tumour risks seeding it and
making subsequent management more difficult. It is
sometimes useful when the cause of a diffuse salivary
gland enlargement remains obscure, or if the diagnosis of
113
Table 14.1
Salivary gland swellings
Discrete
tumours
Diffuse
sialolithiasis
sialadenitis
sialadenosis
Sialolithiasis
Fig. 14.8 Incision for a biopsy of the parotid gland. The
biopsy incision should be placed in part of the standard
parotidectomy incision as shown above, depending on the
part of the gland to be biopsied.
lymphoma is suspected. Very occasionally, an open biopsy
is necessary to make the diagnosis of a tumour involving
a salivary gland. If this is the case, the specimen should
be sent for frozen section to confirm or deny the presence
of a tumour and, if tumour is confirmed, then the
definitive surgical procedure should be performed at the
time of the frozen section. The site of skin incision is
important when performing a biopsy of the parotid gland
and its correct position is shown in Fig. 14.8. It is also
very important to be aware of the position of the facial
nerve when performing a biopsy of the parotid gland so
as not to damage it. Biopsy of minor salivary glands is
discussed in Chapter 34.
Salivary gland swellings
114
Most surgical pathology of the salivary gland presents as
a swelling in the associated gland and it is helpful
clinically to characterise the swelling as one that affects
the whole of the gland or as a discrete swelling that
affects only part of the gland. Most discrete swellings are
caused by a tumour, whereas swellings affecting the
whole of the gland are usually caused by sialolithiasis,
sialadenitis or sialadenosis (Table 14.1). There is
obviously some overlap in this classification but it is
helpful in the clinical context.
Sialolithiasis, or salivary gland stone disease, is caused
by the presence of stones either within the gland itself or
in the duct that is draining the gland, symptoms being
more common when the stones are found in the ducts.
The presentation and diagnosis of these are considered in
detail in Chapter 34.
Stones in the anterior part of the submandibular duct
can be removed via the mouth by opening (and
marsupialising) the duct (see Ch. 34) but if the stone is
further back in the duct, or in the submandibular gland
itself, then it is safer to remove the gland externally by a
neck incision to avoid damage to the lingual nerve.
Recurrent parotid duct stones are rare and if they cannot
be removed through the mouth and are considered very
troublesome then they require a parotidectomy, but this is
very unusual. Dilatation of the parotid duct has been tried
for parotid duct stones, especially when they are
associated with a stricture in the parotid duct, and this is
worth trying as it is a lot less invasive and has lower
morbidity than a parotidectomy, but its effectiveness is
doubtful.
Sialadenosis
Sialadenosis is defined as a non-inflammatory salivary
gland disease due to metabolic and secretory disorders
of the gland parenchyma, accompanied by recurrent,
usually painless, bilateral swelling of the glands due to
acinar enlargement.
Sialadenosis has an equal incidence in the two sexes
and occurs most commonly in the fourth to seventh
decades. The disease is suspected when there is recurrent
enlargement of both pairs of the major salivary glands,
usually the parotids (Fig. 14.9). The gland enlargement
can persist from weeks to months. It is usually associated
with an underlying condition. Sialadenosis has three
major causes:
Table 14.2
Sialadenitis
Acute
bacterial
viral
Chronic
chronic recurrent parotitis
tuberculosis
radiation
Sjögren's
sarcoidosis
Sialadenitis
Sialadenitis is inflammation of the salivary glands, most
commonly the parotid, and can be categorised into acute
and chronic types (Table 14.2).
Acute Sialadenitis
Fig. 14.9 Sialosis occurring in a patient with a history of
alcohol abuse.
• Endocrine: gland enlargement has been described in
most endocrine diseases but it is particularly linked to
diabetes mellitis. It can also occur during pregnancy
and lactation where its cause is thought to be
endocrine in origin.
• Dystrophic/metabolic: this is most commonly seen in
chronic starvation and is thought to be linked to the
deficiency of proteins and vitamins. This is also the
reason it is sometimes seen in alcoholics.
• Neurogenic: dysfunction of the autonomic nervous
system can give rise to sialadenosis and this is most
commonly seen in people taking drugs that affect the
autonomic nervous system, such as some antihypertensive drugs, It may also be the reason it is seen in
patients who are anorexic but there is probably also a
nutritional element in this as well.
The diagnosis is made upon the history and clinical
appearance associated with an underlying cause. A parotid
biopsy is needed occasionally, and histology will then
show acinar enlargement.
The underlying disease is treated but it is very rare
that a parotidectomy will be needed for cosmetic reasons.
Even with treatment of the underlying disease, it is
common for the parotid enlargement to persist.
Acute sialadenitis may be bacterial or viral in nature.
Viral sialadenitis is self-limiting and only bacterial
sialadenitis will be considered here.
Bacterial infection usually presents with a sudden
sense of swelling of the affected gland and there may be
redness of the overlying skin. Pus is often seen exuding
from the salivary gland duct into the mouth and the
patient is unwell. Most acute bacterial infection is related
to a reduction in the flow of saliva and this is commonly
secondary to an underlying disease such as poorly
controlled diabetes mellitis or renal failure and occurs in
older patients. There is often an association with poor
oral hygiene. It used to be a common postoperative
finding but now, with the use of antibiotics and better
fluid management and postoperative oral toilet, it has
become an uncommon disease.
Treatment is usually with antibiotics and correction of
the underlying disease processes if present. Sialogogues
(e.g. citrus-flavoured sweets) are often given to encourage
the flow of saliva. If an abscess develops it may need
draining externally. Care must be taken not to damage the
facial nerve when the parotid gland is affected.
Chronic sialadenitis
Chronic sialadenitis has several causes (see Table 14.2)
and usually presents with persistent inflammation and
enlargement of the affected gland.
115
Chronic recurrent parotitis
This presents mainly as a unilateral or alternating
swelling of the parotid gland, which can be painful. It is
mainly a disease of children and the saliva can be very
milky or purulent. Attacks occur at variable intervals and
in between attacks the child is totally symptom free. The
underlying cause is not known but it is thought that duct
ectasia may be a predisposing factor.
Diagnosis is again made from the history and
sialography can be considered. Duct ectasia supports the
diagnosis when seen on sialography.
Treatment is symptomatic as the underlying cause is
not fully understood. It often involves antibiotics and
analgesia and sialogogues are often given. Most cases in
childhood disappear after puberty. If the attacks continue,
ligation of the parotid duct or a tympanic neuroectomy
can be recommended. It is very occasionally necessary to
perform a parotidectomy.
syndrome to surgical practice is that there is an increased
incidence of malignancy associated with this condition,
especially non-Hodgkin's lymphoma. If there is an associated parotid swelling with Sjögren's syndrome then
there is a 70-fold increase in the development of a nonHodgkin's lymphoma. In patients with no salivary gland
swelling this decreases to a 10-fold increase in incidence
of non-Hodgkin's lymphoma and these patients should
therefore be followed-up to watch for this.
There is no specific treatment for Sjögren's syndrome
apart from symptomatic treatment and treatment of the
underlying connective tissue disease present. A rapidly
enlarging salivary gland should be biopsied to rule-out a
lymphoma.
Sarcoidosis
Sarcoidosis can effect the salivary glands, especially the
parotid glands, causing them to enlarge. Treatment is
usually with corticosteroids.
Tuberculosis
Tuberculosis can present as a chronic sialadenitis,
affecting mainly the parotid or submandibular gland. Its
diagnosis may not be suspected if the patient is not
known to have tuberculosis and is often diagnosed by
biopsy when the cause of a unilateral parotid gland
enlargement remains obscure. Occasionally the disease
can cause a fistula to develop into the skin above the
parotid and this is strongly suggestive of tuberculosis.
Radiation sialadenitis
The salivary glands are very sensitive to the effects of
radiation and this is especially a common problem in
patients who have been irradiated for head and neck
cancer, as the major and minor salivary glands are often
included within the field. They present with a dry mouth
and the presence of thick tenacious saliva, which can be
very distressing. Unfortunately the symptoms tend not to
improve with time.
Treatment is symptomatic and although many types
of artificial saliva are available on the market, their
clinical effectiveness is not high.
Sjogren's syndrome
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A consideration of Sjögren's syndrome is beyond the
scope of this chapter. The significance of Sjögren's
Tumours of the major
salivary glands
Salivary gland tumours usually present as a discrete
swelling or nodule in the associated gland. Over 90% of
salivary gland tumours are epithelial in origin and most
salivary gland tumours are benign. A classification of
salivary gland tumours is given in Table 14.3. Eighty per
cent of tumours arise in the parotid gland, 10% in the
submandibular and 10% in the minor and sublingual
glands.
Most tumours present as a slow growing swelling in
the associated salivary gland and the patient may have
noticed it for some time. It is important, especially in the
parotid gland, not to confuse a swelling in the tail of the
parotid with a swelling in the lymph node. Indeed, in this
region it can be difficult to differentiate a salivary gland
tumour from a lymph node on clinical grounds alone.
This is where fine-needle aspiration and imaging are
useful. When a patient presents with a lump in the parotid
gland, it is important not only to examine the lump itself
but also to document the function of the facial nerve. The
oropharynx should also be examined, as in deep lobe
tumours of the parotid gland they can often be seen
projecting into the oropharynx and pushing the tonsil
inwards. It is also important to examine the neck for any
other associated lymphadenopathy.
Table 14.3
Salivary gland tumours
Benign
pleomorphic adenoma
monomorphic adenomas
Warthin's tumour (adenolymphoma)
duct adenoma
basal cell adenoma
oncocytoma
other adenomas
Malignant
intermediate
mucoepidermoid
acinic cell
carcinomas
adenoid cystic
carcinoma expleomorphic
adenocarcinoma
squamous cell
non-epithelial tumours
metastases
The majority of salivary gland tumours are benign but
malignancy should be suspected if there has been a rapid
growth in the lump associated with pain or if there is an
associated facial nerve paralysis, which is almost always
indicative of malignancy. Malignancy should also be
suspected if there is ulceration of the overlying skin or
there is associated lymphadenopathy present in the neck.
Investigation of the salivary gland lesion should
include fine-needle aspiration, which will help to differentiate a lymph node in the tail of the parotid from a true
salivary gland tumour. It will also be able to give an indication of the type of salivary tumour present, although it
is not 100% sensitive or specific, and indeed interpretation
of parotid tumours by fine-needle aspiration can be
difficult. CT scanning of a parotid swelling is also useful
because it will indicate if there is any deep lobe involvement of the parotid gland and also show if there is any
other associated lymphadenopathy in the neck. It may
also help to differentiate a lymph node from a true
parotid swelling.
Benign salivary gland tumours
Pleomorphic adenoma
The most common benign tumour is the pleomorphic
adenoma (Fig. 14.10). This is a benign tumour that is
most commonly seen in the parotid gland. Histological
examination shows that there are two elements, an
Fig. 14.10
Pleomorphic adenoma of the parotid gland.
epithelial element and a stromal element. There is an
incidence of malignant degeneration in pleomorphic
adenomas of the order of 3%. This is usually in those
tumours that are of longstanding and have been present
for over 20 years. Also, on histological grounds, the greater
the 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 the
superficial lobe of the parotid gland this requires a superficial parotidectomy. The operation consists of removing
the superficial lobe of the parotid gland (i.e. that part that
lies lateral to the facial nerve), but leaving the deep lobe
in situ. However, tumours that arise in the deep lobe
require removal by a subtotal or total parotidectomy. This
first involves performing a superficial parotidectomy and
then carefully mobilising the facial nerve, to allow the
deep lobe to be removed. The pleomorphic adenoma
should not be enucleated as there is an increased chance
of recurrence of the tumour with this. Although, macroscopically, the tumour appears to have a reasonably welldefined capsule, histological studies show that the capsule
is incomplete and there is often breach of the capsule by
117
tumour cells. The tumour should therefore be removed
with a margin of normal parotid tissue. This is sometimes
difficult if the tumour is itself lying against the facial
nerve. As the surgical practice of lumpectomy has greatly
reduced over recent years, the incidence of recurrence of
pleomorphic adenoma has also equally reduced.
Adenolymphoma or Warthin's tumour
(monomorphic adenoma)
This benign tumour often occurs in the tail of the parotid
gland. It has a male predominance and usually occurs
in the sixth and seventh decades. Ten per cent of these
tumours are bilateral and present characteristically as a
soft, fluctuant, mobile mass. The tumour is thought to
arise histologically from duct epithelium. Again, providing
the patient is fit and well, a superficial parotidectomy is
the treatment of choice but if it is absolutely sure the
tumour is an adenolymphoma (confirmed by fine-needle
aspiration) then a lumpectomy will suffice because
recurrence is unusual. Equally, malignant degeneration
does not occur. In elderly patients, in whom this tumour
is common, follow-up is wise to make sure there is no
sudden change in the parotid swelling (which may indicate
another pathology), rather then subject the patient to a
parotidectomy.
118
tumours because, depending on their histology, they can
behave in a relatively benign or aggressive fashion.
The treatment of malignant salivary gland tumours is
excision, if possible. Depending upon the size of the
tumour, its position and its histology, this may require
removal of the facial nerve and other surrounding
structures, including the ear and petrous part of the
temporal bone, and part of the mandible.
Postoperative radiotherapy may be necessary. Radiotherapy can be offered in tumours that are thought to be
inoperable, but this is usually in a palliative role only.
Acinic cell tumour
This tumour is more common in males and tends to
present as a well-localised lesion. Histologically, it is
thought to arise from the boundary zone between the
acinar and intercalated ducts. Overall, with resection,
about 20% may recur. Pathology is very important as
low-grade acinic cell tumours behave relatively benignly,
whereas high-grade acinic tumours behave in a malignant
fashion.
Treatment is excision and, in tumours that are histologically high-grade, postoperative radiotherapy is often
given. If neck nodes are present at presentation then a
neck dissection will also be included in the resection.
Prognosis is generally good, with a 5-year survival of
over 85%.
Malignant salivary gland tumours
Mucoepidermoid tumour
As indicated, malignant salivary gland tumours are
uncommon. Interestingly, of all tumours occurring in the
parotid gland, just 13% are malignant. The incidence
increases in the submandibular gland, where of all
tumours presenting, 32% are malignant. Malignancy is
much more common in the sublingual and minor salivary
glands, with the majority of salivary gland tumours being
malignant (56%). The vast majority of malignant salivary
gland tumours occur in adulthood and are very rare
before puberty. The most common malignant tumour
below puberty is the mucoepidermoid carcinoma. The
aetiology of malignant salivary gland tumours is not
known but malignant degeneration can occur in a
pleomorphic adenoma.
The six most common types of malignant salivary
glands tumour are acinic cell, mucoepidermoid, adenoid
cystic, adenocarcinoma, squamous cell and carcinoma
expleomorphic. The first two – acinic cell and
mucoepidermoid – are often known as intermediate
The mucoepidermoid tumour is again similar to the
acinic cell tumour in that it that it can be classified into
histologically low-grade and high-grade types; the lowgrade type is relatively benign whereas the high-grade
type is a truly malignant tumour. The tumour is thought
to arise from the ductal epithelium. Tumours with a high
mucous content tend to have a low malignant potential
whereas the highly cellular tumours tend to have a high
malignant potential. Treatment is similar to that of the
acinic cell tumour.
Prognosis is dependent on histological type, with
well-differentiated tumours having a 5-year survival of
over 90% but poorly differentiated tumours having a
5-year survival of only 20%.
Adenoid cystic tumour
Adenoid cystic tumours of the salivary gland are
interesting in that they often present with a long history
of a swelling of the affected salivary gland. They are
characterised histologically by perineural spread and are
often associated with pain. Seventy per cent of adenoid
cystic tumours actually arise from the minor salivary
glands. There are three histological types: one with a
tubular pattern, one with a cribriform pattern and one
with 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 adenoid
cystic tumours, they tend to be very slow growing and the
patient can live a long time with this disease. Indeed,
many patients have lung and liver metastasis but can live
for many years even with these present.
Treatment is by excision and postoperative radiotherapy is often given as this is thought to increase local
control of the disease. Whether the facial nerve should be
sacrificed, because of its propensity for perineural spread
in this disease, is controversial. Most surgeons would try
to save the nerve because of the propensity of this tumour
for distant metastases and also due to the difficulty in
obtaining local control despite apparent adequate local
excision. If neck nodes are present then a neck dissection
will also be required.
Prognosis is again dependent upon histological type
and also on length of follow-up. The tubular variety of
adenoid cystic has a 5-year survival of over 95%, with
the 10-year survival being only slightly less than this.
The cribriform and solid types have a 5-year survival of
65% but at 10-year follow-up this drops to 15%, thus
illustrating its propensity for late recurrence.
Adenocarcinoma of the salivary gland
This is a very aggressive tumour and has a poor
prognosis. It is important to exclude metastasis of adenocarcinoma from elsewhere to the parotid gland before
subscribing the tumour to the gland itself e.g. lung and
breast. Treatment is by surgical excision, often combined
with postoperative radiotherapy. Prognosis is poor, with
a 5-year survival of 40%.
Squamous carcinoma
Again, this is usually a disease of elderly males, often in
their eighties. It has a poor prognosis and it is important,
as in adenocarcinoma, to exclude metastasis to the
parotid gland often from the skin before subscribing it as
a primary tumour of this area.
Treatment is usually by surgical excision if possible
and, again, postoperative radiotherapy is usually given,
especially if the tumour is large, the resection was
incomplete or the margins were involved. Prognosis is
poor, with a 5-year survival of 35%.
Carcinoma expleomorphic
This tumour arises from a pre-existing pleomorphic
adenoma and presents as a sudden growth of a known
pleomorphic adenoma. It has a poor prognosis and it is
often associated with facial nerve palsy. Treatment is as
for squamous carcinoma. Prognosis is poor, with a 5-year
survival of 15%.
Complications of salivary
gland surgery
Facial nerve function
The patient should be warned preoperatively about the
risk of damage to the facial nerve. Permanent paralysis of
the facial nerve should be less than 1% in experienced
hands. Some degree of temporary paralysis is not too
unusual after a parotidectomy, and is more common when
the deep lobe has also to be removed, as this requires
much more manipulation of the facial nerve. This
represents 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 facial
nerve and thus prevent injury, the most useful being the
facial nerve monitor and stimulator, which warns the
surgeon when he or she is working close to the nerve, and
also allows the nerve to be stimulated for confirmation. It
is important when using such devices that the patient is
not paralysed, and the anaesthetist should be aware of
this. Unfortunately, technology is not infallible and
experience of parotid gland surgery is the best method
of avoiding damage to the facial nerve. Stimulating the
nerve and seeing the face twitch can confirm that the
facial nerve is working after a parotidectomy.
In submandibular gland surgery it is important to
avoid the marginal mandibular branch of the facial nerve
that runs in the tissue superficial to the submandibular
gland. If this is damaged it leaves the patient with an
unsightly droop to the corner of the mouth. Other nerves
at risk in submandibular gland surgery include the
lingual nerve (supplies taste and touch to the tongue) and
the hypoglossal nerve (supplies motor function to the
tongue).
Other conditions of the
salivary glands
Drooling
Greater auricular nerve
The greater auricular nerve is usually divided in parotid
gland surgery and this leaves the patient with a numb
feeling of the lower half of the ear lobe. This is of no
great consequence to the patient as it will often recover,
but the patient should be warned of it preoperatively. It is
often possible to save a branch of the nerve, which sometimes prevents this from happening.
Frey's syndrome
Following a parotidectomy, the patient may complain of
sweating of the skin over the area of the parotidectomy,
especially on eating. The problem is quite common
following a parotidectomy but is only troublesome in
about 10% of patients. This is thought to occur because
of the inappropriate regeneration of injured autonomic
nerve fibres, which are misdirected and supply the sweat
glands of the overlying skin. Elevating a thick skin flap
when performing the parotidectomy can reduce its
incidence. Most cases are not too troublesome and can be
controlled by the use of an antiperspirant. More troublesome cases may require other procedures such as a
tympanic neurectomy or the interposition of a tissue flap
between the skin and the parotid bed, procedures that
have a variable rate of success.
Salivary fistula
120
This occurs very occasionally after performing a
superficial parotidectomy, and usually presents as saliva
appearing from the wound several days after surgery. The
most surprising thing is that it does not occur more
frequently as functioning parotid tissue is left behind (the
deep lobe). The vast majority settle with conservative
treatment, which usually includes a pressure bandage and
often the prescribing of an anticholinergic drug to
suppress saliva production. It is sometimes confused with
a seroma that can also occur, occasionally, after surgery.
To distinguish a seroma from a salivary fistula, the fluid
should be aspirated and its amylase content measured,
this being very high in a fistula.
Drooling is a normal phenonomen when it is associated
with teething in childhood, but at most other times it is
abnormal. It is often seen in patients with cerebral palsy
but it also may be seen in adults with neurological
diseases such as Parkinson's disease. It can be caused by
the overproduction of saliva or the presence of an
abnormal swallowing reflex. Various surgical treatments
have been described for the treatment of drooling,
including rerouting of the submandibular ducts to drain
into the tonsil fossae and also excision of the
submandibular glands with rerouting of the parotid ducts,
with varying degrees of success. Tympanic neurectomy
also has been shown to be of benefit in the short term but,
like all autonomic nerve surgery, its long-term results are
disappointing.
Branchial cleft anomalies
First branchial cleft anomalies can present as a sinus,
fistula or a cyst, usually in childhood or in the young
adult. The sinus tract often has an external opening in or
near the external auditory meatus. If a true fistula is
present this has an internal opening into the pharynx near
to the posterior tonsillar pillar. It is often seen in association with abnormalities of the ear. One-third of first
branchial clefts are bilateral. They usually present as a
cystic swelling in the region of the parotid gland and they
have a variable relationship to the facial nerve Treatment
is by surgical excision and this usually requires a superficial parotidectomy and exposure of the facial nerve for
their complete removal.
Salivary duct cysts
These usually occur in the parotid gland and are more
common in men often in their seventh or eighth decades.
They present as a swelling in the affected gland, which
on aspiration reveals a clear coloured fluid, and they often
completely disappear on aspiration. Often the diagnosis
is only made when the cyst is removed, as it is not always
easy preoperatively to distinguish this from cystic
degeneration in a Warthin's tumour.
Ranula
A ranula is a sublingual swelling. Most consist of a mucus
filled cyst that lies under the mucosa, just lateral to the
frenulum. It is thought to be a retention cyst that arises
from the obstruction of one of the several ducts draining
the sublingual gland. It presents as an asymptomatic
swelling of the floor of the mouth, but occasionally can
get so large that it interferes with speech or eating.
Treatment consists of uncapping and marsupialising it.
Very occasionally, the ranula can penetrate through the
mylohyoid muscle and into the neck, when it is known as
a plunging ranula. This requires excision, as does a
simple ranula if it recurs after uncapping.
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15
Plastic surgery
Introduction
Plastic surgery techniques are widely used to treat a
variety of diseases and deformities in an effort to
reconstruct both form and function. The basic principles
are fundamental to all surgical practice involving the
head and neck. Advances in plastic surgery techniques
have opened up new possibilities for reconstruction in
the head and neck. Many of these advances have arisen
from an increasing understanding of the structure of
tissues, their anatomy and their vascularity.
This chapter will concentrate on plastic surgery
techniques that are applicable in the face and head and
neck region. This area of the body is one of the most
important in determining body image where deformities
or disfigurement are clearly identifiable. It is also the area
essential for communication with the outside world,
allowing us to express emotions such as happiness or
anger, which are transferred into visible changes in the
face.
A description of the tissues, the skin and facial
muscles will be followed by a consideration of incisions,
lacerations, skin grafts and flaps (Table 15.1).
The skin
122
The skin of the head and neck has several unique features
that differentiate it from other areas in the body. It
communicates with the respiratory tract via the nostrils,
the digestive tract via the oral cavity and the conjunctival
lining of the eyelids. The skin of the head and neck has a
rich blood supply via a complex network of intercommunicating vessels. These can dilate under physical or
emotional stress, changing skin colour and appearance
(e.g. blushing). This high intensity blood supply opens
up plastic surgery techniques that are not routinely
available elsewhere in the body.
Table 15.1
Plastic surgery techniques
Incisions
lines of election
surgical access
Treatment of lacerations
Management of scars
Wound closure
skin grafts
split thickness
full thickness
composite
skin flaps
local
distant
free
Novel methods
prefabrication
tissue engineering
The skin is also not a single entity. There are
variations in skin thickness and in the distribution of hair
growth, the latter being a sexual characteristic. There are
differences in fixity and laxity of the skin with the eyelids
being very thin and elastic to allow free mobility.
Elasticity and mobility is seen in facial expression and in
the development of creases and wrinkles associated with
increasing age. There are also variations in skin colour,
particularly in the face, partly as the result of exposure to
the 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 boundaries
that separate cheek skin from eyelid skin or nasal skin.
These separations have allowed the face to be divided
into cosmetic units and have changed the thinking in
facial reconstructive plastic surgery. Understanding the
special characteristics of the skin of the face is an
essential component of all surgery in this area.
Facial muscles
Muscles of the face can be divided into two broad
groups. The first group concerns functioning of the jaws
and is sometimes termed muscles of mastication. These
include the temporalis muscle, and masseter. These
muscles are innervated by the trigeminal nerve. The
second group of muscles is known as the muscles of
facial expression and forms an extensive network of
interconnecting and interweaving fibres, joined together
to produce a powerful composite muscle complex. The
muscles of facial expression are innervated by the facial
nerve. The muscles are separated from the skin and
subcutaneous tissue by an extension of the superficial
cervical fascia. This specialised layer is known as the
superficial muscular and aponeurotic system (SMAS),
which is continuous with the platysma of the neck
inferiorly and the galia of the scalp superiorly. It is also
attached to the periosteum of the zygomatic arch. This
plane has become increasingly important in face-lifting
procedures. Within this SMAS there are connections
to the overlying skin, which aid the muscles of facial
expression in creating creases and wrinkles and contributing to facial expression. The other importance of
the SMAS is that the facial nerve lies deep to it, therefore
the superficial surface provides an excellent plane for
surgical dissection, without risk of damage to the facial
nerve. The special characteristics of facial skin and the
complexity of the underlying facial musculature, play an
important part in all facial surgery.
Incisions
Incisions are used either for excision or for access to
areas in the head and neck. Such incisions therefore have
to be capable of extension should this be required, but
should 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 underlying
muscular contraction, and therefore is noticeable in
grimacing, showing the teeth, pursing the lips, closing
the eyes tightly or in facial expressions of anger or joy.
Such wrinkle lines are clearly identified in older people
as 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 can
be determined by considering the direction of the underlying muscle. The wrinkle line lies perpendicular to the
long axis of muscle activity. An example is the frontalis,
which works vertically to elevate the eyebrow but creates
horizontal 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 separates
cheek skin from nasal skin and cheek skin from the lips,
and the mental crease, which separates the lower lip from
the chin. Incisions should not cross cosmetic units and
contour lines.
Surgical access
The head and neck has many hidden areas that are
difficult to visualise and thus add to the problems of
surgery. Advances in endoscopy equipment have certainly
123
improved matters but in many tumour situations direct
visualisation requires better access both for tumour
excision and for reconstruction. Such access incisions
should have minimal morbidity, in terms of function and
cosmesis.
Maxillary sinus tumours may be effectively dealt with
by endoscopic surgery, as in functional endoscopic sinus
surgery (FESS) (see Ch. 18). Another approach is via the
upper labial sulcus, which exposes the anterior part of the
maxilla. When more exposure is required, a modified
Weber Fergusson incision can be used. This essentially
splits the lip in the line of the philtrum and extends along
the nasal base and superiorly as a lateral rhinotomy at the
junction between cheek skin and nasal skin. It can be
further extended in a vertical direction to the gabella
frown lines, or in a horizontal direction in a pretarsal line.
This allows the soft tissue to be hinged laterally to expose
the maxilla. This approach can also be used as a midline
facial split by incorporating bone separation of the facial
skeleton and palate which, like the upper face, is
essentially split into two halves.
For the oral cavity, access can be improved by a lower
lip incision placed in the midline in a vertical plane. This
incision can also be extended to curve round the mental
crease, keeping in the contour line and extending down
into the neck, extending laterally in the crease line in the
neck. This, combined with an access osteotomy of the
mandible, allows the mandible to swing out, giving
excellent exposure and access to the oropharynx.
Such incisions used for access stay within the lines of
election, and give excellent functional and aesthetic
results (Fig. 15.2).
Facial lacerations
124
The integrity of the skin can be broken as a result of
sharp or blunt trauma or following abrasion. The extent
of facial lacerations or wounding is often difficult to
determine, partly because of profuse bleeding but also
because of oedema, which distorts the anatomy. The
history and mechanism of the injury are essential, and
further investigations are often required (see Ch.12).
Wounds often require exploration under general
anaesthetic to determine their extent and damage to
underlying structures, notably nerves, vessels and
muscles. There are some differences in the management
of facial lacerations compared with wounds outside the
head and neck area. Wound debridement is usually not as
radical as elsewhere. This is because of the exceptional
Fig. 15.2
Incisions for surgical access: bicoronal, upper
lip and lateral rhinotomy, lower lip and chin.
blood supply to facial structures and because of the
importance of maintaining specialised tissues (e.g. eyelid
and lips). What is vital in debridement is to remove all
foreign material such as gravel. Foreign bodies may
cause problems subsequently and gravel appears as
tattooing of the scar. It is essential that meticulous wound
closure in layers matches anatomical structures (e.g.
eyelids, lips, nostrils, ear), to avoid notching deformities
and irregularities subsequently. It is important to repair
all structures at the time of primary wound closure. If
branches of the facial nerve are divided they should be
repaired using an operating microscope. If the parotid
duct is divided it should similarly be repaired or a stent
inserted, with an approximation of the divided ends. All
muscles should be repaired meticulously, paying particular
attention to orientation of the fibres. The process of
wound healing is covered in Chapter 3.
Management of scars
Scars in the head and neck are not only disfiguring and
noticeable but often have a social stigma attached. Initial
wounds can look quite satisfactory but, as healing
progresses, scar formation develops. This appears as
reddening and increasing size of the scar as it tends to
become wider and raised from the skin surface. The scar
becomes hard and can be associated with itch and pain.
As the scar matures it should become softer paler and
flatter. The final scar should look paler than the surrounding skin, flat and soft and have an atrophic appearance
(i.e. look thinner than the surrounding skin), with no skin
appendages such as hair or sweat glands.
This cycle of scar maturation can take 1–2 years, and
patients often require support throughout this phase.
Occasionally, intralesional injection of corticosteroids
can accelerate the process of maturation; it can also be a
useful treatment for itchy and painful scars. Cosmetically
unsightly scars are usually those that cross the lines of
election. The pull of the muscle tends to widen the scar
with the passage of time and, as these scars do not lie in
the relaxed tension lines, scar maturation tends to be
poor. Cosmetically unsightly scars can require the
direction of the scar to be altered, or the length of the scar
to be broken up. A Z-plasty is a useful way of changing
the direction of facial scars so that at least one limb of the
scar lies in the line of election (Fig. 15.3) and also
breaks-up the length of the scar. Sometimes, facial scars
become soft and flat but retain a red colour; lasers can
sometimes help in this situation.
Wound closure
The details of wound closure and wound healing have
been discussed previously (Ch. 3). As far as plastic
surgery techniques are concerned,wounds may be closed
directly by edge-to-edge apposition or by techniques that
involve the import of tissues. Tissue can be imported
either 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 by
revascularisation from the surrounding tissue. A graft
will therefore not survive in areas of poor vascularity,
such as bare bone (without periosteum) bare cartilage
(without perichondrium) or overexposed joints. Grafts
are also not applicable where protection is required over
major vessels and nerves.
Split thickness skin grafts
These grafts comprise the epidermis and some dermal
elements but leave sufficient dermis to allow rapid
healing with re-epithelialisation of the donor site. Large
amounts of skin can be harvested and such grafts are
useful for resurfacing large areas of skin loss, such as
occurs following burn injuries. The thicker the graft, the
more dermal skin appendages it contains, leading to less
likelihood of subsequent contracture and a more normal
appearance of the skin. Hypopigmentation and poor
colour match in the skin of the head and neck is likely
particularly with thinner grafts. Common donor sites for
split thickness grafts include the thigh the upper arm and
buttock. Due to the raw surface that remains prior to reepithelialisation, donor sites can be painful in the early
postoperative period.
Full thickness skin grafts
Fig. 15.3
A Z-plasty in lower eyelid reconstruction.
These include the full thickness of the skin and dermis
down to the subcutaneous fat, therefore the donor site
requires to be closed. Skin retains the characteristics of
its donor site. To obtain a good colour and texture match,
grafts have to be harvested from the head and neck
region. Common donor sites include the postauricular
skin, the preauricular skin and the supraclavicular skin,
with direct closure of the donor site. Full thickness
grafts, because they contain the dermis, are not prone to
125
contracture and give good quality pliable skin, with a
better colour match, when harvested from the head and
neck region.
Composite grafts
Fig. 15.4 (a) Extensive basal cell carcinoma eyelids(b) planned excision and cervical facial flap; (c) composite
chondromucosal graft (arrowed) from nasal septum(d) postoperative appearance.
126
Composite grafts are peculiar to facial reconstruction and
are used in specific areas. Defects of the nostril, which
involve the skin, cartilage, nostril rim and nasal mucosal
lining, can be reconstructed using a composite graft from
the ear. Excising a wedge from the ear provides two skin
surfaces with a portion of cartilage in between. This can
be inserted to reconstruct the nostril providing skin for
lining for the nasal mucosa, cartilage to give support
and shape of the nostril and skin for external nasal
reconstruction. A similar wedge can be used for reconstruction of the columella and septal lining.
In lower eyelid reconstruction, lining and support can
be provided using a composite graft from the nasal
septum, comprising mucosa and underlying cartilage.
Table 15.2
Advantages and disadvantages of skin graft types
Graft
Advantages
Disadvantages
Thin split-thickness graft
Size - large grafts. Good graft take.
Rapid re-epithelialisation and healing
of donor site
Shrink and contract. Poor colour and
texture match. Often unstable. Painful
donor site
Thick split-thickness graft
Size - large grafts. Less contraction
than thin grafts. Stable
Slow healing of donor site. Donor site
hypopigmentation. Possible scarring at
donor site. Poor colour match for face
Full thickness grafts
Good colour and texture match if
harvested from head and neck.
Not prone to contracture. Stable
Size limited by necessity to close donor
site primarily
Composite grafts
Good tissue match. Composite tissue
Unpredictable graft take. Limited size
Graft success is unpredictable. In nasal reconstruction
revascularisation has to occur from the edges of graft
insertion, since there is no graft bed. Survival can be
improved by enlarging the skin reconstruction element
as a full thickness skin graft, to carry the composite
tissue at its distal end. In eyelid reconstruction, a well
vascularised flap is required to cover the graft and ensure
revascularisation (Fig. 15.4). The advantages of the
different types of grafts are listed in Table 15.2.
Skin flaps
Skin flaps carry with them their own blood supply and
comprise both skin and subcutaneous tissue. Flaps
adjacent to the defect requiring reconstruction are termed
local flaps. Those from further away and not contiguous
with the defect are known as distant flaps. Distant flaps,
which remain attached to the body, are further termed
pedicled flaps, whereas those that are detached from the
body and revascularised by anastomosing the arteries and
veins, are called free flaps.
The success of flaps is totally dependant on their
vascularity. Where the blood vessels supplying and
draining the tissue is known, flaps are given names,
either based on the geographical area (e.g. delto-pectoral
flap), on the vascular pedicle (e.g. deep circumflex iliac
artery flap) or on the tissue types that the flaps contain
(e.g. pectoralis major, myocutaneous flap). Flaps may
therefore be skin flaps (which incorporate skin and fat),
myocutaneous flaps (incorporating muscle and skin),
muscle-only flaps or composite flaps, involving a wide
variety 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 the
flap assumes an indeterminate pattern. These flaps are
called random pattern flaps and are restricted to local
skin flaps. They are particularly useful in the face because
of the intense vascularity of this region.
Local flaps
By definition, these flaps are continuous with the defect
to be reconstructed. Many in the face are random pattern
flaps and are named according to their geometrical design
(e.g. transposition flaps, rotation flaps, rhomboid flaps).
Essentially, local flaps transfer tissue from an area where
it is available into the defect that requires reconstruction.
In the face, common areas of tissue availability are the
glabellar region, the preauricular region and the neck.
When designing local flaps, it is important to pay attention
to the lines of election. Local flaps generally provide a
good colour and texture match in the face but are limited
by tissue availability (Fig. 15.4).
Tissue expansion
One method of increasing the role of local flaps is to use
tissue expansion. An inflatable prosthesis is inserted subcutaneously - and the tissue is gradually distended by
inflating the prosthesis over a period of weeks. This
increases the tissue availability for local flap transfer. It
is most useful in tissues that can be readily expanded
(e.g. forehead and scalp) because of the firm base of the
cranium. In scalp reconstruction, in particular, it allows
reconstruction of hair-bearing skin, thus replacing like
tissue with like.
127
Distant flaps
These flaps have the disadvantage of often being outside
the head and neck area, therefore they do not provide
good skin colour and texture match. However, the
deltopectoral flap, taken from the upper chest, can be
used effectively to resurface the neck and will extend up
to the zygomatic arch. It is certainly adjacent to the neck
skin area and probably provides one of the best colour
matches. This flap has to be taken up in two stages, with
the pedicle divided at 3 weeks and subsequently returned
to its original site (Fig. 15.5). This essentially means that
the blood supply, which enabled the transfer of the flap,
is divided, and the tissue has to survive from ingrowth of
vessels from the original defect.
More useful flaps are those in which the vascular
pedicle can be transferred to the head and neck in a single
stage and maintained permanently in this transferred
128
Fig. 15.5 A deltopectoral flap: (a) incision lines;
(b) transposed flap in place.
position. This retains the blood supply to the transferred
tissue, promoting wound healing. One of the major flaps
of this type is the pectoralis major myocutaneous flap
(Fig. 15.6).
Free flaps
The advent of the operating microscope has opened up
new possibilities in reconstructive surgery. The ability to
revascularise tissue by anastomosing small vessels of
1-3 mm in diameter has enabled the transfer of specific
tissue types. The golden rule of plastic surgery is to
reconstruct like tissue with like. For example, the ability
to reconstruct the jaw with vascularised bone has
revolutionised head and neck cancer surgery (see Ch. 17)
(Fig. 15.7). Similarly, facial paralysis can be improved
by transferring a functioning muscle flap, reconstituting
its vascular and neural supply. Large volumes of skin can
be transferred to resurface defects for the head and neck,
but here the problems of tissue type and colour match
become apparent (Fig. 15.8). A notable feature of these
well-vascularised distant flaps is that they maintain the
characteristics of their original donor sites. A free skin
flap placed for intraoral reconstruction remains as a free
skin flap, with keratinising squamous epithelium, and
does not change its character to mucosa.
Improved understanding of the anatomy of the body
has provided an increasing number of donor sites for
free tissue transfer and surgeons are no longer restricted
by the need to raise flaps in close proximity to the head
and neck. A variety of specialised tissues can now be
transferred in an attempt to replace like with like.
Fig 15.6
flap.
A pectoralis major flap isolated on its vascular
Fig. 15.7 (a) Fibula osteocutaneous flap; (b) radiograph
showing flap restoring mandibular contour.
Free flaps are designed on particular vessels and they
tend to have a very good vascularity, which is dependent
on a successful microvascular anastomosis of both artery
and veins. There is significant evidence of the vascularity
of free flaps, in their ability to heal wounds in the head
and neck, and their ability to tolerate postoperative
radiotherapy in cases of malignancy. Free flaps continue
Fig. 15.8
A scapula flap: (a) flap elevation; (b) showing
poor colour match.
to have a major impact on the cosmetic and functional
outcomes following major head and neck surgery.
Novel methods
Plastic surgery is concerned with excision and the creation
of surgical defects and their subsequent reconstruction.
129
A wide variety of methods are now available but some
specialised tissues in the head and neck are virtually
irreplaceable and it is often difficult to replace like tissue
with like. In an attempt to solve some of these problems,
there has been a move towards prefabrication and tissue
engineering.
Prefabrication
Prefabrication involves multistage surgery to create a
purpose-designed flap to reconstruct a particular defect.
A simple example of prefabrication is to harvest buccal
mucosal grafts and insert these grafts under the skin and
onto the fascia of the forearm. These grafts will take on
130
the fascia and form a mucosal surface. The flap comprising the fascia and this new mucosa can be transferred
subsequently as a radial forearm free flap, to provide
mucosal reconstruction of the oral cavity.
Tissue engineering
Tissue engineering is in its infancy. Specific tissue types
can be grown (e.g. epithelium or bone) under a variety of
growth stimulators. Tissue engineering in essence creates
new tissue, which can be of a specialised nature. These
techniques are being developed in the laboratory and
look promising in the reconstruction of the specialised
tissues of the face and head and neck in the future.
16
Clefts of the lip and palate
Introduction
Clefts of the lip and palate are one of the most common
congenital facial malformations described in humans.
They remain, however, poorly understood and present a
significant challenge for reconstruction.
Early records of successful repairs of clefts of the lip
exist in Eastern texts and the earliest recorded case of
a successful repair of a cleft lip appears to be around
AD 390 in China. Over the centuries, many techniques have
been reported to disguise the visible deformities of cleft
lip or the occlusion with cleft lip and palate, as well as
surgical techniques for their repair.
Surgeons dealing with clefts of the lip and palate today
must recognise that although significant advances have
been made in surgical and anaesthetic technology, the techniques of repair are far from perfect and remain an area
of immense controversy and intense debate.
An understanding of the management of cleft
deformities requires a knowledge of the embryology
of the face and the classification of cleft deformity. The
structural abnormalities that comprise the cleft deformity
dictate the patient management and, in particular, the
surgical procedures employed. These will be discussed in
turn (Table 16.1).
Embryology
The embryological development of the face is a complex
process but occurs very early in fetal life. The face develops from a central or frontonasal process, which grows
forwards and over the developing brain. Two maxillary
processes advance anteriorly between the optic vesicles
and the primitive stomodeum and two mandibular processes advance beneath the stomodeum. The distal end of
the frontonasal process is defined into medial and lateral
nasal processes by the olfactory placodes (Fig. 16.1).
Table 16.1
Management of cleft deformities
Embryology
Classification of cleft deformity
Structural abnormalities of cleft deformity
Patient management
Surgical treatment
Surgical procedures
Philosophy
Fig. 16.1
Development of the face at 5 weeks.
Fusion of the maxillary processes with the frontonasal
process results in the formation of the premaxilla, which
bears the incisor teeth. Facial features become recognisable by the fifth to sixth week of intrauterine life. Fusion
of the maxillary palatine processes with each other and
the premaxilla (between the lateral incisor and canine
teeth) commences at around the eighth week of intrauterine life at the area defined by the incisive foramen and
progresses posteriorly to the uvula by the twelfth week.
It was initially believed that facial clefts occurred as a
result of failure of fusion of the ectodermal processes
131
described above. However, patterns of presentation of
clefts of the lip and palate have resulted in increasing
support for theories suggesting that clefts of this region
are likely to be due to a failure of migration of the
ectomesenchymal cells responsible for the formation of
the deeper tissues, such as the muscles and nerves,
resulting in inadequate tissue support between the two
epithelial layers and consequent breakdown.
The presentation of clefts of the secondary palate is
consistent with failure of fusion of the margins of the
palatal processes.
Clefting may arise as part of a syndrome. Nonsyndromic clefting arises as a result of a genetic link
combined with environmental insults in utero, although
the mechanisms remain unclear.
Classification of the cleft
deformity
The deformity in clefts of the lip and palate can range
widely in severity and extent, rendering attempts to
classify them into a limited set of patterns somewhat
impractical. The various terms used to describe palatal
clefts are defined in Table 16.2.
Clefts of the lip may be barely noticeable, with
minimal surface abnormalities or asymmetry of vertical
height indicating an underlying abnormality of muscle
anatomy, a 'forme fruste' or microform cleft lip. The
Table 16.2
Terms used to describe palatal clefts
deformity can range from this to a complete cleft of the
lip, alveolus, primary palate and secondary palate.
Clefts of the palate alone may similarly manifest a
wide range of severity. There may be no surface or visible
evidence of clefting, but abnormalities of soft palatal
function only displayed by features suggestive of velopharyngeal incompetence. This occult submucous cleft
may occur in an otherwise intact palate with minimal
surface evidence of an underlying abnormality of muscle
anatomy. The clinical features of submucous cleft
deformity are listed in Table 16.3.
Although clefts of the lip and primary palate
associated with clefts of the soft palate and/or the
posterior hard palate with an intervening bridge of intact
hard palate are rare, they have been described. Similarly,
clefts of the palate alone involving the bony palate may
be unilateral with partial or complete attachment of the
vomer to one side.
Structural abnormalities of
cleft deformity
To fully understand the rationale for treatment of clefts of
the lip and palate, it is essential to comprehend the complex nature of the underlying functional and structural
abnormalities associated with this deformity. The
components of the anatomical deformity are listed in
Table 16.4 and these will be discussed in turn.
Table 16.3
deformity
Clinical features of submucous cleft
Primary palate
132
Palate anterior to the incisive
foramen
Secondary palate
Palate derived from the palatal
shelves of the embryo.
(posterior to the incisive
foramen)
Complete cleft palate
Cleft extending to the incisive
foramen
Incomplete cleft palate Cleft not extending to the
incisive foramen
Submucous cleft
Cleft of the muscle layer only in
the soft palate (usually with
notch on the posterior
border of the hard palate)
Unilateral palatal cleft
Vomer attached to one of the
palatal shelves
Bilateral palatal cleft
Vomer totally separated from
the palatal shelves
Bifid uvula
Notching of the posterior edge of the hard palate
Midline translucency of the soft palate
Absence of musculus uvulae
Table 16.4
deformity
Anatomical components of a cleft
Lip
Nose
Alveolus
Primary palate
Secondary palate
Maxilla
Mandible
Other
The lip
There is soft tissue discontinuity of the lip involving the
vermilion and skin. Disruption of the orbicularis oris
with abnormal attachments of the muscle to the skin, the
lateral crus of the alar cartilage and the underlying bone
occurs. Some authorities have proposed that the extent of
muscular abnormality is far more extensive on the affected
side and includes the muscles of facial expression and
nasal sphincters, thus requiring a meticulous restoration
of functional muscular anatomy.
floor. The alveolar arch component on the cleft side
(referred to as the lesser segment) tends to be rotated
mesiopalatally and the primary palatal component on the
non-cleft side (referred to as the greater segment) is
rotated outwards by the action of the abnormally attached
facial muscles. The combination of these deformities can
result in a virtual appearance of a significant tissue deficit
at the site of the cleft. The septal cartilage is also deviated
as the premaxilla is rotated out.
The secondary palate
The nose
The deformity of the nose is minimal or absent in clefts
of the lip that are incomplete with a largely intact
anatomy of the orbicularis oris. 'Forme fruste' nasal
deformities may occur occasionally with otherwise intact
lips, suggesting that components of the nasal deformity
are related to abnormal insertions of the disrupted fibres
of the facial muscles.
There is nasal deformity in more complete clefts of
the lip. The alar cartilage is caudally displaced and the
medial crura and alar domes are separated. This results in
apparent shortening of the columella on the cleft side and
deviation of the nasal tip towards the cleft side. The body
of the cartilage may be elongated and rotated. The caudal
edge of the septal cartilage may be dislocated. The nasal
floor may be stretched and lower in incomplete clefts and
absent in complete clefts. In addition, the nasal lining
may be webbed with a band of skin across the upper
lateral wall.
The alveolus
The premaxillary portion of the alveolus carries the
incisor teeth and forms the primary palate, which is the
part of the palate anterior to the incisive foramen. The
gap in the alveolus usually occurs between the lateral
incisor and canine teeth and extends obliquely towards
the incisive foramen. The extent of alveolar clefting may
range from barely visible notching of the gingiva to a
complete cleft, but the visible manifestations may not
correlate directly with the extent of underlying bony
disruption.
The secondary palate extends posteriorly from the
incisive foramen to the uvula and is composed of the
bony hard palate and the soft palate. Unilateral clefts of
the bony hard palate result in the separation of the palatal
shelf on the affected side from the contralateral palatal
shelf at the midline. The affected shelf is often smaller in
length and width and may also be retrodisplaced. The
transverse deficiency (in width) can be exaggerated by
the cranial tilt of the shelf. The attachment of the vomer
to the contralateral shelf may be variable in extent. The
posterior palatal arch width is greater than normal
because of lateral displacement of the maxillary
tuberosities.
The soft palatal component of a cleft palate results in
a midline deficiency that can be overt (e.g. in a complete
cleft) or submucous, with continuity of the lining but a
deficiency of the muscles in the midline. The muscles of
the soft palate are attached abnormally to the posterior
edge of the hard palate and the edges of the cleft. The
anteroposterior length of the soft palate is reduced.
The maxilla
The maxilla on the affected side is deficient in vertical
and anteroposterior dimensions.
The mandible
The dimensions of the mandible may be smaller in
patients with clefts of the palate, especially as part of the
Pierre Robin sequence and the potential for growth might
be compounded by the existing maxillary deformity.
The primary palate
Other anomalies
Clefts of the primary palate extend posteriorly to the
incisive foramen, resulting in a deficiency of the nasal
The abnormal anatomy of the muscles of the soft palate,
especially the tensor veli palatini, is believed to be
133
responsible for interference with aeration of the middle
ear due to failure of adequate eustachian tube opening
during swallowing, yawning and other pharyngeal
movements.
Patient management
134
The management of clefts of the lip and palate is
multidisciplinary and requires the involvement of several
specialities, which constitute a cleft team. In most centres, the minimum complement of a cleft team involved
in the primary management would consist of a surgeon,
orthodontist, speech and language therapist, ENT surgeon
and audiologist. The participation of several other disciplines is also crucial in the management of the child with
a cleft deformity, including paediatricians, geneticists,
paediatric dentists, hygienists, prosthodontists, psychologists and specialist nurses and dieticians.
The initial management of the child born with a cleft
deformity is essentially supportive. The birth of a baby
with a facial deformity is often a traumatic experience for
the parents and other members of the family. The staff
involved in immediate perinatal care (the obstetricians,
midwives and paediatric perinatologists) must be able to
recognise and deal with the shock and distress of the
parents, as well as with any medical problems that may
arise. It is vital that the parents are visited as soon as
possible by a member of the cleft team to discuss the
long-term management of the condition. A considerable
effort must be made to allay the fears and anxieties of the
parents and relatives with detailed discussions to explain
the nature of the problem and the long-term prognosis of
treatment.
Parents of babies born with clefts are often overcome
by feelings of guilt and self-accusations of punishment
for past sins, as well as with a significant loss of selfesteem generated by feelings that the appearance of
facial deformity in the baby is a manifestation of their
own imperfection. The absence of perceptible emotional
distress should not be considered as evidence of coping.
It is essential to explore the parents' feelings, ideally
with the support of a clinical psychologist, as rejection of
the baby will have significant long-term consequences
for both the parents and the child. Non-syndromic clefts
of the lip and palate are unlikely to present any serious
medical problems and the only immediate concerns
are mainly related to potential airway problems and
feeding.
Airways
Newborn babies are obligate nasal breathers and any
evidence of airway obstruction should be assessed
immediately by careful suction of secretions occluding
the oropharynx, and by measures to prevent the tongue
from blocking the airway.
The Pierre Robin sequence is associated with
micrognathia (a small mandible with obvious lack of
chin prominence), relative macroglossia (a tongue that
appears disproportionately large) with a tendency to
develop glossoptosis (falling backward of the tongue into
the oropharynx) resulting in intermittent airway obstruction, and a cleft palate. Although originally labelled as a
syndrome, it is now recognised that this combination of
features may be associated with a variety of conditions.
Feeding difficulties associated with the respiratory
obstruction are also very common.
Various manoeuvres have been utilised to prevent the
glossoptosis, which is the fundamental cause of the
intermittent airway obstruction. These include nursing in
the prone position in special harnesses, suturing the tongue
to prevent retraction, nasopharyngeal or oropharyngeal
airways, endotracheal intubation and tracheostomies.
The problems of airway obstruction tend to be more
pronounced when the baby is more relaxed or asleep and
are unusual when awake, crying or in the upright
position. Fortunately, severe problems of airway obstruction warranting a tracheostomy or other surgical procedures are relatively rare. However, it is essential to
recognise the condition and institute early appropriate
treatment. Failure to recognise the problem is potentially
fatal because of the possibility of acute obstruction,
progressive exhaustion or brain damage associated with
chronic hypoxia. Pulmonary hypertension and cardiac
failure may result from the chronic hypercapnia and
hypoxia.
In mild cases, simple postural measures are often
adequate and careful supervision with the judicious use
of devices such as pulse oximeters and sleep apnoea
monitors to detect episodes of airway obstruction are
sufficient. The immense emotional and physical stress
imposed on the parents or carers of the child must not be
underestimated. It is essential to ensure that the child is
kept in a suitable high-dependency or intensive care
facility until it has been established that the risk of
apnoea or cyanotic spells is minimal and the parents feel
comfortable about the prospect of managing the problem
at home.
It may be necessary to arrange readmission to hospital
to 'wean' the infant from the apnoea monitor and demonstrate to the parents that the airway problems are unlikely
to constitute a serious risk. A combination of establishing
breathing patterns and the progressive growth of the
mandible often results in fairly rapid improvement in the
situation. In severe cases requiring surgical intervention
such as tracheostomies, it may take a long time to
decannulate the child.
Feeding
Feeding problems associated with clefts of the lip alone
are unusual. Mothers should be encouraged to attempt
breast-feeding as an adequate lip seal over the nipple can
be achieved. Clefts of the palate, and especially the secondary palate, result in an inability to generate sufficient
oropharyngeal negative pressure and tongue compression
against the palate. Milk reflux into the nasal cavity and
associated problems such as respiratory difficulties and
fatigue, as well as frustration on the part of the mother,
compound the problems. Historically, feeding with spoons
and cups have been advocated to allow gravity-assisted
presentation of the feed into the oropharynx, as the ability
to swallow is not affected by palatal clefts.
A wide variety of proprietary teats with compressible
reservoirs and feeding devices have also been designed to
facilitate feeding by minimising the need to suck or by
attempting to obturate the palatal cleft. Feeding plates
comprising an acrylic palatal coverage constructed on a
dental cast and secured with ribbon attached to extraoral
flanges improve sucking ability, but there is less need for
these nowadays with improvements in other feeding techniques, and they are now not generally recommended. In
many instances, a normal teat with an enlarged hole
to permit a steady, gravity-assisted delivery of milk into
the oropharynx is adequate and the mother should be
encouraged to identify, by a process of trial and error, the
best method suited to mother and baby. However, it is
crucial that this process is undertaken under the supervision of a cleft nurse specialist or other member of the
cleft team with a specific interest and knowledge of
feeding problems in babies with clefts.
Feeding may be seriously compromised by associated
respiratory or other problems and it may be necessary to
resort to nasogastric tube feeding if adequate nutrition
cannot be delivered by oral feeds. However, resident
nasogastric tubes are associated with significant morbidity, such as increased risk of respiratory infections,
pulmonary aspiration and gastro-oesophageal reflux. In
extreme cases, percutaneous gastrostomy might have
to be considered. Careful and regular monitoring of
weight gain and development is essential to ensure that
nutritional requirements are being met.
Surgical treatment
The fundamental objectives of surgical treatment for
clefts of the lip and palate are listed in Table 16.5. A wide
range of procedures and protocols for surgical management of this deformity has been described and controversies exist regarding the optimum modalities of
treatment. Rather than becoming immersed in this
debate, it is advisable to grasp the underlying rationale of
treatment (Table 16.6).
Surgical procedures
The evolution of surgical procedures for the treatment
of cleft deformities has only been possible because of
advances in the field of anaesthesia, and especially
paediatric anaesthesia. The earliest repairs of clefts of the
lip consisted of hastily paring the edges of the cleft
deformity without the benefit of anaesthesia and
attempting to suture or appose the edges in an effort to
seal the gap. Palatal clefts were treated with simple
obturators or crude surgical attempts to repair the cleft
Table 16.5
clefts
Objectives of surgical treatment of
The restoration of normal facial appearance and facial
symmetry
Normal speech
Normal occlusion
Normal hearing
Table 16.6 Treatment of the cleft deformity
components
Correction of the surface geometry of the affected
tissues
Restitution of the underlying structural and functional
anatomy
Modulation of growth and development of the jaws and
dentition
Development of normal speech and hearing
135
Table 16.7
Rule of 10s
Age: 10 weeks
Weight: 10 lb
Haemoglobin: 10 g/dL
addressing the geometric deformity and restore the
underlying structural and functional anatomy of the
affected tissues.
The lip
Table 16.8
Stages of cleft repair
Primary surgery
Secondary surgery
Revision surgery
The timing of cleft lip repair ranges from neonatal repair
to delaying surgery to between 6 and 9 months of age.
The advantages and disadvantages of neonatal repair are
listed in Table 16.9.
Lip adhesion
defect. As repair of palatal clefts under such conditions
was associated with risks of considerable blood loss or
other complications, they were often undertaken in adults
and, until the 1970s, repair of palatal clefts was not
recommended before the age of 18 months. Repair of lip
clefts was advocated by the rule of 10s (Table 16.7).
These classic recommendations for the timing of surgery
are still widely applied today in several leading cleft
centres in the world.
Repair of the cleft deformity can be divided into three
categories (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
Table 16.9
Advantages and disadvantages of neonatal repair of cleft lip
Advantages
Disadvantages
Theoretical advantage of scarless fetal wound healing
Reduction of psychological trauma period for parents
and possibly better maternal bonding because of
restoration of facial aesthetics
Higher levels of circulating maternal immunoglobulins
conferring improved resistance to infection
Higher haemoglobin level with possibly better wound
healing
Dimensions of lip and nose are only slightly smaller than
at 3 months. Surgical planning is not compromised
Tissues are more friable and delicate
Need for postoperative intensive care, which may adversely
affect maternal bonding and compound psychological
stress factors
Underlying cardiac or other abnormalities may not be
manifest at this age. Risk of producing a patent ductus
Neonatal jaundice and risks associated with neonatal
anaesthesia
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 unrepaired
cleft may reduce long-term unrealistic expectations
Repair is more difficult in wide or bilateral clefts with no
opportunity to utilise preoperative orthopaedics
Parents take home a baby with a repaired lip cleft
136
Lip adhesion involves merely approximating the skin
without muscle repair. Although it is routine practice in
some leading centres to employ lip adhesion as a primary
procedure at varying times, there is no evidence to
suggest that the procedure confers any long-term benefit
and it has the disadvantage of increasing the total number
of operative procedures if palatal repair is not undertaken
at the time of the definitive lip repair.
Proponents of primary lip adhesion argue that it
serves the same function as preoperative orthopaedics to
mould the component tissues into a more favourable
position without the considerable inconvenience and
cumbersome nature of the process. Lip adhesion may
have a role in wide bilateral clefts or in wide unilateral
clefts if preoperative orthopaedics have failed to narrow
the cleft gap or the risks of breakdown of a definitive
repair are likely to be high.
Underlying alveolus is more malleable and moulded after
repair
Lip repair at 3 months
This is the traditional recommended timing for lip repair.
The anatomical landmarks are well developed at this
stage permitting accurate planning and restoration of the
geometric anatomy of the soft tissues. The nasal tissues
and alar cartilages are also sufficiently developed to
permit dissection for a primary rhinoplasty.
Lip repair at 6 months or later
It is easier to repair the palate and undertake a more
comprehensive palatal repair, especially of the primary
palate and the nasal floor, using the 'working forward
from the back' approach. Some proponents advocate a
one-stage repair of the entire deformity at this age.
'Functional' repair of the muscles of the lip, nose and
palate are believed by advocates of the Delaire functional
repair philosophy to be possible at this stage, when the
component muscles of the orbicularis oris and perinasal
muscle ring can be more readily recognised.
The correction of the vertical dimensions of the
vermilion itself is equally important and the value of
identifying the 'dry' vermilion and restoring the vertical
height of the dry vermilion - and avoiding any use of
'wet' vermilion as a substitute - is being increasingly
recognised.
The importance of the restoration of the muscular
anatomy of the orbicularis oris in maintaining the
proportions of the lip, and especially the symmetry of the
face during dynamic movements, is crucial. Meticulous
attention needs to be directed to the careful detachment
of the abnormal insertions of the muscles into the soft
tissues and bony structures adjacent to the cleft as well as
reconstruction of the superficial and deep components of
the muscle. Some authorities propose that the accurate
reconstruction of the superficial part of the orbicularis
oris, which arises from the muscles of facial expression,
requires radical subperiosteal mobilisation of the facial
soft tissue mask to adequately reposition the muscles of
facial expression and reconstitute the anatomy of the lip.
Reconstruction of the anterior nasal floor and any
associated cleft of the primary palate is desirable at the
time of the primary lip repair as the access to these areas
is considerably facilitated at this time.
The nose
Primary correction of the cleft nasal deformity is now
widely accepted as an essential procedure for the resto-
ration of the symmetry of the nose. Several techniques
have been described. Those utilising extensive incisions
of the nasal lining should be avoided as the risk of
stenosis of the nasal airways is high.
The restoration of the nasal architecture, form and
symmetry can be properly achieved only by utilising the
tissues of the nose. The alar cartilage on the cleft side, or
both alar cartilages in a bilateral cleft, may be mobilised
quite radically through the cleft lip incisions, avoiding
the need for any incisions in the nasal lining. The growth
and development of the nose is very dependent on the
normal flow dynamics of the nasal airways and the temptation to use the lining of the inferior turbinates or similar
structures, which result in gross distortion of the airway
architecture, should be avoided.
The alveolus
Primary repair of the alveolus has been attempted by
many authorities in an attempt to stimulate normal development of the alveolar arch form. Primary bone
grafting, with cancellous bone at the time of lip repair,
has been largely abandoned because of long-term facial
growth problems that result. There is at present some
renewed interest in gingivoperiosteoplasty, which consists of initial orthodontic manipulation to produce
abutment of the gingival cleft edges prior to the lip repair
and a simple restoration of the gingival continuity with
minimal 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 to
as a secondary alveolar bone grafting procedure to distinguish it from alveolar closure undertaken at the time of
lip repair. This is a planned procedure in terms of the
timing of surgery and is undertaken at the age when
sufficient permanent teeth have erupted to allow
preoperative orthodontics with expansion of any collapse
at the site of the cleft and alignment of the alveolar
segments.
Resorption of the alveolar bone graft is likely to occur
if canine descent does not follow soon after the
procedure, and the bone grafting is therefore timed to
coincide as closely as possible with the time of expected
canine eruption at the site of the cleft. At the time of
alveolar bone grafting, it is common practice to augment
the bony foundation of the alar base on the cleft side with
cancellous bone chips or corticocancellous bone block to
improve the projection and symmetry of the nose.
Revision surgery might be indicated also for the lip and
137
the nose to minimise the total number of surgical
interventions.
Table 16.10
The primary palate
Fistula closure
Surgery for speech - pharyngoplasty
Rhinoplasty
Orthognathic surgery
Closure of the primary palate at the time of the lip repair
is recommended as access to this area is extremely
difficult after lip closure. The repair may be a single layer
repair using the mucoperiosteal lining of the vomer. Twolayer closures have been described if the gap is narrow or
using buccal mucosal flaps for the oral lining.
Secondary surgical procedures
fistula does not warrant closure if there is no demonstrable or predicted functional problems likely to be
associated with the fistula.
Surgery for speech
The secondary hard palate
The cleft of the bony secondary palate is often quite wide
and attempts to achieve closure may require extensive
lateral releasing incisions. Studies evaluating facial
growth in patients with unrepaired clefts of the palate or
delayed repairs clearly suggest that surgery of the palate
may be directly implicated in the subsequent restriction
of facial growth.
Some authorities undertake repair of the palate in two
stages by initially repairing the soft palate, which
encourages descent of the hard palatal shelves and
narrowing of the cleft gap, allowing closure at a second
stage with minimal dissection.
The soft palate
Early observations that the anteroposterior length of the
palate was deficient led to the design of passive push
back techniques aimed at lengthening the palate to allow
velopharyngeal contact. Detachment of the abnormal
insertions of the muscle elements into the soft tissues and
posterior edge of the bony hard palate and restoration of
the muscular anatomy of the soft palate is essential to
achieve effective velopharyngeal closure.
Secondary surgery
Secondary procedures in the management of cleft lip and
palate may be grouped chronologically, as listed in Table
16.10.
Fistula closure
138
Fistula closure following palatal cleft repairs is often
undertaken early if it is felt that the fistula may cause
functional problems with speech, swallowing or nasal
regurgitation of ingested foodstuffs. The presence of a
As speech develops, the regular and expert assessment of
a cleft speech therapist is essential to detect and rectify
problems of articulation or other speech problems. Velopharyngeal incompetence resulting from ineffective
closure of the velopharyngeal aperture is often not
correctable by conservative treatment and early surgical
intervention may be warranted.
Pharyngoplasties are designed to reduce the dimensions of the velopharyngeal aperture to facilitate closure
or simply increase the resistance of the airway to
minimise nasal air escape. They are broadly classified as
dynamic - procedures (e.g. orticochea pharyngoplasty),
which are designed to mobilise the palatopharyngeus
muscle bundles in the posterior tonsillar pillars and
attach them to the posterior pharyngeal wall - or passive
- procedures that simply narrow the velopharyngeal
aperture or augment the posterior pharyngeal wall using
implanted materials.
Rhinoplasty
The preschool age is also a common time for parents to
request secondary corrective procedures for the
asymmetry of the nose by a rhinoplasty procedure. If an
adequate primary rhinoplasty was undertaken and the
degree of asymmetry is within expected limits, every
additional procedure undoubtedly confers additional
scars within the nasal tissues, which may compromise
the final result. Secondary rhinoplasty at this age, or in
the preteen age group, should be undertaken only for
gross or obvious deformities causing problems of significant psychological or functional distress.
Secondary rhinoplasty at or nearing the end of the
growth phase is common. If orthognathic surgery is
planned, it is often preferable to undertake the surgery
following the orthognathic procedures to restore the symmetry and aesthetic balance of the face, and especially
the bony foundations of the nose. The procedure can be
combined with the orthognathic operation, if preferred,
to minimise the number of operative interventions.
Orthognathic surgery
With improvements in primary surgical techniques and
the recognition of the potentially harmful effects of
surgery on facial growth and symmetry, it is anticipated
that a smaller proportion of patients will eventually
require orthognathic procedures.
In those patients with gross occlusal problems caused
by restriction of midfacial growth or other facial skeletal
problems, Le Fort osteotomies, bimaxillary surgery, distraction osteogenesis, on-lay bone grafts or other procedures may be indicated. Fixed orthodontic appliances
are required to achieve the optimal occlusal outcome in
conjunction with surgery. The use of osseointegrated
implants and facial reconstruction is becoming more
common in the management of patients with clefts.
Philosophy
The management of the patient with a facial cleft
deformity is a lifelong project. The long-term consequences of each procedure undertaken must be
analysed carefully to weigh-up the potential advantages
and disadvantages with the full involvement of, initially,
the parents or carers and subsequently the patient. All
members of the cleft team should share equal responsibility in the decision-making process. It is essential that
the care of cleft patients is undertaken by dedicated cleft
teams with adequate centralisation of resources and
patient referrals. Continuous and intercentre audit of the
outcome of established protocols of care, which are
strictly enforced, is essential to monitor outcome and
refine techniques. It will also help to identify factors for
poor outcome. The search for the optimum protocol of
care is currently a subject of considerable interest and
speculation.
139
17
Management of orofacial
malignancy
Introduction
Oral cancer is the eighth most common malignancy
worldwide, although the prevalence varies from country
to country. In countries such as India, oral malignancy
accounts for 40% of the total, whereas in the UK around
4000 new cases present every year, accounting for
around 3% of all new malignancies. Around 50% of
these patients will die from their disease and overall
survival rates have not improved over the last three
decades, despite advances in surgical and oncological
techniques.
The incidence of oral cancer has been rising steadily
over recent years; the reasons for which are unclear. Oral
cancer generally appears from the sixth decade and
increases in incidence in subsequent decades. It should
be appreciated, however, that oral cancer can occur at any
age and the recent rise in incidence has been more
apparent in the younger age groups.
Oral cancer is almost exclusively squamous cell
carcinoma, which accounts for 90% of the total; the
remaining 10% is made up by salivary gland tumours
(8%) (see Ch. 14) and oral lymphoma (2%).
140
Over the past 30 years, social deprivation has become
strongly linked with oral cancer. In the early 1970s, oral
cancer was spread relatively evenly over all social
classes. When the detrimental effects of smoking became
clear, the better educated tended to reduce their cigarette
consumption, but those living in deprived areas have continued to smoke to a much greater degree. The aetiology
of oral cancer is, however, complex. The high-risk population is that least likely to attend the dentist and therefore most likely to present with advanced disease.
In the UK, the majority of patients tend to present
with advanced disease and, by definition, a poor prognosis. In many European countries, more than 70% of
patients present with early disease, increasing the chance
of cure and reducing the need for radical treatment.
Despite the fact that treatment for oral cancer has
advanced considerably over the last 30 years, survival
has not improved. This is due to the lack of understanding of tumour biology. Research into tumour
biology is coming to the fore, hopefully allowing the
development of new treatments.
Various aspects of the diagnosis and treatment of oral
cancer are discussed here (Table 17.1).
Table 17.1 The diagnosis and management of
oral malignancy
Aetiology of oral cancer
Aetiology
Morbidity
Premalignancy
Signs and symptoms
Staging of disease
Clinical investigation
Multidisciplinary treatment
Treatment planning
Treatment of the neck
Reconstruction
Quality of life issues
The aetiology of oral squamous cancer is complex. The
main factors associated with this disease are tobacco and
alcohol consumption. Each of these factors increases the
likelihood of oral cancer and both show a strong doserelated increase in incidence. It would seem that heavy
smoking 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 with
oral cancer. The risk of oral cancer is related to the
number of cigarettes per day and the length of time the
Fig. 17.1
The risk of oral cancer by alcohol/tobacco consumption.
patient has smoked, giving rise to the concept of pack
years, where a pack is equivalent to 20 cigarettes:
This formulation allows a calculation of the relative risk
of each patient. The relative risk returns to that of a nonsmoker 10 years after the cessation of smoking. Topical
tobacco, particularly, when mixed with areca nut, slaked
lime, and betel and placed as a quid in the buccal sulcus,
is a potent carcinogen. On the Indian subcontinent, where
the practice of chewing tobacco is common, oral cancer
makes up 40% of the total incidence of all carcinomas; it
is also prevalent in Asian communities in the UK.
Alcohol per se does not appear to be a potent
carcinogen but seems to potentiate the effects of tobacco.
Someone who smokes 30 or more cigarettes per week
has a relative risk of seven-fold that of a non-smoker. A
person who drinks 40 or more units of alcohol per week
has a relative risk of six-fold; if these factors are
combined then the relative risk of oral cancer increases
by a factor of 38.
Recent research suggests that genetic factors play a
significant part in the promotion of oral cancer. Cancer is
prevalent in some families and this can include oral
cancer. There is a cohort of patients who develop oral
cancer in the third or fourth decade. This group, mainly
women, develop aggressive cancers with a poor
prognosis.
Cellular biology investigations show that disturbances
in the regulators of cell growth and cell death (apoptosis)
lead to the development of oral cancer. This is a rapidly
expanding field and it is likely that new prognostic
indicators and cancer treatments will come from this
research.
Other agents that may be implicated in oral cancer
pathogenesis include malnutrition, poor dental hygiene,
infective agents and sunlight in lip cancer.
Oral cancer morbidity
The number of deaths from oral cancer has been rising
over the last 30 years. The death to registration ratio is
0.4, which is higher than many other cancers and similar
to cancer of the uterine cervix and breast. The site in
the mouth is an important prognostic indicator, with the
tongue having the poorest prognosis and highest mortality
(Table 17.2).
141
Table 17.2 Registration and deaths by site in
Scotland 1991-1996
Site
Registrations (%)
Deaths (%)
Tongue
Unspecified mouth
Floor of mouth
Lip
Oropharynx
Ill-defined sites
Gum
25.0
19.2
17.6
14.5
12.5
6.3
4.7
29.9
19.5
12.9
2.4
14.5
16.5
4.2
Cancer surveillance group 1998
Survival rates have not improved over the past
50 years, mainly due to late presentation of patients with
the disease. It has been shown that the delay in presentation correlates well with social deprivation. Education
programmes are required to target the at-risk groups, and
only when lifestyle begins to change is there a likelihood
of an improvement in survival.
Premalignant lesions
The vast majority of oral malignancies arise from
previously normal epithelium. A small number of new
malignancies may develop from abnormal mucosa.
White or red patches may precede the development of
cancer and allow the opportunity of early biopsy. This
will determine whether a lesion is premalignant. The site
and colour of these lesions can give some idea of their
malignant potential. A speckled or red lesion is more
likely to be premalignant than a homogeneous white
lesion. A lesion situated in the floor of mouth or lateral
border of the tongue, irrespective of colour, has a higher
chance of being premalignant. Biopsy is helpful in
determining the malignant potential of any lesion. A
lesion that persists for more that 2 weeks following
removal of chronic trauma should be referred for biopsy.
Many of these lesions are likely to be asymptomatic.
Signs and symptoms of oral
cancer
142
Tumours can be very advanced before patients develop
symptoms that cause them to present to their doctor or
dentist. Early warning signs include soreness in the
mouth, a lump or thickening, a red or white patch or a
non-healing ulcer. Later symptoms include interference
with speech or swallowing, weight loss, trismus, an
infected ulcer, pain referred to the ear, sensory disturbances and the appearance of a neck lump. Tumours
may be of considerable size before the latter symptoms
become apparent.
On examination, oral tumours have a variable
appearance. They may present as a white or red patch,
with or without an ulcer or erosion or as a lump or
thickening with intact mucosa. Classically, the squamous
cell carcinoma presents as an ulcer with a rolled margin
with induration around it. There may be fixation to
surrounding tissue and the ulcer may bleed readily after
minor trauma. Tumours of the oropharynx and tongue
base may first present as a neck lump. To make a diagnosis a biopsy is mandatory.
Staging of the disease
Cancer is staged using the TNM classification, where T
measures the primary tumour size, N the draining lymph
nodes, and M distant metastasis (Table 17.3). Using this
classification, these can be further stratified to stages
(Table 17.4). Using this universal language to identify
the extent of disease helps provide a prognosis, which is
dependent on stage. It also helps in defining treatment
protocols and in the analysis of management and survival
data. Knowing the extent of the disease is of prime
importance for clinicians working in multidisciplinary
teams so that the true extent of the disease is known.
Table 17.3
Tx
TO
T1
T2
T3
T4
NX
NO
N1
N2a
N2b
N2c
N3
MX
MO
M1
TNM staging
Tumour cannot be assessed
No evidence of primary tumour
Tumour <2 cm in greatest dimension
Tumour >2 cm but <4 cm
Tumour >4 cm
Tumour invading adjacent structures (e.g. skin,
cortical bone, deep muscles of tongue)
Regional lymph nodes cannot be assessed
No regional lymph nodes palpable
Single ipsilateral lymph node <3 cm
Single ipsilateral node >3 cm but <6 cm
Multiple ipsilateral nodes <6 cm
Bilateral or contralateral <6 cm
Any node >6 cm
Distant metastases cannot be assessed
No evidence of distant metastases
Distant metastases present
Table 17.4 American Joint Committee on
Cancer Staging guidelines on clinical staging
Stage 0
Stage 1
Stage 2
Stage 3
Stage 4a
Stage 4b
Stage 4c
Tis NO MO
T1 NO MO
T2 NO MO
T3 NO MO
T1-3 N1 MO
T4 NO–1 MO
T1–4 N2–3 MO
T1-4 N1-3 M1
The extent of the disease will determine the prognosis. 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 is
much poorer, with survival rates of around 45% and
25%, respectively. The presence of lymph node metastases can reduce survival by 50% and lymph nodes displaying extra capsular spread reduces the 5-year survival
to as low as 17%.
Initially, disease is staged clinically. However, clinical
examination is a poor indicator of the actual extent of
disease. Palpation of the neck is only sensitive and
specific in around 66% of cases and detection of lymph
nodes smaller than 2 cm is difficult, even under general
anaesthetic.
Clinical investigation
Clinical examination
When a patient presents with oral cancer, the suspicion
needs to be proven histologically. This is straightforward
if the lesion is in the anterior part of the oral cavity and a
biopsy can be harvested under a local anaesthetic. If this
is not possible then it is performed during an examination
under general anaesthetic. The examination under
anaesthetic allows the surgeon to examine the oral cavity,
oropharynx, nasopharynx, hypopharynx and larynx for
second 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 carried
out at this stage.
With oral cancer, almost 70% of second primaries
occur elsewhere in the oral cavity or oropharynx. The
major causes of tobacco and alcohol affect the whole of
the aerodigestive tract. This suggests that the whole tract
is at risk from cancer and more than one area can be
affected at any one time. The term 'field change' was
coined to describe situations where large areas of the
upper aerodigestive tract are affected with malignant or
premalignant change. For this reason, some units carry
out bronchoscopy and oesophagoscopy at this time.
However, these procedures show low pick-up rates for
second primaries and tend to be used only when the
patient has symptoms.
A tumour found initially is known as the index
primary. If a second distinct primary tumour is found at
the same time this is known as a simultaneous primary
whereas a second tumour found within 6 months of the
index tumour is known as a synchronous primary. Any
second primary found after the initial 6-month period is
described as a metachronous primary.
Most patients with oral cancer are likely to be heavy
smokers and drinkers. It is important that all investigations necessary for deciding whether the patient is
physically and mentally fit for treatment are carried out.
Particular attention should be paid to the cardiovascular
and respiratory systems, the nutritional status of the
patient, and his or her social circumstances. A psychological assessment can also be of value. This is to allow
an informed decision to be made on any further
treatment.
Imaging
A plain chest radiograph provides useful information
because many patients suffer from chronic obstructive
airways disease and some even have a second tumour. An
orthopantomogram with other views of the mandible
(e.g. occlusal views) provides information on the
condition and thickness of the mandible and the state of
dentition, and is an essential part in planning treatment
for oral cancer. Sophisticated techniques such as computerised tomography (CT) scans or magnetic resonance
imaging (MRI) are used for assessment of both the
primary and metastatic disease. Many centres favour a
CT scan from the diaphragm to the base of the skull to
identify evidence of second primaries in the aerodigestive tract, the state of the lungs, and the extent of the
primary disease and metastasis in the neck. An MRI scan
is slightly more sensitive and specific than a CT scan for
soft tissue imaging, with sensitivity up to 83% and
specificity of around 85%. Positron emission tomography (PET) scanning is emerging as a useful method
for detecting tumours, and also recurrence in previously
treated areas, with sensitivities and specificities reported
143
as slightly more than 90%. It is poor at anatomically
defining tumours but images can be combined and superimposed on CT or MRI scans to help determine resection
margins.
The use of lymphoscintigraphy techniques in determining nodal involvement and directing sentinel node
biopsy (see below) is showing significant promise in
determining malignant lymph nodes.
The multidisciplinary
approach to treatment
The multidisciplinary approach to the treatment of oral
and oropharyngeal cancer is now fundamental and all
units treating this disease should have a team of
specialists. The surgical disciplines of otolaryngology,
plastic surgery and maxillofacial surgery should all be
involved. A clinical or radiation oncologist with a
specialist interest in head and neck malignancy is also
mandatory. A specialist nurse, speech and language
therapist and nutritionist should also be present and a
cytopathologist should be on hand to give the result of any
fine-needle aspirates while the patient waits in the clinic.
A psychologist and social worker are also helpful in pretreatment assessment and post-treatment rehabilitation.
This multidisciplinary clinic is where all new patients
are assessed. In this environment, the patient's disease
can be discussed and a treatment plan formed and put to
the patient, based on all the information gleaned from the
examination and special investigations. Family and social
problems that might impact on treatment or quality of life
following treatment should also be discussed. Patients
who have been treated are also followed-up at this clinic
and problems with ongoing care can be identified and
treated.
Treatment planning
144
Although there have been advances in treatment, the
survival rates have not really improved. However,
techniques have helped to improve the quality of life for
many cancer patients even if survival has not been
prolonged.
Treatment comprises surgery, radiotherapy or combined treatment (particularly for larger or more aggressive
tumours). These treatments have been the mainstay of
oral cancer treatment for the last 50 years. Radiotherapy
is given in divided doses, usually over a period of 6 weeks.
One local regime is to give 66 Gy in 33 fractions over a
period of 61/2 weeks. Other forms of hyperfractionation
can be given to reduce the length of treatment and increase
the concentration of the radiotherapy effects.
Chemotherapy has a small role to play but, as new
drugs are developed and the biology of the disease
becomes more understood, its role may increase. Chemotherapy seems to be most effective when it is combined
with radiotherapy concomitantly. Currently, the most
effective drugs are platinum-based in combination with
5-fluorouracil. Synchronous chemoradiotherapy seems
to show some survival advantages as well as improved
function in large posterior tumours.
Brachytherapy, or implanted radiotherapy elements,
to the local site may be used to deliver a high dose of
radiotherapy to the index primary tumour while sparing
the surrounding tissues (e.g. the salivary glands). Plastic
tubes are looped through the tumour from the neck and,
after volumetric planning has been carried out, can be
loaded with radioactive wires. If the wires are too far
apart then insufficient radiotherapy levels will be
delivered to the tumour. Conversely, if the wires are too
close then tissue necrosis will ensue. Brachytherapy is an
important option for treating the tongue, particularly the
posterior tongue, because it allows function to be
preserved. The most common side-effect from brachytherapy treatment is pain at the tumour site.
The positive neck is usually treated surgically with the
addition of postoperative radiotherapy dependent on the
extent of neck disease.
In the UK, if combined therapy is required then the
surgery is carried out first in most cases.
When dealing with oral and oropharyngeal tumours, it
is critical that surgical margins should be clear of tumour
by more that 5 mm on the pathological specimen, because
this will have a considerable bearing on the outcome. It
has been shown that survival rates are reduced by 10% on
similar tumours, despite all other remedial treatment, if
the tumour is not completely excised. Many factors seen
on the pathological specimen will affect the outcome and
a specialist pathology service is therefore mandatory.
Tumour thickness, perineural invasion, vascular invasion,
lymphatic invasion, differentiation of the tumour cells
and whether the invasive front is cohesive are important
in deciding further treatment. Tumour thickness has a
bearing on the prognosis, with tumours less than 2 mm
thick having a much better prognosis than those with a
tumour thickness greater than 4 mm. If the invasive front
is cohesive then the prognosis is better than that with a
non-cohesive front, while perineural invasion has been
associated with local recurrence. Not surprisingly,
lymphatic invasion is associated with spread to the lymph
nodes whereas vascular invasion increases the likelihood
of distant metastases. When surgery is performed then
the decision to give postoperative radiotherapy may not
be made until the final pathology is reviewed.
Treatment of the neck
Treatment of the neck in oral and oropharyngeal
malignancy has raised a lot of debate in recent years. The
neck is divided into seven levels to describe the position
of the regional lymph node basin (Fig. 17.2). Only levels
I to V need to be considered when discussing oral
malignancy; levels VI and VII tend to be associated with
thyroid and parathyroid tumours.
Some definitions need to be discussed when referring
to neck dissections. A therapeutic neck dissection takes
place when disease is obviously present in the neck and
the dissection is undertaken to ablate the disease. An
elective neck dissection is used to describe a neck dissection that is undertaken when there is no obvious disease
in the neck but there is a high chance of occult disease
being present or where the neck is opened for access. This
type of neck dissection has become more common since
the advent of free tissue transfer, during which the neck
needs to be opened to facilitate microvascular reconstruction of the oropharyngeal defect. Many terms have been
Fig. 17.2 The seven levels of the neck. Showing the
position of the regional lymph node basin (level VI is deep
and 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 and
can mean different things to different people. It is now
proposed that two terms are used to describe neck
dissections:
• If five levels have been removed then this should be
described as a comprehensive neck dissection.
• Anything less than five levels should be termed a
selective dissection.
As with all neck dissections, the preserved structures
should be described and the dissected levels should be
named in selective dissections. This system tends to
remove any ambiguity when describing the dissection
carried out. In comprehensive neck dissections, the
accessory nerve should be saved if possible, but not at the
expense of good oncological resection, as sacrifice of this
nerve leads to poor shoulder function and pain. Other
structures, such as the internal jugular vein and
sternocleidomastoid, should also be spared if possible.
Surgery is usually the initial treatment for the overtly
positive neck with the possible exception of advanced
neck disease (N3) where preoperative radiotherapy or
chemotherapy can be used to shrink the mass prior to
surgical intervention. For positive disease, most surgeons
favour 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 neck
dissection has been subject to considerable debate. There
is some evidence that elective neck dissection confers a
survival advantage over monitoring the patient and
carrying out a subsequent therapeutic neck dissection
when overt disease develops. Many centres adopt the
protocol where, if the likelihood of metastatic disease is
higher than 20%, elective neck dissection should be
considered.
In the clinically N0 neck, it is perfectly acceptable to
carry out some form of selective neck dissection and, for
oral cancer, most surgeons dissect only levels I to IV
because metastasis in level V in a clinically negative neck
is exceptionally rare. All vital structures should be spared
to maintain as near normal function as possible but it is
important to realise that neck dissection is likely to incur
some morbidity no matter how carefully the dissection is
earried out.
Sentinel node biopsy is currently under investigation
but offers a promising way forward for dealing with the
145
clinically N0 neck. The basis of sentinel node biopsy is
that tumour will migrate to the regional nodes and will
first collect in a node called the sentinel node. The
sentinel node can be identified by using a triple diagnostic approach of lymphoscintigraphy, injection of blue
dye and a hand-held gamma probe for localisation at the
time of surgery. This offers a relatively easy way of harvesting the sentinel node for histological analysis. If the
node turns out to be positive for metastatic tumour, the
patient goes on to have a neck dissection.
wound healing by a mixture of contacture and reepithelialisation. One problem with laser excision is that
any resection specimen will have thermal damage and
pathological examination of margins will be impossible.
In theory, scarring is less and, if selection of the tumour
is correct, then function will be minimally affected. Reepithelialisation is most effective where there is no
possibility of contracture. Raw surfaces can be left in the
hard palate, for example, which will re-epithelialise over
a period of time.
Reconstruction in the head
and neck region
Skin grafts
The main aim of reconstruction around the head and neck
is to maintain form and function. Many techniques have
evolved over the years, resulting in improvements in
function and cosmesis and allowing larger and more
complex defects to be reconstructed. Despite this,
survival rates have not improved, although quality of life
is much better. Depending on the defect, a reconstruction
ladder can be used, starting with the simplest and leading
to the most complex techniques.
A basic principle of reconstruction is to replace like
tissue with like. Unfortunately, this is rarely possible in
replacing oral mucosal lining, which is very specific. The
oral mucosa is moist, sensate, and has specialised
receptors for taste. It is sometimes fixed to bone, as in the
gingiva and hard palate, or is elastic and freely mobile, as
in the buccal area, ventral surface of tongue and floor of
mouth. As there is no ideal replacement for oral mucosa,
most techniques rely on importing skin. The disadvantage of this is that skin is dry, often insensate, and
has no specialised receptors for taste. Often, the best that
can be achieved is to restore the anatomy of the oral
cavity in an effort to maintain form and function.
Primary closure
146
Primary closure is the simplest form of reconstruction
and is particularly helpful in lip reconstruction. It is
possible to resect up to one-third to one-half of the lip
without using any flap reconstruction. Primary closure is
also used after resection of small tumours of the mobile
tongue, floor of mouth and buccal mucosa. Superficial
tumours can be excised using a carbon dioxide or KTP
laser (see Ch. 38). The use of a laser allows the excision
or ablation of tumours without reconstruction, the
It is perhaps surprising that skin grafts can take successfully within the contaminated and wet environment of the
oral cavity. They are best used as split thickness grafts
and in situations where there is a well-vascularised graft
bed such as the muscle of the tongue. The grafts are fixed
by sutures, using a quilting technique to avoid shearing
during movement of the oral cavity. Grafts are also useful
for increasing the height of the labial sulci as in
vestibuloplasty where they can be held in position by
fixed splints.
Other methods of reconstruction, including local and
distant flaps, are discussed in Chapter 15.
Quality of life issues
As mentioned previously, survival has not improved
significantly over the past 20 years and one of the main
treatment goals is to improve the quality of life for oral
cancer patients. The problem is how to measure quality
of life. This is now being resolved with questionnaires to
try to assess this aspect of treatment. These questionnaires look at psychological and social aspects of
patients' lives as well as functional performance. The two
questionnaires usually used are The European Organisation for Recognition and Treatment of Cancer (EORTC)
and The University of Washington Quality of Life
Questionnaire (UW-QOL). The EORTC contains general
questionnaires for all cancers and a head and neck
module specifically for cancer in that region, whereas the
UW-QOL is a head-and-neck-specific questionnaire.
With the use of these questionnaires it is becoming easier
to recognise which treatments help or adversely affect
quality of life. This area of cancer management is still in
its infancy, but will generate a lot of interest and will help
define the best treatments in the future.
18
Otorhinolaryngology
(ENT) surgery
Introduction
Otorhinolaryngology, more commonly known as ear,
nose and throat (ENT) surgery, deals with conditions
affecting the head and neck, upper aerodigestive tract and
organs of special sense. The range of conditions managed
by ENT surgeons is vast and includes conditions as
diverse as neonatal airway obstruction, cerebellopontine
angle tumours and cosmetic rhinoplasty. The scope of
ENT reviewed in this chapter has been limited to that
which may be encountered in dental and oral surgical
practice. Relevant conditions include those affecting the
pharynx, nose, paranasal sinuses and neck. Special
attention is given to management of airway obstruction
and aspects of head and neck malignancy (Table 18.1).
Techniques of examination
in ENT
Like dental surgeons, ENT practitioners can see most
of the organs and areas of interest. Even areas that are
not easily or directly visualised, such as the larynx and
paranasal sinuses, can be examined indirectly using
specialised instrumentation such as mirrors and endoTabte 18.1 ENT conditions encountered in
dental practice
Airway obstruction
Diseases of:
phaarynx
noase
paranasal sinuses
Neack
Epistaxis
Head and neck malignancy
Fig. 18.1
Examination of the larynx and pharynx using
traditional headlight indirect laryngoscopy.
scopes. The special techniques of physical examination
in ENT are difficult to master and trainees in the
specialty spend many months acquiring the basic skills
needed to view the larynx, nasopharynx and posterior
nasal cavity. Traditionally, the pharynx and larynx have
been examined using mirrors and headlight illumination
(Fig. 18.1), but recently fibreoptic and rigid endoscopes
have superseded these techniques (Fig. 18.2).
After an initial review of emergency airway management we will consider some of the more common and
relevant ENT conditions. For reasons of relevance and
brevity, otology has been excluded.
Emergency management of
upper airway obstruction
Perhaps the most challenging clinical situation is a
patient with sudden, severe airway obstruction. Although
147
Acute airway obstruction
Sudden complete laryngeal obstruction is easily diagnosed, as severe respiratory distress is rapidly followed
by cyanosis and collapse. More often, however, laryngeal
obstruction is incomplete and is signified by a less
dramatic increase in respiratory effort, difficulty
speaking and stridor. Stridor is a coarse inspiratory noise
produced as the patient attempts to inhale forcibly
through a narrowing at the level of the larynx. Stridor is
easily distinguished from stertor, which is a rattling
gurgling noise produced by soft tissue obstruction or
retained secretions at the level of the oropharynx.
Fig. 18.2 Modern flexible fibreoptic
nasopharyngolaryngoscopy.
this scenario is fortunately rare, it is important that
clinicians operating in the oral cavity and pharynx have
an awareness of the possible causes of acute airway
compromise and have the necessary equipment and skill
to deal with it. The laryngeal airway is a narrow and
functionally complex system whose most important role
is to separate and protect the airway from the digestive
tract. The diameter of the space between the vocal cords
(glottis) is such that even small foreign bodies can cause
severe and life-threatening airway obstruction. This risk
of airway obstruction is greater in children due to the
relatively small dimensions of the juvenile larynx and the
natural tendency for children to put toys, beads, pen-lids,
etc. into their mouths. Other causes of acute airway
obstruction are shown in Table 18.2.
Immediate management of laryngeal
obstruction
Emergency management depends on the degree of
obstruction and the level of expertise and equipment
available to deal with it. Mild stridor requires urgent
management but allows time for specialist help to be
summoned, whereas acute severe respiratory collapse
demands immediate on-the-spot treatment. It is important
that all practitioners have a rehearsed plan and the
necessary instrumentation available for dealing with
catastrophic airway obstruction, even though most will
never encounter such a case.
The options for treating are shown in Table 18.3. Of
these techniques, only the Heimlich manoeuvre and
laryngotomy are appropriate to non-specialist settings.
Endotracheal intubation and tracheostomy require
advanced skills and instrumentation.
Heimlich manoeuvre
Table 18.2
148
Causes of airway obstruction
Foreign bodies
food bolus
part of a toy, pen top
tooth
Infection
acute epiglottitis
Trauma
laryngotracheal trauma
orofacial trauma
Caustic inhalation/ingestion
Laryngeal tumour
carcinoma
papilloma
The Heimlich manoeuvre is a technique for relieving
airway obstruction caused by an impacted foreign body.
If the patient can cough or speak, then the airway
obstruction is incomplete and the Heimlich manoeuvre is
not appropriate. Stand behind the patient with the arms
encircling the patient's abdomen and crossed at the level
of the patient's umbilicus. A forceable thrust upwards
Table 18.3
Treatment of laryngeal obstruction
Heimlich manoeuvre
Aspiration and endotracheal intubation
Laryngotomy (cricothyrotomy)
Tracheostomy
needle or cannula can be inserted through the membrane
into the airway and this may be sufficient to temporarily
relieve the obstruction. A horizontal stab incision is then
made using a knife or scalpel and, without withdrawing,
the blade is turned through 90° to open the incision. Once
the cricothyrotomy has been performed it can be held
open 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 a
small-bore endotracheal tube and a specially designed
scalpel, are commercially available. General dental
practitioners and others carrying out procedures in the
oropharynx in non-hospital settings would be well
advised to purchase a cricothyrotomy kit and keep a
small emergency tray set up in their surgery to deal with
such an unlikely emergency.
The pharynx
Anatomy and physiology of the pharynx
Fig. 18.3
The Heimlich manoeuvre.
and backwards is used to compress the patient's
abdomen in an attempt to push the diaphragm upwards
and expel the lodged foreign body (Fig. 18.3).
Laryngotomy
If all else fails and the patient is in extremis, an emergency
surgical opening into the airway below the level of the
vocal cords (most likely level of obstructing lesion) has
to be created. The cricothyroid membrane provides an
anatomical window for gaining access to the airway.
Anaesthesia may not be appropriate as, by the time a
decision is made to perform a laryngotomy, the patient is
usually semiconscious.
For laryngotomy, full extension of the neck is
essential. If the subject is a child, lay the patient across
the knee of an assistant with the neck hyperextended and
firmly palpate the midline structures of the neck. Starting
from the prominence of the thyroid cartilage, run a finger
down the midline until the prominent ring of the cricoid
cartilage is palpated. Above the cricoid ring and below the
lower border of the thyroid cartilage lies the cricothyroid
membrane. With the neck sufficiently extended, there
are no intervening structures between the cricothyroid
membrane and the skin. As a first step, a wide-bore
The pharynx is a fibromuscular tube that constitutes
the upper aerodigestive tract. It is formed by the
buccopharyngeal fascia and the overlapping pharyngeal
constrictor muscles, which extend from the level of the
base of the skull to a lower limit at the sixth cervical
vertebra (C6). At C6 the cricopharyngeus fibres of the
inferior constrictor form the upper oesophageal sphincter.
The pharynx is usually divided into three regions: the
nasopharynx, oropharynx and hypopharynx.
The nasopharynx extends from the skull base to the
level of the hard palate. It is lined by transitional respiratory epithelium and contains abundant lymphoid tissue.
The main structures of clinical note in the nasopharynx
are the nasopharyngeal tonsil, or adenoid, and the
eustachian (pharyngotympanic) tubes, which communicate between the middle ear and the nasopharynx.
The oropharynx extends from the level of the hard
palate to the hyoid bone and is lined by stratified
squamous epithelium. Anteriorly, the oropharynx
communicates with the oral cavity at the palatoglossal
folds. Lymphoid tissue is abundant and, in the oropharynx, the most prominent aggregations of lymphoid
tissue are the palatine tonsils and the lingual tonsils.
The hypopharynx extends from the level of the hyoid
bone to the upper oesophageal sphincter (cricopharyngeus
fibres of the inferior constrictor). It is lined by stratified
squamous epithelium and communicates anteriorly with
the larynx.
149
Benign conditions of the pharynx
Nasopharynx
The nasopharynx is often involved in upper respiratory
tract infections, and the common cold is usually associated
with nasopharyngitis. Symptoms of nasopharyngitis consist
of discomfort and pain associated with swelling of the
lymphoid tissue, which leads to nasal obstruction and
seromucinous secretion more commonly referred to as
catarrh. Nasopharyngitis is usually a self-limiting condition
but, in some patients, chronic low-grade inflammation can
occur, leading to nasal obstruction and chronic catarrh.
In children, the nasopharyngeal tonsil, or adenoid, can
occupy almost all of the nasopharyngeal space. Acute
respiratory infections can cause acute adenoiditis with
mucopurulent postnasal discharge, nasal obstruction and
fever. Such episodes of acute infective adenoiditis are
common in childhood and may lead to chronic adenoidal
hypertrophy, mouth breathing, nasal obstruction and
chronic mucopurulent postnasal discharge. The juxtaposition of the eustachian tubes to hypertrophied and
inflamed adenoids is thought to be important in the
causation of middle-ear effusions. The adenoid may
therefore be important in the most common cause of
hearing impairment in childhood – otitis media with
effusion, more frequently known as 'glue ear'. Children
with enlarged and inflamed adenoids often have difficulty
eating because they are obligate mouth breathers.
Symptoms include disturbed sleep, nocturnal cough and
middle-ear effusions. Adenoidectomy offers an effective
treatment in such children.
The adenoid gradually atrophies with age and becomes
relatively less important as the nasopharynx grows, thus
adenoid problems in adults are rare. Symptoms suggestive
of adenoidal hypertrophy in the adult should raise the
suspicion of a nasopharyngeal tumour (see below).
the cause cannot be ascertained, but there appears to be
an association with nasal disease. The treatment of
chronic pharyngitis involves identification of the cause,
treatment of any nasal disease, increased fluid intake and
avoidance of antibiotics, as these can sometimes lead to
secondary candidiasis. In some cases, topical nasal
steroid sprays can help reduce the inflammation.
Tonsillitis
Acute tonsillitis is a common cause of a sore throat.
Although the initial organism may be viral, superinfection with a beta-haemolytic Streptococcus usually
ensues. Acute tonsillitis can also be a complication of
glandular fever. The symptoms are sore throat, pain on
swallowing (odynophagia), systemic malaise, headache
and fever. Because of pain on swallowing, patients tend
to avoid eating and drinking and, therefore, can become
significantly dehydrated and debilitated. Diagnosis is
usually obvious with trismus, tonsillar hypertrophy, and
pus visible in the tonsillar crypts; there will be associated
cervical adenitis. Treatment involves high fluid intake,
analgesics and penicillin. In severe cases the patient may
be unable to swallow oral antibiotics, thus, a short course
of intravenous benzyl penicillin may be indicated (Fig.
18.4). Complications of tonsillitis include a peritonsillar
abscess (quinsy).
Tonsillectomy
Tonsillectomy used to be an extremely common operation
and was often used incorrectly as a treatment for nonspecific sore throat (pharyngitis).
Oropharynx
150
Acute infective oropharyngitis presents as a sore throat,
pain on swallowing and fever. The cause is usually viral
and the condition is self-limiting, responding to symptomatic measures such as paracetamol, saline gargles and
a high fluid intake. Throat swabs seldom yield any
significant growth. Severe, non-resolving pharyngitis
should raise the possibility of glandular fever.
Chronic pharyngitis presents as persistent, dry, sore
throat and irritation and discomfort on swallowing. Often
Fig. 18.4
Acute tonsillitis.
Tonsillectomy is carried out by dissecting the tonsils
from their fossae and ligating any bleeding points
encountered. The most frequent major complication is
postoperative haemorrhage, which occurs in approximately 2% of cases. Minor secondary tonsillar haemorrhage can also occur up to 2 weeks after the operation
and is usually managed conservatively using antibiotics
and saline gargles.
Indicatons for tonsillectomy
Current indications for tonsillectomy include: a clear
history suggesting that the sore throats are due to
tonsillitis on five or more occasions per year over a
period of at least 1 year, or evidence that these episodes
of sore throat are disabling and preventing normal
function at school or work.
Patients often complain of white or yellow lesions on
their tonsils. These are foul tasting and may be associated
with halitosis. Examination shows numerous white
granules occupying the tonsillar crypts; these are often
diagnosed incorrectly as food debris. In fact, the most
frequent cause of this is actinomycotic colonies within
the tonsillar crypts. Actinomycetes are normal oral
commensals but in some patients they 'overgrow' and
form so-called 'sulphur' granules within the tonsillar
crypts. Patients often use antiseptic mouthwashes to
try and cure the problem, but this may well be the cause
rather than the cure! Treatment includes reassurance
and the avoidance of antiseptic mouthwashes. Some
patients, however, are significantly debilitated by this
problem and this may be seen as a rare indication for
tonsillectomy.
Tonsillectomy can also be used in the surgical treatment of snoring. Significant debilitating snoring, which
can lead to extreme social distress, is related to obesity
and, in some cases, tonsillar hypertrophy. Most surgical
procedures for snoring involve modification and
stiffening of the soft palate. The uvulopalatopharyngoplasty (UPPP) operation involves palatal shortening
and tonsillectomy. However, there is no good evidence
that snoring surgery is beneficial, as results are often
poor and snoring recurs within 2 years of successful
surgery in 60% of patients. Snoring alone is not an
indication for tonsillectomy.
Prions have been demonstrated in tonsillar tissue
from patients with new variant Creutzfeldt–Jakob disease
(vCJD; see Ch. 7). Because of the potential risk of
transmission of prion disease, disposable instruments are
now recommended for all tonsillectomies.
Hypopharynx
Benign hypopharyngeal disease often presents as a
feeling of something in the throat with or without
dysphagia. An accurate history needs to be taken from all
patients complaining of pharyngeal discomfort and
dysphagia. Warning signs and symptoms are, weight
loss, pain referred to the ear and dysphonia (hoarseness).
A common benign cause of 'a feeling of something in
the throat' is the globus pharyngeus syndrome, which
used to be referred to as globus hystericus. This condition
is thought to be due to neurological incoordination of the
cricopharyngeus muscle. It is more common in females
and is not associated with pain, referred otalgia or weight
loss. It is important to note that globus pharyngeus is a
diagnosis of exclusion that is made only after normal
endoscopy and/or normal barium swallow investigations.
A pharyngeal pouch is a diverticulum at the lower
part of the pharynx. Cricopharyngeal spasm is implicated
in its causation. Patients present with intermittent
dysphagia and regurgitation of partially digested foodstuffs. A characteristic appearance is seen on a barium
swallow (Fig. 18.5) and the diagnosis is confirmed at
rigid endoscopy. Treatment of pharyngeal pouch can be
carried out by open (excision) or endoscopic means
(drainage of pouch into oesophagus).
Tumours of the pharynx
Tumours of the pharynx will be considered under benign
and malignant lesions affecting the nasopharynx, the
oropharynx and the hypopharynx in turn.
Nasopharynx
Benign tumours of the nasopharynx
Tumours of the nasopharynx present with symptoms
that can be confused with adenoid enlargement or nasal
obstruction. Thus, a high index of suspicion is required
and all cases should undergo pernasal endoscopic
examination.
Juvenile nasopharyngeal angiofibroma (JNA) is a
benign vascular tumour that occurs in adolescent males.
It presents with unilateral nasal obstruction and epistaxis.
151
diagnosis and treatment involves embolisation prior to
resection.
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 middleear effusion secondary to eustachian tube obstruction. In
advanced cases, nasopharyngeal malignancy will invade
the skull base and give rise to cranial nerve palsies.
Nasopharyngeal cancer is usually squamous but poorly
differentiated or anaplastic variants are not uncommon.
Salivary gland tumours (adenoid cystic carcinoma) and
non-Hodgkin's lymphoma also occur.
Nasopharygeal carcinoma is much more common
in parts of Asia than in the UK. In Hong Kong,
nasopharyngeal carcinoma is one of the most common
head and neck malignancies, and its aetiology is thought
to involve an interaction between infection with the
Epstein–Barr virus and racial/genetic predisposition.
Malignancy in the nasopharynx often metastasises early
to upper deep cervical lymph nodes. Presentation is
usually late and curative surgical treatment is seldom
possible. Radical radiotherapy (with or without chemotherapy) can give good results in those patients who are
diagnosed in the early stages.
Oropharynx
Benign tumours of the oropharynx
Fig. 18.5
152
Contrast radiograph of a pharyngeal pouch.
JNA is of unknown aetiology but hormonal influences
associated with puberty are thought to be implicated. If a
tumour is identified in a young male it is important to
consider the possibility of a JNA because biopsy could
prove catastrophic! MRI and angiography confirm the
Benign tumours of the oropharynx are relatively
uncommon. Tonsillar inclusion cysts, which present as
smooth, rounded swellings associated with the upper
pole of the tonsil are commonly mistaken for tumours.
Viral papillomata can be found on the faucial pillars,
tonsil and posterior pharyngeal wall. Their presence
raises the possibility of coexisting laryngeal and genital
papillomatosis. Treatment includes excision or laser
ablation.
A lingual thyroid presents as a smooth swelling in the
midline of the posterior one-third of the tongue. It is due
to a thyroid developmental abnormality that results in
persistence of thyroid tissue in the region of the foramen
caecum.
Tumours of the minor salivary glands may also present
in the oropharynx. Numerically they are most likely to
be pleomorphic salivary adenomas, but low-grade
mucoepidermoid tumours should also be considered (see
Ch. 14).
Malignant tumours of the oropharynx
Malignant oropharyngeal tumours most commonly
involve the tonsils. Squamous cell carcinoma is the most
frequent histology and aetiological factors include
alcohol and smoking. Tonsillar carcinoma often presents
late with spread into the adjacent structures of the soft
palate, tongue base and mandible. There is a high incidence of nodal spread to the deep cervical chain at the
time of diagnosis. Early tonsillar carcinomas can be
treated by radical radiotherapy. More advanced cases
need major surgical resection, which involves
mandibular splitting for surgical access. Excision of the
tumour and adjacent involved structures (mandible,
pharyngeal wall, tongue) and comprehensive neck
dissection (Ch.17) is followed by reconstruction using
radial artery free grafts or pectoralis major
myocutaneous flaps (Ch. 15).
The oropharynx may also be the site of non-Hodgkin's
and Hodgkin's lymphomas arising in the lingual and
palatine tonsils. Treatment of lymphoma includes radiotherapy and chemotherapy.
Hypopharynx
the presenting feature is cervical lymphadenopathy due
to nodal metastases. The symptoms of piriform fossa
tumours are often relatively minor and it is therefore
essential that a high index of suspicion is maintained. In
particular, patients should not be diagnosed as suffering
from globus pharyngeus unless a full endoscopic
examination has been carried out. Piriform fossa tumours
can be treated using radiotherapy (if diagnosed early
enough), but advanced disease requires laryngectomy,
partial pharyngectomy and reconstruction. Adjuvant
radiotherapy is usually required and comprehensive neck
dissection is used to treat nodal disease.
Postcricoid carcinoma has a presentation similar to
other hypopharyngeal conditions. Dysphagia is severe
and progressive, with weight loss in advanced cases.
Clinical examination reveals pooling of secretions in the
hypopharynx and patients will often have cervical
adenopathy. Examination under anaesthesia and biopsy
through rigid hypopharyngoscopes establishes the
diagnosis. Staging relies on the findings at examination
under anaesthesia and computerised tomography (CT) or
magnetic resonance imaging (MRI) results (see Ch. 17).
Early-stage disease can be treated using radical external
beam radiotherapy but more advanced cases require
surgery. Due to a high incidence of synchronous oesophageal malignancy (skip lesions) concomitant resection
of the oesophagus and gastric or free jejunal interposition
is the surgical treatment of choice.
Benign tumours of the hypopharynx
The hypopharynx consists of the piriform fossae, the
posterior wall and the postcricoid region. Benign tumours
of the hypopharynx are extremely unusual and present
with symptoms similar to the globus sensation. Fibromas,
schwannomas, papillomata and benign salivary tumours
can all occur.
Malignant tumours of the hypopharynx
Although any hypopharyngeal site can be involved,
the most common lesions affect the piriform fossa and
postcricoid regions.
Piriform fossa tumours are predominantly squamous
cell carcinomas. They present with vague symptoms of a
feeling of 'something in the throat' and intermittent,
variable dysphagia. As the tumour enlarges and invades
adjacent structures the patient will present with otalgia
due to referred pain. Dysphagia increases and weight loss
and aspiration of secretions ensues. In a high proportion,
Larynx
Benign and malignant disease of the larynx will be
considered after a review of its anatomy and functions.
Anatomy and physiology of the larynx
The larynx occupies the junction between the common
aerodigestive and respiratory tracts. The basic framework
of the larynx consists of the thyroid cartilage articulating
superiorly with the hyoid bone and inferiorly with the
cricoid bone. Superiorly, the epiglottis and aryepiglottic
folds form the laryngeal inlet region, which leads down
to the middle section of the larynx consisting of the false
and true vocal cords. The false vocal cords, or vestibular
folds, lie above and parallel to the true vocal cords and
are separated from them by the shallow gutter of the
laryngeal ventricle. The principal nerve supply to the
larynx comes from the recurrent laryngeal branch of
the vagus nerve, which reaches the larynx after looping
153
round the arch of the aorta on the left, and round the
subclavian artery on the right. The blood supply is derived
from branches of the superior and inferior thyroid
arteries, lymphatic drainage is to the upper deep cervical
nodes superiorly, lower deep cervical nodes inferiorly,
and pre-thyroid nodes anteriorly.
The functions of the larynx are phonation and
protection of the lower airway.
Disorders of the larynx may impair the ability of the
vocal cords to adduct, resulting in aspiration and
weakness of the voice. Inability to abduct the vocal cords
to produce a satisfactory laryngeal airway may result in
airway compromise which will present as stridor and
shortness of breath. Lesions of or on the vocal cords will
alter vocal cord tension and resonance leading to hoarseness (dysphonia) as the presenting symptom.
Examination of the larynx
Traditional indirect laryngoscopy used headlight illumination and an angled mirror. The technique is difficult
and some patients are unable to tolerate the examination.
It is more common today to examine the larynx using a
fibreoptic laryngoscope passed via the nasal cavity (see
Fig. 18.2). This produces an excellent view of the vocal
cords and allows function to be assessed under direct
vision.
Benign laryngeal disease
Acute laryngitis
154
Chronic laryngitis
Chronic, painless dysphonia is more common in people
who smoke and in those who use their voice to excess
such as, amateur singers, teachers and lecturers. In its
simplest form, chronic laryngitis is associated with nonspecific, low-grade inflammatory thickening of the vocal
cords. This produces an alteration in voice quality that
responds slowly to conservative measures. Severe cases
can progress to Reinke's oedema of the subepithelial
space of the vocal cord. This leads to severe dysphonia
and, on examination, swollen oedematous vocal cords are
evident. In extreme cases Reinke's oedema can produce
severe polypoid swelling of the vocal cords.
Vocal nodules are another feature of chronic laryngitis
and appear as small fibrotic thickenings of the central
portion of the vocal cord. Excision can be carried out
using endoscopic microsurgical techniques, or with
endoscopic laser therapy.
Vocal cord papilloma
Viral papillomata of the larynx due to the human
papilloma virus can affect all ages but are more common
in children and young adults than in older people. The
usual presentation is dysphonia but papillomatosis can
also cause respiratory distress.
Vocal cord palsy
Vocal cord palsy presents as painless dysphonia and a
characteristic 'bovine' cough. It is caused by damage to
either recurrent laryngeal nerve. Left recurrent laryngeal
nerve damage is more common due to its longer course
in the thorax. The most common cause of a left vocal
cord palsy is a bronchial cancer and, in all patients
presenting with a palsy, a chest radiograph is mandatory.
Other causes of vocal cord palsy include inadvertent
damage to the recurrent laryngeal nerve during thyroid or
cardiothoracic surgery.
Acute laryngitis is common and often accompanies
upper respiratory tract infections, especially if associated
with simultaneous voice abuse and ingestion of irritants.
Alcohol, cigarettes and voice abuse (shouting or singing)
can cause acute inflammation of the vocal cords, as can
mechanical and chemical irritation. The patient complains of hoarseness and a mild sore throat, sometimes
with pain on swallowing. In the absence of bacterial
superinfection, acute irritant laryngitis usually settles
with voice rest, a high fluid intake and simple analgesics.
Malignant tumours of the larynx
If associated with an upper respiratory tract infection,
Cancer of the larynx is the most common head and neck
acute laryngitis may progress to bacterial infection,
malignancy encountered by ENT surgeons. Any of the
which will present with more severe symptoms and fever.
laryngeal subsites (supraglottis, glottis or subglottis) can
Diagnosis is made on fibreoptic endoscopy. Treatment
be involved but in the UK the glottis is the most common
involves broad-spectrum antibiotics. Failure to respond
site. Even very small tumours involving the vocal cords
within
2 weeks is an indication for referral to an ENT
produce significant dysphonia. The dysphonia produced
department.
by a laryngeal cancer is indistinguishable from that
produced by a vocal nodule or chronic laryngitis and,
therefore, all patients with hoarseness should be treated
seriously and early referral in those who do not resolve
should be routine. Laryngeal cancer is more common in
heavy smokers than in non-smokers, and alcohol intake
appears to be synergistic in supraglottic disease. Patients
present with dysphonia and, in advanced cases, with
respiratory compromise. Squamous cell carcinoma is the
usual histology.
Investigation includes indirect or endoscopic
laryngoscopy.
The treatment of laryngeal carcinoma depends on
the site and stage of the disease. Early tumours can be
effectively treated using courses of radical radiotherapy.
More advanced cases of laryngeal carcinoma almost
invariably require total laryngectomy followed by
adjuvant radical radiotherapy and comprehensive neck
dissection to eradicate disease.
Following total laryngectomy, speech rehabilitation is
required. The most common technique employs a oneway tracheopharyngeal speaking valve, which is placed
between the back wall of the trachea and the reconstructed
pharynx. This allows the patient to exhale air from the
trachea into the pharynx. The shunted air moves the
pharyngeal walls and produces vibrations, which can
then be modulated into a form of speech. Most patients
following total laryngectomy manage to achieve good
voice rehabilitation using these valves.
wall. The nasal cavities communicate with the nasopharynx behind and with the nostrils anteriorly. The
lateral nasal walls are formed by the inferior middle and
superior turbinates with their associated meatuses. The
nasal floor is the hard palate and the roof of the nasal
cavity lies in the region of the cribriform plate. The nasal
cavity has a particularly rich blood supply that is derived
from both the external and internal carotid circulations, a
feature that is in part responsible for the frequency of
spontaneous nasal bleeding (epistaxis).
The nose has five principal physiological functions
(Table 18.4).
Nasal malfunction leads to dry, cold, unfiltered air
reaching the nasopharynx with resultant risks of
inflammation and secondary infection. Nasal conditions
can therefore manifest as rhinorrhoea, nasal airway
obstruction, pharyngitis and mouth breathing, and
abnormalities of olfaction (hyposmia).
Causes of nasal obstruction
Rhinitis
Rhinitis is defined as inflammation of the lining of the
nose characterised by one or more of the following
symptoms: nasal congestion, rhinorrhoea or sneezing
and itching. There are many different causes of rhinitis
but the most prevalent is the common cold (Table 18.5).
Nose
Table 18.4
Anatomy and physiology of the nose
Airway
Filter
Humidification
Heat exchange (warming inspired air)
Olfaction
The nose is divided by the piriform aperture into an
anterior (facial) component and a posterior nasal cavity.
Both components are subdivided into right and left by the
nasal septum. The nasal septum is predominantly bony
in the posterior cavity and cartilaginous anteriorly. The
external nose is covered by skin, subcutaneous tissue and
a musculoaponeurotic layer. The upper 40% of the
external nose consists of paired nasal bones, which
articulate with each other and with the frontal processes
of the maxillae and the maxillary processes of the frontal
bones. The lower 60% of the external nose is cartilaginous
consisting of the paired upper lateral cartilages and lower
lateral cartilages.
Posteriorly, the right and left nasal cavities are
separated by the nasal septum, which forms their medial
Functions of the nose
Table 18.5 A simplified classification of rhinitis
Allergic
seasonal and perennial
Infectious
acute and chronic
Other
idiopathic
occupational
medicamentosa
hormonal
vasomotor
155
The treatment of rhinitis depends on the cause. The
common cold is usually self-limiting and responds to
the short-term use of topically applied decongestants
(ephedrine or xylometazoline), which most patients self
prescribe. Most other forms of chronic rhinitis respond
to potent topical steroids such as beclomethasone or
mometasone, but these drugs should not be used without
medical supervision. Persistent nasal obstruction, rhinorrhoea and nasal congestion, especially if unilateral, should
be seen as a reason for referral to a specialist.
Septal deviation following nasal trauma
The quadrilateral cartilage of the septum may be
fractured, resulting in a septal deviation that can give
rise to nasal obstruction. Characteristically, this produces
unilateral nasal obstruction and examination reveals a
convexity of the septum touching the lateral nasal wall.
The unilateral nature of the symptoms helps distinguish
this from rhinitis. Treatment consists of the operation of
septoplasty, which resects and straightens the quadrilateral cartilage, perpendicular plate of ethmoid and
vomer, and thus recentralises the septum.
Nasal polyps
Nasal polyps are inflammatory masses that originate
predominantly from the lining of the ethmoid sinuses.
Polyps are more common in patients with asthma and, in
a proportion of patients, there is an association with
aspirin allergy. Symptoms are similar to severe rhinitis,
with total nasal obstruction, hyponasal speech, hyposmia
and nasal discharge. Diagnosis is usually easy on nasal
examination. Polyps should be referred for specialist
assessment to exclude tumour. Topical or systemic
corticosteroid medication can shrink polyps but surgical
removal is often required, followed by topical medication
to prevent recurrence.
Fig. 18.6
The paranasal sinuses.
instrumental removal difficult. A suspected foreign body
is a reason for specialist referral and children will
occasionally require general anaesthesia for its removal.
Paranasal sinuses
The nose and paranasal sinuses can be considered to be a
single functional unit. There are eight main paranasal
sinuses, all of which drain into the nasal cavity. Six major
sinuses drain into the narrow middle nasal meatus, which
is, therefore, a key area in the causation and treatment of
sinus disease. Figure 18.6 shows the general positioning
and relationship of the maxillary, ethmoid, frontal and
sphenoid sinuses.
Foreign bodies
156
Children often put foreign bodies into their nose. The
classic presentation is of unilateral, foul-smelling rhinorrhoea (oezena). Common foreign bodies include pieces
of foam rubber mattress or pillow, organic matter such as
peas, and parts of toys, beads, etc. Often, by the time of
presentation there is a secondary vestibular infection,
which makes the nose very tender to touch and makes
Sinusitis
Sinusitis may be acute or chronic, inflammatory or
infective.
Acute inflammatory sinusitis is seen in patients with
acute seasonal allergic rhinitis, commonly known as hay
fever. As such, this condition is seldom diagnosed and
the treatment relies on treating the inflammatory rhinitis
with topical antihistamines and decongestants. It is only
once inflammatory rhinitis becomes chronic and sinus
outflow tracts become blocked with oedematous, swollen
mucosa that chronic inflammatory sinusitis sets in.
Chronic inflammatory sinusitis occurs in people with
allergic nasal conditions (asthma, allergic rhinitis, aspirin
sensitivity). It is usually associated with an allergic or
inflammatory rhinitis, which is characterised by boggy
swelling of the nasal mucosa. Patients present with nasal
obstruction, a feeling of congestion, pressure between
the eyes and over the nasal bridge and postnasal discharge
of mucus. Treatment includes long-term low-dose topical
nasal corticosteroids. Antihistamines may be of value in
acute flare-ups.
Acute infective sinusitis is an almost universal occurrence during the common cold. This is due to rhinovirus
infection and is usually a self-limiting condition needing
only general supportive measures in the form of analgesics
and 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 occur
following viral infection. Bacterial sinusitis is characterised by pain, which may be severe, and poorly localised
(either to the forehead or malar region). There will be a
swinging pyrexia with purulent rhinorrhea. Patients often
complain of upper dental pain due to involvement of the
maxillary sinus. Acute infective sinusitis is a common
sequel to an upper respiratory tract infection and should
be seen as a potentially serious condition. Treatment with
local topical decongestants and systemic antibiotics is
required and failure to improve within 3 weeks necessitates specialist referral. Although most cases of infective
sinusitis respond to the above measures, some go on to
develop complications such as orbital cellulitis, orbital
abscess, frontal lobe abscess, meningitis or cavernous
sinus thrombosis.
Plain sinus radiographs have little or no role in the
investigation of sinusitis, which is mainly a clinical and
endoscopic diagnosis. Nasal endoscopy will often reveal
oedema and pus in the region of the middle meatus.
Failure to respond to conservative measures is an indication for surgical drainage of the infected sinus either
via an external or endoscopic intranasal route.
Chronic infective sinusitis may occur in some patients
as a result of an anatomical abnormality or an unresolved
or inadequately treated infection. Chronic sepsis is most
common in ethmoid and maxillary sinuses and less
frequently observed in the frontal or sphenoid sinuses.
Bacterial infection results in oedema and secondary
development of polypoid mucosa, which ensures that the
sinus ostia remain blocked, impeding sinus drainage,
which in turn prevents resolution of the infection.
Symptoms include nasal obstruction, chronic foul
smelling rhinorrhea or postnasal discharge. Specialist
referral is required and evaluation will include nasal
endoscopy and CT scanning of the sinuses. Surgical
treatment of chronic infective sinusitis aims to secure
unobstructed mucociliary drainage from the major
sinuses. Modern surgical approaches are referred to as
functional endoscopic sinus surgery (FESS). FESS aims
to remove obstructing hyperplastic tissue from the region
of the natural sinus ostia in the middle nasal meatus to
enable drainage of purulent secretions.
Paranasal sinus tumours
Fortunately, tumours of the paranasal sinuses are
uncommon. The most frequently involved sinus is the
maxillary, with the ethmoid being the second most
common site.
Maxillary sinus carcinoma
Carcinoma of the maxillary antrum usually presents late
as the volume of the sinus allows the tumour to enlarge
without causing symptoms. Presentation, therefore,
usually occurs only when the tumour invades beyond the
margins of the maxillary sinus. Symptoms are due to
invasion medially into the nasal cavity, superiorly into
the floor of the orbit and laterally into the cheek, and
inferiorly, into the upper alveolus. Thus, the patient may
present with swelling of the cheek, unilateral epistaxis,
unilateral nasal obstruction or diplopia. Histology is
typically squamous cell carcinoma, but poorly differentiated or anaplastic variants are common. Diagnosis is
made on nasal examination, nasal endoscopy and CT
scanning. Treatment includes radical surgical excision in
the form of total maxillectomy with or without orbital
clearance, followed by radical radiotherapy and treatment of nodal disease.
Ethmoid carcinoma
Ethmoid carcinoma is less common than maxillary sinus
carcinoma but, similarly, presents late. Invasion of the
medial orbital wall, nasal cavity and anterior skull base
leads to the presenting symptoms. Nasal obstruction
157
Section B Specialist Surgical Principles
and epistaxis is universal. There is thought to be an
aetiological association with exposure to lignins, which
are contained within certain hardwoods. Thus, ethmoidal
carcinoma has features of an occupational disease in
carpenters. Diagnosis and treatment is similar to maxillary
sinus carcinoma.
The prognosis in sinus carcinoma is poor.
Epistaxis
Epistaxis is defined as spontaneous bleeding from the
nasal cavity. It is an extremely common condition and
most people will at some point in their life suffer from a
nosebleed. The range of severity is vast, from the mild
self-limiting nosebleed experienced by most people, to
severe torrential arterial haemorrhage that carries a
significant mortality and morbidity. Epistaxis can be
classified into two main groups: childhood and adult.
surprisingly, this condition does not respond to direct
digital pressure over the ala-nasi (Hippocratic method).
The management of a severe epistaxis relies on resuscitation of the patient followed by attempts to identify the
source of the bleeding. The nose is examined using a
headlight, nasal speculum and suction. It is often difficult
to identify the bleeding point because of its posterior
position. If the source cannot be found, otolaryngologists
use endoscopes to examine the posterior nasal cavity and
identify the bleeding vessel, which can then be cauterised
under direct endoscopic vision. In the absence of
specialised equipment, posterior epistaxis is usually
managed by some form of tamponade, using either
specially designed balloon catheters or nasal packing.
Admission to hospital is required and a search for
aetiological factors should be undertaken (aspirin use,
alcohol excess, thrombocytopenia). Unlike childhood
epistaxis, which is recurrent, adult epistaxis tends to be
characterised by a single severe episode of bleeding.
Childhood epistaxis
Childhood epistaxis is common from age four. It is
characteristically minor but none the less alarming.
Nosebleeds occur sporadically, with a predilection for
nocturnal bleeding. The source of the bleeding is usually
on the anterior nasal septum at a rich vascular plexus
known as Little's area. This location has led some to
believe that nose-picking is the main cause, although
there is evidence to suggest other causes may be
important. The management of childhood epistaxis
includes pinching the nostrils over the soft, lower lateral
cartilages, which produces direct pressure over Little's
area (the Hippocratic method). Once bleeding has stopped,
some antibiotic ointment can be applied to the anterior
nares to reduce any associated vestibulitis. Cutting the
child's fingernails can also help. Persistent or recurrent
nosebleeds in children should be referred for specialist
opinion, which will usually lead to the offending blood
vessel being identified and cauterised.
Adult epistaxis
158
Adult epistaxis can be a potentially life-threatening
condition, which has a peak age of onset of 60 years.
This type of epistaxis is characterised by sudden
unilateral severe arterial bleeding. Bleeding in adults
often comes from arterial branches of the sphenopalatine
artery in the posterior reaches of the nasal cavity. This
has led to the term 'posterior epistaxis' being used. Not
The neck
Anatomy
The neck is divided into three zones: an anterior triangle
with its apex inferiorly and two posterior triangles with
their apices superiorly. The anterior triangle is bounded
laterally by the anterior border of the sternomastoid
muscles. Superiorly, its base is formed by the mandible
and, inferiorly, the apex lies in the region of the sternal
notch. The posterior triangles are bounded anteriorly by
the posterior border of the sternomastoid muscle,
posteriorly by the anterior border of trapezius, inferiorly
by the clavicle, and the apices lie posterosuperiorly in the
region of the occiput and mastoid processes. Figure 18.7
shows the triangles of the neck with the associated lymph
node groups that they contain. Neck swellings are
common clinical problems and it is important that a
diagnostic strategy is used when dealing with such
swellings. The majority of neck swellings are to be found
in the anterior triangle and a simple strategy can be used
to 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 the
neck are frequently involved in metastatic spread from
contains squamous carcinoma, is highly undesirable as
the risks of skin implantation with tumour are significantly increased and further curative resection will be
compromised.
Lymphoma involving nodes of the neck is an exception
to the above. Once lymphoma has been diagnosed (using
fine needle aspiration cytology), node sampling is usually
requested in order to histologically type the lymphoma.
However, sampling a known lymphomatous node after
positive cytology is different from exploratory biopsy of
an undiagnosed, possibly carcinomatous, node.
Midline swellings
Fig. 18.7 Triangles of the neck and associated lymph
nodes. 1, submental nodes; 2, submandibular nodes;
3, jugulodiagastric nodes; 4, parotid/facial nodes;
5, mastoid nodes; 6, occipital nodes; 7, upper deep
cervical nodes; 8, mid deep cervical nodes; 9, lower deep
cervical nodes; 10, supraclavicular nodes; 11, posterior
triangle nodes.
cancers of the upper aerodigestive tract and head and
neck. It is, therefore, essential that any patient with an
unexplained swelling in the neck is investigated carefully
to exclude a carcinoma of the head and neck. Examination
of the oral cavity, oropharynx and nasopharynx, and
fibreoptic examination of the larynx and hypopharynx
are essential when assessing lymph node swellings.
Indeed, an isolated lymph node is a common presentation
for tumours of the piriform fossa and nasopharynx.
It used to be common practice to biopsy or excise
lymph nodes to obtain a diagnosis. The practice of
diagnostic excision biopsy of lymph nodes in the head
and neck is generally considered obsolete now that
highly reliable fine-needle aspiration cytology is available. The procedure of fine-needle aspiration cytology
can distinguish between malignant and non-malignant
adenopathy in over 90% of cases. If a malignant cytology
aspirate is obtained, an examination under anaesthesia is
required in combination with detailed imaging of the
upper aerodigestive tract, head and neck, and chest. Once
a primary has been identified, planned curative treatment
can be carried out with nodal disease being treated by
radical radiotherapy or neck dissection. Excision of an
undiagnosed lymph node, only to later discover that it
A midline swelling in the upper neck can represent a
submental lymphadenopamy secondary to oral or dental
sepsis. However, the possibility of metatastatic nodal
spread has to be borne in mind in all patients presenting
with a neck lump and, in the upper neck, a thorough
examination of the oral cavity is essential.
In children, dermoid cysts can present in the upper
midline neck, and these developmental cysts may contain
squamous debris, hair and even teeth! A midline swelling
in the region of the hyoid bone may represent a thyroglossal cyst. This is a developmental abnormality with
cystic thyroid tissue persisting along the thyroglossal
duct. A thyroglossal cyst characteristically moves
upwards on tongue protrusion due to a continuity of the
cyst with the thyroglossal tract leading to the foramen
caecum of the tongue. In the lower neck, midline
swellings are most frequently related to the thyroid
gland. Clinically, it is usually easy to distinguish between
swelling of the thyroid gland and a swelling in the
thyroid gland. Swellings of the thyroid gland may be due
to simple goitre but thyroid cancer must be excluded.
Diagnosis is made by fine-needle aspiration cytology and
appropriate use of magnetic resonance imaging and radioisotope scanning. Occasionally, an early laryngeal cancer
presents with metastatic spread to the midline pretracheal
or Delphian node.
Lateral neck swellings
Lateral swellings in the upper neck may represent disease
of the submandibular salivary gland or inflammatory or
metastatic adenopathy of the submandibular, tonsillar and
upper deep cervical nodes. Inflammatory or neoplastic
disease of the parotid gland can also present as an upper
neck lump. In all of these conditions clinical examination
159
of the upper aerodigestive tract and judicious use of fineneedle cytology will elucidate the diagnosis.
A smooth, firm swelling at the anterior border of
the sternomastoid near the junction of its upper and
middle third is characteristic of a branchial cyst. These
are thought to be developmental abnormalities and are,
therefore, more common in children and young adults
than in older people. Diagnosis is confirmed by fineneedle aspiration, which produces turbid, straw-coloured
fluid, the cytology of which reveals cholesterol crystals.
Treatment of a branchial cyst is by surgical excision.
In elderly patients, atheromatous or even aneurysmal
carotid arteries can present as a pulsatile lateral neck
swelling. Auscultation will often reveal a bruit, and
ultrasound or MRI can confirm the diagnosis. If a carotid
aneurysm is suspected, then fine-needle cytology should
not be performed!
The lower lateral neck is a very common site for
metastatic adenopathy. Hypopharyngeal tumours often
160
spread to the lower cervical chain first. However, spread
from below the clavicles is not uncommon and the
Virchow node of gastric cancer and supraclavicular mass
of Pancoast's tumour should be borne in mind. Again,
clinical examination and cytology will often lead to the
diagnosis.
Tuberculous lymphadenopathy seems to show a
predilection for the lower lateral (posterior triangle)
nodes.
Occasional rarities such as cervical ribs and subclavian
artery aneurysms may present as masses in the lower
lateral neck.
With almost all of the swellings encountered in the
neck, a diagnosis can be made on clinical examination
coupled to judicious use of imaging and cytology. As
has been stressed, all neck lumps should be considered
malignant until proved otherwise, and incisional or
excisional biopsy should be avoided.
19
Neurosurgery
Introduction
Neurosurgeons (previously called neurological surgeons)
are concerned principally with conditions affecting the
central nervous system (CNS), the brain and spinal cord,
in which the management of the patient may be aided
by surgical means. The boundaries of what constitutes a
neurosurgical problem are not clear cut and there are
interesting areas of overlap with several other specialties.
There is an increasing trend for major operations in such
boundary areas to be undertaken by a team of surgeons
from two or three specialties, particularly if skin and
tissue cover or surgical reconstruction is required, or if
the surgical approach to the intracranial lesion is via the
maxilla, oral cavity or petrous bone.
Surgery to the spinal column is undertaken by both
neurosurgeons and orthopaedic surgeons. Some neurosurgeons distinguish between vertebral surgery, that is
surgery to the bones, joints and intervertebral discs of the
spine, and spinal surgery, which involves treatment of
intradural spinal tumours, arteriovenous malformations
of the spinal cord and syringomyelia. Most neurosurgeons
and some orthopaedic surgeons handle vertebral surgery,
the most common surgical procedures being for prolapsed
intervertebral discs and associated spondylitic changes.
Generally speaking, only neurosurgeons would tackle
spinal surgery.
Neurosurgeons have traditionally had close links with
neurologists. The ready availability of sophisticated
imaging techniques has rendered much detailed neurological examination redundant. Nevertheless, there are
still areas where close cooperation is required between
neurosurgeons and their physician colleagues, such as
the surgical treatment of epilepsy, movement disorders
and trigeminal neuralgia.
This chapter will describe the general neurosurgical
approach to problems and outline the common neuro-
Table 19.1
Aspects of neurosurgery
History and examination
Conscious levels
Investigations
Neurosurgical conditions
trauma
intracranial haemorrhage
intracranial neoplasms
intracranial infection
congenital lesions
hydrocephalus
vascular compression syndromes
surgical conditions (Table 19.1). Spinal and vertebral
surgery, although forming a large part of the modern
neurosurgical workload, will not be discussed other than
for the sake of completeness.
Neurosurgical history taking
and examination
In neurosurgical patients the history is of major diagnostic value. A patient who is fully conscious will often
be able to describe clearly any neurological signs and
examination simply confirms the patient's account. The
speed of onset of symptoms is usually important. In a
patient with a reduced conscious level who is unable
to give a history, every attempt must be made to obtain
a reliable history from relatives or other witnesses. In
cases of trauma, the exact mechanism of injury is often
useful.
The details of how to carry out a full neurological
examination will be found in any general medicine
textbook and will not be repeated here. Unfortunately,
students are often taught as if there is such a thing as a
161
routine neurosurgical examination in which all neurological signs and symptoms are tested for. Time constraints alone would preclude such an approach. In
practice, neurosurgical history taking and examination is
not routine or list based, but more heuristic, that is, goal
directed, testing one hypothesis after another. For
example, in a patient with a purulent middle ear infection
and symptoms of intracranial infection (headaches, neck
stiffness, disturbance of conscious level), history taking
and examination should be directed initially at detecting
signs of a lesion, such as cerebritis or abscess, in the area
of brain most likely to be affected. Thus, a middle ear
infection can spread superiorly to the temporal lobe,
giving rise to a contralateral hemiparesis, visual field
defect and, in the dominant hemisphere, dysphasia; or
infection can spread posteriorly into the posterior fossa,
producing cerebellar signs such as ataxia, nystagmus and
ipsilateral incoordination. Therefore these symptoms and
signs would be specifically asked and tested for. Such a
goal-directed approach does, of course, presume a reasonable basic knowledge of neuroanatomy.
It will be clear in the above example that if such a
patient has a limb weakness, detailed testing of individual
limb muscle groups and reflexes will add very little to the
clinical picture and is therefore unnecessary. By contrast,
in a patient with a suspected spinal cord lesion, testing of
individual muscle groups and of reflexes may be of great
value in determining the level of the lesion and which
specific nerve roots may be involved. The examination
performed therefore depends on the clinical question to
be answered.
Neurosurgical history taking and examination is goal
directed, and the goal is in three stages. The first stage is
anatomical localisation, the second is to determine
general pathology and the third is to determine detailed
or special pathology. It is the hallmark of inexperience to
try and make a diagnosis of special pathology in the early
stages of a patient's presentation. The danger of this is
that a patient is labelled with a condition and other
possibilities are ignored.
Anatomical localisation
162
It is usually possible to locate a lesion to one of the three
main compartments of the CNS, supratentorial (cerebral
hemispheres), infratentorial (brainstem and cerebellum)
and spinal.
Certain features always indicate supratentorial pathology. These features are anosmia (inferior frontal lobes),
dysphasia (dominant hemisphere) and seizures (always
arise in the cerebral cortex).
Infratentorial (posterior fossa) lesions are characterised by brainstem or cerebellar signs such as ataxia,
incoordination, nystagmus, dysarthria and dysphagia.
Cranial nerve palsies may often be associated with infratentorial lesions and the presence of a cranial nerve palsy
and a contralateral hemiparesis is virtually diagnostic of
a brainstem lesion. Mass lesions in the posterior fossa
commonly present with signs of raised intracranial
pressure from hydrocephalus secondary to obstruction of
cerebrospinal fluid (CSF) flow through the aqueduct or
the fourth ventricle.
Spinal lesions are characterised first by an absence of
the symptoms and signs characteristic of an intracranial
lesion, and no disturbance of consciousness. Second,
there will often be pain or tenderness at the site of a
vertebral lesion. Third, spinal lesions commonly present
with bilateral limb symptoms or signs, which is less
usual with brain lesions. Fourth, due to the arrangement
of the sensory and motor tracts within the spinal cord,
there are characteristic syndromes associated with lesions
of the spinal cord.
When localising spinal lesions it is important to distinguish between upper motor neuron and lower motor
neuron lesions. The lower motor neuron starts at the
anterior horn cell of the spinal cord. A lesion involving
the anterior horn cell, the nerve root, or the peripheral
motor nerve will tend to cause lower motor neuron signs,
that is hypotonic weakness, muscle wasting, and reduced
or absent reflexes. Lesions of the spinal cord itself will
tend to produce upper motor neuron signs - weakness
with increased tone, increased reflexes and clonus. A
spinal lesion will commonly produce a mixture of upper
motor neuron signs (below the level of lesion) and lower
motor neuron signs (at the level of the lesion) and thus
precise anatomical localisation is often possible.
General pathology
The second stage of the goal of history taking is to
determine, as far as possible, which general pathological
category the patient's complaints suggest. The general
categories are congenital, degenerative, traumatic,
infective/inflammatory, vascular and neoplastic. A history
of trauma in the recent past will be important. A sudden
onset (over a few seconds) of neurological symptoms or
signs 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 of
infection elsewhere; and a more gradual onset (weeks or
months) would point to a neoplastic process or a chronic
subdural haematoma. In younger patients, congenital
lesions will be more likely, although congenital lesions
can present at any age.
The purpose of anatomical localisation and attempting to define general pathology is to help decide which is
the next best investigation to determine special pathology. Modern neuroradiological investigation is sophisticated and accurate but may also be time consuming and
expensive. Therefore it is important to be thoughtful
about the sequence of investigations most likely to yield
useful information.
Special pathology
To make a specific neurosurgical diagnosis usually
requires further investigations. For example, a patient
with sudden onset of dysphasia and a right hemiparesis
has most likely sustained a vascular lesion (general
pathology) affecting the left hemisphere. A computerised
tomography (CT) scan is required to distinguish the
special pathology of an infarct, a haemorrhagic infarct, or
an arterial haemorrhage. If a haemorrhage is detected, a
cerebral angiogram will usually be needed to display an
underlying vascular abnormality such as an aneurysm or
arteriovenous malformation.
The range of neurosurgical investigations that may be
required to make a precise diagnosis are described later.
It is frequently the case, particularly with CNS tumours
or infection, that a biopsy will be required to make a
definitive diagnosis.
Conscious level and
non-localising symptoms
Several common presenting neurosurgical syndromes
allow only the vaguest anatomical localisation.
Symptoms and signs of raised intracranial
pressure (ICP)
The classic presentation of acute raised ICP is headache,
vomiting and papilloedema; with a more chronic buildup of pressure, headache and vomiting may be less
marked, even absent. In babies whose skull sutures have
not formed raised ICP may simply cause the head
circumference to enlarge beyond normal.
Any intracranial lesion can produce raised ICP if it is
large enough, or situated in such a position as to obstruct
the flow of CSF and cause hydrocephalus.
If unrelieved, raised ICP can lead to herniation of the
brain through the tentorial hiatus or foramen magnum
(coning). Raised ICP can lead to decreased cerebral
perfusion; if ICP rises to equal blood pressure, cerebral
perfusion ceases.
Meningism
This refers to the syndrome associated with meningitis,
namely headache and neck stiffness, usually accompanied
by vomiting. Meningitis means simply inflammation of
the meninges. The most common cause in the community is probably viral meningitis, normally a benign,
self-limiting condition. Bacterial meningitis is less
common but is life threatening. Bleeding (from any
cause) into the subarachnoid space also produces
meningism. Chemical (non-infective) meningitis is
sometimes seen following neurosurgical operations
when, for example, cyst contents have escaped into the
CSF. All types of meningitis and most cases of CSF or
intracranial infection (cerebritis or brain abscess) will
give rise to meningism.
Reduced conscious level:
the Glasgow Coma Scale
A pathological reduced conscious level can be caused by
bilateral cerebral hemisphere lesions, brainstem compression or ischaemia, reduced cerebral perfusion,
metabolic disturbance or seizure activity. Most intracranial neurosurgical pathologies can give rise to a
reduced conscious level by reason of pressure, direct or
indirect, on the brainstem, or by causing raised ICP and
reduced cerebral perfusion. Many non-CNS systemic
pathologies will also produce a reduced conscious level,
for example hypoglycaemia, liver failure, hypoxia (cardiac
or respiratory abnormalities) and sepsis. Therefore a
reduced conscious level in itself is not an indication of
primary intracranial pathology.
Conscious level is universally assessed using the
Glasgow Coma Scale (Table 19.2). The three components of consciousness - eye opening, verbal response
and motor response - are assessed individually. When
assessing each of these components it is important that
the examiner starts 'at the top' and works down. Thus,
when assessing eye opening, spontaneous eye opening or
163
Table 19.2
The Glasgow Coma Scale and score
Feature
Scale responses
Score notation
Eye opening
Spontaneous
To speech
To pain
None
Orientated
Confused conversation
Words (inappropriate)
Sounds (incomprehensible)
None
Obeys commands
Localises pain
Flexion - normal
Flexion - abnormal
Extend
None
4
3
2
1
Verbal response
Best motor response
Total Coma score
164
eye opening to speech should be looked for before testing
eye opening to pain.
The correct way to test for a motor response often
causes some difficulty. If a patient does not obey simple
commands, a localising (purposeful) response is tested
for. By convention, painful pressure is applied to the
supraorbital margin and if the patient brings a hand up to
the site of the pain, then the patient is localising. Both
arms are tested by holding one arm down at a time.
If the patient does not localise, the other responses are
tested by applying pressure to the fingernail bed. A
flexion or extension response refers to movement at the
elbow. The intermediate response, abnormal (or spastic)
flexion is charted if there is either preceding extension
movement in arm, or extension in a leg, or two of the
following: stereotyped flexion posture, extreme wrist
flexion, 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, but
is important to record, if present, as a focal sign (Fig.
19.1). If in doubt, record normal flexion.
When recording conscious level, the 'best' motor
response is taken. This means the arm with the best
response, not the best response over time. So if a patient
is localising pain with the right arm but flexing to pain
with the left arm, the conscious level is judged as
localising. However, the flexion response in the left arm
is an important focal sign, indicating a lesion probably
affecting the right hemisphere.
5
4
3
2
1
6
5
4
3
2
1
3
/15 to
15
/15
It is common, especially in trauma patients, to be
unable to record one or more aspects of the Coma Scale.
The patient's eyes might be closed by swelling, or directly
injured, making eye opening not possible. The patient
may be dysphasic, or have an endotracheal tube or
tracheostomy, making verbal response unrecordable.
There may be a high spinal injury, brachial plexus lesion,
or limb fracture, making motor response unreliable. In all
these situations it is important simply to give the reason
for not recording the response, rather than to guess at
what it might be (see Fig. 19.1).
Coma is defined as not obeying commands, not eye
opening even to pain, and not uttering recognisable
words. A severe head injury is one where coma, as
defined, is present for 6 h or more.
Each component of the Glasgow Coma Scale can be
allocated a numerical value, the sum of which can give
the Glasgow Coma (GC) Score (see Table 19.2). The GC
Score was devised in the 1970s to allow information on
large numbers of head-injured patients to be stored and
analysed by computer. The GC Score is useful for
grouping head-injured patients by severity, for displaying
risk factors, and as a form of shorthand used in producing
guidelines. Despite widespread practice to the contrary,
the GC Score should never be used to describe an
individual patient's conscious level in a clinical situation.
To do so often results in confusion and significant loss of
information. In clinical practice, always use the verbal
description of the three components of the GC Scale.
Fig. 19.1 Stylised neurosurgical observation chart of a patient deteriorating with a left-side
extradural 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, the
reason is given (e.g. C, eyes closed by swelling; DYS, dysphasic). The GC Score is not used for
individual patients in a clinical situation.
Neurosurgical investigations
and procedures
The purpose of neurosurgical history taking and examination is to determine anatomical localisation and, if
possible, general pathology. This in turn guides the
investigations that are most likely to assist in further
diagnosis (of special pathology) and management.
Lumbar puncture
This is used to diagnose infection of the CSF, in which
case the white cell count will be raised. Bleeding into the
CSF (from, for example, a ruptured intracranial aneurysm)
is diagnosed by frank blood-staining of the CSF and/or
xanthochromia in the supernatant. Lumbar puncture (LP)
is contraindicated in the presence of an intracranial mass
lesion; an LP in this circumstance may lead to a pressure
differential and subsequent downward herniation of the
brain (coning). This can result in rapid death.
Nerve conduction studies and
electromyography
These are tests performed by neurophysiologists and
may be very useful in distinguishing nerve root abnormalities from peripheral nerve entrapment or peripheral
neuropathy.
Plain radiography
Plain radiographs of the head or spine can be particularly
useful in cases of trauma. Radiographs of the skull can
165
show a fracture, a depressed fracture, air in the head or
foreign bodies following a penetrating wound. Many
head injuries are associated with spinal injury, particularly of the cervical spine, and cervical spine radiograph
is almost routine following any significant head injury.
Some brain tumours contain calcification or cause bone
erosion, which is visible on a skull radiograph. Many
pituitary tumours show erosion or expansion of the
pituitary fossa on a lateral skull radiograph. In babies or
children a skull radiograph can show premature fusion of
the sutures (craniosynostosis), and chronic raised ICP
gives patchy thinning of the skull vault - the copperbeaten appearance. Some spinal cord tumours or cysts
may cause expansion and erosion of adjacent vertebra.
CT scan
This investigation has revolutionalised neurosurgery. No
longer do neurosurgeons need to rely on careful, detailed
neurological examination to identify the exact site of, for
example, a brain tumour.
MRI scan
This gives exquisite anatomical images. The two main
advantages of the MRI scan over the CT scan are, first,
that it is not affected by thick bone and is therefore useful
for imaging the posterior fossa and spine. Second, it can
image in any plane, and this is particularly informative in
sagittal images of the spine.
The disadvantages of the MRI scan is that it is expensive and time consuming. It is contraindicated in patients
with pacemakers, implanted stimulators or ferromagnetic
implants or foreign bodies. Some claustrophobic patients
cannot tolerate lying in the scanner.
Angiography
Carotid and vertebral angiograms are used to visualise
intracranial aneurysms, arteriovenous malformations
(AVMs), and the vascular supply of tumours. Access is
usually via the femoral artery, threading the tracker
catheter along the aorta under X-ray control.
Craniotomy
166
This refers to a flap of bone that is removed with a saw
and replaced at the end of the procedure. The craniotomy
flap may be of any size but is usually greater than 3 cm
diameter. 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 neurosurgical
procedure to gain access to the intracranial contents.
Neurosurgicai conditions
Trauma
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 by
Hippocrates. Head injuries are common and the majority
are minor and do not require investigation or hospital
admission. Nevertheless, the potential for complications
is always present.
Head injuries can be classified anatomically according 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 usually
serious. Blood loss may look frightening but is rarely
enough to cause shock, with the exception sometimes in
babies. The history is always important and may alert the
examiner to the possibility of a penetrating wound or a
depressed fracture, both of which will normally require
neurosurgical exploration. First aid treatment of a scalp
laceration 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 scalp
laceration. A compound (or open) fracture implies
communication of the fracture with the atmosphere. A
compound depressed fracture of the skull vault usually
requires an operation to debride the wound, elevate the
fracture and inspect the underlying dura and brain for
lacerations. The main aim of this procedure is to reduce
the risk of intracranial infection by removing all foreign
material and repairing the dural defect. Penetrating
wounds are dealt with in the same way. Simple depressed
fractures do not require surgery.
Fractures of the skull base are difficult to see with
radiographs but can be diagnosed clinically by the
presence of well-defined periorbital haematomas (racoon
eyes) and subconjunctival haemorrhage with no posterior
Table 19.3
Risk of an operable intracranial haematoma in head injured patients
GCS (/15)
Risk
Other features
Risk
15
1 in 3615
9-14
1 in 51
3-8
1 in 7
None
Post-traumatic amnesia (PTA)
Skull fracture
Skull fracture and PTA
No fracture
Skull fracture
No fracture
Skull fracture
1
1
1
1
1
1
1
1
in 31 300
in 6700
in 81
in 29
in 180
in 5
in 27
in 4
GCS, Glasgow Coma scale
Adapted from Teasdale et al 1990 British Medical Journal, 300: 363-367
limit (in anterior fossa fractures), or bruising over the
mastoid process (Battle's sign) in fractures of the petrous
bone. Petrous fractures can damage the middle or inner
ear and may have associated bleeding from the external
meatus, deafness, dizziness or facial nerve palsy. If the
dura underlying a base of skull fracture is torn, there may
be a CSF leak through the nose or the ear, or air many
enter the subarachnoid space (pneumocephalus). In either
event there is a risk of bacterial meningitis. If the dural
tear does not heal within 1-2 weeks, surgical repair is
usually indicated. Recently published guidelines do not
recommend prophylactic antibiotics for a CSF leak.
The main significance of a skull fracture is that it
indicates a greatly increased risk of the patient harbouring an intracranial haematoma that requires surgical
removal. Table 19.3 illustrates the risks that form the
basis for guidelines on the early management of head
injuries. Table 19.4 lists the criteria for referral of a head
injury to hospital. Further guidelines on the indications
for a skull radiograph, admission to hospital, a CT scan,
and referral to a neurosurgeon can be found in the
Scottish Intercollegiate Guidelines Network (SIGN)
publication entitled 'Early management of patients with
a head injury (No. 46)', published in August 2000.
Table 19.4 Indications for referral of a head
injured patient to hospital
A head injured patient should be referred to hospital if
any of the following is present:
Impaired consciousness (GCS <15/15) at any time since
injury
Amnesia for the incident or subsequent events
Neurological symptoms, e.g. severe and persistent
headache, nausea and vomiting, irritability or altered
behaviour, seizure
Clinical evidence of a skull fracture (e.g. CSF leak,
periorbital haematoma)
Significant extracranial injuries
A mechanism of injury suggesting:
a high energy injury (e.g. road traffic accident, fall
from height)
possible penetrating brain injury
possible non-accidental injury (in a child)
Continuing uncertainty about the diagnosis after first
assessment
Medical comorbidity (e.g. anticoagulant use, alcohol
abuse)
Adverse social factors (e.g. no-one able to supervise the
patient at home).
From Scottish Intercollegiate Guidelines Network (SIGN)
Publication Number 46 'Early management of patients
with a head injury', August 2000.
Brain damage
Brain damage or dysfunction is the subject of most concern following a head injury. Concussion, seizure activity,
mechanical compression and ischaemia, may all render
part of the brain dysfunctional, that is, the axons do not
conduct or the synapses do not transmit. Such dysfunction may be reversible with appropriate treatment over
time. 'Brain damage' is the term used to indicate irreversible
dysfunction, which generally equates with disruption of
the 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 treatment will reverse this. The aim of management is to
prevent further damage, the causes of which are listed in
Table 19.5.
167
Table 10.5
Causes of secondary brain damage
Ischaemia
hypoxaemia
airway obstruction
chest injury
hypotension
extracranial injuries
other causes of shock
Intracranial haematoma
Brain swelling/oedema
Seizures
Infection (meningitis, abscess)
Metabolic/electrolyte disturbance
Hypoxaemia and hypotension are two of the most
common causes of secondary brain damage that can be
treated (or prevented) by a non-specialist. Hence the
emphasis in all guidelines regarding the management of
head injuries on the 'ABC' of resuscitation - the airway
and breathing (i.e. adequate blood gases) always take
priority, followed by treatment of circulatory disturbances.
Treatment of an obstructed airway, or a tension pneumothorax, or bleeding from a ruptured spleen always takes
precedence over a possible intracranial haematoma.
Intracranial haematomas
An intracranial haematoma is the complication that most
people associate with a head injury, but haematomas
requiring surgical treatment are in fact uncommon. The
clinical characteristics of such a lesion are severe headache and vomiting, decreased conscious level, contralateral
hemiparesis and (a late sign) an ipsilateral unreactive
dilated pupil (see Fig. 19.1). Treatment of a significant
haematoma will usually be surgical evacuation via a
craniotomy. An extradural haematoma (i.e. between the
skull bone and the dura) generally carries a better prognosis
because it is less often associated with contusions or
lacerations of the brain substance. An intradural
haematoma is commonly a mixture of subdural blood,
brain contusions or intracerebral haematoma, although
pure subdural or intracerebral haematomas do occur.
Chronic subdural haematoma (CSDH)
168
CSDH is a relatively common but poorly understood
condition. The typical history is of a minor head injury in
an elderly patient, followed weeks or months later by a
gradual 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 to
other causes, such as dementia or stroke. Often there is
no history of a head injury. An overdraining ventriculoperitoneal shunt can also result in a CSDH.
Intracranial haemorrhage
Intracranial haemorrhage is subdivided into parenchymal
(intracerebral) haemorrhage and subarachnoid or intraventricular haemorrhage. Pure intracerebral haemorrhage
may present in the same way as a cerebral infarct (with
sudden onset of neurological signs) although is five times
less common. Hypertension is the commonest cause and
surgery is rarely indicated.
Haemorrhage primarily into the subarachnoid space
or ventricles, or intraparenchymal haemorrhage that
ruptures into the CSF spaces, presents with a very severe
sudden headache, sometimes referred to as thunderclap
headache. There may be accompanying neurological
deficits and/or a decreased conscious level or coma.
Subarachnoid haemorrhage (SAH) is the most common type of intracranial haemorrhage that concerns the
neurosurgeon. The usual cause is a ruptured intracranial
aneurysm. Other uncommon causes include arteriovenous
malformations, tumours and blood dyscrasias. About
12% of all patients with SAH have no cause found.
Usually, such patients are relatively well following the
bleed, make a full recovery in time and rarely rebleed.
The diagnosis of subarachnoid haemorrhage is made
on the history of sudden severe headache. Some patients
liken the onset to being hit on the back of the head with
a baseball bat. A CT scan will show subarachnoid blood
in 90% of cases scanned within 24 h of the haemorrhage.
A cerebral angiogram will demonstrate an aneurysm if
present (Fig. 19.2).
Treatment is directed towards preventing a rebleed.
The aneurysm may be approached through a craniotomy
and a small metal clip placed across its neck to exclude it
from the circulation. Alternatively, platinum coils may be
packed into the aneurysm sac using angiographic
techniques. It is unclear which method gives the best
long-term results.
Aneurysmal subarachnoid haemorrhage is a serious
condition with a high initial mortality and morbidity. In
patients who survive the initial haemorrhage, the risk of
rebleeding is 25% in the first 2 weeks and 60% within
6 months, with a mortality of 60%. Therefore early
referral and assessment of patients with suspected SAH
is important. A common cause of litigation concerns
Fig. 19.2 Anteroposterior (AP) view of a right internal
carotid angiogram showing an anterior communicating
artery aneurysm arising in the midline between the two
anterior cerebral arteries (A). A smaller aneurysm can also
be 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 to
return a week later with a devastating rebleed.
Intracranial neoplasms
Intracranial tumours form a large part of the neurosurgical workload. There are many pathological types of
tumour and detailed discussion of each is not possible.
However, tumours can be grouped broadly into intrinsic
tumours (those that arise within the brain substance) and
extrinsic lesions. The most common adult intrinsic
tumours are gliomas (astrocytomas, oligodendrogliomas,
etc.) and metastatic carcinomas. The most common
extrinsic tumours are meningiomas, which arise from the
arachnoid membrane on the internal aspect of the dura.
In children, the most common neoplasms are medulloblastomas and ependymomas, both intrinsic tumours
arising in the posterior fossa.
Depending on their position, size and rate of growth,
tumours can present with virtually any neurological
symptom or sign. Headache, seizures and confusion are
three of the most common. The key feature of neoplastic
lesions is that the presenting signs will usually be of
gradual onset and progressive. Diagnosis is by CT or
MRI scan, although skull radiograph may give a clue in
some cases. It is often possible to diagnose with a reason-
able degree of certainty the pathological type of tumour
based on the CT scan appearance. However, gliomas in
particular can have a varied appearance and can sometimes look like a metastasis, an abscess, an infarct or a
resolving haematoma. Biopsy is often required.
The management of intracranial tumours depends on
many factors but the key principle of management is to
weigh the likely benefits of the proposed treatment
against the possible morbidity or mortality arising from
treatment. Factors that tend to increase the risk of surgery
are older age, poor clinical condition, location within or
close to an 'eloquent' (i.e. functionally important) area of
brain, and close involvement of important intracranial
arteries or veins.
The usual classification of extracranial tumours into
benign or malignant is not so helpful or relevant with
intracranial tumours. Most meningiomas, for example,
are pathologically 'benign' and have a clear plane of
cleavage from normal brain. However meningiomas can
invade the dural venous sinuses or bone around the base
of the skull, making total removal impractical. Furthermore, meningiomas may have 'atypical' features (such as
mitotic figures) or be frankly malignant, and in all such
situations there is a higher chance of recurrence.
The feature of the majority of gliomas, from low
grade to malignant, is that they invade normal brain. It is
well established that even if the CT scan shows an
apparent clear margin to the tumour, tumour cells extend
at least 2 cm beyond the margin into brain substance.
Most gliomas respond little to radiotherapy and even less
to chemotherapy, and therefore a cure is not possible.
The aim of management must be to try and relieve the
patient's symptoms and extend the length of good quality
life. Attempts at radical resection of the glioma are rarely
justified if this means that the patient is to be left even
more disabled postoperatively. Conservative management is often appropriate.
Secondary tumours within the brain are often multiple
and most are not referred to a neurosurgeon because they
are terminal. Patients with a solitary metastasis in an
accessible area and who are generally well may benefit in
the short-term from surgical excision.
Intracranial infection
Meningitis
Viral meningitis rarely comes to the attention of the
neurosurgeon unless there is suspicion of some other
169
diagnosis such as subarachnoid haemorrhage. Likewise,
most cases of bacterial meningitis will be managed perfectly adequately outside a neurosurgical unit. Diagnosis
is by lumbar puncture.
Meningitis is seen most often by neurosurgeons as a
complication of an open head injury or following
intracranial surgery. Treatment is with the appropriate
antibiotics. Occasionally, bacterial meningitis, especially
tuberculous meningitis, can cause hydrocephalus, which
requires ventricular drainage of CSF. Therefore a patient
in 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 a
result of direct spread from infected sinuses, otitis media
or a penetrating wound, or by the haematogenous route
(Fig. 19.3). Haematogenous brain abscesses are more
likely to be multiple and are thought more likely in patients
with a cardiac septal defect that allows the normal
bacterial filtering action of the lung to be bypassed.
Congenital lesions
Congenital lesions of the CNS may occur in isolation
or in association with other abnormalities as part of a
recognised syndrome. Some lesions are obvious at birth
(e.g. spina bifida), and others cause no symptoms and
remain unrecognised throughout life (e.g. temporal lobe
agenesis). Others, for example, craniosynostosis and
aqueduct stenosis, are only diagnosed when they produce
symptoms or signs.
Craniosynostosis
This refers to premature fusion of one or more of the
skull sutures resulting in abnormalities of the skull shape.
Synostosis may be part of a more generalised
abnormality such as Crouzon's or Apert's syndrome, in
which case there will be facial, dental and ophthalmic
abnormalities to consider, and a multidisciplinary team
approach is required.
Surgery consists of resecting the faulty suture line(s)
and allowing the skull vault bones to 'spring'. Brain growth
will then hopefully mould the skull to a more normal
shape and size. Surgery may also be required to the orbits
and facial bones.
Spina bifida
This term covers a range of abnormalities from asymptomatic spina bifida occulta to large, open, posterior
spinal defects with total loss of cord function. Open
defects need to be closed soon after birth. Less major
(closed) spina bifida defects may only become apparent
as the child grows and develops problems with walking.
An MRI scan is the investigation of choice.
Arnold-Chiari malformation
170
Fig. 19.3Axial computerised tomography (CT) scan
showing an abscess in the region of the thalamus.
In this condition, the cerebellar tonsils are prolapsed
through the foramen magnum. The posterior fossa is
often abnormally shallow. In more pronounced forms the
lower brain stem will also be herniated.
Mild forms are common and often asymptomatic.
Symptoms may range from cough impulse headache to
signs of brainstem compression. Chiari malformations
may be associated with spina bifida and aqueduct stenosis.
Treatment of symptomatic cases is by bony decompression
of the foramen magnum.
Aqueduct stenosis
This can give rise to an obstructive hydrocephalus and
may present at any age. Ataxia is often an early symptom
and headaches are frequently mild or absent even in the
presence of papilloedema. Treatment is by insertion of a
CSF shunt or by making a fenestration in the floor of the
third ventricle.
Hydrocephalus
CSF is actively secreted in the colloid plexus of the
lateral third and fourth ventricles at a rate of 20 mL per
hour. There is a gentle pressure gradient that causes CSF
to flow, in a pulsatile manner, through the aqueduct into
the fourth ventricle and then out of the fourth ventricle
into the basal subarachnoid space. The flow continues
over the cerebral hemispheres to the superior sagittal
sinus, where CSF is absorbed through the arachnoid
granulations by a passive process dependent on differential pressure between the CSF and the venous sinus.
Hydrocephalus refers to the situation where there is an
imbalance between CSF production and absorption,
causing the ventricles to enlarge. In acute hydrocephalus
this causes severe pressure on the brain, decreased
cerebral perfusion, herniation through the tentorial hiatus,
brain stem pressure and, eventually, death. In more chronic
forms there is progressive stretching, ischaemia and
destruction of white matter tracts around the enlarging
ventricles.
Hydrocephalus occurs as a result of a congenital
abnormality (e.g. aqueduct stenosis) or as a complication
of some other intracranial pathology. Almost any intracranial pathology can cause or be associated with hydrocephalus and it is one of the commonest problems in
neurosurgery.
The term 'active hydrocephalus' implies a continuing
imbalance between CSF production and absorption,
leading to ongoing raised ICP. Compensated or arrested
hydrocephalus refers to the condition of large ventricles
(ventriculomegaly), suggestive of previous active
hydrocephalus but with no continuing raised pressure.
Arrested hydrocephalus is common in the community
and although such individuals may have no neurological
deficits they might have large heads and enormous
ventricles on CT scan. It is important to treat the patient
and not the CT scan.
Active hydrocephalus usually requires surgical treatment. The best management in obstructive hydrocephalus
is to remove the cause of the obstruction if possible. As a
temporary or holding measure a ventricular drain may be
inserted to drain CSF into an external reservoir. A shunt
consists of a silastic ventricular catheter connected to a
subcutaneous valve and reservoir, in turn connected to
a tube into the peritoneal cavity (ventriculoperitoneal
shunt) or atrium (ventriculoatrial shunt).
The disadvantages and complications of shunts are
legion and include blockage, infection and over drainage.
Each significant shunt complication requires further
surgery; such patients can become very dependent on
hospital services.
Vascular compression syndromes
Paroxysmal trigeminal neuralgia (PTN)
This is a relatively common condition characterised by
very severe episodes (paroxysms) of shooting pains
affecting one side of the face. The diagnosis is made on
the history alone and the characteristics are listed in
Table 19.6.
In most so-called idiopathic cases of PTN the cause is
a blood vessel compressing the trigeminal nerve at the
position where it enters the pons. There is evidence that
the vessel leads to focal demyelination and ephaptic
transmission. MRI scanning will usually demonstrate the
compressing vessel.
Treatment is by carbamazepine or other anticonvulsant drugs in the first instance. If the patient still
experiences pain on the maximum tolerated dose of
anticonvulsants, it is possible to explore the trigeminal
root 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 cases
where no compressing vessel is evident or, if present,
decompression does not alleviate the symptoms. Clearly
there are other possible causes.
Table 19.6
Features of trigeminal neuralgia
Gradual worsening of severity and frequency of attacks
over the years
Periods of remission
No neurological deficits or sensory disturbance
Often aggravated by chewing
A trigger spot where light touch or cold sets off the pain
Responds to carbamazepine
171
pression procedures will not help but ganglion injection
procedures are effective.
Occasionally, a tumour in the cerebellar pontine
angle, such as an acoustic neuroma, petrous meningioma
or epidermoid cyst may present with PTN. Removal of
the tumour is usually curative.
Glossopharyngeal neuralgia (GPN)
Fig. 19.4 Treatment for trigeminal neuralgia. The lateral
skull X-ray shows a needle entering the foramen ovale and
a Fogarty balloon inflated with contrast in the trigeminal
cistern.
In patients not suitable for the above procedure (i.e.
the elderly or unfit) a destructive procedure can be carried
out to the nerve. This may be a peripheral nerve block
using alcohol or a cryoprobe (usually carried out by oral
physicians), or an injection into the trigeminal ganglion
via the foramen ovale under X-ray control. The ganglion
may be partially denervated by heat (thermocoagulation),
chemical (glycerol) or mechanically (balloon compression;
Fig. 19.4). The initial success rate of these destructive
procedures is high, but so is the recurrence rate.
Patients with multiple sclerosis commonly develop an
identical syndrome to idiopathic trigeminal neuralgia.
Presumably the origin is a demyelinating plaque somewhere on the course of the nerve root. Vascular decom-
172
This is a similar syndrome to PTN except the pain is in
the distribution of the glossopharyngeal nerve that is the
posterior tongue and pharynx on one side. Typically, the
pain of GPN occurs on swallowing and that of PTN on
chewing. Open surgical treatment is highly effective and
there is usually a compressing vessel at the glossopharyngeal root entry zone into the brainstem. If there is
no vessel, or the vessel is technically difficult to separate,
unilateral section of the glossopharyngeal nerve and the
upper roots of the vagus is curative and produces hardly
any neurological deficit.
Hemifacial spasm
This is the third of the curious cranial nerve vascular
compression syndromes. Most people have seen someone with involuntary contractions of muscles on one side
of the face. The syndrome usually starts with blepharospasm but tends to progress over the years to involve the
whole of the side of the face in dystonic contractions.
The patient may effectively lose the use of one eye and
the cosmetic effect is distressing.
Once again there is in most cases a blood vessel
compressing the facial nerve at its root entry zone. A
posterior fossa craniectomy and decompression of the
nerve is usually successful in abolishing the spasm.
20
Temporomandibular joint
investigation and surgery
Introduction
The most common condition affecting the temporomandibular region is temporomandibular dysfunction, or
myofascial pain dysfunction. This may be associated
with a clicking of the temporomandibular joint. This is a
disorder characterised by pain and masticatory muscle
spasm and limited jaw opening, which is treated by
conservative measures such as soft diet, analgesics,
occlusal splint therapy or physiotherapy. Intransigent
cases 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 is
necessary and an overview of this follows, with aspects
of the history and examination of the patient and details
of the investigations that are a prerequisite to appropriate
surgical care. This is followed by a discussion of the
procedures available for the surgical management of
TMJ disorders (Table 20.2).
Table 20.1
Surgical conditions of the
temporomandibular joint
Internal joint derangement
Recurrent dislocation
Traumatic injury
Arthritic conditions
Ankylosis
Tumours
Table 20.2
Surgical procedures for the
temporomandibular joint (TMJ)
Arthrocentesis
TMJ arthroscopy
Meniscal plication
Meniscectomy
Eminectomy
Dautrey procedure
Condylotomy
Condylectomy
TMJ reconstruction
Anatomy of the
temporomandibular joint
(TMJ)
The TMJ is a synovial joint with articular surfaces made
up of fibrocartilage. Fibrocartilage is adapted to take
shearing forces, rather than the compressive forces that
act on the hyaline cartilage in the knee joint. The TMJ
has an upper and a lower compartment separated by a
cartilaginous meniscus. The non-articular surfaces are
lined by a synovial membrane, which produces the synovial
fluid that lubricates the joint and nourishes the cartilage
(Fig. 20.1).
The only time that the joint is loaded is when eating
or clenching. When speaking or relaxed the teeth are
Fig. 20.1
The anatomy of the temporomandibular joint.
A, bilaminar zone; B, condylar head; C, mandibular
eminence; D, glenoid fossa.
173
apart. When the jaws are closed much of the force is
transmitted through the teeth into the facial bones but
some of the forces will go into the jaw joints.
The joints are supported by ligaments, which surround the joint capsule. Movement is by the action of the
masticatory muscles and information from proprioceptors
in the mouth and particularly in the periodontal ligament
allow coordination of all components when chewing or
speaking. Injury or damage to any of these components
affects jaw function.
Investigations
Investigations of the temporomandibular joint include
history, examination and special investigations, and these
are discussed in turn.
History
Special investigations
The patient's presenting symptoms should be noted.
Symptoms might include pain, swelling, clicking,
crackling in the preauricular region and limitation of jaw
opening. There may also be an accompanying generalised
facial ache or a numb sensation over the masseter
muscles. When asked about pain, if a patient points to the
preauricular region then the pain is likely to be in the
TMJ, but if the patient puts a hand over the side of the
face 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 other
conditions in the orofacial regions.
Previous symptoms, duration and potential causes of
the symptoms such as trauma should be elicited from the
patient. Any activity that exacerbates or relieves the condition should be noted. Chewing, yawning or parafunctional habits can aggravate TMJ disease.
A full medical and drug history should be taken, as
well as a family and social history. Of particular relevance
are traumatic life events such as bereavement, a house or
job move or a divorce. Stress is a common factor in TM
dysfunction.
The special investigations which may be considered are
listed in Table 20.3.
Plain radiographs include an orthopantomogram, and
transcranial and transpharyngeal views of the TMJ. These
images give information about the bone structure. Open
and closed views will give some indication about jaw
mobility.
Arthrography is an invasive investigation using a
radiopaque dye, which is injected into the upper joint
compartment, the lower joint compartment or a combination of both. This technique can provide information
about the internal structures of the joint. The cartilaginous
meniscus is outlined. The procedure is usually carried
out under videofluoroscopy so that the joint can be imaged
in motion. Disc displacement and perforations can be
identified. However, extravasation of dye into surrounding tissues will spoil the investigation. With newer
imaging techniques this method is now less frequently
used.
Computerised tomography (CT) scanning can give a
lot of information about the bony relations and bone
Examination
174
Palpation of the TMJs may cause pain and, on movement, clicking or crepitations may be felt or even heard.
On intraoral examination the patient may have limited
opening (normal interincisal opening 40-50 mm). There
may be deviation of the jaw to one side when asked to
open widely due to limitation of movement from that
side (normal lateral movement 10 mm to each side).
Palpation of the masseter muscles and the pterygoid
muscles should be carried out. To palpate the pterygoid
muscles the patient should be asked to deviate the jaw to
the side being examined to allow a finger to be passed
along the upper buccal sulcus backwards between the
ramus of the mandible and the tuberosity of the maxilla.
Behind the tuberosity are the pterygoid plates - the
origin of the pterygoid muscles. This site is often tender
in TM dysfunction, due to muscle spasm and fatigue.
A general examination of the head and neck should be
carried out, paying particular attention to tenderness in
the sternomastoid and temporal muscles. The angle of
the jaw may be tender where the medial pterygoid muscle
is attached.
Table 20.3
Investigation of temporomandibular
joint pathology
Plain radiographs
Arthrography
CT scan
MRI scan
quality of the TMJs. It gives axial views and computergenerated coronal views; it can also give threedimensional images. This method is very helpful in
providing information about trauma to the joint, bony
disease in the joint and ankylosis.
Magnetic resonance imaging (MRI) images the soft
tissues and is helpful in identifying disc position. It can
demonstrate disc perforation and joint effusions. It may
also pick out adhesions within the joint. It does give
information about the bone but it is not as good as a CT
scan.
Surgical management
Arthrocentesis
Arthrocentesis is a method of flushing out the TMJ by
placing a needle into the upper joint compartment using
local or genera] anaesthesia. Ringer's lactate (see Ch. 5)
is injected into the joint. This compartment will take up
to 5 mL of fluid. By filling under pressure, any minor
adhesions are broken down or lysed. A second needle
placed into the same joint compartment allows throughflow of fluid to be achieved. This allows thorough
washing or lavage of the joint. The process is referred to
as 'lysis and lavage' and can produce good therapeutic
outcomes. It has a particular roll in cases of acute closed
lock. In this situation, the meniscus is usually jammed in
front of the condyle, preventing translatory movement.
By ballooning-up the joint the potential space becomes
real and the meniscus may have room to reduce to its
normal position. The lavage will wash-out products of
inflammation, creating a better environment for healing.
Sodium hyaluronate can be injected at the end of the
procedure to improve joint lubrication.
TMJ arthroscopy
TMJ arthroscopy can be used both as a diagnostic tool
and as a treatment modality. The synovium, joint and
miniscal cartilage can be visualised.
The standard technique for TMJ arthroscopy is via a
lateral approach. The upper joint compartment, where
most of the translatory movement occurs, is entered with
a 21 gauge needle posteriorly. After insufflation of the
joint with Ringer's lactate, through-flow of fluid is
established via a second 19 gauge needle placed
anteriorly in the joint space. A trochar and cannula are
then introduced into the space created by the fluid in the
joint. The trochar is removed and replaced by the arthroscope. An outport second cannula may be inserted
anteriorly into the joint for instrumentation - the working
cannula. The upper joint compartment can then be
examined for synovitis, displacement of the meniscus,
adhesions between meniscus and the joint fossa and
other pathology.
If adhesions are seen they can be divided with very
small scissors inserted through the working cannula. It is
possible in some cases to reduce a dislocated meniscus,
biopsy cartilage or synovium, remove loose bodies (fragments of cartilage floating in the joint) and reduce the
joint eminence with rotary instruments. Drugs such as
corticosteroids or sodium hyaluronate may be injected into
the joint to reduce inflammation and improve lubrication
respectively.
Splint therapy, soft diet and analgesics are used as part
of the postoperative management. The patient is also
instructed in gentle jaw stretching exercises.
Meniscal plication
When conservative management has not caused
improvement after a period of 4-6 months, and
arthrocentesis or arthroscopy have failed to correct
meniscal dislocation, then open arthrotomy should be
considered.
The usual approach is via a preauricular incision (Fig.
20.2). Once the joint is exposed, entry is made into the
upper joint compartment and the position of the meniscus
identified. Any adhesions are released and the meniscus
is repositioned and fixed with sutures from the lateral
aspect of the cartilage and posteriorly into the temporal
muscle and fascia. Some surgeons will also enter the
lower joint space to increase the mobilisation of the
meniscus and remove a wedge of retrodiscal tissue, stitch
or plicate the defect created with retrodiscal sutures,
repositioning the meniscus more posteriorly. Sometimes
these procedures are combined with an eminectomy to
increase joint space.
Postoperative management is similar to that of arthroscopy. Physical therapy is important as there is inevitably
a degree of scarring following this surgery.
Meniscectomy
This procedure is not commonly performed in the UK
but there have been reports of successful outcomes in
patients suffering from internal joint derangement by this
175
theory is that by taking away this eminence over which
the joint head sticks, the joint head has no obstruction to
prevent its return into the fossa.
Dautrey procedure
This procedure is another method of stopping TMJ dislocation. The approach is again exposure of the joint via
the preauricular incision. The eminence is again exposed
but in this procedure the anterior part of the eminence,
which is attached to the zygomatic arch, is incised in a
more vertical direction (Fig. 20.4). This anterior portion
is fractured-off and, still attached anteriorly to the zygomatic arch, is swung downwards and wedged against the
remaining eminence to augment the eminence. In theory,
because of the increase in eminence height, the condyle
is unable to dislocate. Other methods of eminence augmentation have been described, for example bone graft
augmentation.
Fig. 20.2 Preauricular incision for exposure of the
temporomandibular joint.
method. Essentially, the approach is the same as that for
meniscal plication. Once the meniscus is identified the
cartilaginous part is excised. There is uncertainty about
long-term effects this may have on the joint.
Eminectomy
This procedure is used for recurrent jaw dislocation. The
approach is the same as for the plication procedure. The
joint eminence, which lies anteriorly to the fossa, has to
be well exposed. The eminence is then excised by a combination of bur cuts and a fine osteotome (Fig. 20.3). The
176
Fig. 20.4
Fig. 20.3 Eminectomy. The hatched line indicates the
bony incision line.
The Dautrey procedure to increase the height of the eminence.
Condylotomy
This technique for treating painful TMJs originally used
a blind external approach using a Gigli saw. Nowadays
this procedure is carried out via an intraoral approach.
The lateral aspect of the ramus of the mandible is
exposed and a cut is made below the condyle with an
oscillating saw. It may be subcondylar or subsigmoid
(Fig. 20.5). This causes reduced pressure on the meniscus
and anterior movement of the condylar head, which
reduces pain and often allows reduction of the displaced
joint meniscus.
Condylectomy
Condylectomy is usually performed when there is either
ankylosis or pathology of the TMJ. A preauricular
approach is used and, once the condyle is well exposed,
it is cut at the neck of the joint and removed. This procedure is generally combined with joint reconstruction.
TMJ reconstruction
On rare occasions the TMJ requires reconstruction. To
date no replacement adequately replaces the normal
TMJ. Indications for joint reconstruction are listed in
Table 20.4.
The goal of treatment is to restore the mandible and
TMJ to as near normal an anatomical state. Partial or
total TMJ reconstruction may be required; partial reconstruction may be indicated. There are fossa prostheses
but these are usually used in conjunction with condylar
replacement.
Various synthetic materials or alloplasts have been
used for meniscus replacement (e.g. Teflon®). These
materials can cause a foreign body giant cell reaction,
which is relentless in its destruction of surrounding
tissues. For this reason, these materials are now rarely
used. Autogenous grafts such as auricular cartilage and
dermis are sometimes used. Potential complications from
these grafts are disruption or displacement, cyst formation
with the dermal graft and fibrous ankylosis.
Ankylosis may be treated with a temporalis muscle
flap, gap arthroplasty or total joint reconstruction.
The usual method in gap arthroplasty is by parallel
cuts approximately 1 cm apart from the sigmoid notch to
the posterior ramus (Fig. 20.6). Interpositional material
can be placed to reduce union. Alloplasts such as Silastic®
or a chrome–cobalt cap prosthesis have been used.
• • • • Two types of incision on vertical ramus
of the mandible for condylotomy
Fig. 20.5 Two types of incision (subcondylar and
subsigmoid) on the vertical ramus of the mandible for
condylotomy.
Table 20.4
Indications for temporomandibular
joint reconstruction
Ankylosis
Joint destruction
Trauma
Infection
Tumours
Previous surgery
Radiation
Developmental deformity
Suturing medial pterygoid and masseter muscles together
above the ramus stump is a biological interpositional
graft.
Most surgery for ankylosis is carried out through the
preauricular approach but when joint replacement is
required a submandibular incision is used for access
to the ramus for a combined approach. A method of
biological reconstruction of the TMJ is the use of an
inferiorly based temporalis muscle flap, which is rotated
anteriorly beneath the zygomatic arch as an interpositional material (Fig. 20.7).
177
Fig. 20.6
excision.
Gap arthroplasty. The hatched area is the bony
Fig. 20.7
Finger flap of the temporalis muscle rotated
anteriorly under the arch of the zygoma into the glenoid fossa.
178
Fig. 20.8
plates.
A costochondral rib graft fixed with mini bone
Total joint reconstruction is required where there is no
functional joint plus loss of ramus height. This may be
necessary where there has been severe trauma, ankylosis,
tumour resection or a developmental abnormality such
as hemifacial microsomia. Costochondral grafts or vascularised free bone grafts such as the second metatarsal
bone from the foot could be used in combination with an
interpositional temporalis muscle graft. The most satisfactory method of total joint reconstruction is the combination of the temporalis muscle flap and an autogenous
costochondral rib graft (Fig. 20.8).
Several prosthetic joint replacement systems have
been devised to replace both glenoid fossa and condyle.
Some have had problems from chronic foreign body
giant cell reactions to the synthetic materials.
Surgery is not the endpoint of treatment. The postoperative phase, as in all surgery, is very important and
neglect in this area is often a reason for failure. Analgesic
and anti-inflammatory medications are usually indicated
and physical therapy is essential, with jaw opening exercises plus lateral and protrusive movement exercises.
PART II
ORAL
SURGERY
179
179
21
Introduction
The oral surgery section of this text focuses on those
areas of surgical practice that are routinely encountered
in general dental practice. Certain procedures, such as
uncomplicated extraction of teeth, will fall within the
area of competence of every dental practitioner whereas
other procedures, such as removal of cysts and certain
wisdom teeth, might be performed only by those who
have an interest in surgical dentistry and who have
developed the necessary competence, through training, to
perform those more complex procedures. Regardless, all
dental practitioners must have a detailed knowledge of
the subject areas covered within the 'oral surgery'
sections of this book because they will encounter patients
routinely who present with signs and symptoms that
require a comprehensive knowledge to diagnose them.
Thus, even if referral to a specialist is the management of
choice, a dentist must be equipped with the knowledge to
180
make a competent referral and to fully inform the patient
of the nature of the problem, the scope of the treatment
and the likely prognosis.
This section therefore covers those areas where
practical knowledge is core information, whereas the
preceding section – 'special surgical principles' - was
concerned with areas where theoretical rather than
practical information is more important.
References to Part I of this book are extensive, thus
minimising duplication of core information relating to
basic principles such as homeostasis, surgical sepsis and
cross infection control.
The subsequent chapter details the process of history
taking and examination and also importantly covers the
issue of the patient consent. Further chapters describe
specific areas of oral surgical interest.
22
History and examination
Introduction
Table 22.1
In oral surgical practice, the same approach to history
taking and examination should be adopted as for general
history taking and examination. The process should be
more focused, however, to the oral region and, for
example, a full systemic history and examination is not
usually required.
History taking
The elements of the clinical history are shown in
Table 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 rapport
to develop with the patient that will facilitate the rest of
the interview and enhance the possibility of achieving an
appropriate diagnosis and treatment plan. Patient contact
at a social level is an important prerequisite to obtaining
the rest of the history and is important before examining
the patient. Premature physical examination of a lesion
may not only reduce the patient's confidence but also
unnerve the surgeon if the diagnosis is not immediately
apparent with visual examination.
As discussed subsequently, consent to history taking
and examination is usually implicit, but nothing should
be taken for granted and all of one's questions and
examinations should be fully explained.
The presenting complaint
The patient should be allowed to describe the complaint
in his or her own words, and then a full history of the
presenting complaint should be established. This should
be carried out using searching questions that do not lead
Elements of the clinical history
History of the presenting complaint
Past medical history including drug history
Family history
Dental history
Social history
the patient into giving false information. Patients wishing
to avail themselves of the best medical attention will
usually 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 patient
with alternatives: 'Is the pain constant?' is more likely to
be answered accurately if the patient is asked 'Is the pain
constant or not?'. Several features of the presenting
problem 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 practice
is that of pain, which requires further specific interrogation to establish its full nature and extent. Key elements
to be ascertained are shown on Table 22.2.
Past medical history including drug history
The importance of obtaining a medical history is paramount not only because it allows the surgeon to enquire
about other general aspects of the patient's wellbeing that
are associated with the presenting complaint but also
because it allows the surgeon to ascertain information
relating to the patient's medical status that might have an
influence on the treatment planning.
181
Table 22.2
Key features in a history of pain
Principle site affected
Radiation
Character
Severity
Duration
Frequency and periodicity
Precipitating and aggravating factors
Relieving factors
Associated features
A number of systemic diseases have a bearing on
surgical practice and these will be discussed below. In
addition, however, a number of standard questions should
be asked relating to the patient's past medical history.
The use of a preprinted questionnaire for this purpose is
helpful because patients are likely to produce truthful
responses when filling in 'their own' questionnaire, and
also because it also provides written confirmation that
these questions have been considered (Fig. 22.1). However, the questionnaire should always be verified by the
clinician and this information should always be included
in the written history that is recorded in the patient's case
record.
A history of smoking should alert the clinician to the
possibility of chronic lung disease and the patient should
be advised to stop prior to any surgical treatment under
general 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 with
coagulation, which may require investigation.
Locomotive system
A history of arthritis, especially rheumatoid disease, is
important. Such patients tend to have problems with the
cervical spine and this may be important, not only for the
anaesthetist if the patient requires intubation but also for
the oral surgeon treating the patient within a dental chair.
Particular care should be taken in patients with Down
syndrome because of their tendency to have atlantoaxial
dislocation.
Neurological system
Neurological symptoms are important to elicit particularly
if there is a history of trauma and these are discussed
fully in Chapter 19.
Cardiovascular system
The cardiovascular status of the patient is particularly
important when general anaesthesia is required. A
myocardial infarction within the previous 6 months is a
contraindication to general anaesthesia and surgery,
unless this is vital (see Ch. 35).
Similarly, patients at risk of endocarditis should
receive antibiotic prophylaxis and it should also be
remembered that many at-risk patients are also on
warfarin; their management must take this into account
(see Ch. 35).
The respiratory system
182
An upper respiratory tract infection is a relative contraindication to surgery and treatment should be deferred
until the infection has been cleared. Patients with chronic
lung disease may need special care. The history of a
productive cough should be elicited, together with sputum
production, which may suggest a current pulmonary
infection that requires active treatment before general
anaesthesia and surgery.
Drug history
It is crucial to know about the drugs ingested by the
patient, including over the counter medication, before
contemplating any surgery. A history of corticosteroid
medication and anticoagulant therapy is particularly
important (see Ch. 35). Care should be taken to ensure
that the patient's medication will not adversely interact
with any medication given to or prescribed for the patient.
Family history
The family history provides information regarding
genetic disease, such as haemophilia, and also provides
an insight into disease susceptibility by enquiring about
concurrent family disease and causes of death in deceased
relatives such as heart disease, stroke or cancer.
Social history
This provides information regarding home support for
patients postoperatively and should also include questions
about smoking and alcohol consumption, as these
Fig. 22.1
Medical history questionnaire.
influence not only disease susceptibility but also will
influence postoperative recovery.
The first is dealt with in appropriate chapters within
this book. The last two can be dealt with by a system of
examination (Table 22.3).
Examination
Examination of the patient is subdivided into three areas:
first, related to the presenting problem; second, to assess
the patient's fitness for the proposed procedure and third,
to detect any associated or coincidental disease.
General assessment
All clinicians should look at their patients at the first
encounter to see whether they think the patient looks
'ill'. This may mean the patient looks cachectic, flushed
183
Table 22.3 System of examination for an oral
surgery patient
General assessment
Hands
Face
Neck
Oral cavity
and feverish, exhausted, pale or jaundiced, or that other
features are apparent. If the patient looks ill, do not
hesitate to ask if he or she feels ill.
When assessing a patient for oral or dental surgery, a
quick and easy check can be performed as described
below.
Examination of the eyes may show arcus senilis, a
ring of cholesterol deposit around the iris of the eye
associated with cardiovascular disease.
Skin rashes may be most obvious on the face associated with allergies, acne, dermatitis, psoriasis, and other
disorders. Lichen planus is more typical on the wrists and
flexor surfaces of the arms.
Facial paralysis may suggest a previous stroke or a
lower motor neuron palsy such as Bell's palsy. A palsy of
one side of the face results in the face being pulled to the
opposite side because of unopposed muscle action.
Again this examination can take place while talking to
the patient and in only a matter of seconds.
Examination of the salivary glands, temporomandibular joints and muscles of mastication should be
carried out when indicated.
Neck
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 deficiency
anaemia), white nails (may suggest liver disease) and
cyanosis or bluish discoloration (may suggest heart or
lung disease).
Examination of the palms of the hands may show
palmar erythema (red and mottled, associated with liver
disease), Dupuytren's contracture of the ring and fifth
fingers (associated with liver disease and epilepsy), pallor
of the palm creases (associated with anaemia) and joint
deformity and swelling will indicate arthritis and its
nature.
The pulse can now be felt recording the rate and any
arrythmia.
Face
184
Jaundice will be obvious from examination of the colour
of the face and conjunctivae. This is a very important sign
for the surgeon. Such patients have associated disorders
of blood coagulation due to clotting factor deficiencies
and are prone to sepsis. If the jaundice is related to viral
hepatitis, the patient may be a major risk to the surgeon
and the theatre staff.
Examination of the conjunctivae will not only demonstrate jaundice but they may also be very pale, indicating
anaemia.
Neck inspection is best performed from the front and
palpation from behind. It may reveal an obvious goitre
especially visible or palpable on swallowing.
Patients receiving treatment for known heart failure
may have distension of neck veins, which suggests that
the failure is not fully controlled.
Enlarged lymph nodes may be visible and palpable
and may be associated with infection, malignancy, or
other less common disorders. These usually need to be
investigated before any other treatment is instituted.
It is important to remember to inspect the sides of the
neck especially in the region of the ears and parotid
gland.
Scars in the neck should alert one to previous surgery
(e.g. thyroidectomy) and enquiry should be made about
this if not mentioned by the patient during the history
taking.
Swelling of the neck or elsewhere in the orofacial
region is often a presenting feature and should be
examined in a rehearsed fashion in order to elicit the
important clinical features (Table 22.4).
Oral cavity
The oral/dental surgeon has the great advantage of being
able to inspect the oral cavity closely and hence to detect
associated diseases that may be apparent here. This is in
addition to the presenting problem. The clinical features
relating to specific oral disease are detailed in the subsequent chapters.
Table 22.4
swelling
Important clinical features of a
Position
Size
Shape
Colour and temperature
Tenderness
Movement
Consistency
Surface texture
Ulceration
Margin
Associated swelling
A full cardiovascular, respiratory, abdominal and
neurological examination does not come under the remit
of the oral/dental surgeon. Suspicion of underlying
disease may be detectable from a clear history and
clinical examination as outlined above. Such a history
and examination should alert the oral/dental surgeon to
an underlying or potential problem and in this situation,
specialist advice should be sought before progressing
with treatment. The patient's GP will often be aware of
the underlying problems and be able to advise on risks
and whether further referrals, investigations and management are necessary. If there is any doubt, advice should
be sought before any oral surgical or dental treatment is
performed.
Conse'nt
The patient must consent to all procedures after full
explanation of the options and consequences. Consent to
answer questions and to be subjected to routine
examination is usually implied. Consent to procedures
under local anaesthesia is commonly obtained verbally
as patient cooperation is a prerequisite to completing the
operation. The consequences, for example, of extraction
of an impacted wisdom tooth, may be lip numbness,
and it is therefore prudent to fully explain the possible
implications and record this in the notes.
Although most dentists will not work on patients
under general anaesthesia - most refer patients for
general anaesthesia and so hence have the responsibilities
of the referring dentist, detailed below - they do have
continuing responsibility for their patients postoperatively
and so must have detailed knowledge regarding their
responsibilities surrounding such referrals.
A detailed discussion about the ethical and legal
obligations upon clinicians is not included here but it is
important to consider the principles of obtaining consent
to treatment.
The use of the term 'informed consent' has led to
much confusion amongst healthcare professionals about
the nature and extent of the information that should be
imparted to a patient. Many clinicians have interpreted
this concept of informed consent as a process that has to
be undertaken to avoid possible legal actions and, as a
result, it is often carried out in a ritualistic way. This
approach is most commonly reflected in cursory clinical
notes recording, for example, 'warning given regarding
possible nerve damage' in association with third molar
surgery.
It may be that the term 'informed consent' is a
misnomer and that the process of obtaining consent to
treatment should, by definition, incorporate all of the
information that a patient requires to make an informed
decision on whether or not to proceed with the proposed
treatment. Rather than thinking in terms of obtaining
informed consent, a clinician may benefit from considering 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 treatment
to be undertaken safely, including sufficient
information about the patient's dental condition, the
treatment options and the material risks and/or
complications arising from the condition itself, or
associated with the patient's medical condition
• requires disclosure of the material and relevant risks
associated with the treatment options under
consideration
• permits discussion about the implications of refusal
of treatment by the patient or withholding of
treatment by the clinician
Before the process of obtaining consent can be broached
with the patient, the clinician must undergo a process of
obtaining all relevant clinical information and recording
the details in the patient record. The patient record is an
invaluable and permanent source of information and it
185
must be possible to rely upon it for accuracy and content
at any time in the future. The patient record should also
contain the information listed in Table 22.5. The prudent
clinician will also record the information listed in
Table 22.6.
Following a structured approach to patient assessment
and recording, the details in the patient record provide
the clinician with all of the information necessary to
facilitate meaningful discussions with the patient about
the clinical situation. The imparting of all relevant information that the patient needs to make a valid decision on
whether or not to proceed with the treatment as proposed
is then readily available.
Competence to give consent
The efficient delivery of dental care and/or treatment
relies on the fact that the law recognises that consent to
every procedure need not be written or even explicitly
given. The medical and dental professions rely on the
fact that a patient implies consent by cooperating with
treatment. However, consenting to treatment is more than
simple acceptance or submission. The principles of obtaining or giving consent involve voluntariness, knowledge
and competence:
• Voluntariness requires the patient freely to agree to
treatment (or not).
• Knowledge requires disclosure of sufficient
information in a comprehensible way to allow the
patient to make an informed choice.
• Competence means that the patient must have
sufficient ability to understand and make an informed
decision. Competence to give consent is a
prerequisite to obtaining valid consent.
Put simply, the ability to give consent is a function of the
patient's age and mental or intellectual capacity. A patient
must be able to do the things listed in Table 22.7.
Patients who are not able to make such autonomous
decisions are young children (due to their lack of maturity),
adults with cognitive difficulties and unconscious
patients. These will be considered in turn.
Children
186
The Family Law Reform Act (1969) in England and
the Age of Legal Capacity (Scotland) Act, as amended,
confirm that a patient aged 16 years and over could give
valid consent to treatment and, by implication, could also
Table 22.5
Essential information contained in
the patient record
Patient's personal details
Current medical history
History of presenting complaint or reason for referral
Symptoms experienced
Patient expectations and/or aspirations
Table 22.6 Desirable information included in the
patient record
Charting of teeth present
Periodontal assessment and charting
Oral cleanliness
Signs and symptoms noted including extra-oral
Special tests undertaken and results
Assessment of radiographs
Diagnosis and treatment options
Assessment of complications and sequelae
Definitive diagnosis and treatment plan
Table 22.7
consent
Requirements for the ability to give
Understand the information
Remember or recall that information
Relate the information to 'self
Make a judgement on whether or not to proceed
Communicate that decision
withhold consent. Although the law does permit a young
person over 16 years to give valid consent, the prudent
clinician undertaking a major procedure on a patient
between 16 and 18 years should consider involving the
parents, but only with the patient's consent.
For young children the consent of the parent or
guardian is sufficient and must be obtained.
For older children, the Children Act (1989), the judgement in the Gillick Case and the Age of Legal Capacity
(Scotland) Act, as amended, effectively permit a patient
under the age of 16 years to give legally valid consent if
he/she has sufficient intelligence and maturity to fully
understand the nature and consequences of the proposed
procedure.
Although the law does permit a child under 16 years
to give consent, it is subject to an assessment by the
clinician of the patient's level of understanding, and
practitioners should always attempt to confer with the
parents of patients under 16 years unless the patient
declines parental involvement.
Mental capacity
There are varying degrees of mental capacity/understanding that affect a patient's ability to understand the
nature and purpose of the treatment and to give valid
consent. Where an adult patient is unable to give consent
then, in an emergency, the law relies upon the 'principle
of necessity'. If emergency treatment is considered
necessary to preserve the health and wellbeing of the
patient then the clinician can proceed without formal
consent. To proceed with treatment on an elective basis
for such patients, a clinician would be wise to take advice
from his/her defence organisation.
Unconscious patients
In the case of temporary incapacity, such as unconsciousness, it is recognised that treatment can be carried out
without consent provided that such treatment is clinically
necessary and in the patient's best interests.
General anaesthesia
As a result of guidance issued by the General Dental
Council, the availability of general anaesthesia for dental
treatment has been removed from the general dental
practice setting. There will be a continuing demand, albeit
a reducing one, for general anaesthesia in the secondary
care sector and an increasing requirement for sedation
facilities, and it is therefore important to define the
obligations on dental practitioners.
The referring dentist
The General Dental Council places the following
obligations on a dentist who refers a patient for treatment
under general anaesthesia:
• to assess the patient's ability to cooperate
• to describe the various methods of pain control,
including an assessment of the relative risks
associated with each
• having decided that the patient requires treatment
under general anaesthesia, or by sedation, to provide
a 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 for
referral.
The referring dentist is also required to ensure that the
provider to which the patient is referred complies with
the General Dental Council guidelines on staff, equipment and facilities for the safe delivery of care.
The operator dentist
Operator dentists are required to ensure that the treatment to be undertaken is not beyond their level of
expertise and knowledge and that the facility complies
with General Dental Council requirements on anaesthetic
and support staff, equipment and drugs and that there is
a protocol in place for the care of the collapsed patient.
Staff training in monitoring of the patient and in dealing
with emergency situations is mandatory and should be
undertaken regularly. Before embarking on the provision
of 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 an
evaluation of the medical history - if general
anaesthesia is deemed necessary
• give appropriate advice about postoperative
complications or sequelae.
When a patient is referred for treatment under general
anaesthesia 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 as
the treatment required
• the operator confirming the need for treatment
and the appropriateness of the request for general
anaesthesia
• in concert with the anaesthetist, obtaining written
consent following an assessment of the patient's
fitness for anaesthesia.
187
Postoperative care
It could be difficult for the patient to find out-ofhours care after a referral for treatment under general
anaesthesia, and this is particularly true if the provider is
188
some distance from the referring practice. The referring
practitioner retains overall responsibility for the care of
the patient and should therefore ensure that the patient, or
a responsible person or carer, is informed of the arrangements for the provision of emergency care.
es
Basic oral surgical
techniques
Introduction
The majority of oral surgery skills can be learnt by
most with good practical training, an awareness of basic
principles of surgery (see Part 1), knowledge of the
anatomy of the region and careful preparation for the
procedure. Whatever surgical operation is being undertaken, the operator must have considered the following
points (Table 23.1).
Preoperative considerations
The surgeon must consider if the procedure is necessary.
For example, oral surgeons over recent years have looked
more critically at the removal of impacted wisdom teeth,
given the unpleasant short-term effects and, more
importantly, the longer-term possibility of inferior dental
or lingual nerve damage. In the light of more careful
scrutiny of these aspects, many surgeons are now
Table 23.1
Preoperative considerations
Equipment for oral surgery
Operative techniques
incision
raising a flap
bone removal
tooth division
elevators
debridement
suturing
types of suture
Postoperative care
postoperative instructions
analgesia
prevention of infection
postoperative bleeding
Follow-up
advising an increasing number of patients not to have
these teeth removed unless quite strict criteria are
fulfilled (see Ch. 27).
The patient must be made aware of other possible,
perhaps non-surgical, treatments. A good example of this
is the treatment of periapical infection by surgical means
where endodontic alternatives may be considered more
appropriate.
The short-term and long-term consequences of the
operation must be explained to the patient, particularly
in relation to known risks. Many surgeons now prefer
to prepare information leaflets on the more common
procedures, such as removal of impacted wisdom teeth,
so that verbal preoperative warnings are reinforced with
written information.
The most appropriate measures for control of pain and
anxiety during the procedure must be considered.
Practically, there must be a decision on whether local
anaesthesia, local anaesthesia with some form of
sedation, or general anaesthesia is the preferred method.
Patients have an important contribution to make when
reaching such a decision but the operator may advise
sedation or general anaesthesia where the procedure
would take an unacceptably long time, where access
might prove difficult in the fully conscious patient, or
where postoperative care would benefit from the expertise
of skilled nurses.
Patients should be urged to accept local anaesthesia,
with or without sedation, for straightforward procedures
given that the additional risk of general anaesthesia,
although small, should be avoided where possible (see
Ch. 10). Only when these issues have been fully addressed
with the patient will he or she be in the position of being
able to give informed consent to the operation. Several of
the points above can be supplemented with preoperative
explanatory literature and the patient's signature is finally
required for documented consent. This is mandatory
189
where sedation or a general anaesthetic is employed but
is implied in many centres where local anaesthesia is used
alone. Informed consent is discussed fully in Chapter 22.
Radiographic viewing screens
Most oral surgical operations require good radiographs
and adequate viewing facilities within the operating
room.
Equipment for oral surgery
Surgical instruments
Although there may be individual preferences for
particular surgical instruments, there is a general consensus on basic items that are commonly used. Figure
23.1 shows a typical oral surgical kit. In oral surgery
there is almost invariably a need for a hand-piece and
drills and, when soft tissue surgery is being carried out, a
bipolar diathermy unit can be invaluable. The use of the
various instruments will be discussed later in this chapter
and the importance of instrument sterilisation has already
been discussed in Chapter 7.
Good lighting is essential to oral surgery and multifocal surgical lamps reduce dark spots and minimise the
head or shoulder shadow of the operator or assistant. Dark
protective spectacles reduce the patient's discomfort from
the glare of a good light, in addition to protecting their
eyes from any possible debris or instruments.
Assistance
Competent assistance is extremely valuable in oral
surgery. Good assistants realise that they can materially
aid the operator's access and vision of the operative site
and are aware of the importance of their role in reducing
tissue damage by careful retraction. They should be fully
aware of the objectives of the surgery being undertaken
and operative problems that might be encountered.
Operative techniques
Incision
For most minor oral surgery, a Swann-Morton number 15
blade is the most common choice for incision of the
mucoperiosteum (Fig. 23.2). The operator should have a
clear picture preoperatively of the access that will be
attained, and the incisions will be made appropriate to
this need. Scalpel blades should be new for each patient
Suction
Suction should be low volume and aspirator heads or tips
should be narrow bore. This combination allows maximum efficiency without undue soft tissue obstruction of
the system.
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 by
pressure onto a bony surface, they can and should be
renewed as necessary intraoperatively. The cut should be
made at right angles to the underlying bone surface such
that the epithelium on each side of the incision is not
chamfered but each edge should lie as close as possible
to 90° to the basement membrane. This will maximise
the chance of good healing when the tissues are
reapposed. Any laxity in the soft tissue that is a feature of
the free rather than the attached gingiva can be tensed
and hence be more stable by a finger stretching the sulcus
and holding it firmly against the underlying bone. The
scalpel should move at uniform speed and with sufficient
firmness to cut through not only the mucosal surface but
also the periosteum overlying the bone. It should be
made, ideally, with one movement, avoiding redefining
or chopping actions, which produce ragged margins.
Raising a flap
This is undertaken with periosteal elevators such as the
Ash pattern or Howarth elevators. Other instruments that
can be used are the small blade end of a Mitchell's
osteotrimmer where the tissues are particularly adherent
to the bone beneath, or the reverse side of the right or left
Warwick James' elevators for careful raising of interdental papillae. The term 'raising a flap' is probably not
well chosen, for it implies that the tissues are lifted up
actively from the bone surface. In fact. the periosteal
elevator should be firmly pushed at approximately
30-45° to the surface of the bone such that the
periosteum is stripped from it. It is important to try to
raise both mucosa and periosteum in one layer and this
does require a considerable force to be applied. Each
push of the periosteal elevator should only be designed
to achieve a movement of about 5–10 mm, with the
emphasis on the sharp edge of the instrument being kept
on the actual surface of the bone. Occasionally, a dry,
sterile swab can be interposed between the periosteal
elevator and the bone, particularly where muscle fibre
attachments are very adherent to the periosteum. This
measure can more effectively clean the bone surface
totally of overlying soft tissue.
Most mucoperiosteal flaps are buccally situated and
are designed to have one horizontal and one vertically
arranged limb. The vertical cut is often known as the
relieving incision. For this reason many refer to this
configuration as 'L'-shaped. For virtually all flaps the
horizontal arm should extend from the distal forward to
the operative site, with the vertical limb anteriorly
placed. This ensures that when the flap is taken back and
retracted, it is being held away from the operator's line of
vision, thus increasing access and visibility. From time to
time there may be a need for a distal (posteriorly) placed
vertical limb in addition to the anterior one, and this can
be an advantage where there is a more marked convexity
to the curvature of the arch such as in the lower anterior
segment. In general, however, the second vertical cut is
avoided because the flap is never as stable when replaced
in such circumstances. Palatal flaps do not require any
vertical relief whatsoever, as the concave configuration
puts no requirement for it whether in the dentate or
edentulous mouth.
In the edentulous patient, horizontal incisions are
made along the crest of the ridge or where there is any
instability due to resorption of the underlying bony
alveolus, slightly to the buccal aspect of the crest.
Incisions around standing teeth require care to avoid
undue damage to the gingival cuff both for buccal or
palatal flaps. The vertical incision needs to be carried
from the attached into the free gingiva to a varying
length, depending on the access needed. It should be
angled forwards such that the base of the flap must
always be longer than its free margin, thus ensuring
adequacy of the blood supply to it. Only the mental nerve
is at risk from a vertical cut in the oral cavity. Care
should always be taken to avoid the mental foramen with
a vertical incision and even the horizontal incision may
need to be swung to the lingual side around this area
where, in the edentulous patient, there has been gross
alveolar bone atrophy and the foramen is lying for
practical purposes on the crest of the ridge.
Finally, in the edentulous ridge, it may be possible
to increase the length of the horizontal (crestal) limb of
the incision such that the need for a vertical relieving cut
is obviated. This is sometimes known as an 'envelope'
flap and it certainly reduces postoperative discomfort
as movement of the lips and cheeks tends not to pull
directly on it, and also where a denture is being inserted
this can be worn more comfortably. This principle (i.e.
increasing the length of the horizontal incision to allow
access without any vertical relief) can also be used in
dentate patients as, for example, in the removal of wisdom
teeth (see Ch. 27).
Buccal retraction can be effected with a variety of
designed retractors. Some of these contain a rake edge,
containing multiple teeth, which should be held against
191
the bone but which can cause considerable damage to the
undersurface of the flap if its teeth are allowed to rotate
and tear into the flap. This might happen if the assistant
tires later on in the procedure. Many prefer, therefore,
to use periosteal elevators, one held by the operator and
the other by the assistant. The main objective of good
retraction is to protect the soft tissues from damage
during the procedure and this includes not only the
mucoperiosteal flap but also the lips and cheeks, which
are particularly liable to frictional burning from bur
shanks if the operator and/or the assistant is not duly
vigilant.
Bone removal
192
Many dentoalveolar procedures require bone to be
removed 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 with
hand instruments such as osteotrimmers, curettes or even
elevators. Under local anaesthesia this may be a less
alarming method for the more nervous patients and can
in some cases eliminate the use of drills. Bone rongeurs
(bone nibblers) can also be used to enlarge existing bone
defects, as for example round cysts, in addition to their
use for trimming sharp edges on completion of the
operation.
A hand-piece and drill is the most frequently used
method for bone removal. For most dentoalveolar
surgical purposes an engine with a capability of 40 000
revs per minute and with good torque is needed, either air
or electrically driven. As oral surgery techniques utilise
direct visualisation, a straight hand-piece is inevitably
the instrument of choice. High-speed air rotors do not
give the same desirable sense of feel to cutting bone and
run the risk of air escape into the wound causing air
emphysema. Air introduced at pressure can be a most
alarming occurrence to both patient and operator as it
causes immediate swelling. Palpation of the resultant
swelling will elicit characteristic crepitus, a creaking
sensation that tends to 'move about', not always being
felt at the same point of the swelling.
A variety of different burs are available but round burs
and fissure burs are most commonly employed. For most
procedures where bone alone is being cut, steel is a good
material but where tooth sectioning is likely, tungsten
carbide burs have faster cutting potential and can reduce
the time spent cutting through enamel, as, for example,
when dividing a tooth. Removal of bone and how much
to remove is a skill learned by experience but, in general
terms, sufficient bone should be removed to allow
adequate further instrumentation to achieve the desired
result. Ideally, bone removal is kept to the minimum
consistent with the provision of satisfactory access.
During the cutting, sterile water or saline should act as a
coolant and aid the successful aspiration of any loose
bony fragments, thus maintaining maximum visibility.
Chisels can be used as hand instruments or with a
hammer. When the latter is employed, the patient would
normally be under a general anaesthetic as the procedure
would be unduly alarming to the conscious patient. The
most common use of the hammer and chisel is in the
removal of lower third molars where the lingual plate is
split (split bone technique) allowing the tooth to be
rotated lingually to effect its removal (see Ch. 27). The
bone must not be unduly brittle as this will increase the
chance of uncontrolled splitting of the bone and jaw
fracture. It is therefore confined to young patients and,
although the split of the bone may be less controlled than
using a drill and hand-piece, it can be a very quick and
remarkably atraumatic technique in skilled hands.
Tooth division
Division of an impacted tooth is usually carried out to
reduce the amount of bone removal that would otherwise
be required to effect its elevation and delivery. Division
of a tooth is normally carried out with a hand-piece and
bur, the latter often being a fissure bur. Teeth may be
divided in any way appropriate to their position, but most
often this involves sectioning of the crown from the root
complex. There are instances where, for example, in a
mesioangular impacted lower third molar there are two
clearly separate roots on radiograph, the tooth may more
easily be divided longitudinally to separate the mesial
root and its adjacent crown from the distal root and
crown. The additional benefit of division of a tooth is the
resultant reduction in its resistance to elevation.
Separation of the roots of a multirooted tooth will
also reduce the mechanical advantage of its resistance to
removal and some teeth do require sectioning of crown
from roots, followed by root from root separation.
Although this clearly requires more use of the drill, the
forces that have to be applied with elevators are consequently reduced and this more than compensates for
the alarm that patients might experience as a result of
excessive forces being used during elevation.
Elevators
A variety of elevators are available for removing teeth or
roots from their sockets: Coupland's chisels (originally
designed 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 'block
and wedge' or 'wheel and axle', and should never be used
as crow-bars (Fig. 23.4). Hence, a dental luxator with its
sharp edge is pushed between the root of a tooth and its
alveolar bone via the periodontal space. This wedging
effect should cause the root to be moved from its socket
as the elevator is advanced. Coupland's chisels can be
used in a similar fashion and are more effective in this
way if their edge is well maintained and sharp.
The other method is accomplished by rotating the
elevator along its long axis such that its edge exerts a
displacing force on the tooth or root. The straight
Warwick James', Coupland's chisels, and, with their
pointed blades, Cryer's elevators are used in this way.
Great care should be exercised to avoid using an adjacent
tooth as a fulcrum for elevators except where several
teeth are to be extracted, when movement of the adjacent
tooth will not be a problem and may indeed be desirable.
Elevators should be applied to teeth with an awareness of the most advantageous point of application so that
the tooth will move along the line of its least resistance.
Hence, as most roots in the lower molar region curve
distally, elevation from the mesial aspect is more likely to
be successful. Similarly, elevation from buccal rather
than lingual is technically more practicable when using
the rotation principle.
Debridement
Fig. 23.3
Elevators left to right Coupland's chisel,
Warwick James' left, straight and right, Cryer's left and
right.
Following the completion of any surgical procedure it is
important to ensure that there are no impediments to good
healing. These can take the form of loose bone spicules
or fragments insufficiently attached to periosteum to
maintain an adequate blood supply, dental fragments
lying loose or hidden under the flap, or infected soft
tissues such as infected follicular tissue around the
removed crown of an impacted tooth. Bony or dental
fragments should be carefully aspirated with thorough
irrigation paying particular attention to spicules hidden
under the retracted flap. Soft tissues should be curetted
or removed with tissue forceps such as 'mosquito' or
Fickling's forceps. Any sharp bony edges can be nibbled
with rongeurs or smoothed with a larger 'acrylic' bur.
Suturing
Fig. 23.4 The correct application of an elevator between
the bone and the tooth.
Inserting sutures into a mucoperiosteal flap allows
accurate repositioning of the soft tissues to their preoperational site. In many cases, this will re-establish the
anatomical position of the flap but in certain circumstances the flap may be moved for good reason. Such a
situation arises where a buccal flap is pulled across an
oroantral fistula to be attached to the palatal aspect of the
socket. This is known as a buccal advancement flap and,
as will be discussed later in Chapter 26, it does require
193
periosteal release by incising the periosteal layer at the
base of the flap to allow sufficient elasticity to move the
tissues across the defect. In the majority of cases, however, sutures hold the soft tissues in the desired healing
position and prevent the wound opening, with the
consequent exposure of bone beneath and encourage
haemostasis.
Materials required
A suturing kit is shown in Figure 23.5 and involves the
following:
Needle holder
These instruments come in a variety of sizes and design
and operators tend to choose one that suits them, having
tried various forms. In general, they will be either ratchet
or non-ratchet designed, the former allowing the needle
to be locked into the beaks of the instrument whereas the
latter requires the operator to actively hold the needle
within the beaks.
Tissue forceps
Sometimes known as dissecting forceps, the important
requirement is that they hold the soft tissues atraumatically so avoiding crushing and with little chance of
slippage. This is achieved by a rat-toothed design, which,
although possibly causing tiny puncture points, is ideal
for the purposes of suturing and holding soft tissues
generally (Fig. 23.6). The use of non-toothed forceps will
194
Fig. 23.5 Suturing kit containing a Kilner's needle holder,
Gillies toothed tissue forceps, suture scissors and suture.
result in crushing of the tissues as, to prevent tissue
slippage from grasp, the instrument must be held too
tightly.
Soft tissue retractor
The relevance of this instrument is obvious but it does
indicate that an assistant is necessary during suturing to
hold the soft tissues aside to allow access and to use the
aspirator.
Needles
These are made of stainless steel and, for oral surgical
purposes, are usually a curved shape from three-eighths
to one-half the circumference of a circle; on cross-section
they are triangular. A full description of suture needles
and sutures appears in Chapter 3. The length of the
needle varies but between 18 and 26 mm is a reasonable
range for intraoral work. The triangular cross-sectional
view of the needle either has the apex of the triangle
facing inwards (i.e. on the concave side) or outwards.
The former (i.e. inward pointing) is known as the cutting
needle and the latter as a reverse cutting needle. These
designs allow minimal soft tissue trauma during needle
insertion as they cut a path through the soft tissues and do
not therefore require excessive force on the part of the
operator.
Fig. 23.6 The head of Gillies toothed tissue forceps
showing the interdigitating nature of the points.
Suture material
There is a wealth of choice of material for suturing
purposes (see Ch. 3) but most commonly in oral surgery
materials such as silk, catgut (now in its softgut format)
vicryl and nylon are used. Sutures are available either as
non-resorbable (e.g. silk and nylon) or resorbable (e.g.
catgut or vicryl). The gauge or thickness of the chosen
material must be determined and this is denoted by O
gradings. As the thickness of the material decreases, the
O grading rises. Hence 2/0 is thicker than 3/0, which is
thicker than 4/0 and so on. Most intraoral suturing is
carried out with 3/0 or 4/0 gauge material but on
extraoral skin surfaces, finer gauge is preferred such as
6/0 or even finer. This helps reduce scar visibility.
Types of suture
Different designs of suture usage can be chosen
according to the particular needs of the clinical situation
(Fig. 23.7). These vary from the simplest, such as the
interrupted suture, to more complex mattress designs to
continuous sutures placed either over the wound or,
particularly with skin surfaces, beneath it. These latter
continuous sutures are sometimes known as subcuticular
sutures. The vast majority of intraoral sutures will be
simple interrupted sutures.
Mattress sutures have particular advantages in certain
clinical situations. The horizontal mattress is often
helpful in reducing the surface area of a bleeding lower
molar socket and exerting pressure on the overlying
Fig. 23.7
mucoperostium. It can also be a useful suture in closing
an oroantral fistula where it encourages eversion of the
margins of the wound, thus ensuring better connective
tissue contact and discouraging epithelial contact which
would prevent healing by primary intention.
The vertical mattress suture also helps the apposition
of connective tissue surfaces and hence trouble free
healing. One example of its application is the interdental
papilla particularly of an anterior tooth where accurate
gingival repositioning of the flap is desired (see Ch. 29).
Suture technique
Flaps are normally 'L'- or inverted 'L'-shaped. Most
operators prefer to suture the angle of the 'L' first as this
will correctly align the vertical and horizontal limits of
the flap. The tissue of the flap should be held firmly by
the tissue forceps and the needle passed through the
mucoperiosteum about 3 mm from the margin, more if
the flap is friable because of chronic infection. The
needle is then pushed through the corresponding tissue
on the other side of the incision, again about 3 mm from
the margin. The suture is pulled through such that there
are only a few centimetres from its entry point to the end
of the suture. The knot should be tied as in Fig. 23.8 and
the ends cut. Where possible, the knots should be drawn
to lie to one or other side of the line of incision and the
tissue should not be drawn too tightly together (which is
usually seen by blanching) as it causes the thread to
'cheese cut' through the flap and produce a painful ulcer.
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) to
create the first tie (c); the suture is then wound counter clockwise to complete the knot (d).
Sutures placed intraorally are normally removed 5-7
days postoperatively. Surface anaesthetic can be very
helpful if the stitch has become embedded. In the
removal of sutures, normal dental tweezers such as
college tweezers should grasp the free ends of the thread
and the suture should be cut by sharp scissors or a suture
blade close to the knot. The suture should then be pulled
though in its entirety.
Postoperative care
196
The responsibility of the surgeon to a patient under treatment does not stop as the last suture is placed. Successful
healing can be enhanced by regimes designed to
minimise pain, prevent infection and reduce the chance
of bleeding. This involves not only necessary prescription
of drugs to patients but also appropriate instruction as
to the measures patients can follow to encourage fewer
postoperative problems.
Postoperative instructions
These can be given orally or by printed instruction sheets;
both compliment each other because oral instructions
given immediately on completion of treatment are
seldom retained fully by patients who have just come
through what to most of them has been an ordeal. Figure
23.9 outlines the information that should be given to
patients. The list of instructions should not be overdetailed and their design should bear in mind the ability
of the patient to understand them. A contact telephone
number is useful and instructions on where to get help
during 'non-office' hours is reassuring even if not
needed.
Analgesia
As far as most patients are concerned, control of postoperative pain is the most important factor during the
early phase of healing.
Fig. 23.9
Postoperative instructions leaflet.
Local anaesthesia
Many operators now administer local anaesthetics to
control immediate postsurgical pain. Under local
anaesthesia with or without sedation, the necessary
injections are given and tested presurgically as a matter
of course. Under general anaesthesia local anaesthetic is
given penoperatively, normally at the start or the
procedure, and many now prefer to use longer-acting
agents such as bupivacaine. It is obviously important to
inform patients that the area in question will be numb
when they first recover consciousness, and this is
particularly important when they have been warned
197
preoperatively of the possibility of nerve damage as a
consequence of the procedure. Even if longer-acting
local anaesthetics are not used, some operators reinforce
anaesthesia with the usual agent on completion of the
surgery, whether under local or general anaesthesia. It
does appear that immediate control of pain for the first
few hours postoperatively seems not only to have an
early benefit but may also reduce the discomfort
throughout the several days following surgery.
Systemic analgesia
The normal agents employed following minor oral
surgery are non-steroidal anti-inflammatory drugs or
paracetamol. Recourse to narcotics is seldom needed,
other than codeine-containing preparations. Opiates may
be needed after more extensive surgery but these patients
will generally be inpatients under the supervision of
skilled nursing personnel. There may be an advantage in
prescribing drugs with an anti-inflammatory action as
well as an analgesic effect. However, certain groups of
patients, such as asthmatics or those with a history of
peptic ulceration, are at risk from these drugs and the use
of paracetamol with or without codeine is more prudent.
All patients should be prescribed adequate analgesics,
and given instructions on their correct usage. There
seems little doubt that, whatever drug is prescribed,
patients should be instructed to take the analgesic before
the local anaesthetic effect has worn off. Some suggest
that analgesics are best started preoperatively, to ensure
that there is an adequate plasma level of the drug when
the local anaesthetic begins to wear off. Many patients
have their 'favourite' preparation and in these circumstances should be encouraged to use a drug that has a
proven success for them.
mandible and infection is consequently a more uncommon
complication and most antibiotics are therefore prescribed
for procedures carried out on the mandible.
Arguments against antibiotic use are based on their
overprescription resulting in increasing numbers of
bacteria that have developed resistance to these drugs,
and in some cases multiresistant organisms such as the
methicillin-resistant Staphylococcus aureus (MRSA)
that now poses such serious problems. The possibility of
more and more organisms having multiresistance is without question a serious and potentially disastrous scenario
of which both the medical and veterinary professions are
becoming increasingly aware. There is good cause, therefore, for all clinicians to consider carefully the perceived
advantages and disadvantages of antibiotic prescription,
particularly where they are being used for prevention of
possible infection rather than the actual treatment of
existing infection. Many clinicians now reduce the length
of time for which antibiotics are prescribed because this
measure in itself will reduce the chance of the emergence
of resistance in bacterial colonies. Amoxicillin or metronidazole are probably the most commonly prescribed
antibiotics when the postoperative risk of infection is
considered significant. Their use for patients with a
reduced capability of coping with infection, such as those
with a reduced immune response (for example, poorly
controlled diabetics, HIV-positive patients or those on
immunosuppressive drugs) in whom the results of
infection can be correspondingly serious, is therefore
uncontroversial. A further discussion of the use of antibiotics in surgery is given in Chapter 8.
Mouthwashes
Patients are universally advised on the use of mouthwashes and they undoubtedly play an important role in
maintaining wound cleanliness if used frequently.
Prevention of infection
198
Antibiotics
Chlorhexidine
Prescription of antibiotics as a prophylactic measure in
this context remains a contentious issue. The evidence
for their use is far from convincing and it is true to say
that most surgeons rely on their clinical experience when
making the decision of whether or not to use them. Many
operators justify their use based on the presence of
infection in the surgical field (see Ch. 8) or the removal
of substantial amounts of bone during the procedure. The
blood supply in the maxilla is more profuse than in the
This is an antiseptic mouthwash which is effective in
controlling plaque but may also have positive benefits for
wounds. With inability to use toothbrushes in the areas of
the surgery, both plaque control and local antiseptic action
are needed and this mouthwash is commonly prescribed
as a routine post-operatively. Use of chlorhexidine is
probably best restricted to 2 or 3 times per day with the
intervening periods covered with simple saline rinses.
Pre- or perioperative use of a chlorhexidine mouthwash
has been shown to reduce the risk of post-operative
infection and reduce the incidence of 'dry sockets'.
Saline mouthwashes
These should be made up with approximately one
teaspoonful of salt to one tumbler of warm to hot water.
They are the mainstay of wound cleanliness and should
be encouraged. Their use should initially be gentle rather
than vigorous but, as the days progress, a more vigorous
use should be encouraged. In addition to increasing the
use of mouthwashes after the first 24 h, patients should
also be encouraged to keep their mouths moving so that
stagnation of saliva does not result, as this can encourage
infection. Mouthwashes upwards of six times per day
should be discontinued only if bleeding from the wound
Postoperative bleeding
Bleeding from intraoral wounds is seldom due to a defect
in the haemostatic mechanism or in the clotting process
(see Ch. 6) but is more commonly due to leakage from
small vessels in bone or periosteum. It is more frequently
seen within a few hours of surgery and may in some
cases be reactive bleeding resultant upon the dilatation
of vessels previously constricted by local anaesthetic
containing adrenaline (epinephrine). Another contributory
factor may be inappropriate exploration of the wound by
fingers or tongue and by mouth rinsing too soon after the
surgery.
Control of such bleeding is usually affected by use
of local haemostatic agents such as regenerated oxidised
cellulose, further suturing of the wound and direct masticatory pressure via a suitably placed swab.
Secondary haemorrhage caused by wound infection is
characteristically seen around 10 days postoperatively
but is very uncommon in dentoalveolar wounds.
Follow-up
Following surgery, most patients will be seen between
5 and 7 days later to ensure that healing is progressing
satisfactorily. Sutures are removed when necessary and
debris may need to be irrigated from the wound area if the
patient's oral hygiene measures have been inadequate.
For some patients, results of histological examination of
tissue can be explained and, if necessary, further appointments arranged. For many patients, however, there is no
further 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 used
in the surgery, some operators see only those patients
who have continuing problems. Where this format of
management is used, a full postoperative leaflet is issued,
which indicates the particular problems that could occur
and might need further consultation. The required
contact telephone numbers are a necessary inclusion in
such a leaflet.
199
24
Local anaesthesia
Introduction
200
Achieving good local anaesthesia is a prerequisite for
virtually all dental surgery, and in oral surgery the
confidence this gives is mandatory from both the
patient's and the operator's point of view. The ability to
administer a comfortable local anaesthetic to any patient
is a fundamental skill that dental surgeons should strive
to achieve. This will allow stress levels in both giver and
receiver to be greatly reduced, and technique must be
constantly reviewed and revised to this end.
Not only is the actual injection of local anaesthetic
important, the operator must give the drug adequate time
to block nerve transmission and must have confidence
in his or her ability to recognise the subjective changes
it will bring about before testing its adequacy. One of
the most common faults is testing the effect of local
anaesthetic before reasonable time has elapsed, when
lack of necessary depth of anaesthesia causes discomfort.
This immediately results in loss of confidence by the
patient, who becomes more apprehensive and may therefore be far more difficult to convince that adequate
anaesthesia, even after further administration, is finally
attained.
Patients must be told before the testing of an
anaesthetic that all sensation is not, and will not, be lost,
and that it is specifically pain that will be abolished. This
is particularly true in oral surgery practice, where the
procedure may often involve causing a very real feeling
of pressure that can be alarming to patients who have not
been fully briefed on what the local anaesthetic can and
cannot do. If patients are asked to report 'feeling anything' during the testing procedure they might truthfully
say that they feel something, and this could lead to
further, and possibly unnecessary, administration of local
anaesthetic. Finally, awareness that good local anaesthesia
is one of the most important criteria by which patients
judge their operator makes this subject worth studying
and knowing well.
Uses of local anaesthesia
The uses of local anaesthesia are listed in Table 24.1 and
these are discussed in turn.
Diagnostic use
Administration of local anaesthetic can be a useful way
of finding the source of a patient's pain. An example of
this is the pain of a pulpitis, which can be very difficult
for both the patient and the dentist to isolate because of
its tendency to be referred to other parts of the mouth or
face. Particularly useful is the infiltration technique,
which achieves a localised action and can discriminate
between maxillary and mandibular sources, and even
between individual upper teeth provided they are not
immediately adjacent. Another example is the patient
with myofascial pain who is convinced that an upper
tooth is causing the problem. Local anaesthesia may help
this patient and the surgeon in this situation to eliminate
the tooth as the cause of pain and may thus avoid its
unnecessary treatment.
Table 24.1
Uses of local anaesthesia
Diagnostic: to isolate a source of pain
Therapeutic: to reduce or abolish the pain of a
pathological condition
Perioperative: to achieve comfort during operative
procedures
Postoperative: to reduce postoperative pain
Therapeutic use
Local anaesthetics can, in themselves, constitute part of a
treatment regimen for painful surgical conditions. The
ability of the dentist to abolish pain for a patient, albeit
temporarily, is a therapeutic measure in its own right.
The use of a block technique to eliminate the pain of dry
socket (localised osteitis) (see Ch. 26) can be immensely
helpful to the management of this very painful condition,
particularly in the first few days. Inferior dental blocks of
long-acting local anaesthetics such as bupivacaine can
give total comfort for several hours, allowing patients to
catch up on lost sleep and perhaps reduce the use of
systemic analgesics to avoid overuse. Moreover, the
patient can return for further local anaesthesia if the pain
once more becomes too demanding. Although it would
be impossible to keep administering local anaesthetic
blocks, there is enough, albeit anecdotal, evidence to
suggest that when the pain returns after the block wears
off, it is not at the same level of intensity.
Blocks of the inferior dental, mental or infraorbital
nerves can also be used for the treatment of trigeminal
neuralgia when pain breakthrough, despite medication
such as carbamazepine, has become unacceptable. Longacting local anaesthetic in this context seems, in some
patients, not only to give comfort during the duration of
the anaesthetic but also to break the pattern of breakthrough in the longer term.
Additionally, however, local anaesthetics are often
given to patients undergoing oral or maxillofacial surgery
under 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 when
significant afferent stimulation is taking place. This
can be seen, for example, when a tooth is being
elevated.
• It also provides local haemostasis to the operative site
and provides immediate postoperative analgesia.
Postoperative use
After surgery with either local or general anaesthesia, the
continuing effect of the anaesthetic is a most beneficial
way of reducing patient discomfort. It helps to reduce
or even eliminate the need for stronger (often narcotic)
systemic analgesics, which have their own drawbacks.
Many operators now use longer-acting agents, such as
bupivacaine, to prolong the immediate postoperative
analgesia. There is some evidence to suggest that this
measure, allied to early prescription of systemic
analgesics, can more effectively control pain and that this
early benefit may well be sustained throughout the days
following surgery.
Local anaesthetic agents
Perioperative use
The provision of pain-free operative surgery is by far
the most common use of local anaesthetics, and provides
an effective and safe method for almost all outpatient
dentoalveolar oral surgical procedures. It can, in conjunction with sedation techniques, allow more difficult
or protracted procedures to be carried out without the
additional risks of general anaesthesia, and this may be
particularly of value in patients with significant cardiovascular or airway disease (see Ch. 11).
Table 24.2
Table 24.2 shows the commonly used local anaesthetic
agents. In oral surgery there is a distinct advantage in
using a local anaesthetic with adrenaline (epinephrine),
which, by its vasoconstrictive action, improves the
visibility of the surgical site by reducing small-vessel
bleeding.
Action
Both lidocaine (lignocaine) and prilocaine hydrochloride
are good local anaesthetic agents and account for the vast
Commonly used local anaesthetic agents
Anaesthetic drug
Vasoconstrictor
Duration (ID block)
Lidocaine (lignocaine) hydrochloride 2%
Prilocaine hydrochloride 3%
Bupivacaine hydrochloride 0.5%
Adrenaline (epinephrine) 1 :80 000
Felypressin 0.03 international units
Adrenaline (epinephrine) 1 :200 000
2.5-3 h
2.5–3 h
6–8 h
201
202
majority of local anaesthetic administrations in oral
surgery. They are both tertiary amines that form hydrochloride salts for use in solution. When injected into the
tissues, these agents dissociate into cationic quaternary
amides with a positive chemical charge, although some
remains in the uncharged base form. It is this uncharged
lidocaine (lignocaine) or prilocaine that passes through
the nerve membrane to once again dissociate into the
cationic form. These intracellular cations of the anaesthetic agents are believed to be primarily responsible for
blocking the sodium channels in the membrane, which in
turn blocks the rapid sodium inrush to the cell during
nerve impulse propagation. Distortion of the axon
membrane by uncharged local anaesthetic also appears to
have a role in blocking this transmission.
pain breakthrough, and that for oral surgical purposes the
relatively bloodless field they produce is a significant
advantage.
In general terms, the maximum safe dose can be
expressed as 4.5-5.0 mg per kg body weight of lidocaine
(lignocaine) with 1:80000 adrenaline (epinephrine) and
3 mg per kg body weight of prilocaine. When translated
into millilitres of 2% lidocaine (lignocaine) with adrenaline (epinephrine) or 3% prilocaine with felypressin in a
fit 70-kg adult patient this means that a maximum of six
cartridges of lidocaine (lignocaine) (or four of prilocaine),
each of 2.2 mL, is well within the safe limit. The preoccupation with volume is misleading as it tends to cause
unthinking administration, and not consideration of each
patient's individual situation allied to safe technique.
Maximum safe dose
Local anaesthetic
technique
Local anaesthetics such as lidocaine (lignocaine) and
prilocaine are extremely safe given their extensive use in
both medicine and dentistry. The addition of adrenaline
(epinephrine) to lidocaine (lignocaine)and of felypressin
to prilocaine reduces the rate of uptake from the site of
injection, thus reducing the possible toxic effects of
the local anaesthetic agent and increasing, in theory, the
volume that can therefore be used. Apart from the actual
amounts used, three other considerations should be taken
into account: (1) the avoidance of intravascular injection
by use of an aspirating syringe; (2) the rate of administration of the local anaesthetic - a slow rate reduces the
chance of overload and hence possible toxic effects; and
(3) the status of the patient. Extremes of age, physical
size and medical background should be determined for
each individual patient, all of which may modify what
could be considered a safe quantity.
Most authorities do now acknowledge that the toxic
effects of the local anaesthetic agents - which mainly arise
from central nervous system depression, and in particular
respiratory depression - must be balanced against the
possible undesirable effects of adrenaline (epinephrine)
where that is included in the solution. The action of
adrenaline (epinephrine) on the heart (causing increase in
myocardial excitability, rate, force of contraction, and
stroke volume) is potentially undesirable, particularly in
patients with known heart disease. It is in this group of
patients that many operators prefer to use adrenaline
(epinephrine)-free local anaesthetics. Others argue that
lidocaine (lignocaine) and adrenaline (epinephrine)
provide a more profound anaesthesia with less chance of
There are a variety of techniques used in local
anaesthetic administration and these will be discussed in
turn (Table 24.3).
Infiltration
This can be used to achieve anaesthesia of upper teeth
and lower anteriors. It is achieved by depositing the
solution around the apex of a tooth on its buccal aspect in
the sulcus. The porosity of the bone allows it to diffuse
through the outer plate of bone to affect the apical nerve
or nerves. It normally achieves anaesthesia within 1-2 min
and has the added surgical advantage (where adrenaline
(epinephrine) is in the solution) of small-vessel vasoconstriction, which provides reduction in bleeding and
Table 24.3
Local anaesthetic techniques
Infiltration
Block anaesthesia
inferior dental block
mental nerve block
posterior superior alveolar block
infraorbital block
greater palatine block
nasopalatine block
Other injection techniques
periodontal ligament block
intraosseous injection
intrapulpal injection
increased visibility as a consequence. Administration
should be considered as a two-part technique:
1. needle insertion
2. deposition of local anaesthetic.
Needle insertion
To achieve minimal discomfort, topical local anaesthetic
should be applied 2-3 min before the injection. The
index finger or thumb of the 'free' hand should pull the
lip or cheek such that the sulcus tissues are taut, as this
will minimise discomfort on introduction of the needle.
The tip of the needle needs to be advanced only 3-4 mm
into the tissue adjacent to the tooth to be anaesthetised
(Fig. 24.1).
Deposition of local anaesthetic solution
The solution should be deposited slowly because the
lumen of a dental needle is very fine and undue force of
the solution being injected can lead to unwanted pain and
tissue damage. This therefore takes time and patience but
is essential in reducing discomfort.
For palatal anaesthesia, the greater palatine (or nasopalatine) nerve anteriorly supplies the mucoperiosteum.
Only a small quantity of local solution should be
introduced and use of topical anaesthesia and strong
finger-pressure adjacent to the point of entry of the
needle can help to reduce this notoriously unpleasant
injection. The injection is normally given adjacent to the
surgical site but many consider that the area midway
between the midline of the palate and the gingival margin
of the tooth is less tightly bound down to the underlying
bone, and is therefore less uncomfortable.
Another technique is to achieve buccal anaesthesia in
the usual way, then pass the needle from buccal to palatal
through both the interdental papillae (anterior and
posterior) of the tooth under treatment. This does appear
to reduce discomfort even if an additional palatal injection
is necessary to be quite sure of adequate anaesthesia.
Block anaesthesia
Several block injections of nerve trunks can be used for
oral surgical purposes. By far the most common is the
inferior dental block, but others include the mental block,
the posterior superior dental block and the infraorbital
block. The hard palate can be anaesthetised by greater
palatine and nasopalatine blocks if more extensive areas
of palate require to be anaesthetised.
Inferior dental block
Several techniques have been suggested but only two will
be described here, the first being a standard block and the
second a closed-mouth technique that can be very useful
if restricted opening is a problem.
The nerves affected are: (1) the inferior dental nerve,
which provides sensation to the pulps and periodontal
membranes of first incisor to third molar, the bone
investing the teeth, the buccal gingivae and the sulcus
from premolars to incisors, lower lip and chin; and (2)
the lingual nerve, which supplies the anterior two-thirds
of the tongue, the floor of mouth and the lingual gingiva.
Technique
Fig. 24.1 Position of the needle for the infiltration of local
anaesthetic to achieve anaesthesia of an upper lateral
incisor.
The precise technique will vary but the following will
serve as a guideline for administering an inferior dental
block injection.
The patient should be seated with good head and neck
support and with the neck slightly extended such that the
lower occlusal plane will be approximately horizontal on
fully opening the mouth. With the mouth widely opened,
203
the finger or thumb of the 'free' hand should pass along
the lower buccal sulcus until it rests posteriorly in the
retromolar triangle, which lies between the (external)
oblique line of the mandible and the continuation of the
mylohyoid ridge or internal oblique line.
The pterygomandibular raphe should then be identified
as an almost vertically running soft tissue line. This takes
its origin from the pterygoid hamulus and runs downwards to its insertion on the lingual aspect of the mandible
in the third molar region. The raphe gives rise to muscle
attachments running laterally (buccinator) and medially
(superior constrictor).
The syringe should be introduced from the lower
premolar teeth of the other side parallel to the lower
occlusal plane such that the needle penetrates the tissues
lateral to the pterygomandibular raphe and at a level
halfway up the finger or thumb lying in the retromolar
triangle (Fig. 24.2).
The 'long' dental needle (3.4 cm) should be advanced
about 2.5 cm until bone is touched lightly. The needle
should then be withdrawn a millimetre or two and
aspiration performed. If blood in the form of a smoky red
trail is noted in the cartridge, the needle should be
withdrawn 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 local
anaesthetic being deposited on slow withdrawal to
'catch' the lingual nerve, which lies anteromedial to the
inferior dental nerve.
This technique introduces a local anaesthetic solution
to the inferior dental nerve as it enters the mandibular
foramen on the medial aspect of the ramus. In patients
who, for a variety of reasons, have trismus and cannot
open sufficiently to allow this technique, a closed
technique can sometimes be useful.
The patient should be seated such that the occlusal
plane is approximately horizontal. The cheek should be
retracted with the index finger or thumb of the 'free' hand
and the needle advanced horizontally at about the level of
the gingival margins of the upper molar teeth. The needle
should penetrate to a depth of 1–1.5 cm before aspiration.
Slow deposition of most of the 2.2 mL cartridge is
normally required.
This technique leaves the local anaesthetic solution at
a level higher than the standard technique, which means
that it is deposited above the mandibular foramen but still
below the level of the mandibular notch.
Determination of adequate anaesthesia
As mentioned in the introductory paragraph, it is
important not to embark on surgery until full anaesthesia
is achieved. This is normally done by asking the patient
what subjective changes he or she feels in the lower lip
and chin of the affected side. A feeling of pins and needles
or a tingling sensation denotes early-stage changes, which
would normally progress to a numb, swollen, thick or
rubbery sensation. At this point the area can be tested
objectively with a sharp probe passed between the tooth
to be extracted, or operated upon, and the attached
gingiva. Patients must be told that the sensations of
touch, and especially pressure, will not be totally
abolished, although pain should not be felt. Patients
should always be advised that, once the surgery begins,
they must immediately indicate if there is any pain
breakthrough because more local anaesthetic can be
given.
Buccal injection
204
Fig. 24.2
block.
Position of the needle for an inferior dental
The sulcus region in the lower premolar and molar
regions may have innervation from the buccal nerve and
this must be covered by a separate injection.
The buccal injection can be given more comfortably
by waiting for the inferior dental block to become
effective. Rather than a single block given in the cheek at
the level of the crown of the third molar at the anterior
border of the ramus, many operators simply infiltrate
around the surgical site, for example, in the sulcus of the
third molar region where an impacted third molar is
being treated since this will have the added benefit of
haemostasis of the flap.
Complications of inferior dental block
Systemic complications such as allergy, fainting or
inadvertent intravascular injection with cardiac or central
nervous system effects are rare, with the exception of
fainting, which can usually be averted by placing the
patient in the supine position. Specific to this injection,
however, are certain local complications and these are
listed in Table 24.4.
Facial nerve paralysis (palsy) occurs when the
injection is given too far distally and the parotid gland is
penetrated, allowing diffusion of the local anaesthetic
through the loose glandular tissue, which then affects all
five terminal branches of the facial nerve. The effect is
seen in the lack of the corrugation of the forehead,
inability to close the eye or blink, and inability to raise
the corner of the mouth or puff the cheeks. Patients may
feel that something is wrong but be unable to identify
exactly what the problem is, and it is usually the operator
who notices these specific changes. Patients should be
informed, reassured as to the transitory nature of the
palsy, and the eye should be protected with a loose pad
such that the cornea is protected until the protective blink
reflex returns. Recovery often occurs in a relatively short
time (within an hour), unlike the inferior dental nerve
itself, which can take up to 3 h.
Postinjection trismus may also arise. The diagnosis of
this distressing complication is normally fairly easy in
that the trismus occurs within hours of the injection. It is
believed to be due to damage to the medial pterygoid
muscle, resulting in its spasm and consequent inability of
the muscle to relax and allow opening. It is not painful
but many patients are extremely anxious and do need
reassurance. In terms of technique, it may be attributed to
an injection at too low a level and perhaps using too
Table 24.4
Complications of inferior dental block
Facial nerve paralysis
Postinjection trismus
Prolonged anaesthesia
Visual impairment
much force to deliver the anaesthetic solution. If undue
resistance to any injection is felt (as when in a muscle
bed) excessive force should be avoided and the needle
withdrawn. The free-running of the cartridge plunger
should be checked and the needle reinserted at a higher
level. Trismus can also occur after the extraction of teeth,
unrelated to the anaesthetic technique. This is especially
so with mandibular third molar teeth (see Ch. 27).
If the problem does occur, some prescribe a benzodiazepine to try to alleviate muscle spasm. The mainstay
of management, however, is reassurance and encouragement to the patient to try to gain further opening. Use of
wooden spatulae may be a convenient method for the
patient to measure progress. The trismus may last for
weeks and even months, and resolution may occur slowly
or quite dramatically over a day or two after even a
prolonged period of limitation.
Prolonged anaesthesia is a rare and poorly documented
complication. It can affect the inferior dental nerve or
lingual nerve, and very occasionally both. It may
represent physical trauma to the nerve by the needle or an
idiosyncratic reaction to the local anaesthetic. Prognosis
is difficult to judge as there is little evidence of outcome
and resolution appears unpredictable.
Visual impairment is a reported complication but is
very rare. Its cause is unknown although vasospasm has
been suggested as a possible factor. Any impairment of
vision warrants immediate referral to an ophthalmic
specialist.
Mental nerve block
This injection will anaesthetise the pulps and periodontal
membranes of the lower incisors, canine, first premolar
and variably the second premolar. For surgical procedures,
it must be remembered that the lingual mucoperiosteum
will require separate infiltration as the mental block
anaesthetises the teeth through the incisive branch of the
inferior dental nerve and the peripheral distribution of the
mental nerve.
Technique
In dentate patients, the mental foramen lies below and
between the apices of the lower premolar teeth, approximately half way between the cervical margins of the
teeth and the lower border of the mandible. The injection
is similar in all respects to an infiltration injection, and
the objective is to deposit the solution at or near the
205
needle should be angled inwards towards the buccal plate
as much as possible, given that the opening of the mouth
will restrict this. The other angle to remember is the
alignment of the needle at approximately 45° to the
occlusal plane after entering the sulcus in the second
molar region.
Infraorbital block
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 totally
unnecessary and often causes haematoma formation
through damage to the mental blood vessels.
In edentulous patients, the foramen may lie nearer the
crest of the ridge as a result of alveolar resorption and
due allowance for this should therefore be made before
the injection is given.
This injection, although given infrequently, can be a very
valuable technique for achieving anaesthesia in the
anterior part of the maxilla. The local anaesthetic solution
is deposited around the infraorbital foramen, where it can
diffuse back along the infraorbital canal to affect the
anterior and, where present as a separate nerve, the middle
superior dental nerve. Ideally, therefore, in addition to
anaesthesia of the soft tissues of the upper lip, side of
nose, cheek and lower eyelid, the upper incisors, canine
and premolars will be affected together with the adjacent
sulcus and gingivae.
For oral surgery purposes this injection can be given
to avoid injecting into inflamed tissues in the incisor or
canine region, but can also achieve a more dependable
and profound anaesthesia for larger lesions such as cysts.
Use of a long-acting agent such as bupivacaine to achieve
control of trigeminal neuralgic pain breakthrough also
makes knowledge of this technique valuable.
Technique
Posterior superior alveolar (dental) block
This block is intended to anaesthetise the posterior
superior dental nerve as it penetrates the posterolateral
aspect of the maxillary tuberosity before it pierces bone.
As such, a close relationship exists between the site of
the injection and pterygoid venous plexus lying laterally
and above and which can easily therefore be entered by
the needle. This can cause an immediate and alarming
haematoma visible both in the sulcus and externally in
the face just below the zygomatic arch.
Technique
206
The technique, which is in effect high infiltration, is
seldom, if ever, really necessary as diffusion of
anaesthetic from the conventional infiltration is almost
always effective. If it is considered necessary, then the
Although several techniques can be used, the most
commonly employed, which uses the upper first and
second premolar as the key landmark, is described.
The buccal sulcus is tensed with the finger or thumb
of the 'free' hand in the premolar region. Some operators
suggest that a finger be placed over the infraorbital
foramen on the face to 'feel' the local anaesthetic as it is
administered 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 the
long axis of the premolars; it penetrates the lateral aspect
of the sulcus about 1–1.5 cm from the buccal bone surface
and it is advanced upwards approximately 1.5 cm into the
tissues (Fig. 24.4). After aspiration, the local anaesthetic
is slowly introduced to the tissues when 1.5–2.0 mL of
the preferred solution is normally sufficient.
Alternative techniques include direct injection through
the skin to the foramen. The lower orbital margin rim
prophylactically covered with appropriate antibiotic in an
endocarditis at-risk patient.
Intraosseous injection
This technique will achieve excellent anaesthesia limited,
however, to the immediate locality of the injection. The
local is administered through a trephined hole best
prepared with a specially designed bur through the outer
cortical plate of bone. Initial infiltration anaesthesia of
the area is hence a prerequisite and, after the entry is cut,
a short needle is introduced into the medullary space
before injecting a small quantity of solution. The diameter
of the trephined hole should ideally be matched to the
needle to prevent leakage. Again, the advantages of the
technique are the small quantity of local anaesthetic used
and the ability to achieve a good depth of anaesthesia
where access may be limited through trismus.
Fig. 24.4
Position of the needle for an infra-orbital block.
Intrapulpal injection
should be palpated carefully before injecting about 1 cm
below this landmark, and at the midpoint of the infraorbital bony margin. Administration of local anaesthetic
in this way can be alarming to a patient, and careful
explanation of what is being done is necessary. The eye
should be protected by the fingers of the 'free' hand, with
one finger carefully palpating the lower orbital bony
margin.
Other injection techniques
This injection is normally used where, despite apparently
good anaesthesia by other conventional means, the tooth
remains painful on manipulation. This again is a feature
of some pulpal or apical infections. In oral surgery, the
tooth is normally being extracted and either the pulp
canal(s) are already accessible or can be accessed using
a small round bur. The technique is imprecise and escape
of the solution is almost invariable. It can, however, be
remarkably successful if sufficient local can be introduced. Discomfort during its administration is often a
reliable indication that it will prove of benefit.
Periodontal ligament injection
This technique introduces local anaesthetic directly into
the periodontal space and, as the force required is quite
substantial, specialised syringes are available to achieve
this. In oral surgery, the intraligamentous injection is
most frequently used if pain is being felt despite the
normal techniques of infiltration or block anaesthesia.
This can occur when a tooth is 'hot' through acute
pulpitis or apical infection. It may also be of value if
limitation of jaw mobility makes block injection difficult
or impossible. One of its advantages is the small volume
of local solution needed, but it is often uncomfortable to
administer and will cause a bacteraemia which should be
Difficulty in obtaining anaesthesia
The above techniques can all be helpful in achieving
sufficient anaesthesia where prior, more conventional,
methods have been unsuccessful. One other measure is
the use of a stronger local anaesthetic solution, such as
4% prilocaine. The higher concentration appears in some
cases to obtain a more profound depth of anaesthesia. If
an inferior dental block fails to allow surgical comfort
despite all the subjective features of adequacy, it may be
useful to consider giving a second block with the
stronger anaesthetic solution rather than simply repeating
the procedure with the same agent.
207
25
Extraction techniques
Introduction
208
and producing more space for forcep application. They
can be very helpful but care must be taken due to the
potential soft tissue damage. They should be used to
'unscrew' the tooth, not to elevate it.
Teeth are extracted for a number of reasons, including
caries, trauma, periodontal disease, impactions and
orthodontics. Tooth extraction techniques improve with
clinical experience. Two aspects of tooth extraction are
important in successful completion of the operation:
equipment and technique.
Technique
Equipment
Every clinician will develop specific techniques for tooth
extraction, but all follow the same basic pattern (listed in
Table 25.2), and these will be discussed in turn.
Most teeth are extracted with dental forceps of which a
variety of types are available.
Lower forceps have their blades at 90° to the handles
and upper forceps have the blades either angled slightly
forwards or straight in relation to their handles (Fig. 25.1).
Forcep design has developed over many years and is
based around the principle of creating a displacing force
on the roots of the tooth, not the crown. When teeth
fracture during extraction it is most commonly the result
of poor forceps placement. Forceps are therefore designed
around the root morphology of the tooth they are intended
to remove (Fig. 25.2). The appropriate forceps choice is
outlined in Table 25.1.
Root forceps that have smaller beaks for smaller teeth
or fractured roots are available. There are other specific
forceps with more limited application, such as upper third
molar forceps, which have an elongated 'gooseneck' for
access to the posterior maxilla.
Elevators may be used as an alternative method of
mobilising or extracting teeth, and these are discussed in
Chapter 23. There has been a recent increase in the use of
instruments known as luxators to assist with extractions.
Luxators are designed to help the operator gain space for
application of the forceps. They are very sharp-bladed
elevators that are used to increase the gap between the
tooth and the surrounding bone, thus loosening the tooth
Application
Having chosen the forceps that best fit the root
morphology of the tooth to be removed, surgeons must
first position themselves and the patient to achieve good
access and vision, as well as allowing the surgeon to
Table 25.1 Types of forcep
Forcep
Tooth
Upper universals
Upper straights
Upper molars (R/L)
Lower universals
Upper incisors and premolars
Upper canines
Upper molars (R/L)
Lower incisors, canines and
premolars
Lower molars
Lower first and second molars
Lower molars
Cow-horns
Table 25.2
Extraction technique
Application of forceps
Consolidation of grip
Displacement of tooth
Postdelivery care
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.
209
Quadrant
Patient
Operator
time as forcing the handles together. This avoids the
beaks of the forceps sliding around the root of the tooth
on rotation rather than the efficient transfer of forces
from operator to tooth.
Upper right and upper left
Lower left
Lower right
Supine
Upright
Upright
In front
In front
Behind
Displacement
Table 25.3
extraction
Operator–patient position for
put appropriate force on the tooth. For a right-handed
operator this is outlined in Table 25.3. It is usual practice
to remove lower teeth before upper teeth, and posterior
teeth before anterior teeth, to avoid blood obscuring the
operator's view if a number of teeth are to be extracted.
The patient's head should be at the level of the
surgeon's elbow. The next stage is to position the
surgeon's non-dominant hand. This is important because
it improves access by retracting soft tissues and allows
the surgeon to place a counterforce on the jaw to assist
tooth extraction. For example, when buccally expanding
an upper molar it is necessary to have an opposing force
provided by the operator's passive hand. It is conventional
to place a finger and a thumb on either side of the tooth
to be extracted.
Application of the forceps is the most important stage
and the basic principle of tooth removal must always be
borne in mind: application of the beaks of the forceps to
the root rather than the crown of the tooth. It should
usually be as easy to remove a tooth fractured at gingival
level as a fully intact tooth because the forcep blades are
placed on the root face not on the enamel of the tooth.
This application involves the placing of the blades
under the gingivae, taking care to minimise soft tissue
damage. The forceps should then be pushed apically,
completing this stage of the procedure. This may require
considerable force.
There are exceptions to these general rules, for
example, cow-horn forceps fit into the bifurcation of lower
molars and, because of their unique design, produce an
upwards force. Their application is therefore different.
Consolidation
210
To remove the tooth efficiently, the forceps must be
pushed together firmly to engage on to the root surface,
with the handles of the forceps being gripped with the
palm of the hand with an apical force applied at the same
Displacement depends on root morphology. Teeth can be
removed in two ways: by rotational movement or buccal
movement (expansion).
Upper incisors and lower premolars can be rotated.
All other teeth are best removed by controlled buccal
expansion. Upper first premolars are an exception as they
often present with two thin roots. The best extraction
technique is a combination of gently wiggling the teeth
and slight expansion, both bucally and palatally.
Rotational movement involves increasing destruction
of the periodontal ligament by a circular movement both
clockwise and anticlockwise. Buccal expansion involves
the enlargement of the bony socket allowing tooth
delivery. This is usually a staged process where the tooth
is forced bucally and, with sustained pressure on the
buccal alveolar bone, the tooth is extracted.
There are variations of the above basic movements:
lower molars can often be removed efficiently by a
combination of rotation and buccal expansion (a figureof-eight movement is often suggested); also lower third
molars can be expanded lingually where the lingual plate
is 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 of
procedures: sockets that have been expanded should be
squeezed to replace the bone to its original position;
sharp pieces of bone can be removed and the patient
should be instructed to bite on to a damp piece of gauze
to aid haemostasis. Once haemostasis has been achieved,
postoperative instructions should be given (Ch. 23). Postoperative instructions should include leaving the socket
undisturbed for 4-6 h and then gentle rinsing with hot
saline mouthwashes after each meal. Patients should also
be advised of control measures if bleeding occurs postoperatively and how to contact the appropriate emergency
service in case of complications.
Risk assessment in tooth
extraction
Examination
Teeth should be assessed preoperatively to anticipate
potential difficulties with extractions. Preoperative assessment can be carried out using the history, examination
and special investigations.
Clinical examination will reveal gross caries, which can
make forceps placement very difficult. Imbrication or
crowding can make forceps placement and delivery of
the tooth difficult. Wear facets, indicating increased
occlusal load, increase supporting bone strength making
extractions more difficult.
History
Radiography
A history of difficult extractions or postoperative
complications can give an early indication of potential
problems. The age of the patient is also important: the
bone of older patients is less flexible than that of younger
patients, making standard techniques such as buccal
expansion more difficult.
Radiographs are helpful in showing the number, shape
and relationship of the roots of the tooth. They also reveal
whether the roots of a lower molar tooth are convergent
or divergent. Radiographs can also indicate areas of hypercementosis and bony pathology that may complicate the
extraction.
211
26
Complications of extractions
Introduction
Complications can arise during the procedure of extraction or may manifest themselves some time following the
extraction. These will be discussed in turn. Problems of
local anaesthesia are discussed in Chapter 24.
Immediate extraction
complications
These occur at the time of the extraction and are listed in
Table 26.1.
Fracture of the crown of a tooth
This may be unavoidable if the tooth is weakened either
by caries or a large restoration. However, the forceps may
have been applied improperly to the crown instead of to
the root mass, or the long axis of the beaks of the forceps
may not have been along that of the tooth. Sometimes,
crown fracture arises from the use of forceps whose beaks
are too broad (see Ch. 25) or as a result of the operator
trying to 'hurry' the operation. The management of this
complication is to remove all debris from the oral cavity
and review the clinical situation. Surgical extraction of the
remaining fragment may then be necessary (see Ch. 23).
Fracture of the root of a tooth
212
Ideally, it should be possible to ensure that the whole
tooth is removed every time an extraction is carried out.
However, when a root breaks a decision about management of the retained piece of root has to be made.
Further management depends on the size of the root
fragment, whether it is mobile, whether it is infected, how
Table 26.1
Immediate extraction complications
Fracture of tooth:
crown
root
Fracture of alveolar plate
Fracture of mandible
Soft tissue damage
Involvement of maxillary antrum:
oroantral fistula
fractured tuberosity
loss of root (or tooth) into antrum
Loss of tooth or root:
into pharynx
into soft tissues
Damage to nerves or vessels
Dislocation of temporomandibular joint
Damage to adjacent teeth
Extraction of permanent tooth germ with deciduous
tooth
Extraction of wrong tooth
close it is to major anatomical structures such as the maxillary antrum or inferior dental canal, patient cooperation
and the ability of the surgeon to successfully complete
the procedure taking into account the constraints of time,
equipment and surgical expertise.
If the decision is made to leave the root then this must
be written in the case notes and the patient fully informed.
If the procedure is deferred, the root fragment should
have the pulp removed and a dressing placed.
If a deciduous tooth is being removed, it must be kept
in mind that the roots are usually being resorbed with the
roots being pushed towards the surface by the permanent
tooth. It is often prudent therefore to leave these fragments, as injudicious use of elevators can cause damage
to the underlying permanent tooth.
Fracture of the alveolar plate
Involvement of maxillary antrum
This is a common complication and is often seen when
extracting canine teeth or molars. If the alveolar plate has
little periosteal attachment and is hence liable to lose its
blood supply then it should be carefully removed by
stripping off any remaining periosteum with a periosteal
elevator. If, however, it is still adequately attached to the
periosteum, a mattress or simple suture over the socket
margin will stabilise the plate and allow its incorporation
into the healing process.
Oroantral fistula (OAF)
Fracture of the mandible
This is an uncommon complication of dental extraction,
which is usually heralded by a loud crack. The most
important thing is to stop the extraction and reassess
the situation. The patient should be informed of the
possibility that his or her mandible might be broken and
a radiograph should be taken. If a jaw fracture is confirmed then the patient should be referred to a maxillofacial centre as an emergency. It would be advisable to
administer another inferior dental block injection. If this
involves a significant delay, then further analgesia should
be provided and appropriate antiseptic mouthwashes and
antibiotics prescribed.
Soft tissue trauma
Soft tissues must not be crushed. For example, the lower
lip is at risk from the handles of the forceps when
removing maxillary teeth. It should be ensured that
recently sterilised instruments are not too hot and the
patient's eyes should be protected from instruments and
fingers using safety spectacles. Soft tissue damage is
more likely to be encountered when the patient is under
a general anaesthetic and cannot communicate. Care
should be exercised to avoid application of the beaks of
forceps over the gingival soft tissues, especially lingually
in the lower molar region where the lingual nerve may be
damaged. Protective finger positioning is required when
using elevators that may slip and damage the tongue,
floor of mouth or the soft tissues of the palate. The soft
tissues at the angle of the mouth may also be damaged by
excessive lateral movement of forceps particularly when
extracting an upper tooth when an ipsilateral inferior
dental block has been administered or where the patient
is having general anaesthesia.
The roots of the maxillary molar teeth (and occasionally
the premolar teeth) lie in close proximity to, or even
within, the maxillary antrum. When the tooth is
extracted, a communication between the oral cavity and
the antrum may be created. The operator may be aware
of this possibility from the study of a pre-extraction
radiograph (Fig. 26.1) or may suspect the creation of an
OAF by inspection of the extracted tooth or the socket.
An upper molar may have a saucer-shaped piece of bone
attached to the trifurcation of the roots, indicating that
the floor of the antrum has been detached. The socket
itself may show abnormal architecture such as loss of the
interradicular bony septae. To confirm the presence of an
OAF the patient can be asked to pinch the nostrils
together and blow air gently into the nose. The operator
can then hold cotton wool in tweezers under the socket
and look for movement of the fibres. Sometimes, the
blood in the socket can be observed to bubble or the noise
of the air moving through the fistula can be detected.
Some operators favour inspection of the socket with
good lighting and efficient suction using a blunt probe to
explore the integrity of the socket. The noise of the
suction often becomes more resonate if a communication
exists between socket and sinus.
Once confirmed, an OAF can be treated in two ways:
if small, the socket can be sutured and a haemostatic
agent such as Surgicel® can be used to encourage clot
formation. Strict instructions should be given to avoid
nose blowing because this can increase the intrasinus
pressure and break-down the early clot that covers the
defect. The patient should be prescribed an antibiotic
Fig. 26.1 Radiograph of the upper molar region showing
the close association of the maxillary antrum to the upper
molar roots. On the right side a root apex has been
displaced into the maxillary antrum.
213
Fig. 26.2
A buccal advancement flap: (a) and (b) show a
buccal flap, which is inelastic due to the underlying
periosteum; (c) and (d) show the flap advanced to cover
the fistula after incising the periosteum.
because of the risk of infection, which would prevent the
sinus healing and lead to a chronic oroantral fistula. The
patient should be reviewed 1 week later to check progress and then 1 month later to ensure that the socket has
healed.
If the OAF is large then it should be closed immediately by means of a surgical flap. Most commonly
this is done by means of a buccal advancement flap. This
is a U-shaped flap with vertical relieving incisions taken
from the mesial and distal margins of the socket. The flap
is mucoperiosteal, which means that the periosteum lies
on its inner aspect. Periosteum is a thin sheet of osteogenic soft tissue that has no elasticity and must therefore
be incised to allow the whole flap to be advanced to the
palatal margin of the socket (Fig. 26.2). The incision is
made horizontally along the whole length of the base of
the flap; it need not be deep because the periosteum is
relatively thin. Some surgeons reduce the height of the
buccal plate of bone to reduce the length of the advance.
Horizontal mattress sutures encourage wound margin
eversion and aid primary healing. A prophylactic
antibiotic would normally be prescribed and the patient
asked to avoid nose-blowing.
the operator should stop the extraction and assess the
problem, as continuing to extract the tooth will lead to
tearing of the soft tissues and displacement of the fractured segment. Assessment can be carried out clinically
by palpating the area to gauge the size of the bone
fragment. This can be confirmed by taking radiographs
including periapicals, oblique occlusals or panoramic
films. It must be decided whether to retain the fractured
piece of bone or to remove it with the associated tooth, or
teeth. The principal consideration is size of the defect
that will be left when the segment is removed, as this can
complicate future denture provision. If the decision is
made to remove the tooth and the bone, then a mucoperiosteal flap should be raised and the segment
dissected out carefully. The soft tissues can then be
sutured and the wound closed completely. As there is a
breach of the maxillary antrum, antibiotics and analgesics
should be prescribed for the patient.
The more common management is to retain the tooth
and bone in position and allow the fracture to heal. First,
the segment must be reduced if it is displaced, and this
can normally be done with digital pressure or through
forceps on the tooth. The tooth that has been giving rise
to pain will have to have appropriate pulp extirpation
or obtundent dressing. The next stage is to take an
impression for construction of an appropriate splint to
hold the fractured segment in position and protect it from
trauma from the mandibular teeth. Alternatively, a segment of preformed arch bar can be wired to the buccal
aspects of the fragment, extending forwards as far as the
canine. Orthodontic wire can be used in much the same
way, either using brackets or more simply attached with
composite. The patient should be prescribed analgesics
and antibiotics. The splint should be kept in place for
approximately 4 weeks, after which time healing should
be assessed. If the fragment is firm and there is no sign
of infection, the tooth should be removed surgically by
raising a flap, removing buccal bone and dividing the
tooth into separate roots to avoid applying lateral
pressure to the relatively weak tuberosity segment.
Loss of the root (or tooth) into the antrum
Fractured tuberosity
214
The maxillary tuberosity is the posterior part of the
tooth-bearing segment of the maxilla. Occasionally,
during extraction of a maxillary molar tooth a segment of
bone becomes mobile. As with the fractured mandible,
Another complication involving the antrum is pushing
part or all of a tooth into the antral cavity. Normally the
operator should arrange for the removal of this root as the
patient is again at risk of the development of maxillary
sinusitis with or without an oroantral fistula. The patient
should have radiographs taken to confirm the presence of
the root in the antrum and the operator should then raise
a buccal flap from the mesial and distal margins of the
socket. Access to the antrum should then be increased by
bone removal with bone nibblers and drills. The root can
then be removed from the antrum by a variety of techniques including suction, the use of small caries excavators or direct removal by tweezers. If these methods
are unsuccessful then the antrum can be flushed-out with
sterile saline in an attempt to 'float' the root out, or the
antrum can be packed with ribbon gauze, which might
dislodge the root when it is removed. Once the root has
been removed from the antrum, the resulting defect
should be closed with a buccal advancement flap, as in
the closure of an oroantral fistula. In the rare circumstances where a whole tooth is dislodged into the maxillary antrum, its removal is often paradoxically easier.
Loss of tooth/root
Occasionally, during removal of a tooth, parts of the
tooth can be dislodged and disappear. If this happens, a
search should be instituted, using good suction. The
patient may be aware of swallowing the tooth, or part of
the tooth. If the tooth or root cannot be located then a
radiograph, first of the abdomen, should be arranged to
check whether the tooth or root has been swallowed,
which is most likely. It is important to ensure that the
object is not in the patient's airways.
Roots that are elevated incorrectly can occasionally
be pushed through a very thin bony plate overlying the
socket and disappear — bucally or lingually—into the soft
tissues. This is more problematic when a root (often an
additional third root) is pushed through the lingual plate
in the lower third molar region, because these can be very
difficult to recover.
Damage to nerves or vessels
This complication applies more commonly to the surgical removal of teeth rather than simple extractions but
one must always be aware of difficulties when operating
in the region of the inferior dental, lingual or mental
nerves.
Dislocation of the temporomandibular joint
Occasionally, a patient will open the mouth so widely
during an extraction that the mandible is dislocated; or
the operator might apply force to an unsupported mandible, causing it to dislocate. In this event, the operator
should try, as quickly as possible, to reduce the dislocation
by pushing the mandible downwards and backwards. If
this is not done relatively quickly, muscle spasm of the
powerful elevator muscles of the mandible will ensue and
the patient will require sedation, or indeed even a general
anaesthetic, to reduce the dislocation. When extracting
teeth under general anaesthesia the mandible can dislocate due to the loss of muscular tone. It is important to
ensure the mandible is repositioned before the patient
recovers from the anaesthesia. Recurrent dislocation of
the temporomandibular joint is discussed in Chapter 20.
Damage to adjacent teeth
When extracting teeth, fillings from adjacent teeth may
become dislodged and this should be dealt with appropriately. Inexperienced operators sometimes damage teeth
in the opposing jaw when the tooth being removed comes
out of its socket rather more quickly than expected. It is
important to recognise that damage has been caused and
to deal with it appropriately.
Extraction of a permanent tooth germ along
with the deciduous tooth
When extracting deciduous teeth there is occasionally a
significant amount of soft tissue attached to the apex of
the deciduous root. It is often difficult to ascertain
clinically whether this is a granuloma or abscess, or
whether it is the permanent tooth germ attached to the
root. If there is concern, the specimen should be sent for
histopathological investigation to confirm whether the
permanent tooth germ has been removed.
Extraction of the wrong tooth
Extraction should be considered to be an irreversible
procedure and therefore extreme vigilance should be
employed to ensure that the correct tooth is extracted.
The most vulnerable clinical situation is where one is
extracting teeth for orthodontic reasons and the teeth
have no obvious clinical problem. Extracting the wrong
tooth is medicolegally indefensible.
Postextraction complications
Postextraction complications can occur a variable length
of time after the extraction. They are listed in Table 26.2
and will be considered in turn.
215
Table 26.2
Postextraction complications
Haemorrhage
Dry socket
Osteomyelitis
Swelling, pain, echymosis
Sequestra
Trismus
Prolonged anaesthesia
Actinomycosis
Chronic oroantral fistula
Infective endocarditis
Postextraction haemorrhage
216
Haemorrhage is one of the complications that clinicians
worry about most and it can seriously complicate the
extraction of teeth. Prevention of haemorrhage is
desirable. To achieve this, the patient must be questioned
carefully as to any previous history of excessive haemorrhage particularly in relation to previous extractions (see
Ch. 6). If a history of postextraction haemorrhage is
elicited it is important to try and ascertain for how long
the bleeding continued and what measures were used to
stop the bleeding on previous occasions. It is also important to discover when the bleeding started in relationship to the time of the extraction. General questions
regarding a history of prolonged bleeding after trauma or
other operations, or a family history of excessive
bleeding or known haemorrhagic conditions may be
relevant. It is also important to question the patient about
the use of drugs, such as anticoagulant drugs. If there is
any doubt regarding the existence of a haemorrhagic
abnormality the patient should be investigated as
discussed in detail in Chapter 6.
A postextraction haemorrhage is first dealt with by
removing any clot from the mouth and establishing from
where the bleeding is originating. The patient can then be
asked to apply firm pressure by biting on a gauze pack for
10–15 rnin. It is advantageous to infiltrate local anaesthetic
with a vasoconstrictor into the region, as this will make
any manipulation of the socket more comfortable and the
vasoconstrictor in the local anaesthetic will also aid in
reducing the haemorrhage. Suturing is essential in the
management of a postextraction haemorrhage and a
horizontal mattress or interrupted sutures should be used
to tense the mucoperiostem over the underlying bone so
that the haemorrhage can be controlled (see Ch. 23). The
use 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
Infection
Extraction trauma
Blood supply
Site
Smoking
Sex
Systemic factors, e.g. oral contraceptives
bony walls of the socket. Although postextraction haemorrhage can be dramatic, significant blood loss is unusual.
Patients should, however, be assessed for evidence of
shock if bleeding appears significant (see Ch. 4).
Dry socket
Dry socket is also known as focal or localised osteitis and
manifests clinically as inflammation involving either the
whole or part of the condensed bone lining the tooth
socket (lamina dura). The features of this are a painful
socket that arises 24-72 h after extraction and may last
for 7-10 days. Clinically, there is an empty socket with
possibly some evidence of broken-down blood clot and
food debris within it. An intense odour may be evident
and can be confirmed by dipping cotton wool into the
socket and passing it under the nose. The overall incidence
of dry socket is about 3% but this figure is much higher
if the definition of postextraction pain is used as the sole
diagnostic criterion.
The aetiology of this condition is incompletely understood but many predisposing factors exist and these are
listed in Table 26.3.
Infection
This could occur before, during or after the extraction.
However, many abscessed and infected teeth heal without leading to a dry socket. The oral flora in some patients
can be shown to be haemolytic and these individuals may
be more susceptible to recurrent dry sockets.
Extraction trauma
Excessive force may be associated with an increase in the
incidence of dry socket. This is not always the case and
it may occur after very easy extractions. The difficulty of
extraction may be important, as the bony wall of the socket
may be burnished during the extraction, crushing small
bony blood vessels and so impairing the repair process.
Blood supply
Vasoconstrictors in local anaesthetics may predispose to
a dry socket by interfering with the blood supply to the
bone and dry sockets certainly occur more frequently
after extractions with local anaesthetic than after those
using general anaesthetic.
Dry sockets are much more common in the mandible
than in the maxilla. The relatively poor blood supply of
the mandible predisposes to the development of this
problem and food debris also tends to gather in the lower
sockets more readily.
Site
The incidence of dry sockets increases further back in the
mouth with the highest incidence in the mandibular
molar region. The most common tooth involved is the
lower third molar, where the incidence may be significantly more than 3% (see Ch. 27).
Smoking
Tobacco use of any kind is associated with an increase in
dry socket. This may occur, in part, due to the significant
vasoconstrictor effect of nicotine on small vessels that
occurs in smokers.
Sex
Dry sockets are significantly more common among
females.
should be anaesthetised and irrigated gently and all
degenerating blood clot and food debris should be
removed. A dressing should be inserted into the socket to
protect it from further irritation by food debris. The most
appropriate dressing is a matter of personal choice but
Whitehead's varnish pack, a zinc oxide pack or the use of
proprietary agents such as Alvogyl® are commonly used.
Analgesics are an essential part of the management, as is
the use of regular mouthwashes to keep the area clean.
It is important that the patient is reviewed regularly to
ensure that healing is progressing. When pain is intolerable, long-acting local anaesthesia such as bupivacaine
blocks may afford relief and allow patients to sleep.
Osteomyelitis
This rare complication is often a result of an immunecomprised state or a reduction in the blood supply, usually
of the mandible following radiotherapy. The patient is
usually systemically unwell: there is an increase in
temperature and severe pain. Often the mandible, which
is more commonly involved, is tender on extraoral palpation. The onset of disturbance of labial sensation after an
extraction is characteristic of acute osteomyelitis. The
patient will often be admitted to hospital for management
of this condition. The principles of treatment are the
drainage of pus, the use of antibiotics and the later
removal of sequestra once the acute infection has been
controlled. Prevention is best achieved, in a predisposed
patient, by ensuring primary closure of the socket by
bone trimming and suturing (see Ch. 33).
Systemic factors
It has been suggested that systemic factors are involved,
although these have not been elucidated. Oral contraceptive use is associated with an increased incidence of
dry sockets.
In an attempt to reduce the incidence of this painful
condition, the teeth to be extracted should be scaled to
remove any debris and preoperative flushing with 0.2%
chlorhexidine may reduce the incidence. The operator
should use a minimum amount of local anaesthetic and
the 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 of
pain and secondly resolution of the condition. The socket
Swelling, pain, echymosis
Some swelling, pain or bruising can be expected after
any surgical interference and it is important for the
operator to realise that if the soft tissues are not handled
carefully these features can be exacerbated. The use of
blunt instruments, excessive retraction or burs becoming
entangled in the soft tissue all predispose to increased
swelling and discomfort. If sutures are tied too tightly,
postoperative swelling due to inflammatory oedema or
haemotoma formation can cause the sutures to cheesecut through the soft tissues, causing unnecessary pain. It
is helpful for the patient to bathe the area with hot saline
mouthwashes in an attempt to reduce debris around the
wound. Surgeons must be aware of the possibility of
wound infection and be prepared to institute drainage and
consider antibiotic therapy.
217
Sequestra
There will be occasions when small pieces of bone
become detached and cause interruption to the healing
process. The patient will return, complaining of something
sharp in the area of the socket and may feel that the
operator has left a root fragment behind. These sequestra
can be dealt with either by reassuring the patient and
await shedding of the piece of bone or by administering
some local anaesthesia and removing the piece of loose
bone with tweezers. In some cases, granulation tissue
may be apparent with pus discharging especially on probing
the socket. This will respond well to a curettage of the
socket, thus removing the sequestrum in the curettings.
Trismus
Trismus is a common feature after the removal of
wisdom teeth (see Ch. 27) and may be associated with
other extractions. It can also be related to the use of
inferior dental block local anaesthesia (see Ch. 24). It is
important to ascertain the cause of the trismus and then
to manage it appropriately. On most occasions the
trismus will resolve gradually over a period of time,
which will vary depending on whether the condition is
due to inflammatory oedema or perhaps direct damage to
the muscles following local anaesthesia. The management is discussed in Chapter 24.
Prolonged anaesthesia
This is usually a feature of the removal of difficult or
impacted teeth, particularly wisdom teeth, and is
considered in detail in Chapter 27.
Actinomycosis
This is an uncommon chronic suppurative infection
caused by Actinomyces israelii and classically characterised by swelling in the neck with multiple sinus formation and widespread fibrosis. The common site of
presentation following extraction is the region around the
angle of the mandible. Extraction wounds from lower
teeth or fracture of the mandible provide pathways for
the entry of the organisms. A detailed consideration of
cervicofacial actinomycosis is given in Chapter 33.
Chronic oroantral fistula
218
This complication arises when a communication between
the socket of an upper molar (or more rarely premolar)
and the maxillary air sinus has not been noted at the time
of extraction and infection both in the socket and the air
sinus occurs. The patient may present with a variety of
symptoms and signs either within a week or two following the extraction or many months (and even years) later.
Common to all, however, is failure of the normal healing
process and persistence of the socket. As infection of the
air sinus becomes acute, symptoms of diffuse unilateral
maxillary pain, nasal stuffiness, bad taste and intraoral
pus discharge may occur; these can be intermittent in
character.
On examination, the socket can appear empty or be
filled with granulation tissue. Occasionally, distinctly
polypoidal tissue can grow down from the opening,
reflecting the sinus origin of the tissue. In other cases, the
socket can appear almost totally closed, with only a very
small opening into the sinus. Diagnosis by careful
probing is normally straightforward and an occipitomental radiograph will show the extent of infection
within the sinus.
The management involves two stages. First, the acute
infection must be controlled, then the opening should be
closed surgically. Initially, any accumulation of pus in
the sinus should be drained. This often requires excision
of the infected granulation tissue and polyps from
the socket to allow free drainage and also to ensure histologically that the formation of the fistula is not related
to downgrowth of an antral neoplasm. Nasal decongestants and antibiotics also help to control more acute
infections.
Once the acute phase is controlled, most fistulae can
be closed using the buccal flap advancement. The
margins of the opening must be freshened by excising a
rim of soft tissue, because epithelium will often have
grown-up into the opening and, if not removed, will
prevent healing. Where infection is limited to the
immediate vicinity of the fistula, a limited curettage is
carried out. However, where the whole sinus is filled with
polypoidal granulation tissue, a more thorough exploration
of the sinus may be required, and this often is performed
under general anaesthesia.
Infective endocarditis
Infective endocarditis may arise in susceptible patients
with cardiac lesions who are not given appropriate
antibiotic prophylaxis. A detailed consideration of
antibiotic prophylaxis for dental procedures is given in
Chapter 35.
27
Wisdom teeth
Introduction
Third molars are the last teeth to erupt in the human
dentition and are popularly known as wisdom teeth. They
frequently give rise to problems when they are erupting
and the management of these problems has become
colloquially known as the 'bread and butter' aspect of the
speciality of oral surgery. Through evolution, the human
jaws are occasionally no longer large enough to accommodate all of the permanent dentition and therefore the
last ones to erupt are short of space. Most of the problems
associated with wisdom teeth occur between the ages of
18 and 25 but adults of any age can have problems.
A consideration of the criteria for removing wisdom
teeth will be followed by discussion of pericoronitis. The
clinical assessment and management of impacted wisdom
teeth will then be outlined, including preoperative
assessment, the procedures used to remove wisdom teeth,
postoperative care and -finally- complications of surgery
(Table 27.1).
Criteria for removal of
wisdom teeth
Over recent years there has been debate over the
advisability of removing symptom-free wisdom teeth or
leaving them in place. The trend in recent years has been
to be conservative in the management of these teeth and
this has been driven, to some extent, by the incidence of
complications associated with their surgical removal, and
particularly the small, but measurable, risk of damage to
the inferior dental nerve or the lingual nerve.
The controversy surrounding wisdom teeth has led to
the publication of guidelines, the most recent of which
are 'Management of unerupted and impacted third molar
teeth' a National Clinical Guideline from the Scottish
Table 27.1
Management of impacted third molars
Criteria for removal of wisdom teeth
Pericoronitis
spread of infection from pericoronitis
treatment of pericoronitis
Clinical assessment
Radiographic assessment
Clinical management
preoperative information
techniques
lower third molars
upper third molars
Postoperative care
Complications of surgery
Table 27.2
teeth
Indications for removal of wisdom
Infection
pericoronitis
untreatable caries
untreatable pulpal or periapical pathology
periodontal disease
Cystic change
External or internal resorption
Wisdom tooth in tumour resection
Intercollegiate Guidelines Network (SIGN) and
'Removal of wisdom teeth' guidance from the National
Institute for Clinical Excellence (NICE). These guidelines inform the decision on whether to remove wisdom
teeth.
Surgical removal of impacted third molars, it is
recommended, should be limited to patients with
evidence of pathology. These are listed in Table 27.2 and
will be discussed in turn. Further possible indications to
be considered are listed in Table 27.3.
219
hTable 27.3 Further possible indications for
removal of third molars
Transplantation
Fractured mandible
Atrophic mandible
Denture or implant design
Access to dental care
Medical condition
Orthodontic considerations
Orthognathic surgery or reconstructive surgery
Use of general anaesthesia
Age of patient
Infection
these cysts is low but is also unpredictable and gives rise
to a clinical dilemma of how often radiographic assessment of unerupted third molars is necessary to diagnose
a cyst before its size makes the management more
complicated.
External or internal resorption
A less common reason for removal of third molars is
external resorption of the second molar due to pressure
from the unerupted third molar. As with the formation of
the dentigerous cyst, this resorption can be extensive
before the patient experiences symptoms. Internal
resorption within the wisdom tooth is also an indication
for removal.
Pericoronitis
The most common reason for recommending removal of
wisdom teeth is that patients have experienced significant
infection associated with them. This usually manifests
itself as pericoronitis and a discussion of the clinical features and management of this will follow. Pericoronitis is
only an indication for extraction if the first episode is very
acute or there has been more than one episode.
Untreatable caries, pulpal or periapical pathology
Another common indication for removal of wisdom teeth
is the development of caries either in the wisdom tooth
itself or in the adjacent second molar. This occurs because
the patient is unable to clean the distal aspect of the
second molar or the area around the wisdom tooth, which
is often partially erupted. This leads to the accumulation
of food debris and plaque and then caries of the adjacent
tooth surfaces. This may lead to untreatable pulpal or
periapical pathology.
Periodontal disease
As a result of the unsatisfactory relationship between the
second and third molars, the area is prone to periodontal
disease, which may compromise the second molar. This
can be improved by the removal of the third molar.
Wisdom teeth in tumour resection
If an impacted wisdom tooth is associated with a tumour
at the angle of the mandible, or is within the tumour
resection margins, it should be removed.
Transplantation
When a patient presents with a heavily restored or
carious first molar tooth and a partially erupted third
molar tooth it is possible to transplant the third molar into
the socket of the first molar. This procedure is complicated
by the difficulty of removing the third molar without
damage and also because the root morphology of these
teeth is different, which causes problems accommodating
the third molar in its new site. Once transplanted, the tooth
will often require to be splinted for a period and, with a
low success rate, this procedure is rarely carried out.
Fracture of mandible
If a fracture of the mandible through the angle occurs, an
opportunity may arise to remove the third molar when
surgical access is being made to treat the fracture itself.
Some authorities consider that unerupted third molars
should be removed in those individuals who participate
in contact sports like rugby and boxing, in whom the risk
of mandibular fracture is increased.
Cystic change
220
When third molars are unerupted they may be the source
of a dentigerous cyst, which can enlarge considerably
before giving rise to symptoms. The risk of developing
Atrophic mandible
It has been argued that an unerupted third molar in an
already atrophic mandible might be a potential site for
fracture and consideration should be given to removing it
in a controlled manner before a fracture occurs.
Denture or implant design
Restorative dentists can request the removal of unerupted
third molar teeth to facilitate denture design or the
accurate placement of implants.
mouth should be removed when general anaesthesia or
sedation is being used for the removal of a symptomatic
third molar tooth. The fact that the tooth is present is not
sufficient reason to remove it while the patient is
anaesthetised. However, as in all situations regarding
third molars, all four teeth should be subject to a
risk-benefit analysis.
Age of patient
Access to dental care
Where patients are in a situation where they do not have
easy access to dental care, it is appropriate to consider
the removal of potentially troublesome third molar teeth.
This could for example, include submariners or occupations that involve working in isolated areas where
dental help may be difficult to find. With modern means
of travel and communication, this reason for removing
third molar teeth has assumed less significance.
Medical conditions
Removal of third molars may be indicated in certain
medical conditions, such as prior to cardiac surgery or in
those scheduled to have radiotherapy of the jaw. Removal
of third molars following radiotherapy increases the
likelihood of the development of osteoradionecrosis, and
is therefore better carried out before such treatment (see
Ch. 36).
Orthodontic considerations
Orthodontic treatment plans may include the removal of
impacted lower and upper third molars in an attempt to
prevent or reduce imbrication of the incisor teeth. There
is no evidence, however, that third molars contribute to
this problem (see Ch. 31).
Orthognathic or reconstructive surgery
Third molars may also need removed when orthognathic
surgery is being planned, particularly with procedures
such as sagittal split osteotomy (see Ch. 13).
General anaesthesia
More rigorous criteria for removal of lower third molars
can lead to further difficulties in determining whether
symptom-free third molar teeth on the other side of the
Finally, removing third molars in young fit patients and
not leaving them until an older age when the bone is
denser and more difficult to manage, and when the
patient may have medical problems related to older age
groups, is still a common point of view. Contrary to this
argument is the view that the small but significant morbidity following removal of wisdom teeth supports a more
conservative approach, and so removal for this reason
alone can no longer be condoned. The more conservative
approach is now more commonly adopted but many oral
surgeons are mindful that they may be storing up
difficulties for later years, both for their patients and for
their surgical successors. Time alone will answer this
question
Pericoronitis
This condition is characterised by inflammation around
the crown of a tooth and only occurs when there is communication between the tooth and the oral cavity. The
tooth is normally partially erupted, and hence visible, but
occasionally there may be little evidence of communication between it and the oral cavity and careful probing
of the gingiva immediately distal to the second molar
may be necessary to demonstrate some communication,
however small.
The patient's main complaint will be pain, which
initially may be of low intensity. As the condition
develops the pain increases in intensity. Swelling over
the affected site may develop and this will cause further
discomfort when the patient occludes with the opposing
teeth. As the swelling increases, the pain on occluding
becomes more severe and the patient will be discouraged
from bringing the teeth together. The 'lid' of gum over
the involved tooth is known as the operculum and this
may show evidence of trauma from the cusps of the
opposing maxillary teeth. There may be pus formation
and a bad taste. There will be marked inflammation in the
221
tissue adjacent to the affected tooth and this can lead to
trismus and difficulty in swallowing. The patient may be
generally unwell, with lymphadenitis and pyrexia. There
will often be marked halitosis.
Spread of infection from pericoronitis
On occasion, pus associated with an impacted lower
wisdom tooth will track buccally forwards above the
buccinator attachment forming a sinus in the region of
the first permanent molar. This may lead to some confusion as to the source of the infection and can lead to
unnecessary removal of the first permanent molar. This
condition is referred to as a migratory abscess.
Pericoronitis can also be associated with acute ulcerative
gingivitis causing marked halitosis and gingival
sloughing and ulceration. Spread of infection can occur
in various directions (Table 27.4), including laterally into
cheek, or distobuccally under the masseter muscle to give
rise to a submasseteric abscess characterised by profound
trismus. It can also spread to the sublingual or submandibular region and also into the area around the
tonsils and parapharyngeal space (see Ch. 33). Less
commonly, it can ascend through the anterior pillar of
fauces into soft palate causing marked dysphagia. Early
and competent management of acute pericoronitis will
hopefully limit this spread.
Treatment of pericoronitis
The management of pericoronitis is similar to the management of any acute oral infection. It is essential to
provide drainage for any pus. Once drainage is adequate
it is important to clean the area beneath the operculum.
Table 27.4 Spread of pericoronal third molar
infection
Region
222
Direction of spread
Migratory abscess of sulcus Forwards, bucally above
buccinator
Soft tissue of cheek
Laterally
Distally and bucally
Submasseteric
Sublingual space
Lingually above mylohyoid
Submandibular space
Lingually below mylohyoid
Parapharyngeal space
Distally and lingually
Soft palate
Upwards through anterior
fauces
This can be carried out mechanically by irrigation with
warm chlorhexidine or saline solution. This should
remove any accumulated food debris and plaque.
Application of antiseptic or mildly caustic solutions
underneath the operculum may be beneficial. Examples
include Talbot's iodine and trichloracetic acid. These
agents are astringents and will cause soft tissue damage,
and must therefore be used with caution. If the maxillary
third molar has overerupted and is causing trauma to the
operculum, the single most effective treatment is its
removal. This can be carried out easily, even in the
presence of some degree of trismus, and often leads to
resolution. The patient's general condition needs to be
assessed and a decision made regarding the prescription
of an antibiotic (see Ch. 33). The patient should be
encouraged to use regular hot saline mouthwashes and
discouraged from applying heat to the cheek area extraorally. Arrangements should be made for early review of
the patient's condition (within 2-3 days), when some
resolution should have occurred.
Clinical assessment
Once the symptoms of pericoronitis have settled the
patient needs to be assessed fully regarding the future
management of the wisdom teeth. It is important to consider all four third molars as a unit and to make a decision
on each of them. A general assessment of the mouth
should be made, including caries activity and the level of
periodontal disease. The patient's oral hygiene should be
checked with particular reference to the accumulation of
debris around the third molars. The eruption status of each
of the four third molars is made using three categories unerupted, partially erupted or fully erupted. Note should
be taken of the patient's age because the management of
third molars can be significantly influenced by this
factor. It is also important to assess the surgical access to
the third molar region by asking the patient to open
widely and to note the space available between the distal
aspect of the second molar and the vertical anterior border
of the ascending ramus. This is particularly important
when removal of these teeth under local anaesthesia is
being contemplated.
Radiographic assessment
Radiographs are an essential part of the assessment of a
patient's wisdom teeth. When removal is contemplated it
is important that the entire tooth and the surrounding
bone can be seen clearly using a panoramic view of the
oral cavity. A periapical radiograph may be helpful if
lack of detail in the panoramic view compromises
assessment of the root morphology or its proximity to the
inferior dental canal.
Table 27.5 lists the information which should be
available from the radiographs.
Most operators initially assess the depth and the
position of the impacted tooth. The simplest method of
depth assessment can be made by looking at the position
of the crown of the impacted tooth relative to the second
molar (Fig. 27.1). A crown-to-crown relationship
indicates a superficial impaction, crown-to-crown-androot of the second molar indicates intermediate depth and
crown of wisdom tooth to the roots only of the second
molar implies a deep position. The angulation should be
assessed by comparing a line joining the mesial and
distal images of the cusps of the wisdom tooth with the
curve of Spee formed by joining the cusps of the premolar and molar teeth. If the lines are parallel then the
wisdom tooth is vertical in position. However, if the
wisdom tooth line, when extended posteriorly, would
meet the Spee line then the tooth is mesio-obliquely
impacted (Fig. 27.2). Conversely, if the wisdom tooth
line when extended posteriorly would never meet the
curve of Spee, then it is disto-oblique in position. The
most common position is mesio-oblique and the most
difficult to remove is the deep disto-angular impaction,
because its path of removal impacts into the ramus of the
mandible and there is often little space to elevate the
tooth from its mesial aspect.
The crown may show evidence of distal bone loss or
follicular enlargement, which is indicative of chronic
pericoronal infection and often facilitates removal of the
tooth.
The crown of the impacted tooth should also be
examined for evidence of caries, as caries will tend to
weaken it and make fracture more likely on elevation.
Paradoxically, a carious crown is also more difficult to
section and split than an intact crown. The size, number
and 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 in
elevation and removal compared to converging or
diverging roots with apical dilacerations.
The relationship of the roots to the image of the
inferior dental canal should be scrutinised carefully
(Fig. 27.3). Features likely to indicate close proximity
Table 27.5 Information obtained from
radiographs of wisdom teeth
Angulation of the wisdom tooth (for example
mesioangular, distoangular, vertical or horizontal)
Depth of the wisdom tooth
The relationship to the inferior dental canal
Crown features
The root morphology
The texture of the surrounding bone
Any associated pathology (e.g. dentigerous cyst)
Surgical access
The state of the second permanent molars (including
root morphology, presence of caries or extensive
restoration)
Fig. 27.1 Depth assessment of an impacted wisdom
tooth on a radiograph: (a) superficial impaction;
(b) intermediate depth; (c) deep position.
223
Fig. 27.2 Angulation of a wisdom tooth on a radiograph: (a) vertical: the
intercuspal 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) distooblique: the intercuspal line of the wisdom tooth is diverging from the line of Spee.
224
include narrowing of the canal as it passes across the
outline of the root, loss of continuity of the radio-opaque
roof of the canal or deflection of the normal arc of the
canal as it passes across the root(s). Additionally, the
apices of the roots may show severe dilacerations as they
approach 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 images
of roots and the inferior dental (ID) canal with interposed
bone on any radiographic view indicates lack of close
approximation because, if the root(s) were anatomically
close, such a separation could not be shown radiographically, 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 distal
restorations present in the second molar should be noted
as forces carelessly applied to the third molar may cause
movement to this tooth or risk dislodging the restoration.
Clinical management
Once the decision has been made to remove a patient's
wisdom tooth, the options for anaesthesia should then be
considered. Consideration of either local anaesthesia
and sedation or general anaesthesia may be indicated.
Decisions regarding the form of anaesthesia used will
depend upon the patient's anxiety about the procedure,
the number and the degree of difficulty of removal of the
wisdom teeth and the availability of patient-care options.
Preoperative information
Before treatment commences, the patient should be given
information regarding the possible complications of the
removal of wisdom teeth. This is best done not only
verbally on a one-to-one basis with the clinician but also
by the use of written information, which the patient can
study and discuss with the surgeon before the procedure.
The information provided to the patient should include a
description of the discomfort that follows removal of
these teeth and the associated swelling and difficulty in
opening the mouth for a short period. Bruising of the face
at the angle of the jaw can cause alarm. Dry socket is
more frequently experienced when lower wisdom teeth
are removed than other teeth (see Ch. 26). The most
serious complication is numbness of the tissues supplied
by the inferior dental or lingual nerves. It is mandatory
that the patient is advised of this possible complication
prior to their procedure. Around 15% of patients who
have lower wisdom teeth removed will experience some
temporary alteration in sensation along the distribution
of the lingual or inferior dental nerves but permanent
numbness occurs in under 1%. It is important that the
case record is fully documented with the information that
has been given to the patient regarding the possible complications and also to indicate whether written information
has been given to the patient.
Techniques
Lower third molars
Access to the tooth is gained by lifting a buccal
mucoperiosteal flap (Figs 27.4 and 27.5). Raising the
flap lingually can lead to stretching of the lingual nerve,
225
Fig. 27.6
Fig. 27.4
Flap design for removing an impacted wisdom
tooth: (a) occlusal view; (b) lateral view; unerupted; c)
partially erupted.
Fig. 27.5
Envelope flap (no vertical relief) for removing an
impacted wisdom tooth.
226
which is anatomically close to the lingual aspect of the
lower wisdom tooth and, in many cases, can be avoided
if sufficient visibility and access are gained without it.
Once the lower wisdom tooth is adequately exposed,
consideration should be given to bone removal to
facilitate delivery of the tooth. Bone removal is most
commonly achieved using drills and burs and is carried
out on the buccal aspect of the tooth and onto the distal
aspect of the impaction. The intention is to create a deep,
Removal of pericoronal bone.
narrow gutter around the crown of the wisdom tooth (Fig.
27.6), and not a shallow, broad gutter. Bone should be
removed to allow correct application of elevators on the
mesial and buccal aspects of the tooth. The operator can
then assess the possibility of removing the tooth in its
entirety with the use of elevators or a combination of
elevators and forceps. If it proves impossible to remove
the tooth in this way and adequate bone has been
removed, sectioning the tooth using burs is carried out
(Fig. 27.7). Most commonly, the crown of the tooth is
sectioned from the roots and the crowns and roots are
then removed as individual items. Further separation of
the roots with burs may also be necessary. Where the
roots are separate, the tooth may be sectioned longitudinally, allowing removal of the distal portion of the crown
and distal roots, followed by elevation of the mesial half
of the tooth.
In younger patients under general anaesthesia, the
lingual wall of the third molar socket may be removed
using a hammer and chisel (the split bone technique).
This often allows the tooth to be delivered in one piece
by rotating it lingually. Clearly, this technique does
require a lingual flap to be reflected but in skilled hands
it can be a very successful and rapid technique.
When tooth removal is completed, any debris is
cleaned out and any follicular tissue - especially that
hidden behind the second molar - is curetted free. After
smoothing any sharp bone, irrigation of the socket is
carried out with saline. The flap is then sutured using
either resorbable or non-resorbable materials.
Fig. 27.7
Methods of sectioning an impacted wisdom tooth.
examples with diverging roots in large patients can be
more than a little challenging.
Postoperative care
Fig. 27.8
'Anatomical' closure of a flap after surgical
removal of an impacted wisdom tooth.
Although it is possible to suture the flap across the
socket to the lingual side, many operators prefer to return
the flap to its original position, leaving a socket that is
more easily kept clean by the patient postoperatively, and
may well also reduce swelling (Fig. 27.8).
Upper third molars
These teeth are generally easily removed by elevation
from the mesiobuccal aspect using a curved Warwick
James elevator or Coupland's chisel. If undue resistance
to elevation is encountered then excessive force can
cause fracture of the posterior aspect of the tuberosity,
and forceps should be used if possible in this circumstance. If this is not possible due to only partial eruption
of the tooth, a buccal flap can be raised with appropriate
bone removal.
Upper third molar removal should not be underestimated and access to grossly carious, partially erupted
The overuse of antibiotics is being recognised and, in
particular, there is controversy about their use prophylactically in the removal of wisdom teeth. Some routinely
prescribe antibiotics to the patient whereas others withhold antibiotics and use them only if infection occurs. No
clear evidence is available to support either viewpoint.
Some operators provide antimicrobials where there is a
history of repeated episodes of pericoronitis or if there
has been a recent acute episode. Others prescribe if
extensive bone removal is necessary or there is extreme
difficulty in removing the tooth.
The antibiotic may be administered preoperatively,
perioperatively or immediately postoperatively. Regimes
and choice of antibiotic vary but the most commonly
used are amoxicillin or metronidazole, and they should
be prescribed for as short a period as possible. The use of
corticosteroids during the removal of wisdom teeth is
more evidence-based and more clinicians are now using
them to reduce postoperative swelling. The provision of
postoperative analgesia is an integral part of treatment.
Chlorhexidine mouthwashes twice daily and frequent hot
saline rinsing is beneficial. Patients should be encouraged to keep moving the jaw, despite the swelling and
discomfort, as this reduces stagnation and consequent
infection.
Complications of surgery
These can be considered under perioperative and postoperative complications.
227
Perioperative complications are similar to those occurring with any other dentoalveolar surgery and include
excessive bleeding (see Ch. 26). Certain complications
are more specific to the third molar region and include
fracture of the mandible, loss of a root in the lower jaw
into the lingual space or in the upper jaw displacement of
the tooth into the maxillary air sinus or into the pterygoid
space (see Ch. 26). Direct trauma to the inferior dental
neurovascular bundle may occur and can be difficult to
avoid where anatomically the roots are intimately related
to the canal tissues. The most obvious example of this is
the rare situation where the inferior dental canal actually
passes through the root. Even here, it may be possible to
split the root around the neurovascular bundle leaving the
bundle relatively undamaged.
Postoperatively, the majority of patients will have
swelling at the angle region, trismus and discomfort. This
generally peaks after 48 h and will resolve within a week
228
to 10 days. Infection in the form of localised osteitis (dry
socket) can occur and should be managed in the usual
symptomatic way (see Ch. 26). Occasionally, the wound
may become infected with pus production and this is
more likely if there has been haematoma formation in the
cheek or other adjacent soft tissue spaces.
Anaesthesia (complete loss of sensation), paraesthesia
(partial loss) or dysaesthesia (an altered sensation often
painful to the patient) are more worrying sequelae. Where
lingual nerve damage has been sustained taste perception
is also frequently altered and can be an additional distressing symptom. The prognosis for resolution is good
but a small number of patients have to accommodate to
permanent loss or alteration of sensation in the distribution of the particular nerve. Recovery of normal
sensation may take from a few days to several months,
but after a year little improvement will occur.
28
Cysts of the jaws
Introduction
A cyst, by definition, is a pathological cavity that is
usually lined with epithelium and which contains fluid or
semi-fluid.
The vast majority of cysts of the jaws form within
bone and grow slowly. They may therefore attain a
relatively large size because they are often initially
Table 28.1
symptom free. Diagnosis of a cyst is not uncommonly
made when the cyst becomes acutely infected, or it is
found 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 considered in more detail here, discussing their clinical
features, diagnosis and treatment.
Features of cysts of the jaws
Type
Site
Epithelial source
Frequency
Radiographic
appearance
Radicular (apical or
dental)
Dentigerous
Any non-vital tooth
Debris of Mallassez
Most common of all
Unerupted teeth
Reduced enamel
epithelium
Relatively common
Keratocyst
Angle of mandible but
anywhere possible
Periodontal pocket
Dental lamina
Relatively common
Round or oval
radiolucency
Radiolucency around
crown of unerupted
tooth
Multilocular when large
Debris of Mallassez
Uncommon
Nasopalatine
Midline anterior
hard palate
Epithelium nests at
nasopalatine
fissure
Uncommon
Nasolabial
Nasolabial fold
(not intrabony)
Very rare
Solitary bone cyst
Mandibular body
Possibly epithelium
from the
nasolacrimal
duct
Not epithelium lined
Staphne's idiopathic
bone cyst
Mandibular body on
lingual aspect
Very rare
Aneurysmal
bone cyst
Usually mandible
Not cystic but
submandibular
salivary gland
inclusion
Not cystic
Periodontal
Rare
Rare
Round or oval
radiolucency
Midline palatal
radiolucency, lamina
dura of centrals
intact
May cause depression
of nasal lateral wall
Radiolucency often
scalloped around
roots of lower
molars
Small round shadow
below inferior dental
canal
Multilocular, soapbubble apearance
229
Radicular cysts
A radicular cyst is by far the most common cyst of the
jaws. Its synonyms are dental cyst, periapical cyst or simply apical cyst. From time-to-time the teeth responsible
for the formation of a radicular cyst may be extracted but
the cyst remains and may well increase in size subsequent to the extraction. In this circumstance the name
residual cyst is commonly used.
A radicular cyst develops when epithelial debris of
Mallassez in a granuloma at the apex of a non-vital tooth
is stimulated to proliferate. The epithelium forms a ball
or mass of cells, which may break down centrally, perhaps
due to lack of nutrients, to form a liquefied central area.
Alternatively, the epithelium cells may form strands and
sheets that encompass part of the granuloma, with a
similar resulting breakdown of the enclosed granulomatous
content to form the fluid centre of the cyst. Whichever
method occurs, the effect is the formation of an epithelial
semipermeable lining to the cyst content that allows
fluids to enter the lumen by osmosis and leads to its
gradual enlargement. This whole process is sometimes
known as cystic degeneration.
Clinical features
230
Initially, the cyst will be contained within the alveolar
bone around the apex of the non-vital tooth. At this stage
the bone increases its density peripherally around the
lesion in an attempt to wall it off. This is possible due to
its slow rate of growth and explains why, radiographically,
there is a sharp radio-opaque line surrounding the
radiolucent shadow of the cyst.
With continued growth, the cyst eventually approaches
the surface of the alveolar bone and as the apices of most
teeth lie closer to the buccal than the palatal or lingual
plates, it is the buccal plate which is usually first affected.
Lying on the surface of the bone is the periosteum, and
this layer of osteogenic tissue in turn reacts to the
encroaching cyst by laying down new bone over its
advancing front. The first real evidence of a cyst is
therefore a bony swelling, known as bony expansion, in
the buccal sulcus. Occasionally, especially with an upper
lateral incisor, the expansion may be palatal, reflecting
the palatal inclination of the apex. This expansion will
feel hard to palpation and its presence may be convincing
only on comparison with the contour of the bone on the
other side of the jaw. With further growth, this
enlargement will continue until the periosteum can no
longer lay-down bone sufficiently rapidly and the cyst
erodes through an ever-thinning bony buccal covering
until it presents as a soft fluctuant (fluid-filled) swelling
in the sulcus, which often appears slightly blue in colour.
When the overlying expanded bone is very thin,
palpation may elicit the characteristic eggshell crackling
though this is rarely felt in practice.
Acute infection can supervene at any time during this
process of evolution and this will convert the cyst, as far
as its clinical features are concerned, into those of an
acute apical abscess. If the acutely infected cyst bursts
and discharges into the mouth, the continued discharge
may lead to formation of a sinus.
Loosening or tilting of adjacent teeth is only
encountered in very large cysts, and resorption of roots
usually results from repeated infection of the cyst and is
relatively uncommon.
Unless a radicular cyst becomes infected, it will
remain painless and vital structures will be gently moved
aside to accommodate it. This can be seen clearly in
larger mandibular cysts, which push the inferior dental
canal downwards to the lower border of the mandible. No
anaesthesia will be noted of the lip or chin unless the
pressure within the cavity rises rapidly as with an acute
infection. With large cysts occasionally the tooth
responsible for the lesion elicits a rather hollow note on
percussion.
Diagnosis
As mentioned above, many radicular cysts are found
either by chance radiographically or because of acute
infection. However, other clinical features may present.
Expansion of bone is usually buccal and hard to palpation. Later it is soft, fluctuant, and bluish in colour.
The tooth will be non-vital. Radiographic features will
show the classic appearance of a round or oval-shaped
radiolucency (Fig. 28.1) surrounded by a sharply
delineated thin white line of increased bone density. The
affected tooth will show loss of its apical lamina dura.
Very occasionally there may be evidence of resorption of
adjacent teeth and this reflects repeated acute episodes of
infection within the cyst. Similarly, such infection can
cause a haziness in the sharp radio-opaque delineations
of the margin of the cyst. In larger mandibular cysts there
may be clear evidence of the inferior dental canal having
been displaced downwards by the advancing lesion.
Aspiration of the cyst contents may be possible in
larger cysts with little or no bony covering. Classically,
enucleation, with marsupialisation tending to be reserved
for certain categories of patients, usually with larger
cysts.
Enucleation
Fig. 28.1
A radicular cyst associated with a lateral incisor
showing as a round radiolucency.
the fluid appears as straw-coloured in which a shimmer
may be seen due to its cholesterol content. However, if
the cyst has been infected, this characteristic appearance
may be lost and the fluid may well consist of pus or
blood-stained pus. Many authorities have alluded to the
difference between the higher soluble protein content of
the radicular cyst and the dentigerous cyst compared with
the lesser amount contained in odontogenic keratocysts.
Such analyses are in practice seldom, if ever, carried out
because of their cost and due to the fact that the
differences between aspirates are visible to the naked eye
and the use of a simple cytological smearing of suspected
keratocysts makes such expensive tests unnecessary.
With very large cysts, especially in the mandible, it
may be prudent to obtain some lining for histopathological examination, as this may allow differentiation
between a large radicular (or residual) cyst, a keratocyst
or a cystic ameloblastoma, especially when considering
the differential diagnosis of a radiolucency of the angle
of the mandible.
Treatment
There are two main methods of treatment for cysts:
enucleation (removal of the lining in total) and
marsupialisation (creation of a permanent opening into
the cyst cavity). The vast majority of cysts are treated by
This is suitable for all small to moderate-sized cysts and
the majority of large cysts.
Root-treating and conserving the tooth causing the
cyst may be worthwhile and surgery may therefore be
preceded by endodontic treatment.
A standard mucoperiosteal flap is raised buccally with
the vertical relieving incision placed anteriorly (see
Ch. 23). The thin bone is then removed with bone rongeurs
(nibblers) or burs to allow surgical access to the fluidfilled sac. The cyst lining is then separated with periosteal elevators or curettes from its bony wall and 'shelled'
out. The lining should be sent for histopathological
investigation. After irrigating with sterile saline the flap
is sutured back to its anatomical position. If the tooth has
been root filled, an apicectomy should be performed at
the same time with retrograde sealing of the canal if
appropriate.
The operation is for all but very large cysts usually
carried out under local anaesthesia with or without sedation
according to the patient's preference. Postoperative complications are rare, although breakdown of the wound in
large mandibular cysts can occur. The patient is normally
recalled about 4-6 months postoperatively, when a radiograph should show evidence of bony infilling of the cyst
cavity.
Marsupialisation
As the name implies, marsupialisation means creating a
pouch. The rationale of this treatment is the permanent
destruction of the integrity (wholeness) of the cyst. This,
in effect, depressurises the cyst cavity, stops its continued
expansion and encourages a shrinkage of the lining by
new bone formation around its periphery. It is more
suitable for large cysts where enucleation may endanger
vital structures such as the inferior dental nerve or there
is a risk of fracture during enucleation. The limited surgery
involved is very suitable for outpatient care under local
anaesthesia and it can therefore be particularly appropriate for elderly or medically compromised patients
who would be at risk from a general anaesthetic. Any
decision to marsupialise a cyst cavity should be preceded
by histological evidence that confirms the lesion as a cyst
231
and this involves a small incisional biopsy or retrieving
tissue from the cyst cavity at the time of the procedure.
Marsupialisation may be achieved most simply by
extraction of the tooth responsible for the cyst, aspirating
the contents through the socket, then irrigating the cyst
lumen before packing the opening with a surgical pack.
Sterile ribbon gauze soaked in Whitehead's varnish is
excellent for this purpose, as the antiseptic content will
protect the cyst cavity from infection. The pack is later
substituted for a partial denture with a root-shaped acrylic
bung extending into the cyst cavity from the socket. The
patient is then given syringes with which to irrigate the
cyst cavity with warm saline on a twice-daily basis. With
the lining no longer complete, the bone heals inwards
around the cyst, reducing it progressively in size. Some
operators remove the cyst by enucleation when it has
reduced to a more manageable size.
If no tooth is involved - as in a large residual dental
cyst - then a small semilunar flap is raised over the most
expanded part of the cyst to allow part of the lining to be
excised, and the cyst contents to be aspirated and washed
out. The flap is then turned into the cyst and sutured to
its lining, and the opening maintained initially with a
surgical pack and later by a denture or prosthesis with an
acrylic bung.
Marsupialisation of a large cyst may take many
months for healing to occur and the onus is therefore on
the patient to maintain cleanliness by frequent irrigations
of the cyst cavity, as described above.
Diagnosis
Radiographic imaging and aspiration are often fairly
conclusive (Fig. 28.2). A very large dentigerous cyst in
the lower third molar area can displace the wisdom tooth
and may require to be differentiated from other lesions
such as a keratocyst or ameloblastoma. Although both
these lesions are classically described as being
multilocular radiolucencies on radiograph, it must be
remembered that unilocular lesions do exist. Aspiration
may not be sufficient to differentiate a dentigerous cyst
from a keratocyst, particularly if there has been infection.
Similarly, an ameloblastoma may have within it areas of
cystic degeneration, even in the more solid tumours, and
a variant of the ameloblastoma – known as the cystic
ameloblastoma – can be very similar to the dentigerous
cyst in its clinical appearance, radiographic image and
aspirated fluid content. If any doubt exists, then biopsy of
a small portion of the lining will be diagnostic in most
cases, although in the cystic ameloblastoma the tumour
may only be evident histologically in a small area of the
cyst lining and the sample taken may therefore be
misleading.
Dentigerous cysts
These cysts are developmental odontogenic cysts, which
arise when cystic degeneration occurs in the reduced
enamel epithelium (dental follicle). They are seen around
unerupted teeth and are therefore most frequently found
in the third molar areas, both upper and lower, the upper
canine region and, less frequently, around lower second
premolars. They may also arise in relation to supernumerary or supplemental unerupted teeth.
Clinical features
232
These cysts grow slowly and have the same effect as
radicular cysts on surrounding bone. A bony expansion
occurs initially and at a later stage a soft fluctuant swelling
over the area of the unerupted tooth will develop. As
with radicular cysts, dentigerous cysts are usually
asymptomatic until infected.
Fig. 28.2 Radiograph of a dentigerous cyst in the lower
third molar area showing downward displacement of the
inferior dental canal.
Treatment
Treatment will either be enucleation along with extraction of the unerupted tooth or marsupialisation.
Marsupialisation is the method of choice if it is hoped to
encourage eruption of the buried tooth, but it is
remarkable how seldom the involved tooth is in a satisfactory position in terms of its angulation and depth to
make this the preferred choice. The vast majority,
therefore, are enucleated with the unerupted tooth.
periodontal space of an adjacent tooth. It is important to
realise that, unless infected, these sometimes very large
lesions are painless and do not exert sufficient pressure
on vital structures such as the inferior dental nerve to
cause anaesthesia of the lip and chin. When infected,
however, they can become very painful, cause anaesthesia
and may discharge into the mouth, with consequent bad
taste and bad breath as additional clinical features.
Diagnosis
Keratocysts (odontogenic
keratocysts)
Keratocysts are believed to be derived from remnants of
the dental lamina. They can be found anywhere in the
jaws but the most common site is at the angle of the
mandible. Unlike other cysts of the jaws, their epithelium
is a keratinising stratified squamous epithelium and their
contents are therefore filled with desquamated squames
and keratin, which form a semisolid material that has
been likened to cottage cheese. Their mode of growth is
also different from the other cysts in that the lining
appears to be more active, with passive fluid ingress of
little significance. Keratocysts are also characterised by
the formation of microcysts or satellite cysts which protrude into the surrounding fibrous tissue and tend to be
left behind during enucleation. This increases the risk of
recurrence and dictates a different management
approach.
Clinical features
The active growth of keratocysts appears not to be evenly
distributed, so the cyst does not expand uniformly as a
sphere or oval-shaped lesion. Different rates of activity
within areas of the lining probably account for the formation of locules, which, once the cyst has achieved a
moderate size, will give rise radiographically to the typical
multilocular appearance. They appear to grow selectively
within the looser medulla of the jaw initially and
although eventually the outer cortical plates do show
expansion, the cyst may be by that time a considerable
size. Lingual as well as buccal expansion is often noted.
Infection often only occurs when the cyst is quite
large and where soft tissue trauma allows ingress of
bacteria. It is not infrequent to find that with expansion
the cyst communicates with the surface through the
As with other cysts, the diagnosis is based on clinical
features, radiographic findings and the results of aspiration
and biopsy. Two extraoral radiographic views at right
angles to each other, such as an orthopantomogram and
posteroanterior mandibular view, may be required with
large keratocysts. Classically, the appearance is of a
multilocular radiolucency with marked expansion of both
buccal and lingual plates. Unerupted wisdom teeth may
well be pushed into bizarre ectopic positions such as
inverted high into the ramus of the mandible. The inferior
dental canal may be difficult to see and may reflect the
more active growth of these cysts around the canal with
less evidence of significant repositioning as is seen with
radicular cysts. Displacement or tilting of the teeth can
be a feature, as can resorption of roots, although this is
again probably a result of infection. Infection within a
cyst also accounts for many becoming symptomatic.
As previously indicated, the soluble protein content of
the aspirate obtained from a keratocyst is lower than that
of other cysts and this is due to the fact that keratin is an
insoluble protein. Aspiration will yield a 'dirty' creamcoloured semisolid material composed of keratinised
squames. These can be confirmed histologically and
provide good evidence that the lesion is a keratocyst.
As the differential diagnosis may well include
odontogenic tumours such as ameloblastoma, many
surgeons prefer to make a small flap incision and remove
some lining of the cyst to confirm the diagnosis.
Treatment
Keratocysts have a higher recurrence rate than other cysts
and especially when they are large and multilocular.
Enucleation is suitable for most keratocysts but may
be difficult in large ones where, for example, they extend
upwards into the vertical ramus of the mandible. Surgical
access may be difficult and with the multilocular pattern
of growth it may be impossible to ensure that the whole
233
lining is removed. It is known that small clusters of
epithelium known as microcysts, or satellite cysts can lie
outside the epithelial lining and within the fibrous wall,
and leaving even a small amount of this fibrous wall may
well account for eventual recurrence. For this reason,
some operators have in the past used chemicals such as
mercuric salts or, more recently, cryotherapy techniques
(particularly liquid nitrogen sprayed around the bony
cavity) to try to ensure that no viable soft tissue remnants
remain (see Ch. 38).
Marsupialisation can be used particularly with large
keratocysts where it can be very effective (Figs 28.3
and 28.4). It has the same advantages as mentioned
previously with radicular cysts and probably reduces the
chance of recurrence. Again, it may be appropriate in
234
Fig. 28.3
some cases to use the technique to reduce the size of the
lesion before enucleating it. Whatever method is used,
follow-up is required for years to ensure that there is no
recurrence, and this is mainly radiographic.
Gorlin-Goltz syndrome
Gorlin-Goltz syndrome, or multiple basal-cell naevi
syndrome, is an inherited (autosomal dominant) condition
in which multiple keratocysts of the jaws form part of the
overall syndrome. Other aspects in these patients are the
presence of many skin lesions in the form of basal-cell
naevi or carcinomas, and skeletal abnormalities affecting
the vertebral column and the ribs. Calcification of the
falx cerebri is also a noteworthy feature.
Marsupialisation of a large keratocyst showing (a) cyst cavity; (b) denture with extension.
A radiograph of a nasopalatine cyst causing
Fig. 28.5
displacement of incisor roots.
Clinical features
These cysts cause swelling of the anterior aspect of the
midline of the hard palate. They may become infected
and cause pain and overlying tenderness and can, on
occasion, discharge forming a sinus. However, as with
most cysts, they are painless unless infected and may
grow to a considerable size.
Diagnosis
Fig. 28.4
Radiograph of keratocyst at left angle of
mandible: (a) at presentation; (b) 6 months after
marsupialisation.
Nasopalatine cysts
These cysts arise from epithelial remnants within or near
to the nasopalatine foramen. They are not odontogenic
but are classified as fissural cysts, and they represent by
far the most common example of fissural cysts of the
jaws.
Presence of a midline anterior palatine swelling is the
only usual clinical finding. However, many are again
diagnosed through chance by radiographs of the teeth in
this region. It can be difficult when such radiolucencies
are found on routine radiographic assessment of the
central incisors, to know if the image seen is within
normal anatomical limits of the nasopalatine foramen. A
radiolucency of approximately greater than 8 mm in
diameter is more likely to represent cystic degeneration
but, where doubt exists, a further radiograph 6 months to
1 year later may be more conclusive. The normal radiographic image is a round or inverted pear-shaped
radiolucency with sharp radio-opaque margins (Fig.
28.5). When they are large, they can cause separation of
the central incisor roots, but the laminae dura of the teeth
remain intact. If there is doubt whether the cyst is a
radicular cyst related to one or other incisor, pulp testing
can be carried out and close examination of the apices
radiographically should show an intact lamina dura.
Treatment
These cysts should be enucleated - never marsupialised
because marsupialisation in this area can lead to a
235
This bony surface is normally very gently convex in
appearance but may show concavity where the cyst has
caused saucerisation of the bone in this region.
Confirmation may be obtained by aspiration and the
normal treatment would be surgical enucleation.
Solitary bone cyst
Fig. 28.6
cyst.
Palatal flap raised to expose a nasopalatine
permanent cavity that will show no evidence of
restoration of the normal contour. Normally, enucleation
is carried out with a palatal flap taken around the gingival
margins of the premolars on one side to the premolars of
the other (Fig. 28.6). After enucleation, interdental
interrupted sutures are used to replace the flap and in
larger cysts. It is sometimes useful to have constructed a
palatal plate from preoperative impressions to support
the flap and prevent the formation of a painful haematoma.
This used to be known as a traumatic bone cyst or a
haemorrhagic bone cyst. It is usually found in the
mandibular body and appears radiographically as a
radiolucency that not infrequently shows scalloping
around the roots of the lower molar and premolar teeth.
It causes no expansion of the bone and even on
radiographic examination the outline of the radiolucency
is less well defined than would be obtained from other
cysts. This cyst is not a true cyst in so far as it has no
epithelial lining and, in fact, the majority have apparently
no content whatsoever. When surgically explored, they
tend to heal spontaneously after the surgery.
Staphne's idiopathic bone cyst
Although usually discussed with cysts of the jaws, this is
not in fact cystic at all. It consists of submandibular
salivary gland tissue that occupies a recess on the lingual
aspect of the mandibular body. These cavities are usually
found by chance on routine radiography of the lower jaw
where they appear as round or oval-shaped radiolucencies
Other cysts
The other cysts of the jaws are very uncommon and, as
they are so rare, it is only necessary to know a few facts
about them.
Nasolabial cyst
236
This is a fissural cyst that is thought to form by cystic
degeneration of epithelium from the lower part of the
nasolacrimal duct during embryological development.
Clinically, they may present as painless swellings in the
nasolabial fold, where they may be palpated either
externally on the skin surface or intraorally high in the
buccal sulcus anteriorly. Radiographically, although they
are not intrabony cysts they may, if they attain a
reasonable size, cause a depression of the radio-opaque
margin of the floor and lateral wall of the nose, which is
best viewed by an oblique anterior occlusal radiograph.
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 most
clinicians would take a further radiograph 6 months to
1 year later to confirm that the shadow of this cavity
remains unchanged.
Globulomaxillary cyst
This cyst was originally thought to be a separate clinical
entity. It was believed to be a fissural cyst formed
between the upper lateral and canine teeth, but many now
consider it to be a radicular cyst derived from the lateral
incisor.
Aneurysmal bone cyst
This is discussed in Chapter 36.
237
29
Periradicular surgery
Introduction
The term 'periradicular surgery' has superseded the older
term of 'apicectomy' and reflects the fact that the surgery
might not always be related to an apical problem but can
affect the side of the root, as when a post has perforated
into the periodontal space. Virtually any tooth can be
treated in this way although anterior teeth, being
strategically and aesthetically more important, are more
common. The indications for periradicular surgery will
be discussed, followed by a consideration of surgical
techniques and post perforations.
Indications for surgery
filling problems may also arise. Underfilling of the canal
often reflects preparation of the root canal short of the
true apex with necrotic tissue perpetuating the infection
(Fig. 29.1). Overfilling of the canal may occur and the
material used and the quantity of material through the
apex will determine the likelihood of the need for surgery. 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 endodontic
and surgical sealing if the apex is funnel-shaped.
Miscellaneous examples of endodontic failure include
significant lateral canals, often near the apex, poor
natural drainage and difficult canal morphology. This can
lead to difficulty in controlling infection and may need
apical surgery in addition to endodontics.
In general, too many teeth are treated by periradicular
surgery and this is a direct result of inadequate endodontic techniques. There are, however, several indications
for periradicular surgery, including endodontic failure,
which may be unavoidable. These will be discussed in
turn (Table 29.1).
Endodontic failure
Obstructions to instrumentation, such as calcified root
canals, dilacerated (hooked or curved) roots, broken
endodontic instruments or root fractures may occur; root-
Table 29.1
238
Indications for periradicular surgery
Endodontic failure:
canal obstruction
problems with root filling
other, e.g. canal number and shape
Pathology
Post-crowned teeth
Fig. 29.1 Radiograph of an underfilled root canal.
Fig. 29.2 Radiograph of an overfilled root canal (and
lateral perforation).
Fig. 29.3
Pathology
Surgical technique
The presence of a radicular cyst requires enucleation
after endodontic sealing of the canal. Also there may be
associated pathology such as infection from an upper
lateral incisor spreading to the follicle of an unerupted
canine.
Post-crowned teeth
Post-crowned teeth can fail due to any of the above
reasons and there may be additional considerations in
the decision to carry out periradicular surgery. Often, the
correct treatment would be to root treat the tooth again,
but this would involve destroying the existing crown and
removing the post. This may be unattractive to the
patient, especially if the crown is good functionally and
aesthetically. The pragmatic solution may therefore be to
leave the crown and post undisturbed and carry out the
surgery, unless the endodontic filling is very poor.
Minimising the risk of post perforations and their
management will be discussed later (Fig. 29.3). It is,
however, likely that the infection is initiated by the
acidity of the cement used to retain the post causing
tissue necrosis in the periodontal space and this subsequently becoming infected.
Lateral perforation of a root with a post.
Periradicular surgery is a simple minor procedure and is
outlined in Table 29.2.
Anaesthesia
Infiltration with an adrenaline (epinephrine)-containing
solution is preferable and significantly improves visibility
by its haemostatic effect. Even where a block anaesthetic
is given, additional infiltration is wise. Palatal or lingual
infiltration is needed for full gingival margin flaps to
allow suturing but may be necessary for larger lesions in
any case, e.g. upper lateral incisor where the infection
has eroded palatal bone.
Table 29.2
Periradicular surgical technique
Anaesthesia
Flap design
Bone removal
Apex removal
Curettage
Retrograde root filling
Wound closure
Follow-up
239
Flap design
An 'L' or inverted 'L'-shaped flap from the gingival margin is the flap of choice (see Ch. 23). Only one vertical
incision is normally required and the access afforded is
excellent (Fig. 29.4). The only perceived disadvantage
may be gingival recession postoperatively, but this can be
minimised by careful suturing.
The older semilunar flap avoids the risk of recession
but has several disadvantages (Fig. 29.4). It gives less
surgical access, is more difficult to suture accurately and,
by cutting across the gingivae, can lead to dysaesthesia
(painful altered touch sensation) of the gingivae, which
may be long lasting.
Fig. 29.4
flap.
Flap design for apicectomy: older L-shaped
Fig. 29.5
Retrograde sealing of a root canal.
Bone removal
It may be necessary to remove bone over the apex of the
tooth to gain surgical access. This is relatively easy when
the pathology has destroyed bone, but accurate assessment of the location of the apex is required when the area
of infection is smaller, and good radiographs may be very
helpful. The apical third of the root should be found by
using a fast-rotating round bur with good suction and
light, and bone then removed over the apex and sufficiently above it to allow access.
Removal of apex
Normally, 3 mm of apex is removed using a narrowtapered fissure bur. Ideally, the cut across the root should
be at right angles to the long axis of the root and this
stage should be carried out early in the procedure to clear
the field for curettage of the existing infection.
Curettage
Large to medium-sized caries excavators are ideal for
curettage. The cavity should be clean but it is probably
unnecessary to spend too much time removing every
fragment of soft tissue. Ideally, curettings should be sent
for histopathology.
and probing will almost inevitably indicate the
requirement.
The root canal needs to be prepared and cleansed to a
depth of 3 mm (Fig. 29.5). In practice, this can be accomplished with a small rose head bur (a small contra-angle
hand-piece may be helpful) or by ultrasonic preparation
using specially designed tips.
After drying the canal, various sealants can be used,
including zinc oxide and Eugenol® preparations, ethoxy
benzoic acid cement (EBA) and, more recently, mineral
trioxide aggregate (MTA). No material will produce a
hermetic seal, although this must be regarded as the
ultimate objective of the procedure. Excess filler should
be removed carefully to reduce foreign body reactions.
Wound closure
Retrograde root filling
240
The vast majority of teeth treated require retrograde
sealing of the root canal. This need may be obvious from
the outset with good radiographs but visual inspection
After thorough irrigation with sterile saline the wound
should be closed. In the anterior region, especially, a
finer gauge of suture and smaller needle may facilitate a
neater result. Great care should be exercised to ensure
that the interdental papillae are repositioned accurately.
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 vertically
arranged mattress suture can be very helpful in holding
the papilla firmly on either side of the tooth. Time spent
in the closure of these wounds is well spent as the
aesthetics of the end result can depend largely on accurate
suturing.
Table 29.3
surgery
Reasons for failure of periradicular
Inadequate apical seal
Inadequate tooth support
Vertical tooth fracture
Follow-up
Sutures are usually removed 5-7 days postoperatively
and patients are normally seen 3-6 months after this to
assess the longer-term results. Absence of pain, tenderness of the sulcus sinus formation and undue mobility are
indicative of success. Radiographs should show the
retrograde seal in good position and a reduction in the
radiolucency compared with the preoperative film.
Reasons for failure
The reasons for failure of periradicular surgery are listed
in Table 29.3.
The procedure will fail if the apical seal is inadequate
and release of toxins and bacteria continues. The seal
may be poorly placed at surgery or it can be displaced
when, for example, a new post is being prepared for the
tooth. The possibility of extra root canals or bifid root
apices may be missed and hence not sealed.
Inadequate support may cause undue movement of
the tooth and may cause reinfection. This may result
Fig. 29.7 The root of a tooth supporting a post crown
showing a vertical split.
from an existing periodontal lesion, undue forces acting
on the tooth or overzealous removal of the root apex.
A vertical split in the tooth may be the result of
excessive forces acting on a large post (Fig. 29.7). A
vertical fracture may be suggested if the post has had to
be recemented on several occasions and the radiolucency
evident on the radiograph may correspond with the post
rather than the apex of the tooth. If a vertical fracture is
diagnosed, the tooth must be extracted.
Post perforations
Fig. 29.6 Suturing of an L-shaped apicectomy flap.
Suture between 23 is interrupted and tied over the contact
point. The suture between 12, having no contact point
interdentally, is a vertically arranged mattress suture.
The risk of post perforation during preparation of the root
canal for the posts can be minimised by ensuring the
preparation is carried out without local anaesthetic. If an
inadvertent perforation occurs, the patient will feel pain
and bleeding may be evident from the canal. In addition,
root-filling material should be removed carefully using
hand-driven non-dentine cutting instruments. Finally,
good quality radiographs should always be available.
241
Perforations which do occur should be gently
irrigated, dried and the correct alignment re-established.
The false channel should normally be sealed on filling
the canal.
Diagnosis
This may be obvious if the post has perforated mesially
or distally, when the rarefaction can readily be seen on
periapical radiograph (Fig. 29.3). If the perforation has
been labial or palatal (or lingual) then the use of a
'profile' (i.e. lateral) periapical radiographic view may be
useful. The site of the radiolucency can be a valuable
clue, as it will generally appear on the lateral side of the
root at the level of the top of the post. This appearance
can also be seen where there is a vertical split.
Management
To curette the abscess and seal the perforation from the
surgical aspect will normally be unsuccessful in the long
242
term. Better results demand removal of the post and
thorough cleansing of the false channel. Root filler
should then obliterate this channel and, as excess filler
may be extruded into the abscess cavity, curettage should
be arranged very soon afterwards. Sealing the defect can
lead to complete healing and resolution of the defect. If
the original post is otherwise satisfactory, it may be
reduced in length before recementing, or a new post
could be fitted along the correct line of the root canal.
Surgical access is achieved in the usual way, the cavity
curetted of infected tissue together with any excess root
filler. If the perforation is directly palatal or lingual,
access may be virtually impossible and the prognosis
will hence be poorer.
Some clinicians have extracted inaccessible perforated
roots, sealed the perforation outside the mouth and
reimplanted it with appropriate splinting. This is clearly
'last chance' treatment but can be remarkably successful,
at least in the short term.
35
Preprosthetic surgery
Introduction
In the normal course of events, the extraction of teeth
will be the final surgical procedure undertaken before the
provision of a prosthesis, whether this is a full or partial
removable appliance or a fixed system. The presence of
'hidden' pathology in the form of unerupted teeth or
roots, or residual infections or cysts, should also be
ascertained and dealt with appropriately before prosthodontic work is undertaken, as this may well avoid
embarrassing complications at a later date, which might
compromise the prosthesis. However, certain situations often anatomical rather than pathological - will benefit
from minor surgical modifications, which can greatly
improve the provision of a more stable and comfortable
prosthesis. Additionally, dental implants have opened up
new horizons for increased stability and hence patient
acceptability of both fixed and removable crowns, bridges
and dentures, and this topic will be discussed in more
depth in Chapter 38.
Preprosthetic surgery can conveniently be divided
into three subtopics: extraction of teeth; soft tissue
surgery and bone surgery (Table 30.1), and these will be
discussed in turn.
Extraction of teeth
Standing teeth
Standing teeth should be extracted with an awareness
that preservation of the bony socket and attached gingiva
will materially promote healing by preserving the
maximum amount of tissue on or within which future
replacement of the lost unit(s) will be based. Good
technique ensures that soft-tissue damage by forceps is
minima], as does firm digital support of the alveolus
during extraction. Compression of expanded buccal plate
Table 30.1
Preprosthetic surgical procedures
Extraction of teeth
standing teeth
unerupted teeth
Soft tissue surgery
fraenal attachments
vestibular denture-induced hyperplasia
palatal hyperplasia
leaf fibroma
fibrous tuberosities
flabby ridges
Bone surgery
alveolectomy or alveolotomy
bony exostoses and bone undercuts
sharp bony ridges
torus palatinus
torus mandibularis
sharp mylohyoid ridge
genial tubercles
ridge augmentation and vestibuloplasty
and judicious use of sutures over the socket margins, or
where minor soft tissue tears have occurred, can also
benefit the healing process.
It is clearly beneficial that teeth are extracted without
root fracture, but this may be unavoidable. Surgical
removal of any such roots requires awareness by the
operator that the ridge form can be influenced by the
technique employed to remove the fragment. It is unwise
to persist in attempting to elevate a root through the
socket if this causes damage to the soft tissue margins or
destroys bone in an uncontrolled fashion. A mucoperiosteal
flap can often not only preserve soft tissue health but also
reveal the underlying root in such a way as to minimise
bone loss. In some cases, bone may be preserved around
the coronal aspect of the socket by gaining application
points for elevators further apically, in a manner similar
to bone removal for apicectomy. This will help to
preserve the ridge height. Careful wound debridement is
essential and the flap should be sutured back anatomically to maximise ridge form. Drawing a buccal flap over
the socket on completion will effectively reduce both
ridge height and also the stronger attached gingiva, which
is better able to cope with future prostheses. In some
situations, periodontal bone loss and gingival recession
may combine to leave spurs of interradicular bone lying
proud to the socket margin, and careful trimming with
bone rongeurs will allow the blood clots to cover all the
underlying bone.
Unerupted teeth
Before provision of any prosthesis, it must be ascertained
that no buried teeth that could compromise longer-term
success are present. The most commonly found are
wisdom teeth, upper canines and lower premolars, and an
orthopantomogram is an ideal radiograph to reveal such
potential problems. A judgement is needed as to whether
it is likely that an unerupted tooth could, within the
lifetime of either the patient or the proposed prosthesis,
cause a problem that would prejudice the appliance. This
assessment may be relatively easily made where there is
related pathology such as dentigerous cyst formation
around the crown or evidence of communication, however minimal, with the surface. In many cases, however,
it may well be in the patient's best interests to leave such
a tooth, especially where its depth makes it improbable even with resorption over many years - that it will ever
interfere with a prosthesis. Further, its surgical removal
might risk damage to nerves or involve a considerable
amount of bone removal resulting in a poorer ridge form.
If removal is deemed necessary, planned removal of bone
in which sectioning of the tooth may well reduce this
need can better preserve the ridge contour and height.
So-called osteoplastic flaps can, in a limited number of
situations, help to preserve bone. This technique usually
involves hinging the buccal plate (with its periosteum
intact) from the underlying tooth to gain surgical access,
and then suturing the intact plate of bone, still with its
blood supply through the periosteum, back to its
anatomical site.
Soft-tissue surgery
244
Several soft-tissue impediments to provision of a good,
stable prosthesis can be rectified surgically and are
relatively minor surgical procedures.
Fraenal attachments
These anatomical fraenal bands are composed not of
muscle but of fibrous tissue. They may form an attachment on the ridge, which is near the crest, and cause
instability to removable appliances when adjacent
muscles are in function and they become tense.
Surgically, they may be excised (see Ch. 31) or their
attachment to the ridge may be incised close to the
alveolar ridge and a surgical pack sutured over to prevent
reattachment. Alternatively, if the patient has an existing
prosthesis, this may be lined with gutta percha or a zinc
oxide-based periodontal pack to hold the incised fraenum
away from the ridge during the healing phase.
Vestibular denture-induced hyperplasia
Several forms of denture-related hyperplastic soft-tissue
lesions are recognised but they all arise as a result of loss
of denture fit and are therefore more often seen in the
'old denture' wearer, who is often the satisfied denture
wearer.
Aetiology and clinical appearance
The most common form is the result of alveolar resorption
over a considerable number of years. This causes the
periphery of the flange of the denture to impinge on the
sulcus depth or adjacent lip or cheek tissue. As this is a
very gradual process, the tissues have time to react to the
irritation by a protective hyperplastic reaction. This
results in a characteristic sausage-shaped roll of excess
tissue, which can lie in function either on the outer aspect
of the flange or between the flange and the alveolar ridge
where there is a space (Fig. 30.1). This can result, on
occasion, in two parallel rolls of tissue lying across the
sulcus region, and sometimes - when progressive loss of
fit causes trauma further into the lip or cheek - in several
flaps of redundant tissue. Hyperplasia of this kind can
occur anywhere along the periphery of a denture, and
even along the line of the post-dam, but it is most
common in the lower labial anterior sulcus, reflecting the
more extensive resorption of alveolar bone in this region.
A less common but distinctive group of patients with
this problem are the immediate denture wearers, whose
dentures have not been adjusted appropriately for the
more rapid loss of fit that is caused by initial resorption.
These patients often complain of pain - in marked
contrast to the 'old denture' wearer - because the tissues,
often oedematous and elimination of further trauma
produces a dramatic resolution.
In both cases, provision of new dentures is the ultimate aim.
Palatal hyperplasia
Aetiology and clinical appearance
Fig. 30.1
Denture-induced hyperplasia of the lower labial
sulcus in a patient with a loose-fitting denture.
having had less time to react to the loss of fit, ulcerate in
addition to forming a hyperplastic protective overgrowth.
Management
In the established denture wearer, the roll of tissue is
usually composed of very mature connective tissue,
which, even if the flange is trimmed back, will not shrink
appreciably and resolve. However, trimming of the flange
should always be carried out at the time of presentation,
with or without the use of a tissue-conditioning lining to
maximise the retention of the prosthesis. Surgical trimming of the excess tissue is almost always needed and
this is usually done under local anaesthesia. The surgeon
can manipulate the roll of tissue better by passing a
suture through the lesion, allowing accurate incision
along its margins. When the incision on the outer and
inner aspects of the role of tissue is completed, its base
can often be simply lifted and separated using a scalpel.
It is undesirable to cut down to deeper tissues, as this can
cause excessive scarring on healing thus reducing sulcus
depth. When the base of the wound extends into lip or
cheek, superficial 'tack' sutures can be used after careful
undermining of the margins, but in some cases the base
is left open and covered by a surgical pack, or the
previously trimmed old denture lined over the wound
with gutta percha or a zinc oxide-based periodontal pack.
In the more 'acute' immediate denture hyperplasia,
denture adjustments with appropriate soft lining can often
obviate the need for surgery, because the hyperplasia is
This reactive condition results from movement and loss
of even contact of the upper denture base on the palatal
epithelium and underlying connective tissues. The
clinical appearance can vary between a multitude of
small papillary projections, to an appearance of cobblestones, to areas of surface hyperplasia with slit-like clefts
between the 'blocks' of hyperplastic mucosa. This latter
form is more commonly seen under partial dentures. This
clinical appearance represents a hyperplastic type of
denture stomatitis (Newton's classification Type III) and
is infected with Candida. The tissues may be significantly
red 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 toothbrush
night and morning
• the use of systemic antifungals, such as fluconazole.
The dentures should be lined with tissue conditioner for
daytime use.
Total resolution by such means is unusual and
removal of the hyperplastic tissue either with diathermy
loop or laser may be needed. The resultant raw surface
created by surgery is best covered with the denture lined
with a zinc oxide-based periodontal pack.
Leaf fibroma
Aetiology and clinical appearance
This lesion is not, as its name implies, a true neoplasm
but is again the result of chronic frictional irritation of the
palatal soft tissues by movement or irregularity of the
245
palatal coverage of an upper denture. Were it not covered
by the denture, it would grow evenly as a rounded
exophytic non-ulcerated swelling but, because of its
position, it is flattened into a leaf shape by the denture. It
is a perdunculated lesion, which means that it has a stalklike attachment, and on occasion can be of considerable
size, having lain unseen in the vault of the hard palate
(Fig. 30.2). Gentle probing can often cause it to lose its
adhesion to the true vault and it then hangs from its
narrow 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 of
the upper molar regions are usually bilateral, although
often asymmetrical. They may be so bulky that they
contact the lower alveolar process in edentulous patients
and hence prevent provision of adequate dentures.
Grossly enlarged tuberosities may be due to bony
overgrowth rather than fibrous tissue and it is important
to ensure by clinical examination and radiographs which
tissue is present in excessive quantity. Fibrous overgrowth may often be moveable on palpation, unlike bony
overgrowth, but if doubt exists as to the extent of the soft
tissue component, a sharp probe can be used for assessment after appropriate local anaesthesia has been given.
Fig. 30.2 Leaf fibroma: (a) lying against hard palate;
(b) demonstrating pedunculated attachment.
Management
Surgical reduction can be undertaken in which a wedge
of soft tissue is excised through an elliptical surface
incision (Fig. 30.3).
After removal of this wedge of tissue, the margins
require to be undermined by further cuts and 'filleting' on
either side of the original excision to allow the edges to
be approximated and sutured without undue tension.
'Flabby' ridges
Aetiology and clinical appearance
246
Flabby ridges are the result of fibrous replacement of the
bony ridge. This is most commonly seen in the upper
anterior segment where a full upper denture is opposed
by natural lower teeth but with free end saddles not
compensated with a partial lower denture. The resultant
tipping action induced by the protrusive chewing action
results in bony resorption and fibrous replacement of the
ridge. The ridge becomes excessively mobile reflecting
the lack of underlying hard tissue.
Management
Surgery is seldom indicated, as most prosthodontists
would prefer more rather than less of this tissue given
that 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-section
showing undermining of the wedge to allow suturing without tension from 'A' to 'B'.
can be 'tightened' by a wedge excision similar to the
fibrous tuberosity reduction.
Bone surgery
Alveolectomy or alveolotomy
Aetiology and clinical appearance
The indications for these procedures are rare but may be
of value where excessive anterior projection of the ridge
in the upper premaxillary area might pose problems for
future denture aesthetics or stability. Class II, division I
maloclusions are therefore most likely to benefit from
such surgery.
Management
Alveolectomy involves reduction in both the height and
width of the ridge and is mainly accomplished by
reduction of the labial plate. The mucoperiosteum is best
raised with a 'U'-shaped incision to allow access. Bone
rongeurs or larger 'acrylic' burs can be used to reduce the
labial plate prominence and, on occasion, also the interdental septae. The bony margin is then smoothed with a
file and the wound closed with sutures.
Transeptal or interseptal alveolotomy reduces the
labial prominence but maintains the height of the ridge.
Following extraction of the incisors and canines, the
interdental septum is removed between each socket and
the labial plate is then fractured inwards with firm digital
pressure. A vertical cut may be needed over the canine
prominence labially to facilitate this fracture. The labial
plate will still be attached to its overlying periosteum and
should therefore remain viable.
These operations may be facilitated by cooperation
with the prosthodontist, who can provide the surgeon
with a template of acrylic that is made on the cast
trimmed to the desired contour. Unless the patient desires
an aesthetic change, these procedures are becoming less
frequent.
Bony exostoses and bone undercuts
Aetiology and clinical appearance
Surgery is indicated where the bony morphology, either
through localised excessive growth or as a result of
unusual resorption of the ridge, gives rise to impediments
to denture construction.
Management
A simple mucoperiostial flap is taken, the bone impediment is reduced with rongeurs or burs, and the flap is
closed with sutures.
Sharp bony ridges
Aetiology and clinical appearance
These are usually found in the lower anterior region
where resorption of bone has produced a pointed, often
razor-sharp, bony ridge, described as a knife-edge or
feather-edge ridge.
247
Management
The incision to gain surgical access is often best made on
the buccal aspect of the crest of what is often a very thin
line of attached gingiva forming the soft tissue crest of
ridge. This allows the underlying bone to be smoothed
but prevents undue disruption to the stability of the overlying 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 normal
bone but its presence may make palatal coverage with a
denture impossible or, if a denture is made over, it can
cause fracture of the denture. In some dentate patients,
repeated trauma caused by the swallowing action on its
posterior aspect may result in ulceration of the overlying
soft tissues and this would merit surgical reduction.
with one anteroposterior fissure bur cut and crossed by
several lateral cuts. This conveniently divides the mass
into smaller blocks, which can be chiselled free. A final
smoothing with a round 'acrylic' bur precedes wound
closure. Some soft tissue reduction of the margins may
be needed, as there will be excess soft tissue. Suturing
may be difficult and the prior construction of a plate to
cover and hold the flap is very helpful, as this will reduce
the chance of a painful palatal haematoma and will help
the patient to eat in the first few days after the operation.
Large palatal tori are better removed under general
anaesthesia or at least under local anaesthesia with
sedation.
Torus mandibularis
Aetiology and clinical appearance
Mandibular tori present on the lingual aspect of the
alveolar process in the premolar region (Fig. 30.6). Often
bilateral, they may or may not be symmetrical and the
excess bone may be a single dome-shaped mass or several
Management
A preoperative impression allows construction of a
palatal splint in dentate patients or the existing denture, if
available, can be used as a postoperative covering. An
incision is made anteroposteriorly along the midline of
the torus and relieving 'Y'-shaped incisions are made at
the anterior and posterior extensions (Fig. 30.5). The
overlying mucoperiosteum should be reflected with care
as it is often very thin. The bony mass is then divided
248
Fig. 30.4
A torus palatinus.
Fig. 30.5
torus.
Incision to allow surgical trimming of a palatal
Fig. 30.6
Bilateral torus mandibularis.
protuberances. Surgical reduction is only indicated if
they impede denture design.
increase postoperative swelling and haematoma formation
is more likely. Patients require to be warned preoperatively of this possibility.
Management
In the edentulous patient, a straight incision over the crest
of the ridge with no relieving incision is needed. This
allows the raising of the mucoperiosteum from the torus.
The excess bone can then be trimmed using a combination of a narrow fissure bur with a chisel or simply
with a flame-shaped acrylic smoothing bur. Flap retraction
should be combined with protection of floor of mouth
and underlying soft tissue. The flap is then sutured back
with no need for trimming.
In dentate patients, the procedure is essentially the
same but surgical access caused by the presence of teeth
in the area can make for difficult surgical access.
Sharp mylohyoid ridge
Aetiology and clinical appearance
With continued alveolar resorption in the lower molar
region, most of the alveolar process may eventually be
lost, with the denture base then being constructed over
more basal bone. On the lingual aspect of the molar
region, the mylohyoid ridge of bone can be covered by
the lingual flange of a denture, which may cause discomfort and even overlying soft tissue ulceration due to
its sharp upper surface.
Management
If the denture cannot be relieved adequately to reduce
pressure 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 premolar
region, allows a lingual flap to be raised to expose the
sharp upper aspect of the ridge. Often, minimal smoothing using a bur, or even a hand file, without stripping the
muscle off the affected area is successful and can be
judged by running a finger over the ridge. If muscle
stripping is thought necessary, this will undoubtedly
Genial tubercles
Aetiology and clinical appearance
Gross alveolar resorption following extractions can cause
the upper tubercles to be traumatised by the lingual flange
of a lower denture in the midline. Recurrent ulceration,
hyperplastic tissue formation or simply discomfort may
be the stimulus to surgery.
Management
An incision along the midline of the crest of the alveolar
ridge allows a lingual flap to be raised to expose the bony
tubercle. Simple smoothing with a bur is normally
sufficient, and stripping of the genioglossus should be
unnecessary because it is important to maintain the
function of this muscle.
Ridge augmentation and vestibuloplasty
These minor surgical procedures can be of great benefit
to the patient. It will be apparent that many problems
arise as a result of alveolar resorption and surgeons have
in the past devised many surgical procedures to make
good this loss of ridge, either by augmenting the ridge or
by deepening the sulcus (vestibuloplasty). Augmentation
using bone, hydroxyapatite or allelograft material
often failed due to infection or the inability of the soft
tissues to accommodate the increased ridge bulk.
Vestibuloplasties were probably more successful in that
they increased sulcus depth rather than trying to increase
the resorbed bony ridge. In recent years, however, such
operations have largely been superseded by the use of
dental implants. The success rate with implants is high
and involves relatively minor surgical operative procedures. This rapidly growing field will be discussed in
Chapter 37.
249
31
Orthodontics and oral surgery
Introduction
When jaw relationships such as severe skeletal base
abnormalities result in a malocclusion that is beyond the
scope of orthodontic treatment, orthognathic surgery or
distraction osteogenesis should be considered to effect
correction. These are described in Chapter 13.
Dentoalveolar surgery may be required, often in
conjunction with orthodontic treatment, to deal with
specific localised problems of eruption or crowding.
Where several options exist, the risks of surgery, and
perhaps general anaesthesia, must be weighed against the
benefits of a successful outcome. It is for the surgeon and
orthodontist together to explain the options and advise
when a surgical approach is in the best interest of the
patient.
The most common orthodontic problems with surgical
treatment options are crowding, failed eruption, spacing
and ankylosis. The orthodontist may have several treatment options so it is important for the surgeon to have a
good appreciation of the orthodontic problem. A good
history is essential. Clinical and radiographic examination
reveal the nature of the malocclusion or orthodontic
problem and the state of oral and dental health. Discussion
of the surgical aspects with the patient and parents reveals
their attitude to treatment, and helps to finalise the 'treatment plan.
Some causes of the orthodontic problems alluded to
above are listed in Table 31.1.
Treatment options
A number of surgical treatments exist for orthodontic
problems and these should be considered as part of the
treatment-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 impaction
teeth relatively large for arch size
early loss of deciduous teeth allowing mesial drift
supernumerary and supplemental teeth
odontomes
Failed eruption
crowding or early loss of deciduous teeth
retained deciduous teeth
congenital absence
supernumerary teeth/odontomes
fibrous tissue (scar) due to previous trauma, surgery
or infection
ectopic development or dilaceration due to trauma
cysts and other pathology
cleft palate
cleidocranial dysostosis
Down syndrome or hypothyroidism
gingival hyperplasia or fibromatosis
Spacing
tooth size/arch size disproportion
small teeth
prominent fleshy frenum
proclined incisors
partial anodontia
Ankylosis
trauma
infection
Non-surgical extractions
Extractions are the most common requirement for relief
of crowding. There may be an indication for general
anaesthesia in very young or nervous children, and those
with learning difficulties. Local anaesthesia, with or
without sedation, should be used wherever possible,
bearing in mind that in most cases orthodontic treatment
is elective. In some cases, it is better to delay treatment
until the patient is more cooperative. On the other hand,
correct timing of extractions can be a significant
advantage, often removing the need for later orthodontic
appliance treatment. For example, timely removal of
carious or heavily restored or hypoplastic first permanent
molars may not only relieve crowding but also removes
teeth of doubtful long-term prognosis.
Surgical removal of teeth
Surgical removal may be indicated when a tooth is
unerupted. There is no need to remove a buried tooth
unless there is a positive indication such as interference
with the orthodontic movement of other teeth, or associated pathology such as cyst formation, or resorption of
an adjacent tooth.
Surgical exposure of teeth
Surgical exposure is used to encourage eruption or to
allow access for orthodontic traction. It involves removal
of overlying soft tissue, bone and scar tissue. It is
important to use a technique that will result in good
gingival contour and minimise postoperative scarring.
Adequate exposure is important otherwise the tissues
will cover the tooth again. Orthodontic traction using a
gold chain bonded to the exposed tooth can also be used.
Fraenectomy
Fraenectomy may be requested when there is a
diastema or a localised periodontal problem. Upper labial
fraenectomy or lingual fraenectomy are the most common
of these procedures. A prominent fraenal attachment can
cause a diastema, which is most common where there is
a thick, fibrous, upper labial fraenum. When this is present,
blanching of the palatal gingiva when the lip is pulled up
to create tension confirms the need for fraenectomy, as
does the presence of 'V notching interincisally on a
maxillary anterior occlusal radiograph. A radiograph
should always be taken to exclude a midline supernumerary tooth or any other pathology. A tight lingual
fraenum can pull on the gingival margin and cause a
pocket or contour defect together with tongue restriction.
Tooth transplantation
Tooth transplantation can be considered when orthodontic movement cannot achieve the desired result, or
sometimes to expedite the outcome in impacted canine
cases. There are, however, inherent problems in the transplantation of teeth.
A transplanted tooth must not be left in traumatic
occlusion or it will quickly fail. Unfortunately, transplants have a high failure rate. After a promising start
many develop internal and external resorption after about
4 years. This often progresses to abscess formation
despite root canal therapy. Root treatment soon after
transplantation is advocated by some but the failure rate
is still high. Alveolar bone is removed when the socket is
created and abscess formation can cause further damage.
The resulting depression in the alveolus causes a cosmetic
problem with a subsequent denture or bridge, and leaves
insufficient bone for an osseointegrated implant. For the
above reasons, transplantation is now rarely the best
option. It is often better to temporise and consider an
adhesive bridge or implant later. Autotransplanation,
where a tooth is extracted from one site, such as a lower
premolar, and inserted into the upper central region after
traumatic loss, has a good success rate, however, and
should be considered.
Surgical management of
specific orthodontic
problems
The aforementioned treatment options can be applied
to several teeth with orthodontic problems related to
crowding and impaction. The problems of spacing and
ankylosis will also be discussed followed by a consideration of the individual surgical procedures.
Incisors
Maxillary central incisors may be impacted. There may
be 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 tooth
germs. The tooth may subsequently develop in an ectopic
position and the crown or root may be deformed. Also,
trauma to the alveolar mucosa or bone may result in scar
tissue, which later prevents eruption. Supernumerary teeth
and odontomes are another common obstacle to eruption.
Scar tissue formed following their surgical removal may
also result in eruption problems. Further space can be
lost by drifting of adjacent teeth if eruption is delayed.
251
Occasionally there are systemic factors such as
cleidocranial dysostosis, Down syndrome or chemotherapy to cause a delay in eruption. Also, gingival overgrowth due to hereditary fibromatosis, or secondary to
drugs such as phenytoin or cyclosporin may inhibit
eruption.
Scar tissue or a supernumerary tooth frequently holds
the incisor in a fairly normal pre-eruptive position, but
following intrusion trauma it is more often displaced
upwards and forwards and lies horizontally under the
anterior nasal spine. Very occasionally there is a palatal
inclination. It is important to realise that a tooth will only
erupt through attached mucosa. If gingival mucosa has
been lost through previous trauma or the tooth is
attempting to erupt under the unattached sulcus mucosa,
surgical exposure will be required.
The choice of treatment depends on the position of the
tooth, the space available and patient cooperation. If the
patient is unlikely to accept appliance therapy, or if oral
hygiene is poor, it may be better to accept the space and
construct a partial denture. Alternatively, the space could
be allowed to close as far as possible and the defect
disguised by building up, by restorative means, adjacent
teeth. The tooth can be left in situ unless there is any
associated pathology, but surgical removal is often
indicated.
Ideally, the incisor should be aligned unless radiographs suggest that the tooth is hypoplastic, markedly
dilacerated or in an unfavourable position. Surgical
exposure is performed to encourage eruption and create
orthodontic access. This would normally be by a labial
flap, either apically repositioned, or replaced after attachment of a gold chain.
Removal of supernumerary teeth normally requires a
palatal flap as they are almost always palatally situated
relative to the permanent incisors.
Canines
252
Impacted maxillary canines have a prevalence of about
1.7% in Caucasians. Ideally, they should be detected
before the teenage years, as timely interception can reduce
the severity of the problem. Canines can be palpated in
the labial sulcus at around 10 years of age. Eruption is
expected at about 12 years of age in girls and 13 years
of age in boys. Any deviation from this normal pattern
warrants investigation. Extraction of the deciduous canine
can encourage the successor to resume a normal path of
eruption in more than 60% of cases depending on several
factors such as canine height, inclination, mesiodistal
position and crowding.
Unfortunately, resorption of the roots of adjacent
permanent incisors can occur and it is claimed that the
incidence may be as high as 12% for incisors adjacent to
ectopic canines. It would not be practical or defendable
to remove every buried canine for this reason and the best
advice is to be vigilant. Root resorption, if it is going to
happen, generally occurs at 10 or 11 years of age and it
is rare for this complication to occur after 14 years of
age, unless there is a general delay in dental development.
The management of the unerupted upper canine can
be in one of four ways.
No surgery
The most common option is to leave the buried canine
alone. The first premolar can be disguised by reducing
the palatal cusp or by its orthodontic alignment provided
this is not obstructed by the unerupted canine. The
deciduous canine may be kept and often lasts for many
years where alignment of the permanent tooth is not
feasible. Later, an adhesive bridge or implant can be
considered, although overeruption of an opposing tooth
can cause difficulty.
Surgical exposure
Surgical exposure may be requested where space is
readily available or where it is decided this will provide
the optimum aesthetic result. The position of the tooth
must be ascertained by clinical examination and radiography. The tooth may be palpable on the buccal or
palatal aspect and the position and inclination of adjacent
teeth often gives guidance. For example, the lateral
incisor may show undue prominence of its root outline
on the labial aspect and be almost retroclined due to the
palatal presence of the canine crown exerting pressure on
it. A panoramic film is most useful but other radiographs
such as periapical or occlusal views may be required for
localisation. It can be difficult to know whether the canine
is inclined buccally, palatally or lies in the line of the
arch. Parallax methods may help localisation but clinical
assessment is often more reliable. Approximately threequarters of impacted canines lie with crowns palatal to
the arch line.
The principle of parallax is that the image of two
parallel objects will alter with differing angulations of
radiographic views. If, on comparing the image of the
unerupted canine relative to the lateral incisor on a
panoral film with its position on an oblique occlusal film,
the canine appears to move upwards, then it is palatal to
the lateral incisor. Put more simply, if the buried tooth
moves with the position of the tube (i.e. the source of the
X-rays), then it is palatal. The depth and inclination are
relevant not only to the difficulty of surgery but also to
the prospect of successful orthodontic alignment in
reasonable time. Availability of space and overeruption of
opposing teeth must also be considered.
Surgical removal
Surgical removal is required when the buried canine is
not suitable for alignment and there is an indication, such
as interference with proposed orthodontic treatment, or
associated pathology, such as dentigerous cyst formation
or resorption of the roots of the incisors. Often, a first or
second premolar would need to be extracted to make
space for alignment of the canine and the patient may
prefer to avoid more prolonged appliance therapy by
accepting space closure. As with exposure, the position
of the tooth must be assessed by clinical and radiographic
examination. Difficulties such as dilaceration of the root
and proximity of adjacent teeth must be assessed.
Reimplantation
Reimplantation of canines is another option. If space is
available or can be created and the impacted canine can
be removed intact and with minimal trauma, it may be
reimplanted into a surgically prepared socket. The
transplanted tooth may need to be stabilised with a
cemented splint or an orthodontic bracket. This technique
is usually successful in the short term, although it is often
difficult to place the canine in the optimum position
unless additional space to that previously occupied by the
deciduous canine is obtained preoperatively by orthodontic means. Commonly, the lower canine has overerupted and this can also lead to difficulty in positioning
free of occlusal contact. As described previously, the
failure rate is high and transplantation is seldom the
preferred option.
Premolars
In the maxilla the second premolar is occasionally
excluded from the arch due to crowding. It is usually
found in the palate, where it may remain harmlessly or
eventually erupt. The tooth can be left unless it interferes
with orthodontic treatment or if it erupts and becomes
a threat to periodontal health by encouraging food
trapping.
In the mandible, premolars may be impacted due to
crowding and can be buccal, lingual or in the line of the
arch. The second premolar is usually lingually inclined,
in which case it can be left in situ or removed if there is
a good indication. Surgery on the lingual aspect of the
mandible can be awkward because of difficulty of access
and of reflection of the delicate lingual mucosa. Generally,
therefore, a lingually inclined premolar is removed via a
buccal approach.
If lower first permanent molars have been lost early,
the adjacent premolars have a tendency to drift backwards
and may even become horizontally impacted against the
root of the second molar. Surgical exposure and orthodontic alignment may be appropriate in a well-motivated
patient.
First and second permanent molars
If one or more carious first permanent molars require
extraction it is often beneficial to carry out balancing
extractions. Ideally this should be done in children
around the age of nine years.
Removal of second permanent molars at an
appropriate time during development is still accepted as
a method of encouraging wisdom teeth to erupt into a
functional position but this is not always successful
especially where there is severe crowding. Removal of
second molars in late adolescence to allow eruption of
wisdom teeth is not wise, as the eruption of third molars
is unreliable and these teeth may be of poor quality.
Third molars
Imbrication of lower incisors often occurs around
20 years of age but prophylactic removal of third molars
is no longer regarded as effective in preventing lower
anterior crowding. There are only rare occasions when
wisdom teeth should be removed for orthodontic reasons.
Possible indications are proposed distal movement of
second molars or orthognathic surgery involving the
mandibular ramus.
Guidelines advise that the risks of damage to inferior
alveolar or lingual nerve, as well as the trauma of
surgery, should be undertaken only when there are valid
indications. In our present state of knowledge it is not
253
possible to predict the behaviour of lower third molars. If
it were possible to predict which ones would need
removal, this could be done much more easily during the
teenage years, before their roots are fully formed and
difficult impactions have developed.
Removal of lower third molar tooth germs at around
12 years of age, before calcification of enamel and dentine,
used to be fairly common practice. This procedure, known
as lateral trepanation, was fairly simple but a general
anaesthetic was required. There is no evidence that this
operation was worthwhile. Extraction of third molars is
considered further in Chapter 27.
Spacing
Spacing is normal in the deciduous dentition and as the
jaws increase in size to accommodate the permanent
teeth. Spacing of permanent teeth may be due to small
teeth or partial anodontia. There are usually restorative
treatment options but implants may also be indicated.
Ankylosis and submerged deciduous teeth
254
Although most commonly seen in the upper incisors,
ankylosis of other teeth also occurs. The causes are
trauma and infection.
Upper incisors are frequently traumatised and
ankylosis is especially common after reimplantation. An
ankylosed tooth does not move as jaw growth progresses,
so that, if reimplantation occurred at an early age, the
reimplanted tooth is significantly palatally and apically
displaced by adulthood. The tooth can function normally
for many years, but frequently internal and external
resorption results in abscess formation or complete loss
of the root. An implant should be considered if no simple
restorative option is available.
Submerged deciduous molars are also a result of
ankylosis. Some children have submerged teeth in several
areas, the cause of which is often unknown. It has been
suggested that there is a lack of growth potential in these
areas. The ankylosed tooth remains static while alveolar
bone growth continues, so that it may become completely
buried. The adjacent permanent teeth erupt and often
the submerged tooth becomes impacted between them.
The submerging tooth is prone to caries and eruption of
the permanent successor is prevented. Removal becomes
more difficult as they become more deeply embedded so
it is better to extract them early.
Failure of a permanent molar to erupt may be due to
ankylosis. The cause is again unknown but trauma to the
Table 31.2
Orthodontic surgical procedures
Upper labial fraenectomy
Removal of supernumerary teeth
Exposure of incisors
Exposure of palatal canines
Exposure of buccal canines
Removal of impacted premolars
area by a mouth gag during dental extraction or other
surgical procedures under general anaesthesia is a
possibility, as is primary failure of eruption. Surgical
exposure is sometimes successful if there is soft tissue
obstruction or a small odontome preventing eruption, but
results are poor if there is true ankylosis or long delay
after normal eruption time. These teeth are often partially
erupted and develop caries and surgical removal is then
indicated. Cyst formation can also occur.
Several of the surgical procedures discussed above are
described in other chapters. Some, however, are specifically used only as an adjunct to orthodontic treatment
(Table 31.2) and these are described below.
Surgical procedures
Upper labial fraenectomy
When the lip is pulled upwards, a fibrous band between
the inner surface of the upper lip and the crest of the
maxillary alveolar ridge can be palpated just underneath
the mucosa. An incision is made around the fibrous band
and the fraenal attachment on the ridge. The incision is
superficial on the lip and fraenum but extends down to
bone between the central incisors. The fraenum is
grasped with forceps and detached by sharp dissection
from the lip. The fibres entering the bone are detached
with a small excavator or curette. Some operators mill
the crestal bone surface with a bur.
When the fraenum has been removed, further dissection is required to recontour the sulcus. A Z-plasty can
be performed but this can cause excessive swelling. It is
simpler and kinder to hitch the midline of the incision to
the periosteum overlying the anterior nasal spine with a
resorbable suture. The fatty tissue on the anterior aspect
of the alveolus is mobilised by inserting scissors superficial to the periosteum and opening the blades. This
allows the bulky tissue to be displaced laterally so that a
good 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 the
incisors and this will also cover the adjacent small defect
in the alveolar mucosa, but this is often unnecessary.
Removal of supernumerary teeth
Supernumerary teeth may occur anywhere in the
maxillary or mandibular alveolus but it is most common
to find one or two in the midline of the anterior maxilla.
They are almost always on the palatal aspect. A parallax
view should confirm the position, but occasionally a
lateral radiograph of the anterior maxilla is helpful.
It is better to wait until there is some root formation
in the permanent centrals before surgery than to risk
damage to the tooth germ. Bear in mind that many supernumeraries erupt and a surgical approach is then avoided.
There is no need to remove those that have no associated
pathology and are not in the way of orthodontic tooth
movement.
The normal surgical approach is by a palatal flap
using a gingival margin incision. The incisive vessels and
nerve can usually be preserved. Larger supernumeraries
are usually easy to find due to altered bone contour.
Small ones can be very difficult to find, especially if the
follicle is small or the enamel is hypoplastic. It is a mistake to look too high because the root of an inverted
supernumerary is often found between the roots of the
centrals, near the amelocemental junction. Bone overlying 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 decision
should be made on whether surgical exposure is
indicated. It may well be opportune to avoid a further
anaesthetic but many orthodontists prefer to wait for
eruption, as the gingival contour may be uneven following surgical exposure. Healing after removal of a large
supernumerary often produces a barrier of scar tissue,
however, and patients may require surgery if the incisor
fails to erupt.
A labial flap with parallel sides is taken. The
horizontal arm of the incision must include attached
mucosa, as this will be used to form the gingival margin
when the flap is repositioned. The flap is carefully
dissected 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 palatal
mucosa and follicle to ensure that the incisal edge
remains exposed. The flap is then repositioned apically
and sutured in position. It is important to place the flap
high enough to ensure that the tissues do not heal over
the tooth. In this situation, the flap can be inverted so that
the attached mucosal edge of the flap is brought close to
the amelocemental junction of the incisor. A resorbable
mattress suture placed high in the vertical incision will
usually stabilise the flap. The flap will have less tendency
to slide back over the crown if this suture enters and exits
on the mucosal surface, as this helps to invert the margin.
When the above technique is not feasible a gold chain
may be attached. There are alternatives, such as brackets
or wire loops, but these are less effective. Gold chain is
used only because stainless steel chain is not readily
available. A small circle of stainless steel mesh is welded
to one end of the chain to facilitate bonding to the enamel.
Corrosion between gold and stainless steel can result in
detachment of the chain and so it is better to add a ligature
of fine wire around the weld.
Attachment of the chain is easy if the enamel surface
is isolated. A section of a surgical rubber glove makes a
convenient sterile 'rubber dam'. The enamel is etched in
the normal way and the surface is irrigated with sterile
water and dried using the surgical suction. The mesh is
attached to the tooth using a light-cured orthodontic
bonding agent. After testing the bond with a gentle tug,
the flap is replaced with the chain emerging in the proposed path of eruption (usually at the crest of the ridge).
With normal healing, orthodontic traction can begin
after a couple of weeks. If there is a long delay, scar
tissue forms around the chain and makes alignment more
difficult. Patients should be warned that traction might
take many months.
Exposure of incisors
Upper permanent centrals are usually on the labial aspect
of the alveolus. The object of surgery is to leave a portion
of the crown exposed to allow natural eruption or orthodontic traction. Alternatively, if the tooth is high and
simple exposure is not possible, an attachment such as a
gold chain can be cemented via a surgical approach.
Exposure of palatal canines
The hard palate is covered by keratinised mucoperiosteum
so that it is not necessary to preserve and reposition a flap
to achieve a gingival margin.
If the surgeon is confident that the crown of the
unerupted tooth lies palatally, an ellipse of overlying
mucoperiosteum can be excised. The amount of further
tissue to be excised becomes clear as the operation
proceeds. Alternatively, a palatal gingival margin flap is
raised and an ellipse of tissue is excised after the tooth
has been uncovered. Overlying bone is removed with a
bur or hand chisel, taking care not to uncover root
dentine or damage adjacent teeth. The amount of soft
tissue and bone removal should be sufficient to prevent
mucosa reforming over the canine. The crown of the
tooth should be visible within a saucerised cavity.
There may be brisk haemorrhage from the palatal
aspect. Digital pressure or artery forceps will control this
during the procedure. A suture should be placed around
any identified vessel if bleeding persists at the end. A
Whitehead's varnish pack is held in place using nonresorbable sutures. The pack is left in situ for 1-2 weeks,
depending on the extent of the surgery. The orthodontist
often waits for some eruption before commencing
appliance therapy.
An alternative method is to attach a gold chain once
the tooth is uncovered and replace the palatal flap
without excising the overlying mucoperiosteum. This is
technically more challenging due to difficult access and
haemorrhage, which makes creating a dry field for attachment of the chain more problematic.
Exposure of buccal canines
It is sometimes difficult to get a good result, particularly
if the tooth is high in the buccal sulcus. Ideally, an
256
apically repositioned flap should be carried out, as for
buried incisors. Unfortunately, the only attached mucosa
may be the gingival margin of the lateral incisor, but this
cannot be used as it would leave an unsightly defect. If
there is a gap, however, sufficient mucosa may be available on the ridge.
Overlying mucosa in the sulcus may be excised and a
pack inserted, but often the tissues close over or the tooth
is tethered by unsightly scar tissue. A better option is to
take a normal flap and attach a gold chain as described
above or simply to close the flap over the surgically
exposed crown.
Removal of impacted second premolars
The impacted maxillary premolar is normally palatally
placed and may be removed by raising a palatal
mucoperiosteal gingival margin flap. Elevation is then
often sufficient to remove the tooth but occasionally bone
may need to be removed to gain adequate elevation.
Impacted lower premolars are usually lingually
inclined and, if sufficiently erupted, can be removed by
gentle elevation and forceps. Fine beaked upper forceps
are often ideal for this purpose. If a surgical approach is
needed, a buccal flap is raised and bone removed to
expose the crown buccally and several millimetres of the
root. The crown can then be sectioned and delivered
lingually and the root subsequently elevated into the
space vacated by the crown.
32
Tissue sampling and soft
tissue lesions
Introduction
Tissue sampling
A biopsy is defined as a procedure whereby tissues are
sampled from a patient for the purpose of histopathological, microbiological, or other laboratory analysis.
Results from such investigations may confirm a provisional diagnosis or establish one. They may also help
in the determination of a prognosis, which in turn is
defined as a likely outcome of the disease encountered
and is based on previous knowledge.
The word biopsy may have unwanted connotations
for many patients, who regard this procedure as a test
for malignant disease, and it may be better avoided or
explained more fully. Any abnormal tissue removed from
the mouth should undergo routine analysis, with the
possible exception of caries or periodontally infected
teeth, where selection of particular cases may at times
also be worthwhile. If a surgeon considers that removal
of soft tissue is indicated even though the nature of the
pathological process is certain, this is best confirmed with
appropriate histological examination. Various methods
may be used to sample tissue and some representative
examples will be discussed (Table 32.1). This will be
followed by consideration of individual soft tissue
lesions.
Aspiration techniques
Table 32.1
Tissue sampling techniques
Aspiration techniques
blood
pus
cysts
radiolucencies
fine-needle aspiration
Surgical biopsy
excision
incision
punch
frozen sections
Aspiration of blood, cavity fluids and solid tissue can all
provide diagnostic information, as discussed below.
Blood
A venous blood sample can yield a vast amount of
information on disease processes relevant to oral surgical
practice. Most common is the full blood count, which
indicates total numbers of red cells, white cells and
platelets. The differential count of white cells will indicate
the numbers of neutrophils, lymphocytes and eosinophils
within the white-cell population. The haemoglobin level
is also included in this analysis.
Blood serum can also be examined to determine biochemical parameters such as electrolytes, proteins and
enzyme levels, which may alter significantly in disease.
Within the globulin fraction of the serum, antibody levels
may be determined, which may reflect a patient's previous
exposure to viral or bacterial infection. Glucose levels,
if raised, may raise suspicion of diabetes mellitus and
indicate further investigation.
Aspiration from pathological lesions
The most common example of this is the aspiration of an
abscess presenting either in the soft tissues of the submandibular or submental regions, or intraorally in the
buccal sulcus or palate. The advantage of aspirating a pus
sample is that the technique avoids gross contamination
of the aspirate by other organisms, especially in the mouth
where there is a commensal population. Additionally,
by drawing the pus into the partial vacuum of a sterile
syringe, the viability of the anaerobic bacteria is protected
and they are therefore more likely to grow in the labora-
257
tory. Anaerobes are extremely common in dentoalveolar
infections and their survival from any sampling procedure is important, allowing a more accurate assessment
of the antibiotic sensitivity of the infection.
Cystic lesions are also often easily aspirated to determine both their fluid nature and contents. Keratocysts,
which contain keratin and shed epithelial squames, can
be differentiated from inflammatory or other odontogenic
cysts, which contain a proteinaceous fluid. More sophisticated assessment of the contents of keratocysts and of
other cysts involves assessment of soluble protein content
(the keratocyst has less than the dental cyst) although, in
practice, this is seldom needed (see Ch. 28).
Aspiration of radiolucent areas of the jaw may also
indicate that a presumed pathological cyst cavity is not,
in fact, cystic. If no fluid is present then the aspiration
will yield nothing, which may indicate a need for an
incision biopsy of the tissues within the cavity because
the implication is that the lesion is solid. Occasionally, in
the maxilla, air may be aspirated from a radiolucent
image. This might indicate that the maxillary air sinus
has been penetrated and incorrectly diagnosed as a pathological cavity. Very occasionally blood may be aspirated
from a lesion, which may indicate the presence of an
intrabony 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 such
as in salivary glands or the neck. Cytology is more
difficult to interpret than an incisional biopsy but it can
be a valuable guide as to the nature of a swelling.
Surgical biopsy
Two types of biopsy can be taken from abnormalities of
the soft tissues of the mouth: the excision biopsy and the
incision biopsy, using either a scalpel or a punch biopsy.
Excision biopsy
258
This procedure removes all the clinically abnormal tissue
that is evident. It is therefore normally carried out on
relatively small swellings or lumps for which the clinician
would have normally made a confident provisional diagnosis. Lesions such as papillomas, fibrous hyperplastic
overgrowths and mucocoeles are common examples of
lesions normally removed in total by this means.
Incision biopsy
A representative piece of tissue is removed from a lesion
whose total removal would not be practicable as an outpatient procedure, either because of its size or because its
nature is not known and requires to be identified
histologically to allow a correct treatment plan to be
formulated. Such lesions as widespread erythroplakia or
leukoplakia, larger swellings either arising as soft-tissue
lumps or within bone are examples of the appropriateness of this technique.
Punch biopsy
This may be a useful way of sampling a lump before
deciding on its definitive treatment. The punch is a hollow
trephine of 3-4 mm in diameter, which can remove a
small 'core' of soft tissue with minimal damage and does
not normally require suturing.
Sample disposition
Accurate orientation of the sample may be important
when sending the specimen to the histopathology laboratory, especially if the lesion is thought to be neoplastic.
Correct disposition into 10% formalin is also needed to
preserve the tissues in the best possible condition and
undue trauma during the surgery should be avoided for
the same reason. All relevant clinical information should
be included on the specimen form for the information of
the pathologist.
In widespread lesions it may be prudent to take more
than one biopsy sample, especially where there is a
clinical variation in the appearance in different areas of
the abnormal tissue. An example of this would be a white
patch but within which there are areas of redness
denoting atrophic epithelium or superficial ulceration.
At one time, it was considered necessary to provide
an incision biopsy that contained the transitional area
between clinically normal and abnormal soft tissue. This
is now considered of less importance than providing an
untraumatised, representative sample of the lesion itself.
Where there are extensive areas of soft tissue abnormality and there is therefore a choice of site for incision
biopsy, certain areas should be avoided. The orifices of
the parotid and submandibular ducts may cause fibrosis
and contraction if surgically traumatised, and this in turn
may lead to obstruction of salivary flow and resultant
swelling 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 vessels
or nerves such as in the region of the mental foramen
or the deep lingual veins on the ventral surface of the
tongue.
Almost instant histopathological assessment can be
achieved by freezing the specimen rapidly rather than
fixing it in formalin. This is known as a frozen section
and can provide information to the clinician within
minutes. It can be a very appropriate way of ensuring that
margins of tumour excision are clear during the operation
and can therefore be acted on while the patient is still
anaesthetised. However, the clarity of the prepared
specimen may not be as good as the paraffin prepared
sections. For this reason, frozen sections are not
indicated for routine diagnostic biopsies. Immunofluorescence cannot be performed on formalin-fixed
tissue and so fresh tissue for frozen sections is required
for immunopathology using fluorescent techniques.
Table 32.2
Oral soft tissue lesions
Carcinoma
Denture-induced hyperplasia
Fibrous epulis
Fibrous overgrowth
Giant-cell epulis
Haemangioma and lymphangioma
Lipoma
Pregnancy epulis
Pyogenic granuloma
Squamous cell papilloma
Salivary gland lesions
Soft tissue lesions
Soft tissue lesions that may present on the buccal mucosa
or gingivae are listed in Table 32.2. Oral carcinoma is
discussed further in Chapter 17 and denture-induced
hyperplasia is considered in Chapter 30. Minor salivary
gland swellings are considered in Chapters 14 and 34.
Fig. 32.1
A fibrous epulis.
Fibrous epulis
An epulis may be defined as a swelling or lump arising
from the gingivae, and the fibrous epulis is the most
common type. The lesion is basically a hyperplastic
response to irritation to the attached gingivae. In some
cases, the stimulus or irritant is very obvious, such as an
overhanging restoration or subgingival calculus. In
others, however, it may be more difficult to detect and
only careful examination may reveal a small developmental defect in the enamel or dentine of the tooth at the
gingival margin. Clinically, they present as smoothsurfaced, rounded swellings, normally pink in colour and
often pedunculated in attachment (Fig. 32.1). In older,
more mature lesions, the surface may show stippling
reflecting the attached gingival origin of the overgrowth.
Treatment is by surgical excision, with removal of any
irritant focus found. The base of the wound is often
dressed with a periodontal pack or if larger with a ribbon
gauze impregnated with Whitehead's varnish. This may
be sutured over the raw surface.
Fibrous overgrowth
Fibrous overgrowths or fibroepithelial polyps are
relatively common in the mouth and are usually the result
of trauma or frictional irritation. By contrast, fibromas,
which are benign neoplasms, are extremely rare. They
are most often seen in the cheeks or lips where such
irritation from the dentition can be encountered. Sometimes known as polyps, they may be semi-pedunculated
or sessile in their attachment and are similar in colour to
the surrounding normal tissue unless they have been
traumatised frictionally, when they may show a whitened
keratinised surface. They do not, however, have the cauliflower hyperkeratotic surface of the papilloma, being
smooth-surfaced and hence easily distinguished from
the papilloma (Fig. 32.2). Treatment is simple surgical
excision. As, histologically, they are simple hyperplasias,
there is no requirement to remove a margin of normal
tissue nor to extend the excision deeply into the under-
259
lying tissues. A suture may be needed to ensure adequate
haemostasis in the larger lesions.
Giant cell epulis
Fig. 32.2
A fibroepithelial polyp of dorsum of tongue.
This epulis is sometimes known as a peripheral giant-cell
granuloma and, as its name implies, the tissue consists of
a mass of multinucleated giant cells in a vascular stroma.
Many are seen in teenagers or adolescents and are
usually found in the anterior regions of the mouth. They
may represent an overgrowth of osteoclasts derived from
the resorptive process encountered during the loss of the
deciduous dentition. They can, however, arise in the
older patient. These lesions are typically deep red or even
purplish in colour and are often quite broadly based,
unlike the paler coloured, often pedunculated fibrous
epulis (Fig. 32.3). If suspected of being a giant-cell
lesion, radiographs should be taken to ensure that it is
a peripheral and not a centrally, i.e. bony, originating
lesion, which would appear as a radiolucent area (see
Ch. 36). If it is a peripheral epulis then surgical excision
with curettage or cautery to its base is normally curative.
The base of the lesion can be covered by a periodontal
pack if small, or a Whitehead's varnish packing may be
used for larger lesions. If a central giant-cell lesion is
evident on the radiograph, it must be distinguished from
the brown tumour of hyperparathyroidism by appropriate
assessment of blood calcium, phosphate and parathormone levels (see Ch. 36).
Haemangioma and lymphangioma
260
Fig. 32.3
A giant cell epulis.
Fig. 32.4
A haemangioma of cheek.
These lesions, which may appear in any of the soft
tissues of the mouth, are regarded as hamartomata. They
are developmental overgrowths of either blood vessels or
lymphatic vessels. In some patients they may achieve a
considerable size, particularly in the tongue. Typically,
however, the haemangioma will appear as an exophytic
multilobular swelling, deep blue in colour, and often
likened to a small bunch of grapes (Fig. 32.4). Gentle
finger pressure on the surface of the haemangioma
empties the blood-filled vessels leaving the swelling flat
and pale in colour. If the malformation is likely to be,
or has been, traumatised repeatedly, it may either be
removed surgically or treated by cryotherapy. This latter
method may be very successful but, as no pathological
confirmation of the diagnosis is possible, the clinician
must be quite sure of the diagnosis before treatment is
carried out in this way (see Ch. 38). Provided they are
symptom free and not subject to direct trauma, some are
simply kept under observation.
Lipoma
This is a benign neoplasm of fat; true intraoral lipomas
are quite rare. They may present with a soft swelling,
which is often pale or yellow in colour, and they are
normally sessile. These lesions may, on occasion, grow
into muscle layers and be quite difficult to dissect out
surgically. The treatment, however, is normally that of
Squamous cell papilloma
This is not an uncommon lesion of the oral mucosa and
may arise at virtually any site, but more commonly on
palate, buccal mucosa or lips. It is a benign neoplasm of
epithelial tissue and most squamous cell papillomata
present as pedunculated (stalked attachment) lesions with
characteristic white, hyperkeratinised, crenated surfaces,
which can be likened to a cauliflower (Fig. 32.6). They
are normally small, usually less than 0.5 cm in diameter.
Treatment is simply excision at the base of the stalk
Pregnancy epulis
This lesion is histologically indistinguishable from the
pyogenic granuloma, being essentially a vascular overgrowth of granulation tissue. It may be related to an
obvious focus such as calculus but it may equally arise
from an extraction socket. Hormonal changes during
pregnancy are believed to enhance the reactive tissue
response to irritation and although many lesions remain
small and do not require surgical intervention, some can
grow alarmingly fast and attain considerable size even to
the point of being traumatised by the opposing teeth.
These lesions are therefore surgically excised with
appropriate curettage or diathermy to their bases. If small
they tend to resolve following the pregnancy.
Fig. 32.5
A pyogenic granuloma.
Fig. 32.6
A squamous cell papilloma of the soft palate.
Pyogenic granuloma
The pyogenic granuloma is a lesion that arises from a
failure of normal healing causing an exuberant overgrowth of what is essentially granulation tissue. They
may grow in relation to extraction sockets or from
traumatic injuries to soft tissues, most often tongue or
palate. They can be regarded as reactive lesions and
obvious irritational factors may be evident clinically or
from the patient's history. Foreign bodies related to
extraction sockets, such as fragments of filling material
or indeed of small bony sequestra, may form the stimulus,
whereas in soft tissues there is occasionally a history
of self-medication with a variety of remedies that could
be attributed as causal. Clinically they appear as red or
speckled-red overgrowths of tissue that closely resemble
granulation tissue on visual examination (Fig. 32.5).
Treatment is surgical excision with curettage or diathermy
to the base of the lesions where appropriate.
261
attachment. A very similar lesion may be attributed to a
viral origin and is sometimes known as a viral wart. In
these cases it is sometimes possible to see finger warts
262
that have clearly been responsible for transmitting the
virus to the oral cavity. These can also be treated
effectively with cryotherapy (see Ch. 38).
33
Pyogenic dental infection
and its spread
Introduction
Dental disease, both caries and periodontal disease, is an
infective process occurring in a bacterial oral environment. It is therefore not surprising that pyogenic dental
infections are common. The most common causes of pusproducing infection in the mouth are listed in Table 33.1.
A dental abscess, otherwise known as an apical
abscess or periapical abscess, arises from an infected
pulp, which is most commonly the result of caries but
may also be due to trauma, either physical or chemical.
A periodontal abscess arises from a periodontal pocket
and may involve the bifurcation or trifurcation of molar
teeth. Pericoronitis results from infection involving the
follicle and overlying gingivae (operculum) of a partially
erupted and usually impacted tooth. This infection was
discussed in Chapter 27. Salivary gland infection is
usually the result of obstruction to a major salivary gland,
most commonly the submandibular gland. The infection
is said to be 'ascending' from the oral cavity along the
duct. Management was discussed in Chapter 14.
Dental abscess
The dental abscess accounts for the majority of pyogenic
infections in the mouth. Acute infection may arise directly
from spread of acute pulpal infection or it may represent
re-ignition of an existing chronic abscess or granuloma
by more virulent bacterial contamination or through a
lowering of the patient's natural resistance as, for
example, after influenza. Dental abscesses are normally
polymicrobial. This means that there are several
organisms present and anaerobic bacteria predominate.
Clinical features
Pain
The dominant symptom is pain, which can be described
variously as throbbing, unremitting or unresponsive to
simple over-the-counter analgesics. Unlike pulpal-derived
pain, thermal irritation tends not to be a feature. Severity
is usually sufficient to cause sleep loss. In function, the
pain is made worse as the abscess will be under considerable pressure because of the acute inflammatory reaction.
Interestingly, the pain may be slightly reduced by gentle
occlusal pressure from the opposing tooth and this may
be due to pressure increasing to the point that nerve
endings become non-functional. When the abscess has
achieved sufficient size, it breaks out of the bone into the
soft tissues and at this point the pain reduces dramatically
as the pressure eases.
As the soft tissue reacts to the infection, acute inflammation within these tissues will eventually again cause
pain as swelling in the soft tissues increases and pressure
even in the more lax soft tissue spaces rises. This may
take up to 2-3 days to occur.
Swelling
Table 33.1
Infections
Common pus-producing oral
Dental abscess
Periodontal abscess
Pericoronitis
Salivary gland infection
Early abscesses are confined within the unyielding
alveolar bone and at this stage no swelling is evident. It
is only when the abscess bursts through alveolar bone
that swelling may become apparent, together with
redness and surface tenderness. The site of the swelling
varies and may be intraoral and/or extraoral. The sulcus
on the labial or buccal aspect of the tooth is the most
common intraoral site of swelling because the apices of
most teeth are closer to the buccal plate surface. The
minority of upper lateral incisors have apices closer to
the palatal bone surface and can therefore present as
palatal swellings. In later presentations, the sulcus
swelling may become soft and fluctuant, or even have
discharging pus through a sinus, and this heralds
reduction in both swelling and pain.
Spread of infection
When dental abscesses escape the confines of alveolar
bone, the infection passes into soft tissues and in turn
provokes in these tissues an acute inflammatory reaction
and eventually pus formation. Where this happens
depends largely on the anatomy of the region in which
the apex or apices lie. The length of the root is therefore
relevant, and how it relates in certain cases to muscle
attachments. In acute abscesses of deciduous teeth, therefore, the short roots often dictate that the infection passes
not into the facial structures but intraorally, forming a socalled 'gumboil'. Where spread of infection causes facial
or cervical swelling it is often characteristic of the
quadrant of the mouth involved, and these will be
considered in turn.
Maxilla
Anteriorly from incisor to canine, the patient may show
upper lip swelling, obliteration of the nasolabial fold and
puffiness of the lower eyelid. In extreme cases, the eye
may be almost totally closed with oedematous swelling
(Fig. 33.1).
Posteriorly, the swelling will be evident in the upper
part of the cheek, with swelling around the eye occasionally but will not distend the nasolabial fold or cause
significant lip swelling (Fig. 33.1). Spread upward from
molar or premolar infection seldom passes into the
maxillary air sinus. The buccinator muscle attachments
in the molar region may determine whether the infection
passes above it into the cheek or below into the sulcus,
although both are frequently present, as this muscle will
form only a partial barrier.
Mandible
264
Spread from incisors or canine teeth may cause mental or
submental swelling (Fig. 33.2). Lower canine infections
Fig. 33.1
Facial swelling and closure of the eye due to
infection spreading from an upper incisor.
Fig. 33.2
Mental abscess arising from infection
associated with a lower incisor.
do sometimes pass into the floor of mouth, resulting in
swelling here in addition to the swelling of the chin.
Posterior teeth infections may pass either buccally
or lingually through the bone, and the attachments of
buccinator laterally and mylohyoid lingually will have a
bearing on the direction of spread. If buccal spread
occurs above buccinator, the swelling will largely be seen
in the sulcus but, if below, it will cause swelling on the
lateral aspect of the jaw externally, which may gravitate
downwards into the upper part of the neck. Occasionally,
infection may spread deep to the masseter muscle. This
usually arises from a pericoronal infection around a
wisdom tooth, as described in Chapter 27. If the infection
passes lingually, the swelling will be in the submandibular
space if below the mylohyoid or in the floor of mouth
if above this muscle. Although the muscles direct the
route of spread into the various tissue compartments, it is
important to be aware that both intraoral and extraoral
spread can occur from any tooth. It is therefore not
unusual to see swelling in both the sublingual and submandibular space from a lower molar tooth or, for that
matter, both sulcus swelling and facial swelling from an
upper tooth.
When infection spreads into whichever of the soft
tissue spaces, the initial reaction of these tissues will be
an acute inflammatory reaction. The fluid exudate of this
reaction causes the early swelling, which is therefore
mainly oedematous, and this phase can be known as a
cellulitis complicating the original bony abscess. As
the soft tissues continue to react to the infection, pus will
be formed, which may collect within the compartment,
giving rise to, for example, a submandibular or a submental abscess (Fig. 33.3). A well-recognised complication of lower jaw dental infection is the rapid spread of
submandibular and sublingual infection across the
midline of the neck. This is a life-threatening situation
known as Ludwig's angina and requires immediate
hospital admission for appropriate drainage and intensive
antimicrobial therapy.
Pus within the soft tissues of the upper part of the face
seldom presents as a facial external abscess but usually
collects within the upper buccal sulcus.
Management
Management of the acute dental abscess is shown in
Table 33.2.
Drainage
Fig. 33.3
A submandibular abscess.
Table 33.2
abscess
Management of an acute dental
Drainage
tooth
extraction
root canal drainage
incision
intraoral
extraoral
Removal of source of infection
endodontic treatment
extraction
periradicular surgery
Supportive antibiotic therapy
severe spreading infection
systemic toxicity
medically compromised
Provision of drainage remains the most important
measure where pus has formed.
Root canal drainage
Extraction
Extraction of the tooth is usually carried out if it is
unconservable or if the acuteness of the condition
warrants it. This provides excellent drainage, especially
in upper teeth. If the abscess is still confined to the
alveolar bone, or even where spread to soft tissues is in
its early oedematous phase, extraction is often sufficient
to allow resolution. There is no justification whatsoever
in delaying the extraction on account of swelling because
this is one of the best ways of achieving good drainage,
and thereby speeding resolution.
Opening of the root canal can, in the early intrabony
abscess, be sufficient in itself. When opened and pus is
obtained, it is prudent not to close the canal immediately
but allow sufficient time for adequate drainage to occur.
This may take only 12–24 h but gross contamination and
even caries within the root canal can occur if the tooth is
left 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
265
anaesthesia within the outer wall only of the abscess
is normally sufficient to allow incision with a pointed
scalpel blade (number 11), which should be used with a
stab action and a cut of suitable size made on withdrawal.
If the pus is deeper, fine artery forceps may be introduced
to explore the abscess and gently open it to encourage
free flow of pus. This may require more extensive local
anaesthesia. Palatal abscesses may require excision of a
small ellipse of soft tissue or insertion of a small drain
after incision as this mucoperiosteum tends to rebound
and seal following the release of pus, thus preventing
further free drainage.
Incision of extraoral abscesses
266
This is usually carried out by a specialist surgeon and,
unless the abscess is very superficial, under general
anaesthetic. Provision of a general anaesthetic for some
of these patients is a skilled procedure when trismus is a
marked feature and laryngeal oedema masks the normal
anatomy (see Ch. 10).
The presence of pus is confirmed clinically by eliciting
fluctuation on careful palpation of the swelling. Finger
pressure of one hand on one side of the swelling causes
fluid movement to be detected by the pulps of the fingers
of the other hand. This can be difficult to determine,
especially in deeper lying pus collections. Generally, the
abscesses requiring such treatment will be submental or
submandibular.
The key points of treatment are that the skin overlying
the abscess should be prepared with surface antiseptic
and isolated with sterile drapes. A wide-lumen needle
should be introduced into the abscess cavity to obtain an
uncontaminated sample, and it may also help to 'find' the
pus. An incision is made below the maximum convexity
of the swelling, parallel to the lower border of the
mandible, if possible using a skin crease line to minimise
later scar visibility (see Ch. 15). The incision should be
through skin only and normally an incision of about 2 cm
is sufficient. Blunt dissection is then carried out with
blunt scissors or Hilton-type forceps into the cavity,
which should be explored thoroughly with the blunt
instrument or a finger. A drain is then inserted into the
abscess and sutured to the skin surface. A dry sterile
dressing is finally taped over the drain. This allows
frequent assessment of the continuing discharge. The
drain is removed after the dressings are seen to contain
no further pus.
Removal of source of infection
This will be accomplished immediately if the tooth is
extracted in the process of gaining drainage but may be a
later procedure in the form of either endodontic treatment or periradicular surgery.
Supportive antibiotic therapy
The decision to prescribe antibiotics for acute abscesses
will depend upon a number of factors and is not
invariable. Extraction of a maxillary tooth or incision of
a well-localised sulcus abscess may well be sufficient to
allow resolution of the acute infection without antibiotic
supplemental treatment. Clinical experience is invaluable
but some features may well influence the decision to
prescribe an antibiotic (Table 33.3).
The swelling may encroach on the airway as, for
example, in a submandibular or sublingual infection.
Difficulty in swallowing normally implies that the tongue,
floor of mouth or parapharyngeal spaces are affected. If
incision and drainage have yielded poor quantities of
pus, this suggests that management may be inadequate
without antibiotics. Regional nodes are often late to react
to 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 particularly
if the immune system is compromised, patients may not
have the capability to respond adequately to this type
of infection. Patients with conditions such as diabetes
mellitus, HIV infection, or who are receiving treatment
with corticosteroids or cytotoxic drugs, can be included
in this group. Where infection is evident in the floor of
the mouth, there appears to be an increased likelihood
of rapid spread. The patient may feel unwell, with an
elevated temperature and a tachycardia, signifying
systemic toxicity. Most severe infections will cause a
Table 33.3 Factors influencing antibiotic therapy
in the management of acute dental abscess
Airway
Dysphagia
Lack of drainage
Medically compromised
Site of spread
Systemic toxicity
Trismus
degree of trismus by simply stretching the soft tissues,
but profound trismus often implies infection affecting
muscles either directly or indirectly involved in jaw
movement.
The choice of antibiotic is initially empirical, as the
results of antibiotic sensitivity testing will not be available. The penicillin group is often chosen in non-allergic
patients, with the wider-spectrum amoxicillin being a
common choice. Metronidazole is becoming more popular
as a first choice antimicrobial because anaerobes are the
predominant pathogens. Cephalosporins, erythromycin
and, where antibiotic sensitivity indicates, clindamycin
are all possible useful agents. In severe acute infections,
it is sometimes considered necessary to prescribe two or
more antibiotics. Metronidazole and amoxicllin have
proved to be a popular choice where two antibiotics are
deemed necessary.
Finally, management of the acute abscess requires
meticulous follow-up to ensure that the treatment is
having the desired effect. In the early stages, this may be
as an outpatient and require daily assessment until it is
evident that resolution is being achieved. If the dentist,
from the initial presentation, feels that the infection is
very severe, early referral to a specialist is appropriate,
because a number of patients will require admission to
hospital for appropriate drainage and perhaps intravenous
antibiotic therapy.
Ludwig's angina
This severe complication has been described above and
requires immediate admission to hospital for drainage
and appropriate intravenous antibiotic therapy.
Necrotising fasciitis
This combination of virulent pathogens can cause massive
soft tissue necrosis with formation of multiple sinuses.
It can arise from a dental infection.
Orofacial sinus
This complication arises when the pus has discharged
onto the face or neck, either through lack of treatment or
inadequate treatment (Fig. 33.4). If the condition remains
untreated it can cause disfiguring soft tissue fibrosis
around the intermittently discharging sinus. Epithelium
from the skin can grow into the sinus, complicating the
treatment in that surgical revision of the opening may be
necessary. The dental source must be removed as soon as
possible.
Osteomyelitis
This is very rare and may be an indication of an immunocompromised state or previous irradiation of the jaw,
which has reduced the blood supply to the bone (see
Ch. 36).
Complications
A number of complications may arise from a dental
abscess as listed in Table 33.4.
Cavernous sinus thrombosis
Spread of infection through emissary veins from the
periorbital region and upper face can, in theory, cause
thrombus formation within the cavernous sinus. With
modern antibiotics, this complication is seldom seen
nowadays.
Table 33.4
Complications of dental abscess
Cavernous sinus thrombosis
Ludwig's angina
Necrotising fasciitis
Orofacial sinus
Osteomyelitis
Septicaemia
Fig. 33.4
abscess.
An orofacial sinus arising from a lower premolar
267
Septicaemia
This is discussed in Chapter 8.
Periodontal abscess
This arises from a periodontal lesion and the clinical
features are therefore different from the apical lesion.
Clinical features
Pain and swelling
The swelling in this type of abscess being further coronal
than the apical abscess normally discharges eventually
through a periodontal pocket or through a sinus in the
alveolar process. Spread to soft tissues is therefore
relatively rare but can involve particularly the floor of
mouth.
Mobility of the affected tooth
This feature may not be particularly helpful in diagnosis
if other teeth also have mobility reflecting a generalised
periodontal 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 pulp
testing.
Management
Extraction is often the logical treatment. This provides
good drainage and also removes the source of infection.
Occasionally, if the abscess involves a strategically
important tooth and the patient's general periodontal
condition is considered capable of control, then curettage
and root planing may be appropriate.
are rare, they are important to recognise and manage
successfully. Both are somewhat unusual in that they are
due to one organism rather than the polymicrobial nature
of most pyogenic oral infections.
Cervicofacial actinomycosis
Different species of actinomyces microorganisms can be
found in mixed dental abscesses related to infected teeth,
and do not require particular management other than
appropriate drainage with additional antibiotic therapy if
considered necessary. Cervicofacial actinomycosis is a
distinct clinical entity and arises subsequent to either
mandibular extractions or jaw fracture.
Aetiology
The infecting organism is the strictly anaerobic
Actinomyces israelii. This microorganism is found in
dental plaque and appears to gain access to the soft
tissues through an extraction socket or fracture through
the tooth-bearing area of the mandible.
Clinical features
Most commonly, a swelling forms either at the lower
border of the mandible or in the neck. It classically
presents a week or so (and up to 6 weeks) after the
wound in the mouth, which will normally appear to have
healed well. Severe pain is not a feature and, if not
treated, the infection may develop with several swellings
and skin sinus formation. The related skin is said to have
a dusky, bluish tinge. Tissue planes are not followed and
the tissues respond by forming a granulomatous reaction
around the infected area. If a sinus is active, closer
examination of the pus may reveal small, yellow, seedlike granules in the discharge. These are known as
sulphur granules.
Diagnosis
Less common pyogenic oral
infections
268
Less common infections that produce pus are cervicofacial actinomycosis and submandibular staphylococcal
lymphadenitis of childhood. Although these infections
Microscopic analysis of a granule by crushing it between
glass slides and Gram staining shows typical Grampositive branching mycelia with related pus cells.
Anaerobic culture will later reveal the typical 'molar
tooth' colonies of Actinomyces israelii on blood agar.
Occasionally, another small Gram-negative bacillus may
be found: Actinobacillus actinomycetemcomitans.
Management
Where pus is formed, incision and drainage should be
carried out. Antibiotics should be prescribed for 6 weeks
because they take a considerable time to penetrate the
granulomatous fibrous tissue reaction in the soft tissues.
Shorter courses may result in a recurrence of the infection and it is therefore important to stress to the patient
the importance of continuing the antibiotic for the full
prescribed period. Actinomyces israelii is sensitive to
most commonly used antibiotics and, being a narrowspectrum antibiotic, penicillin is a sensible choice. If
cervicofacial actinomycosis presents late or is treated
inadequately, it can gravitate from the neck into the
mediastinum, and this is clearly a serious complication.
Less serious but disfiguring is the scarring that results
from the fibrotic reaction in the neck.
Acute submandibular staphylococcal
lymphadenitis
This acute infection occurs in children between the ages
of 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 down
the lymphatics to settle in submandibular lymph node.
The child may not have been previously exposed to a
staphylococcal infection and, the immune reaction being
insufficient to deal with this challenge, the node is overwhelmed and becomes an abscess itself.
Clinical features
This is similar to any acute inflammatory swelling at the
lower border of the mandible. There may be surface
reddening and it will be tender to palpation; the
temperature may be elevated. Dental examination shows
no carious focus and this generally will raise suspicions
of a staphylococcal infection. There may be evidence of
infection of a hair follicle on the face on that side or a
history of recent nasal congestion such as a head cold.
Management
If there is evidence of accumulation of pus, such as
fluctuation, then incision and drainage is necessary.
Aspiration prior to the incision, will allow an accurate
microbiological analysis. If no pus is formed, then a
beta-lactamase-resistant form of penicillin, such as
flucloxacillin or erythromycin, may be effective in
allowing resolution.
269
34
270
Salivary gland diseases
Introduction
Submandibular duct (Wharton's duct)
Surgery of the major salivary glands has already been
discussed in Ch. 14, but there are some conditions that
are treated by minor surgery within the oral cavity. These
procedures are mainly related to pathology of the minor
glands but, where the major gland ducts are involved, it
is often possible to treat the condition by less radical
surgery intraorally.
When the major gland ducts are involved, it is often
possible to treat obstructive sialadenitis intraorally.
Obstruction of the minor salivary gland ducts can also
be managed by minor surgery and these conditions are
considered here, after a review of their applied anatomy.
This duct is between 5 and 6 cm in length. It originates
from the deep surface of the gland just behind the
posterior limit of the mylohyoid muscle. It runs upwards
and forwards between mylohyoid and hyoglossus, and
then between the sublingual gland and the genioglossus
muscle, before ending on the sublingual papilla beside
the fraenulum of the tongue and just behind the lower
incisor teeth. Its important relation is the lingual nerve,
which crosses its lateral surface on its earlier course
before running upward on its medial side where the nerve
is already beginning to divide into its smaller terminal
branches. As the duct runs forwards, it becomes
progressively more superficial.
Applied anatomy
Sublingual ducts
An awareness of the location of the minor glands and the
anatomical course of the ducts of the major glands is
needed and these will be considered in turn. The gross
anatomy of the major glands has been discussed in
Chapter 14.
The sublingual gland lies fairly superficially beneath the
mucosa of the floor of the mouth, which it raises to form
the sublingual fold. It has many ducts (around 12), some
of which run directly up to open onto the floor of mouth,
whereas others may join the submandibular duct.
Parotid duct - (Stenson's duct)
Minor salivary glands
This duct is approximately 6 cm in length and is formed
within the anterior part of the gland by the joining of two
main branches. After emerging from the gland it runs
horizontally forwards over the surface of the masseter
muscle to the anterior border of that muscle and then
turns inwards, passing through the buccinator and buccal
pad of fat, before ending in a slightly raised papilla
adjacent to the upper first or second molar tooth on the
buccal mucosa. The accessory parotid gland lies closely
related to its initial third and the buccal branches of the
facial nerve may be in close relationship to it.
Around the mouth are aggregates of minor salivary
glands, which are mucus secretors. They lie superficially
in the submucosal regions and are most easily felt by
passing the tongue along the inner aspect of the lower lip,
where they are felt as a multitude of small lobules. They
are most numerous in the lower lip but are plentiful in the
upper lip, buccal mucosa and floor of mouth. In lesser
numbers, however, they may also be found in the palate,
the posterior aspect of both the hard palate and soft
palate, and also on the ventral surface of the tongue. They
open onto the surface of the mucous membrane by tiny
ducts and their secretion is an important contribution to
the lubrication of the soft tissues.
Obstructive sialadenitis
Obstructive sialadenitis in a major gland is due either to
a stone or, less commonly, stenosis of the duct. Minor
gland obstruction gives rise to a mucocoele.
Major gland obstruction
Aetiology
Obstruction to the free passage of saliva from a major
gland can clearly cause problems to a patient. The most
common cause of this is blockage of the duct by a stone
that is sometimes known as a sialolith. This is relatively
uncommon in the parotid gland and is more frequently
seen close to the orifice of the duct. In the submandibular
gland, the stone may form either within the duct or the
gland itself, but duct stones are more common. A certain
number of obstructions within the duct are poorly
calcified, if at all, and are referred to as mucous plugs.
Other less common causes of obstruction are stenosis
(probably a developmental occurrence) and pressure
effects from space-occupying lesions, such as malignant
disease, arising either from the epithelium of the floor of
mouth or within the gland itself. In the parotid gland,
there may be another cause related to the trapping of
the duct as it pierces the buccinator muscle, and this has
been described as more often occurring in children or
adolescents.
Submandibular duct stones are relatively common
and their presentation may vary from patient to patient.
Clinical features
Characteristically, the stone may become apparent by
swelling and discomfort in the submandibular gland
region. The swelling is palpable at the lower border of
mandible in the submandibular triangle. It is often made
worse at meal-times and, typically, pain may last for a
couple of hours. Although this can occur at each mealtime for several days, it often settles and the patient may
report being quite symptom free for weeks or months. It
is not unknown for large stones occupying most of the
floor of mouth to present with no history whatsoever of
discomfort or swelling in the gland.
More dramatically, however, infection may supervene
because the duct is not being 'washed out' with saliva.
Bacteria from the mouth may pass along the duct and
gain access to the gland around the obstruction. This is
known as ascending infection and it can give rise to acute
sialadenitis of the submandibular gland. When this occurs,
the patient experiences severe pain and swelling of the
gland, which becomes extremely tender with dysphagia
and, often, high temperature. Pain is made worse on
attempting to eat or drink and the patient may complain
of a bad taste in the mouth. Intraorally, the floor of mouth
may be severely swollen with a raised, red, wheal-like
line along the length of the duct. Small amounts of
pus may be expressed from the orifice of the duct on
occasion.
Diagnosis
This is made fairly straightforward with a clear history
but clinical examination by visual inspection of the floor
of the mouth may show a yellowish coloured, rounded or
fusiform-shaped lump of varying size along the line of
the duct. This is more often seen when the stone is close
to the orifice of the duct or is fairly large. If it cannot
be seen, bimanual palpation of the floor of the mouth
with the 'outside' hand pushing the floor of the mouth
upwards while the line of the duct is palpated with the
index 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 lateral
view (lateral oblique jaw or orthopantomograph) and
occlusal view, the latter being most useful (see Fig. 14.4).
If no stone is noted on the radiograph, it may indicate that
the obstruction is not calcified. In these circumstances, a
sialogram – where a radio-opaque dye is passed along the
duct prior to the radiograph being exposed - may reveal
this type of obstruction and also strictures within the duct
(see Fig. 14.5).
In the acute presentations, the clinical features are
fairly conclusive but radiographs should be taken to
allow accurate location of the stone.
Management
Acute sialadenitis should be treated vigorously with
aspiration, incision and intraoral drainage if possible, and
antibiotics. Amoxicillin is commonly prescribed with a
271
high initial dosage, and this can usually be administered
orally. Clindamycin may be appropriate in cases
unresponsive to more commonly described antibiotics, as
it is secreted through the salivary glands and perhaps has
a more direct effect.
Removal of the stone may often be done on an
outpatient basis with local anaesthesia. However some
patients have great difficulty in relaxing their tongue
sufficiently to allow the surgery, particularly if the stone
is further back in the mouth. Large stones are normally
easy to treat but some small stones can be very difficult
technically. The nearer to the duct orifice the stone lies,
the less difficult it will prove to remove. Anaesthesia is
best carried out with a lingual nerve block, as infiltration
can often distort the surgical site and with small stones
may obscure them from easy vision and palpation.
The technique involves passing a suture behind the
obstruction underneath the duct and tightening this
sufficiently to prevent the stone being pushed inadvertently
backwards during the procedure. There is often dilatation
of the duct up to the point of the obstruction and this
displacement therefore is a real possibility, with the
added complication that it may pass from the duct into
the gland itself.
An incision is then made over the stone parallel to the
duct and slightly lateral to it. A blunt dissection is then
carried out to expose the duct. An incision is made in the
duct over the stone, which is removed. There is often a
release of pus and saliva at this point. The wound should
not 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 on
healing, which may itself cause obstruction. Patients
should be encouraged to rinse copiously postoperatively
and a free flow of saliva should be encouraged with citrus
drinks.
Aetiology
Mucocoeles are caused either by damage to the minor
duct leading to leakage of saliva into the submucosal
layer (mucous extravasation cyst) or by blockage of the
duct, normally by a mucus plug (mucus retention cyst).
By far the more common is the extravasation cyst.
On occasion, small stones can cause obstruction to
minor salivary glands. This is more commonly seen on
the upper lip or buccal mucosa and secondary infection
of the gland can occur, causing a localised raised tender
swelling. On the top of this dome-shaped swelling it may
be possible to see or feel the small stone. Treatment is
simply surgical excision of the lesion.
Clinical appearance
Clinically, mucocoeles present as soft, bluish, fluid-filled
swellings that often burst or leak, only to reform, and
patients normally are little inconvenienced by them. The
most common site is the lower lip (Fig. 34.1), probably
reflecting its greater tendency to trauma and ductal
damage, but the floor of mouth is also quite a common
site.
In the floor of mouth, they may be related to the sublingual gland and can rapidly assume quite a large size.
The ballooning lesion in the floor of the mouth may be
described as a ranula (frog's belly) and may be a
nuisance to the patient, although they frequently rupture.
Mucocoeles
272
Mucocoeles are the most common cause of minor
salivary gland problems. Neoplasms arising from minor
salivary glands are relatively uncommon but both benign
and malignant varieties can be found. They can occur at
any site where minor glands are found but the most
common intraoral location is at the junction of the hard
and soft palates. Swellings in the upper lip are usually
neoplastic rather than mucocoeles, which are rare in the
upper lip.
Fig. 34.1
A mucocoele affecting the lower lip.
More precisely, however, a ranula merely implies a
sublingual swelling regardless of aetiology.
Diagnosis
The diagnosis is very straightforward, as the history is
usually typical. Occasionally, mucocoeles resemble minor
salivary gland tumours, especially if they have become
fibrosed and more walled off. Their bluish colour can
make them similar to a superficial haemangioma but they
tend not to deflate on sustained digital pressure, as would
most haemangiomas.
Management
The majority of mucocoeles are surgically excised but
some in the floor of mouth may be marsupialised.
Excision is carried out under local anaesthesia. An
incision over the swelling must be executed with care or
the lesion will burst and the subsequent removal may be
more complicated. Extravasation cysts do not have
epithelial lining and, if the cyst is ruptured, it may be
difficult to visualise. A blunt dissection around the cyst
frees it very simply if it remains intact and minor glands
at its base are usually also removed. One or two sutures
may be needed to close the wound.
Marsupialisation of a larger floor of mouth mucocoele
is preferable to dissecting the lesion out and removing it.
This may be done by passing a suture through the lesion
to lift it. A small incision can then be made over the
maximum convexity and the contents aspirated. Sterile
ribbon gauze is then packed into the now empty cavity
through the small incision to 'reconstitute' the swelling,
and the mucosal roof can then be removed with scalpel
or scissors. The opening into the cavity must be kept
patent by suturing its margins to the oral mucosa, or the
pack may be soaked in Whitehead's varnish and sutured
to 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 does
close over rapidly. If floor of mouth mucocoeles do
repeatedly recur, it may be necessary to remove the
sublingual gland, (see Ch. 14).
Minor salivary gland biopsy
In Sjögren's syndrome, it has become established that the
lymphocytic aggregates around minor glands are a direct
reflection of the pathology in the major glands that
causes the reduction in saliva production. Histological
examination of minor salivary glands therefore avoids
the more invasive major gland biopsy. An incision is
made in the mucosa of the lower lip - along the lines of
the mental nerve branches rather than across them, to
minimise nerve damage. The minor mucous glands will
extrude through the open wound and can be excised
before wound closure (Fig. 34.2).
An incision in the lower labial mucosa showing
Fig. 34.2
the minor salivary glands protruding through the wound.
273
35
Oral surgery in the medically
compromised patient
Introduction
Patients who require an oral surgical procedure will have
their medical status questioned as a matter of routine
during the history taking. Certain conditions have a direct
bearing on the management and treatment of these
patients, which may have to be altered or modified as a
result. Thus the treatment plan may have to be modified
for the patient's safety.
Most medical conditions do not interfere with minor
oral surgical procedures carried out under local anaesthetic. The major problems are with patients who have
bleeding tendencies, allergies, are on corticosteroids or
have cardiac disease.
Those requiring general anaesthetic will be treated in
the secondary care system under the supervision of a
consultant anaesthetist.
Not only can systemic disease influence the oral
management of a patient, but systemic disease may arise
from the mouth, usually as a result of infection. An
example of this is infective endocarditis arising in a
patient with valvular or other cardiac disease; immunocompromised patients, such as those taking cytotoxic
chemotherapy, are also at special risk of infection. Moreover, a number of acute medical emergencies may arise
while oral surgical procedures are being carried out and
the surgeon must have the necessary agents available for
the appropriate management of the patient. The main
systemic diseases that impact on the practice of oral
surgery are listed in Table 35.1, and these will be
discussed in turn.
Blood disorders
274
Haematological disease, particularly anaemia, is not
uncommon. Except in severe cases and those requiring
general anaesthesia, anaemia is not a significant problem
Table 35.1
Systemic disease and oral surgery
Blood disorders: haemorrhagic disease
Cardiovascular disease
Endocrine disease
Liver disease
Neurological disease
Pregnancy
Radiotherapy
Renal disease
Respiratory disease
because blood loss during minor oral surgical procedures
should be controlled and not excessive.
A number of bleeding disorders can occur (see
the discussion in Ch. 6) and the specific management of
postextraction haemorrhage is considered in detail in
Chapter 26. In addition, it should be noted that aspirin
is being taken by an increasing number of patients for
prophylaxis against thrombotic disease such as coronary
artery disease or cerebrovascular thrombotic incidence.
Normally, a dose of 75 mg daily is prescribed, which
has the desired effect of reducing platelet adhesiveness.
In theory, this should also cause more bleeding after oral
surgery, but in practice it seldom seems to have a
significant effect. Occasionally, continued oozing may
prompt haemostatic measures such as suturing or use of
regenerated oxidised cellulose but in most cases firm
pressure is all that is necessary.
When patients are taking higher doses of aspirin for
chronic pain (e.g. patients with osteoarthritis or rheumatoid arthritis), then more major oral surgery may require
the use of alternative analgesics for about 2 weeks before
surgery, as the effects on platelets might prove more
troublesome in these circumstances.
Patients taking anticoagulants, such as warfarin, for
cardiac arrythmias or those with prosthetic heart valves,
should have their INR (International Normalised Ratio)
estimated on the day of surgery. A higher INR can be
accepted before minor oral surgical than before general
surgery (Ch. 6). Some suggest that an INR of <4 can be
accepted, but most oral surgeons would wish the INR to
be between 2-3 for elective procedures other than single
tooth extractions. Haemostasis should be secured with
local measures including Surgicel®, suturing and pressure
packs.
Surgeons must also be aware of the effect of prescribed
drugs on anticoagulated patients. Most antibiotics and
some antifungals will enhance the anticoagulant effect of
warfarin, and non-steroidal anti-inflammatory drugs such
as aspirin not only enhance the activity of warfarin but
risk more severe bleeding from the stomach by their
action on the gastric mucosa.
a consequence of its effects on the valves. Although
damage is not invariable, these patients are regarded as
'at risk' unless there is proof to the contrary. This should
include those with developmental septal defects and those
with prosthetic heart valves following cardiac surgery.
Patients with cardiac pacemakers are not at risk and antibiotic therapy is not required. The remainder are at risk
of endocarditis as a result of bacteraemia, which will be
resultant upon oral surgery. Antibiotic cover is, therefore,
a preoperative requirement and the regime is dependent
on whether the patient is being treated under local or
general anaesthesia, whether the patient is allergic to
penicillin and whether penicillin has been prescribed on
more than one occasion in the previous month. Patients
at a particular high risk are those who have had a
previous episode of endocarditis. The appropriate regime
for managing these patients is listed in Table 35.2.
Cardiovascular disease
From an oral surgical viewpoint, patients with cardiovascular disease can be considered in two groups.
Those with vascular disease
Hypertension is probably the most common consequence
of peripheral vascular disease. Patients may be taking a
variety of medications, ranging from diuretics to betablockers, calcium-channel-blockers or angiotensinconverting-enzyme (ACE) inhibitors. In general terms,
treatment of the hypertensive patient will be largely
unaltered other than under a general anaesthetic. Most
dentoalveolar surgery can be carried out with no
problems under local anaesthesia, although adrenaline
(epinephrine)-containing local anaesthetics are known to
cause a reduction in the blood potassium level and, in
patients 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 considered
under two headings.
Valvular disease
Although rheumatic fever is now extremely rare, valvular
disease of the heart is still seen in the older population as
Ischaemic heart disease
Patients at particular risk are those with severe hypertension, those with angina or those who have had a
previous myocardial infarction. Anxiety or pain can cause
an outpouring of adrenaline, which can increase the strain
on the heart and also precipitate dangerous arrhythmias.
The patient should, therefore, be exposed to minimum
stress and prescribed sedation if required (see Ch. 11).
The most effective agent for local anaesthesia is
lidocaine (lignocaine) 2% with adrenaline (epinephrine)
(see Ch. 24). Doses of local anaesthetics should be kept
to a minimum and treatment sessions should not be
prolonged.
If it is unavoidable, general anaesthesia should be
given by an expert anaesthetist in a hospital setting,
because cardiovascular disease is the chief risk of death
under anaesthesia.
A number of measures should be considered when
treating patients in an outpatient environment under
local anaesthesia. Patients should be advised to continue
their normal medication before and after procedures.
Patients should bring their glyceryl trinitrate (GTN)
spray to the surgery, if they use one, because they may
wish to use it prophylactically. Oxygen should be
available on a continuous flow delivery system and staff
should be trained in the appropriate care for the
collapsed patient.
Where possible, surgical treatment is best deferred for
3-6 months after myocardial infarction, depending on
Table 35.2
Prevention of endocarditis1 in patients with heart-valve lesion, septal defect, patent ductus, or
prosthetic valve
Dental procedures2 under local or no anaesthesia, patients who have not received more than a single dose of a
penicillin in the previous month, including those with a prosthetic valve (but not those who have had endocarditis), oral
amoxicillin 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, oral
clindamycin3 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 a
single dose of a penicillin in the previous month), either i.m. or i.v. amoxicillin 1 g at induction, then oral amoxicillin
500 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 under
5 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 adult
dose, 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 years
teicoplanin 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. clindamycin
150 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 Association
and 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 chlorhexidine
gluconate 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.
the severity of the attack and the patient's rate and degree
of recovery.
Endocrine disorders
276
A number of endocrine disorders can complicate the
management of the patient undergoing minor oral
surgery. The most prevalent of these conditions is diabetes
mellitus, which can occur in the insulin-dependent form
or in the non-insulin-dependent, maturity-onset form. In
addition, an increasing number of patients take corticosteroid drugs for the management of autoimmune
conditions. The management of these groups of patients
will now be discussed.
Diabetes mellitus
If oral surgery requires a general anaesthetic, the requirements of preanaesthetic starving and the difficulties with
postoperative food intake will need appropriate management. This needs to be carried out on an inpatient basis
in cooperation with the patient's physician and using a
balance of dextrose infusions and soluble insulin.
Under local anaesthetic, patients should be encouraged
to maintain their normal regime with regard to eating and
insulin injections. Effort should be made not to delay
treatment such that the normal dietary intake is disrupted.
Diabetic patients have a compromised response to
infections. Certain procedures may, therefore, warrant an
antibiotic prescription to cover them over the initial
healing period. For the straightforward extraction in a
well-controlled patient, however, this is not necessary,
particularly where good oral hygiene can be relied upon.
Certain non-steroidal anti-inflammatory drugs have
an effect on blood sugar levels and paracetamol, with or
without codeine, may be a wiser analgesic choice.
Corticosteroid treatment
Corticosteroids have important effects when given in
sufficiently large doses, and these include depression of
adrenocortical function, which will lead to collapse under
stress. Depression of the inflammatory and immune
responses may lead to an increase in opportunistic
infections and impaired wound healing.
The need to give additional steroids for those patients
taking systemic corticosteroids, or having used them in
the previous 2 years, is controversial. Where clinical
concerns exist regarding the risk of hypotensive shock,
patients should be treated by increasing oral steroid therapy
or by intravenous or intramuscular hydrocortisone.
Liver disease
Normal liver function is essential for production of
several blood-clotting factors and for the metabolism and
detoxification of many drugs. Viral disease also has
implications in terms of cross-infection (see Ch. 7). It is
important to assess coagulation defects preoperatively to
ensure that adequate haemostasis will occur (see Ch. 6),
and to be aware of the possibility of reduced drug breakdown when administering or prescribing agents. The
British National Formulary contains valuable information
on prescribing for such patients and should be consulted
appropriately.
Neurological disease
The most significant neurological problem presenting
routinely in minor oral surgical practice is that of grand
mal epilepsy.
Most patients with epilepsy will be taking antiepileptic
drugs such as carbamazepine or phenytoin for the control
of the seizures. Oral surgery can be carried out under
local anaesthesia without any problems if control is
satisfactory and patients should be advised to continue
their normal antiepileptic drug unchanged. If general
Table 35.3
pregnancy
Oral surgical considerations in
Risk to mother
increased gingivitis and epulis formation
risk of hypotension if supine
risk of hypertension
vomiting especially with general anaesthesia
aspirin may cause neonatal haemorrhage
Risk to fetus
radiography hazardous
respiratory depression with sedatives
tooth staining with tetracyclines
prilocaine rarely causes methaemoglobinaemia
some drugs are teratogenic
anaesthesia is required, the anaesthetist should be made
aware of the history to allow for the use of appropriate
volatile agents for anaesthetic maintenance.
Pregnancy
Minor oral surgical procedures can be carried out during
pregnancy, which, it should be remembered, is a physiological state. The potential risks to the mother and fetus
are outlined in Table 35.3.
In the later stages of pregnancy, patients should
normally receive treatment in a more upright position
rather than supine because the weight of the fetus and
uterus can interfere with blood return via the inferior
vena cava.
Although radiographs in the region of the jaws do not
cause direct irradiation of the abdominal area, these
should be restricted to clinical necessity, as should all
radiographs. Patients who have non-acute problems
should defer radiographic imaging until after pregnancy.
Protective shielding where radiographs are needed
should be used as much for reassurance as for their actual
benefit. In acute conditions, radiographs will often be
necessary and patients should be reassured that the risk is
minimal.
Prescription of drugs should be carefully considered
and reference to the British National Formulary is
necessary to allow a choice of drugs that have been
proven safe during this period. Lidocaine (lignocaine)
plus adrenaline (epinephrine) is an appropriate anaesthetic
and some clinicians prefer to avoid prilocaine with
felypressin, which may (in theory) have a mild oxytocic
277
effect. During the first trimester of pregnancy, particular
care should be taken with any prescription as this is the
time when drugs administered to the mother can have the
most serious consequences on the child's development.
Necessary dental treatment should continue during
pregnancy, especially such measures as extraction of
unrestorable, grossly carious teeth where delay could
lead to acute pain and spread of infection. Prompt treatment under local anaesthesia may well avoid the need for
later use of antibiotics and painkillers, and even the need
for general anaesthesia where gross infection precludes
the 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 during
the middle trimester of pregnancy or deferred until after
the pregnancy.
Most pregnancies are trouble free, but if there are
related problems surgeons should communicate with the
consulting obstetrician if there is any doubt as to the
appropriateness of dental treatment.
Radiotherapy
Radiotherapy in the head and neck region may not only
cause mucosites and xerostomia but also reduces the
vitality of bone, which increases susceptibility to
osteoradionecrosis. This is discussed in Chapter 36.
Renal disease
Renal disease is becoming more important to the dental
surgeon as more patients are now receiving renal dialysis
278
or renal transplantation. Patients receiving regular haemodialysis are heparinised before dialysis and haemostasis
is impaired for 6–12 h thereafter. These patients are also
at greater risk of carrying hepatitis viruses. Furthermore,
the permanent fistula formation that is required for
haemodialysis is susceptible to infection and antibiotic
cover should be provided for these individuals.
In addition, the kidney is a major organ of excretion
and many drugs may have reduced elimination leading to
possible toxic effects if renal function is impaired. The
British National Formulary should be consulted before
prescribing drugs for any patient with a history of renal
disease.
Respiratory disease
Long-standing or severe obstructive pulmonary disease
poses general anaesthetic problems not only because of
the compromised gaseous exchange but also because of
the possible related right-sided heart failure problems.
The conditions most likely to cause chronic obstructive
pulmonary disease are bronchitis, bronchiectasis and
asthma.
Treatment that is to be carried out under local
anaesthetic should be staged to reduce stress and fatigue.
Asthmatic patients should be counselled to bring their
salbutamol or corticosteroid inhalers to the surgery and
to use them if the need arises. Salbutamol and oxygen
should be kept in the surgery, with a suitable method of
delivery as an emergency measure.
Worsening of asthma can be related to non-steroidal
anti-inflammatories and caution should be exercised in
their prescription.
36
Diseases of bone
Introduction
Central giant-cell granuloma
The health of the bone of the jaws is important to the
integrity of the oral cavity and the teeth. Among them, a
number of conditions, primarily of bone, exist which
may be genetic, metabolic or due to some other
aetiology. Often, however, bone disorders have a mixed
aetiology which makes their classification problematic:
cherubism is a genetic condition but is also a fibroosseous metabolic bone disease. A list of bone disorders,
categorised according to their known aetiology is shown
in Fig. 36.1. These will be discussed in turn.
The clinical appearance in the jaws of this lesion may be
exactly the same as the brown tumour described later in
hyperparathyroidism. However, it is not a parathyroidrelated problem but appears to be an endosteally originating resorptive process causing a cyst-like lesion filled
with a very vascular fibrous tissue rich in multinucleated
giant cells.
Achondroplasia
Achondroplasia is the most common genetic skeletal
disorder and is characterised by failure of epiphyseal
cartilage growth. This leads to short limbs and a retrusive
middle third of the face due to defective growth at the
base of the skull. The facial deformity leads to
malocclusion.
This very rare condition affects the mandible rather than
the maxilla. It is characterised by expansion of the
mandibular inner and outer cortical plates with a very
vascular fibrous tissue that contains osteoclasts and areas
of immature bone. The lesion may appear radiographically as multilocular radiolucencies with a soapbubble type of appearance and with evidence of marked
expansion in larger lesions. Treatment is by curettage
locally and some operators prefer to freeze the periphery
of the bony cavity with liquid nitrogen. Occasionally,
very aggressive aneurysmal bone cysts may require more
radical treatment in the form of local resection of the
affected part of the jaw.
Clinical presentation
There is normally a bony expansion of mandible rather
than maxilla and there may be mobility of related teeth
and resorption of roots.
Diagnosis
Radiographically and histologically, the giant-cell
granuloma is indistinguishable from the brown tumour,
and bone biochemical tests must be carried out to
exclude hyperparathyroidism. The diagnosis is therefore
made on histological grounds supplemented by negative
serological findings of parathyroid disease.
Management
These lesions are treated conservatively by local
curettage. They do have a tendency to recur and many
operators now freeze the bony walls of the cavity with
liquid nitrogen after curettage in an attempt to prevent
this recurrence. In children, where there may be quite
gross deformity, the lesions may respond to calcitonin
injections, which are given over a prolonged period such
as a year. When successful, such treatment may avoid the
need for extensive surgery and the consequent aesthetic
problems that can, in turn, require later surgical
reconstruction in the form of bone grafting.
279
Fig. 36.1
280
Diseases of bone according to aetiology.
Cleidocranial dysostosis
Clinical appearance
This is also a very rare inherited disorder. It is characterised by partial or complete agenesis of clavicles, by
frontal bossing, ocular hypertelorism (excessive spacing
between the orbital cavities) and late closure of skull
fontanelles. Dentally, there may be multiple supernumerary teeth, lack of eruption of teeth generally and
thin dilacerated roots. It would appear that normal
resorptive activity during eruption is compromised
leading to the unerupted teeth lying in crypts covered
with overlying bone which does not resorb. Dental treatment involves exposure of teeth and removal of obstructing supernumeraries where these are impeding normal
eruption. However, even after exposure, the teeth may
not erupt satisfactorily.
In the monostotic form, the usual presentation is of a
painless enlargement of the maxilla on the affected side.
Buccal and palatal aspects of the alveolar bone may be
enlarged and expanded and this may cause spacing
between the teeth compared to the unaffected side. The
occlusion, however, is seldom significantly affected other
than the spacing and the teeth erupt normally and are not
unduly mobile. The overgrowth can usually be seen as a
facial asymmetry with fullness of the cheekbone and
nasolabial fold.
Fluorosis
Excessive intake of fluoride can lead to mottling of the
teeth. Skeletal sclerosis can also occur and this is
histologically similar to Paget's disease.
Fibro-osseous lesions
These form a group of lesions with diverse aetiologies
with a range of clinical presentations. Fibrous dysplasia
is the most important.
Diagnosis
The diagnosis is normally made on three grounds: the
age of the patient and clinical features described; the
radiographic appearance and the histopathology. Radiographs of the affected bone or bones typically show a
granular appearance that has been likened to ground
glass. There is an obvious excess of this abnormal bone
and it merges with the normal appearance of bone without a clearly defined separation. A bone biopsy will
generally show the typical histological picture of islands
of irregularly shaped bone with vascular fibrous tissue
interspersing.
Bone biochemistry is normally unhelpful, with
calcium, phosphate and alkaline phosphatase levels
within normal limits. The alkaline phosphatase level,
which is a measure of osteoblastic bone formative
activity, may be raised if the sample is taken during an
active growth phase of the child, and its relevance is
therefore almost impossible to determine.
Fibrous dysplasia
This condition affects children and is, as the name
implies, a replacement of normal bone by an immature
bone not unlike woven bone with extensive vascular
fibrous tissue elements. The abnormality may affect
many bones (polyostotic) or one bone (monostotic), and
the maxilla is far more commonly affected than the
mandible. Two rare variants are also identified, one being
cherubism and the other Albright's syndrome, which is a
form of polyostotic fibrous dysplasia with additional
features of skin pigmentation and precocious puberty in
females. Fibrous dysplasia is usually self-limiting and
tends to 'burn out' on completion of skeletal growth. It
can, however, cause quite marked disfigurement in severe
cases and in the polyostotic form can encroach on bony
foramina leading to compression of nerves.
Management
Unless there is unacceptable disfigurement, most surgeons prefer to defer treatment until growth is complete.
The surgery is normally in the form of recontouring of
the excess bulk of bone. In more gross cases, surgery
may be needed at an earlier stage but may require to be
repeated when maturity is reached.
Cherubism
This is regarded as a form of fibrous dysplasia that is
familial and carried by a dominant gene. It is characterised by an increased width and fullness of the angles
of mandible bilaterally. The bone itself is immature in
281
these regions with areas of vascular fibrous tissue. Radiographically, it appears as bilateral multilocular cyst-like
radiolucencies. Although normally seen in the mandible,
the maxilla can be affected also. The condition is first
seen in childhood and becomes less active on maturity.
Cemento-ossifying fibroma
These rare lesions can grow to a considerable size. They
are essentially fibrous overgrowths that become filled
with either a bony or cement-like calcification. They are
generally painless and are found as swellings usually in
the buccal sulcus. They may be encapsulated but these
capsules are not invariably present. Surgical removal of
the lesion may be difficult as the boundaries of the lesion
may be almost impossible to ascertain. They are more
common in the mandible and generally present in young
adults.
Cemento-ossifying dysplasia
This process is similar to fibrous dysplasia but lesions
resemble cemento-ossifying fibromas and probably arise
in the periodontium. The condition may be multifocal or
generalised. Single lesions are called cementomas and
florid lesions are termed gigantiform cementomas. They
are more common in women and black patients and
undergo progressive periapical calification. This leads to
difficulties with extractions and the subsequent risk of
osteomyelitis.
Gigantism
Excess growth hormones arising from a pituitary
adenoma will cause increased growth in height before the
epiphyses are closed. Subsequent growth causes
acromegaly with prognathism and increased soft tissue
growth leading to coarse facial features and macroglossia.
The bone quality is normal.
Hyperparathyroidism
282
This may be primary and due to overproduction of
parathormone often by an adenoma in the parathyroid
glands or secondary to conditions that reduce calcium
levels in the blood, such as chronic renal disease. Where
increased levels of parathormone are present, calcium is
mobilised from the bony skeleton to raise blood levels of
calcium. In the primary form of the disease, this leads to
hypercalcaemia, and renal calculi may develop if the
problem is not identified. In the bone, however, where the
jaws can be affected, cyst-like spaces known as 'brown
tumours' may develop. The bone in these tumours is
resorbed by vascular fibrous tissue with multinucleated
giant cells in profusion. This has given rise to the other
name of this condition, osteitis fibrosa cystica. In the
jaws, the mandible is more commonly affected by such
lesions than the maxilla.
Clinical features
In the mandible, the presence of a brown tumour may
give rise to expansion of the outer and/or the inner
cortical plates of bone. Occasionally, the soft tissue of the
brown tumour may grow through the upper border of the
alveolar process and appear as a dark red or purplecoloured mass under the oral mucosa. The lesion is
usually non-painful but may be tender to palpation.
Diagnosis
Radiographs will show a well circumscribed area of
radiolucency with a less defined lamina dura surrounding
it than is normally found in a true cystic lesion. The outline may have a scalloped margin and some authorities
also describe a lack of definition of the lamina dura
around all the standing teeth. This, in fact, is difficult to
discern and tends to be a rather subjective finding.
An incision biopsy of the lesion reveals the typical
histological appearance of fibrous vascular tissue with
large numbers of multinucleated giant cells.
Serum biochemistry will reveal elevated parathormone
levels and, in the primary form of the disease, this will be
accompanied by a raised serum calcium and lowered
phosphate level.
Management
Primary hyperparathyroidism is normally treated
surgically by removal of usually an adenoma of the
parathyroid gland. The bone lesions usually resolve
spontaneously following this surgery.
Hypophosphatasia
This rare recessive genetic disorder can be of early or late
onset. It is characterised by bony fragility and a rickets-
like condition. Defective cementogenesis can lead to
shedding of the teeth.
Infective bone conditions
Infection in bone is relatively uncommon in the jaws
given the large number of dental abscesses that occur and
also the amount of bone exposed by extractions that heal
without apparent problems. It is probably a reflection of
the good blood supply in the mouth generally, and particularly in the upper jaw, which seldom becomes
infected. The use of antibiotics also limits the occurrence
of bone infection compared with preantibiotic days.
Osteomyelitis is so rare nowadays that most clinicians
look for underlying reasons for its occurrence. Conditions
that have rendered the patient immunocompromised,
such as diabetes mellitus, HIV infection, immunosuppressive drug therapy and blood dyscrasias should be
excluded. Local factors, such as previous radiotherapy to
that region of the jaw or lack of a normal blood supply
(as encountered in osteopetrosis), are also relevant as
predisposing factors. A number of distinct bony infections can occur (Table 36.1) and these will be considered
here.
that found in dental abscesses with anaerobes predominating. It differs in this from osteomyelitis in a long
bone, which is often of staphylococcal origin and is said
to be haematogenous, meaning that the bacteria have
circulated in the bloodstream from other sources such as
skin infections.
Clinical features
These reflect the results of a sudden increase in pressure
within the medulla of the bone in which the intact
cortical plates do not allow any release in the early
stages. This rapid increase in pressure is brought about
by the inflammatory reaction in response to the presence
of infection. Patients therefore complain of severe
throbbing pain, trismus, swelling over the mandible and
paraesthesia or anaesthesia in the distribution of the
mental nerve. More variably, a bad taste or discharge
through sinus formation may be seen. In severe cases
there may be pyrexia with consequent malaise and
anorexia. Lymphadenitis may be relatively late but may
be palpable and tender in the submandibular and upper
cervical chain of nodes. Later features may include sinus
formation on the skin and shedding intraorally of
necrotic bone.
Localised osteitis (dry socket)
Radiographic features
This is discussed in Chapter 26.
Initially, there may be little evidence of changes within
the bone, other than possible dental foci of infection. In
the later stages, areas of patchy radiolucency are present,
within which there may be irregular areas of increased
density that signify bony sequestra (Fig. 36.2). Sequestra
are areas of dead bone formed by thrombus formation in
the nutrient blood vessels to these areas of bone brought
about by the increased pressure on these vessels. The
areas of necrotic bone further enhance the inflammatory
reaction, as the body attempts to shed them in the same
way as any foreign body.
Acute osteomyelitis
By definition, this is an acute inflammatory reaction to
infection within the medulla of the affected bone. It
rarely affects the maxilla, which has a more profuse
blood supply, being primarily a mandibular infection. It
is comparatively rare and may well be an indication of
other disease that reduces the normal defence mechanisms.
The source of most mandibular osteomyelitis is dentoalveolar infection and the microbial profile is similar to
Management
Table 36.1
Infective bony conditions
Localised osteitis
Acute osteomyelitis
Chronic osteomyelitis
Chronic sclerosing osteomyelitis
Subperiosteal osteomyelitis
Osteoradionecrosis
Initially, the management of osteomyelitis follows the
principles of any acute pyogenic infection: incision and
drainage of any collection of pus together with appropriate vigorous antibiotic therapy. If possible, pus should
be sampled by aspiration for culture and antibiotic
sensitivity testing but antimicrobial prescriptions should
not be delayed for this laboratory analysis. Commonly,
metronidazole and amoxicillin are used together but
283
and pain that responds to non-steroidal antiinflammatory drugs, which are often used together with
antibiotics, although the latter are usually prescribed
before any accurate diagnosis is made. Systemic corticosteroids can also be helpful in controlling the acute
symptoms. Some investigators have suggested that the
condition, which is chronic and intermittent in character,
may be related to excessive tooth clenching or grinding,
and will therefore respond to interocclusal splinting of
the teeth. Surgery often involves decortication of the
outer lamellar bone and this is normally followed by an
osteosclerotic reaction. The condition frequently remits
spontaneously with the affected region or regions showing increased radiodensity on radiographic examination.
Subperiosteal osteomyelitis
Fig. 36.2
Radiograph showing acute osteomyelitis
3 months after removal of an infected lower third molar.
these can be changed to reflect the bacteriological findings
if required. Clindamycin has good bone-penetrating
qualities and is effective in many anaerobic infections, it
is therefore a useful drug if there is a poor clinical
response. Once the acute phase has been brought under
control, surgical sequestrectomy, which removes any
areas of dead bone and curettage, is carried out. If significant loss of bone has occurred, bone grafting may be
considered at a later stage but only after total resolution
of the infection.
Chronic osteomyelitis
Features of chronic infection are less florid that in the
acute form, and hence pain is less marked, disturbance of
nerve transmission is much less likely and generally the
presentation is more subtle. Management is normally by
surgical means with sequestrectomy and curettage.
Chronic sclerosing osteomyelitis
284
This is a rare and ill-understood condition in which areas
of bone in the mandible show radiographic evidence
of rarefaction often giving patchy round or oval
radiolucencies in the affected region. It does not appear
to be due to bacterial infection although there is some
dispute over this, and surgical curettage reveals chronic
inflammatory changes but no histological evidence of
microbial presence. The condition may cause swelling
This is more commonly seen in children or young adults
where infection usually through an infected tooth causes
pus to form under the periosteum of the bone. The
periosteum is hence lifted off the bone and reacts by
forming a layer of new bone known as an involucrum.
Patients have a fairly hard bony swelling formed of this
new bone beneath which pus may be trapped. Radiographically, this is often best illustrated by occlusal or
posteroanterior mandibular views, which show the outer
cortical plate with a thin overlying wafer of new bone
where the periosteum has been raised from the surface
and formed new bone in an attempt to wall-off the
infection. Treatment consists of removal of the source of
infection, normally a tooth, and curettage of the area with
appropriate removal of the overlying involucrum bone.
Osteoradionecrosis
Irradiation to the jaws may occur as a result of radiotherapy for malignant disease of the mouth, pharynx or
salivary gland regions. Damage to the cells within the
bone, the osteocytes, and to the nutrient blood vessels
within bone, renders the bone less vital and hence more
open to infection. In the blood vessels there is an
endarteritis and periarteritis that significantly reduces the
blood supply to the bone and this particularly affects
mandibular bone, which has a less profuse vascular
network than the maxilla. Where irradiation has been
extensive, which is now less commonly seen due to
better zoning of the beam and protection of adjacent
tissues, a form of avascular necrosis can occur with
exposed bone failing to sequestrate normally and heal
with granulation tissue. Creation of a wound such as an
extraction wound can, therefore, result in infection very
easily, and this may be difficult to control. Added to this
problem is a dry mouth and high caries rate if the salivary
glands have been affected by the radiation.
Table 36.2
Neoplasm in bone
Osteoma
Osteosarcoma
Cemento-ossifying fibroma
Odontogenic neoplasms
Management
Prevention is preferable to treating exposed or infected
bone and careful preradiation assessment of restorative
needs is essential. Unrestorable teeth should be extracted,
if possible 3 weeks before the start of radiotherapy. Strict
oral hygiene measures should be stressed to reduce the
chance of subsequent caries and tooth loss and this
should be in conjunction with regular dental treatment
including preventive measures.
When extraction is unavoidable after radiation, most
clinicians use antibiotics for a week to 10 days after the
extraction. Care should be taken to cover any exposed
bone such as interradicular septa and, if necessary, such
uncovered areas need to be protected with a Whitehead's
varnish ribbon gauze pack or covered with a surgical
flap. More recently, hyperbaric oxygen therapy has been
used with some success in the management of these
problems. The treatment involves the patient entering a
pressure chamber where the atmospheric pressure is
increased to about 2.5 atmospheres for a period of 90
min. This has to be done daily for several weeks but does
appear to help the healing process significantly. It has
also been shown that surgery to remove necrotic bone
following hyperbaric oxygen treatment increases the
chance of successful healing. The success of hyperbaric
oxygen therapy underlines the ischaemic cause of the
problem consequent to radiotherapy.
Neoplasms
Neoplastic disease
Neoplasms derived from bone itself are relatively
infrequent in the jaws. The benign osteoma and the
malignant osteosarcoma are very uncommon. However,
the jaws may be affected by neoplasms of dental origin,
such as odontogenic tumours, secondary metastatic
deposits in bone from primary tumours such as breast,
thyroid or lung, or more commonly from direct invasion
of the oral squamous cell carcinoma arising from the
overlying mucosal epithelium. Neoplasms in bone give
rise to radiographic changes in the form of radiolucencies
and therefore bone loss unexplained from the more common infective causes should always arouse suspicion. In
these situations, a biopsy of the area is the only satisfactory method of eliminating the possibility of neoplastic
disease. The neoplasms to be discussed are listed in
Table 36.2.
Osteoma
This is a benign tumour of bone and, unlike bony
exostoses, is very uncommon. It can arise from compact
or cancellous bone in the form of a painless hard swelling.
Radiographically, a round or oval-shaped radiodense
image is seen and although a capsule is classically found
in benign tumours it is seldom seen clearly on such
radiographs. If the swelling is interfering with function it
can be surgically removed.
A more rare condition, Gardner's syndrome, is
characterised by multiple osteomata of the jaws. The
condition is important because the syndrome exhibits
multiple intestinal polyposis and these polyps have the
potential for malignant transformation. Urgent referral to
a gastroenterologist is therefore needed.
Osteosarcoma
This is - fortunately - a rare malignant tumour of the
jaws. It is more common in young people under the age
of 30 but can occur in older patients and a small number
of people with Paget's disease develop osteosarcoma as a
rare complication. The age of presentation of the disease
appears to be significantly older in the jaws than in other
bones, and it may affect maxilla or mandible. Jaw lesions
also appear to differ from those in other bones in that
metastases usually to lung or brain are less prevalent. The
poor prognosis of the disease appears to be more related
to local aggressive recurrence.
Clinical appearance
This varies according to the site of origin but normally
consists of a fairly rapidly enlarging swelling, which can
be painful and cause loosening of related teeth. Anaesthesia
may also occur if the tumour grows in relation to the
inferior dental canal or infra orbital canal causing altered
sensation peripheral to the point of tumour pressure or
infiltration.
Radiographs may show clear evidence of bone
destruction although areas of radio-opacity, which may
be quite dense, can be seen within the radiolucent region.
The periphery is indistinct reflecting the rapid growth
and both widening of the periodontal membranes and
resorption of the roots of teeth may be evident.
Diagnosis
Table 36.3
Odontogenic tumours and odontomes
Epithelial in origin
Ameloblastoma
Calcifying epithelial odontogenic tumour (Pindborg
tumour)
Adenomatoid odontogenic tumour
Mesenchymal in origin
Odontogenic myxoma
Cementoma
Odontomes
Invaginated odontome (dilated composite odontome
and 'dens in dente')
Compound composite odontome
Complex composite odontome
Germinated odontome
This is confirmed by incision biopsy of the lesion.
Management
The lesion is treated by radical excision of the affected
bone and wide margins of soft tissue are also removed.
More recently, better responses have been claimed by
presurgical chemotherapy and, if necessary, postsurgical
chemotherapy or radiotherapy.
Cemento-ossifying fibroma
This neoplasm has been discussed in the section on fibroosseous lesions.
Odontogenic neoplasms
This is a collection of neoplasms derived from toothforming tissue and may arise from epithelial or
mesenchymal tissue. They are rare, although the most
aggressive of them - the ameloblastoma – is the most
common. At the other end of the spectrum of these
neoplasms are the odontomes, which are best considered
hamartomas (which means that they are abnormal toothlike structures that generally do not continue to grow
once their development is complete). There are many
histological types of odontogenic tumour, the more
common of these are listed in Table 36.3.
Ameloblastoma
286
The ameloblastoma is the most common of the odontogenic tumours and can present at any time from childhood to older age groups but is more often seen in the
middle-aged adult population. It occurs in both mandible
and maxilla but is far more common in the lower jaw,
with an approximate ratio of 3:1. In the lower jaw, the
angle and ramus is the most frequent site, with over
two-thirds of occurrences.
The tumour is variable in its aggressiveness and
spreads by local destruction of bone. If untreated, it will
eventually spread into soft tissues and this may make it
very difficult to eradicate surgically. It does not tend to
metastasise other than the extremely rare malignant
ameloblastoma variant. There are several histological
variants of this tumour, the two most common being the
plexiform and the follicular forms, but these different
appearances do not appear to produce differences in
behaviour or prognosis.
Clinical features
Gradual swelling of the jaw is the usual initial symptom
of this tumour, although it may be diagnosed through a
radiograph before this becomes apparent. Loosening and
displacement of teeth can occur, although pain or altered
sensation is not usually reported. In the earlier stages, the
swelling will be in the form of expansion of buccal
and/or lingual cortical plates and is hence hard to
palpation. With further growth, however, the swelling
may be softer but firm denoting that the lesion has eroded
through the bone into the adjacent soft tissues.
Radiographs classically show a multilocular 'soap
bubble' round or oval-shaped radiolucency with welldemarcated radio-opaque margins (Fig. 36.3). The sharp
delineation of the radiolucent areas reflects the slow rate
of growth of these neoplasms. It may displace the outline
of the inferior dental canal and may also cause displacement and/or resorption of the roots of the teeth.
Fig. 36.4
Radiograph of a cystic ameloblastoma.
the fluid content, it may not be taken in an area that is
showing neoplastic change and it is therefore important
that, when any presumed cyst is enucleated, the whole
pathological specimen is examined by a pathologist who
is aware of such variations of the ameloblastoma (see
Ch. 28).
Irrespective of histological differences in this neoplasm,
most authorities advise total resection with around 1 cm
clearance of the affected bone. In smaller lesions this
may still allow preservation of the lower border of the
mandible and this clearly has significant advantages with
regard to aesthetics. The resultant defect may be filled
with a bone graft and, where necessary, supported by a
reconstruction plate.
Fig. 36.3
Radiograph of an ameloblastoma showing
(a) soap-bubble appearance; (b) expansion.
One recognised variant of the ameloblastoma is the
cystic ameloblastoma, which most frequently occurs at
the angle of mandible. Radiographically, this is indistinguishable from a dentigerous cyst related to an
unerupted wisdom tooth and is a fluid-filled cystic cavity
with nodules of ameloblastoma within certain areas of
the lining of the cyst (Fig. 36.4). Even if an incision
biopsy of the cyst lining is taken following aspiration of
Calcifying epithelial odontogenic tumour (Pindborg
tumour)
This rare neoplasm can occur at any site in the upper or
lower jaw but is most commonly found in the mandible.
It causes painless expansion of the affected area and is
frequently related to an unerupted tooth. Radiographs
show a radiolucency, which may be multiloculated, and
there may be areas of radiodensity within the central area
of the radiolucency. Demarcation of the tumour from
normal bone is not always clear. The lesion is locally
invasive into the surrounding bone and is treated by a
localised resection with a small margin of normal bone
around it to reduce the chance of recurrence.
287
Adenomatoid odontogenic tumour
This benign neoplasm is commonly found in the maxilla
and is often related to an unerupted canine tooth. Radiographically, it can be indistinguishable from a dentigerous
cyst around the crown of the unerupted tooth. Conservative curettage is its method of treatment.
Odontogenic myxoma
These slow-growing tumours are benign and are most
frequent in the second and third decades. They occur in
either jaw but are more common in the mandible. They
erode bone and enlarge to form multilocular, radiolucent
regions that can be very difficult to differentiate from
other multilocular lesions such as ameloblastoma or
odontogenic keratocysts. Treatment is conservative by
thorough bony curettage. Recurrences can occur and,
therefore, although the treatment is generally conservative, follow-up is required. These tumours do not
appear to metastasise.
Fig. 36.5 Radiograph of an invaginated odontome with
related radicular cyst.
Cementoma
These lesions are composed of cementum and may occur
singly or may affect many teeth in the dentition. They are
a form of cemento-ossifying dysplasia. They are asymptomatic and are usually diagnosed by radiographic appearance. In the early stages they cause radiolucency, which
later mineralises into cement-like tissue. The teeth affected
are vital throughout this process.
Odontomes
Odontomes are relatively infrequent occurrences in the
dentition but, when they do occur, they often impede the
normal eruption of adjacent teeth or, in the case of the
invaginated form, directly affect the vitality of the tooth.
They are best regarded as malformations of development
of the tooth from its dental lamina or as hamartomas,
which cease their growth at completion of their
formation and do not alter thereafter.
Invaginated odontome
288
This malformation is most often seen related to the upper
lateral incisor tooth. It is formed by an ingrowth of
enamel epithelium forming a blind-ending, enamel-lined
pouch that is in direct communication with the surface of
the tooth, most commonly at the cingulum. The labial
surface of the tooth may look entirely normal and the
entrance to the invagination may be a minute pit, but the
ingress of saliva and bacteria usually results in pulpal
death and the development of an apical lesion. Such
invaginations may be so small as to be difficult to image
even with good radiographs but in some cases the malformation may be so great that the whole clinical crown
is taken up by the dilated nature of the ingrowth and the
appearance on radiograph can then be likened to a tooth
within a tooth or 'dens in dente' (Fig. 36.5).
When the invagination is small the tooth may well be
amenable to conventional root canal treatment and, where
an apical cyst has developed, periradicular surgery. However, the malformation may be so gross that extraction is
the only practical solution.
Complex odontome
This developmental aberration results in a random
laying-down of all the dental elements in a totally
haphazard fashion. Radiographically, it gives rise to an
irregular radiodense image. Enamel, dentine, cement and
pulpal tissues are all represented and the radiographic
image 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 teeth
from normal eruption and they are better removed as
early as possible to reduce this chance.
Compound odontome
In this abnormal manifestation of development, there is
more organisation of the dental tissues and the lesion
consists of numerous small denticles massed together
within an outer capsule (Fig. 36.7). The odontome may
be small, with only a few tiny teeth, or it may be of
considerable size and contain many denticles. As with
the complex odontome, the compound form should be
removed where it is affecting normal eruption of the
dentition.
Germinated odontome
This defect of development arises from either a complete
or partial fusion of adjacent tooth germs or by a splitting
or dichotomy of one germ. The result is a fusion of the
resultant tooth that may affect only the crown or the
crown and root together. They can pose both aesthetic and
orthodontic 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 largely
be dependent upon aesthetic and orthodontic criteria.
Although not a developmental problem, fusion of
teeth by excessive production of root cementum can lead
to what is referred to as pathological germination or
concrescence. The most common teeth to be joined in
this fashion are upper second and third molars, especially
where the upper wisdom tooth has developed with a
disto-oblique angulation. Concrescence of teeth is
fortunately very rare as they pose considerable problems
in removal since they are usually only detected at
extraction.
289
Osteogenesis imperfecta
This is a group of rare, usually autosomal dominant
conditions of varying severity affecting the formation of
all bony tissue. The condition is sometimes referred to as
brittle-bone disease because the inherent weakness of the
structure of the tissue can lead to fracture of the bone
with even minimum trauma. The condition arises due to
defective biosynthesis of type I collagen, leading to
inadequate amounts of bone formation by osteoblasts. In
addition to the weak nature of the bones, they tend to be
thinner than normal, although growth may be relatively
unaffected. Multiple fractures can lead to deformity. The
sclerae of the eyes are typically a bluish colour and many
cases also have a related defect in dentine structure,
dentinogenesis imperfecta. This dentine is poorly
attached to the overlying enamel and this can lead to
rapid loss of the enamel and subsequent wear of the
unprotected dentine. Patients may often therefore require
extractions, and these need considerable care in their
execution, although fracture of the jaw during such
extraction is relatively uncommon.
Table 36.4
Risk factors for osteoporosis
Physiological
Pathological
Ageing
Female sex
Alcohol
Corticosteroid drugs,
Cushing's syndrome
Early menopause
Multiple myeloma
Immobility
Diabetes mellitus rare
Underweight
Hypogonadism
causes
Childhood maturation failure Thyrotoxicosis
Smoking
with increasing age accounts for the apparent increasing
prevalence of this disorder. The risk factors for osteoporosis are listed in Table 36.4.
Treatment is unsatisfactory. Prevention is preferred
and hormone-replacement therapy (HRT) is effective in
postmenopausal women. Patients with osteoporosis have
increased alveolar resorption if they are edentulous.
Paget's disease
Osteopetrosis
This inherited but very rare condition is sometimes
known as marble bone disease because of the density of
the bone that encroaches upon medullary spaces and may
therefore compromise haemopoesis. The condition arises
due to inactivity of osteoclasts. The problem can affect
the jaws where the lack of vascularity of the tissue may
lead to infection. The avascular bone makes eradication
of infection by antibiotics difficult because adequate
levels of such antibiotics may not be effective in the
affected area because of the lack of blood supply.
Similarly, surgical removal of affected bone can be
followed by very poor healing and the risk of reinfection.
Extractions may not only be difficult, therefore, but may
also lead to infection. Reduction of the medullary spaces
compromises haemopoesis, which then takes place in the
liver and spleen. Regardless, anaemia is progressive
without marrow transplantation.
Osteoporosis
290
This disorder is characterised by loss of bone density.
The composition of the bone is normal and there are no
demonstrable metabolic changes. Physiological bone loss
This disease can affect the jaws but is normally more of
a problem in the weight-bearing bones. It is characterised
by irregular resorption of bone with subsequent
redeposition and it therefore disrupts normal bony
architecture. During the resorptive phases, areas of bone
may be severely resorbed, leading to distortion under
normal weight bearing function. There may be pain in
the bones, large vascular regions in the medullary spaces
and 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 the
relative avascularity following redeposition of bone can
then 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 particular
the maxilla. Deformity can result from vertebral column
and lower limbs being unable to deal with the forces and
deforming as a result. This deformation led to Paget's
disease being known as 'osteitis deformans', but this
term is now rarely used. Enlargement of the jaws, where
they are affected, may result in loss of fit of prostheses
and the teeth themselves may show excessive deposits of
cement known as hypercementosis.
trimmed and covered by soft tissues with appropriate
suturing.
Diagnosis
Rickets
Blood samples may show very high levels of alkaline
phosphatase with normal values for calcium and phosphate. Radiographs show patchy areas of radiolucency
interspersed with radio-opaque density. The descriptive
term 'cotton wool' has been used to describe these
changes and is an accurate reflection of the radiographic
changes seen. Bone biopsy may show irregular areas of
resorption or evidence of previous resorption in the form
of reversal lines. These are heavily staining haematoxilin
lines, which denote the boundary of previous resorptive
activity.
Rickets arises as a result of defective calcium and
phosphorus metabolism during bone growth. After
cessation of bone growth the condition causes osteomalacia. It may occur in three ways (Table 36.5).
Biochemistry reveals a low normal calcium and
phosphate (both maintained by parathyroid activity) and
an increased bone alkaline phosphatase level. Treatment
is with oral vitamin D.
Management
In the general management of Paget's disease,
bisphosphonates are the usual form of treatment. These
drugs appear to have a direct effect on hydroxyapatite
crystals, which make the bone less receptive to resorptive
activity and hence reduce the rate of turnover. Dental
problems may be encountered in the form of excessive
bleeding if the area of the jaw affected is undergoing
active resorption, and infection can be a complication
where the bone has reformed and become relatively
avascular. Added to these problems may be hypercementosis of the roots resulting in large-rooted teeth
that may be difficult to extract conventionally. Prophylactic antibiotics are often prescribed for extractions if
the bone is sclerotic and areas of exposed bone such as
prominent interdental or interradicular septa should be
Scurvy
Scurvy is caused by vitamin C deficiency. This is now
not seen in clinical practice but, historically, caused bone
defects due to defective collagen formation, which also
caused bone pains due to periosteal haemorrhage.
Table 36.5
Vitamin D deficiency
Reduced intake/
absorption
Skin synthesis impaired
Metabolism abnormal
Poor dietary content of
vitamin D
Fat malabsorption steatorrhoea
Lack of exposure to sunlight
Pigmented skin
Impaired renal activation of
25-hydroxyvitamin D to
1,25-dihydroxy vitamin D;
e.g. chronic renal failure
Interference by anticonvulsant
drugs
291
37
Dental implants
Introduction
Dental implants are now increasingly used to attach
crowns, bridges or dentures by anchorage to bone. Extraoral implants are also available for attaching facial
prostheses such as artificial ears or noses, and for bone
anchored hearing aids.
Placement of implants requires careful patient selection
and treatment planning. Although the surgical techniques
are straightforward, they are exacting and practitioners
should only embark on implant treatment after appropriate
training and experience.
Types of implant
292
Early implants were unreliable because the attachment to
bone was by a layer of connective tissue. A variety of
pins, screws and blades were tried but epithelial downgrowth frequently led to rejection. The resulting loss of
alveolar bone led to an even more difficult restorative
problem.
Subperiosteal implants were less damaging but
required a general anaesthetic to expose the bone surface
for impression taking. Chrome-cobalt frames were constructed in the laboratory and a further anaesthetic was
then required for insertion. They were often in function
for many years but epithelial downgrowth usually resulted
in failure. Removal of failed implants was difficult due
extensive scar tissue.
Transmandibular implants appeared to have some
advantages but an extraoral incision was required and the
surgical technique was demanding. They were obviously
unsuitable for routine use as they required specialist
expertise and hospital facilities.
The progression to modern implantology followed the
discovery of osseointegration, with the predictable
success of titanium implants. Osseointegration implies
Table 37.1
Osseointegrated dental implants
Osseointegration
Indications for implant treatment
Patient selection
Treatment planning
Surgical technique
Augmentation of bone
Complications
Success rates
contact between the implant surface and bone without
any intervening connective tissue layer. It is, in fact, an
ankylosis of implant to bone and some prefer the term
'functional ankylosis'. The bone does not recognise the
implant as a foreign body, which becomes, in effect, part
of the bone. Thus an osseointegrated implant forms a
direct bone anchorage for a prosthesis.
Osseointegration is therefore a prerequisite to successful implant placement and a consideration of the requirements for this is followed by a description of the indications
for implant placement in dentistry. Discussion of patient
selection and treatment planning will be followed by a
description of the surgical techniques involved in implant
placement including augmentation techniques, complications and a consideration of success rates (Table 37.1).
Osseointegration
The requirements for successful osseointegration of an
implant are listed in Table 37.2. Suitable implant materials
are discussed below.
Implant materials
Ideally, an implant should be non-toxic, biocompatible,
strong and aesthetic.
Table 37.2
Requirements for osseointegration
Suitable implant material
Minimal surgical trauma
Primary implant stability
Adequate bone volume and quality
Delayed loading (healing phase)
Metals such as nickel and chromium used in stainless
steel are corroded in living tissue and taken into the bloodstream. There is concern about possible neurotoxicity.
Titanium is also absorbed and may be detected in tissues
at very low concentrations, but there is no evidence of
toxicity.
Implant materials can be biotolerated, bioinert or
bioactive. Stainless steel, chrome cobalt and other alloys
are tolerated by bone but are linked by a connective tissue
layer rather than an intimate bond. Titanium implants
make direct contact with bone but are regarded as bioinert
because there is no chemical bond. Bioactive materials
such as calcium phosphate and hydroxyapatite allow a true
chemical bond to develop as the bone surface remodels.
The material should be able to withstand occlusal forces
and be capable of accurate machining into cylinders with
screw threads for initial stability in bone, and with suitable abutment connections. Unfortunately, a bioactive
material with adequate mechanical properties has not yet
been developed.
Surface characteristics can modify the properties of
the material. Correct pore size is important in osseointegration of ceramics. Surface roughness may affect the
reaction of tissues to implants enhancing osseointegration
as well as increasing the surface area in contact with
bone.
gas at high temperature in an electric arc. Plasma-sprayed
implants have a much greater surface area and mechanical
resistance to rotational forces. Abrasion of the surface
with titanium pellets or grit blasting and acid etching
may also achieve similar effects. Some workers claim
that these surface modifications promote a chemical and
mechanical attachment to bone. Rough surfaces exposed
to the mouth will be difficult to keep clean and plaque
formation will result in peri-implant disease. Transmucosal
elements and abutments are therefore made smooth. A
'gingival' cuff attachment is achieved by reorientation of
connective tissue fibres and possibly by adhesion of
epithelial cells.
Ceramic
Ceramic implants had good biological and aesthetic
properties but lacked mechanical strength. In practice the
incidence of implant fracture was unacceptable and they
have been discontinued. It is possible that better ceramics
will be developed.
Hydroxyapatite
Hydroxyapatite can be used as a coating on titanium
implants because it is osteoinductive. It enhances, and
reduces the time for, osseointegration. It is also used in
particle or block form to augment bone for placement of
implants. It does have mechanical weakness and disruption of the surface occurs in function, although these
microfractures do not seem to result in loss of implants.
Fractures can also occur at the interface between
hydroxyapatite and titanium.
Implant system
Titanium
Titanium is the best material available at present. It is a
highly reactive metal that oxidises in the atmosphere to
form an inert surface layer of titanium oxide. It has good
mechanical properties and can be machined. Implant
fractures can occur but these are minimised by careful
implant design and avoidance of a traumatic occlusion. A
disadvantage of titanium is its grey colour, which may be
visible at crown margins if there is recession and may
discolour thin mucosa. The surface can be polished and
anodised and surface roughness can be achieved by
addition or subtraction processes. In plasma coating,
titanium powder is sprayed onto the implant as an inert
Many implant systems are available and many factors
need to be considered when making a choice. These are
listed in Table 37.3.
Surgical principles
Initially an implant bed must be prepared by drilling a
hole in the bone to receive the implant. It is essential to
minimise tissue damage when preparing the implant bed.
Mucoperiosteal flaps should be well designed, carefully
reflected and gently retracted, so that healing is optimal.
Healthy soft tissue cover enhances osseointegration by
providing a barrier to infection and restoration of blood
293
Table 37.3
system
Criteria affecting choice of implant
Use commercially pure titanium
Components proven to withstand masticatory load
Physiological response of bone when loaded
One- or two-stage system
Type of surface, i.e. plain, plasma sprayed, roughened
or hydroxyapatite coated
Plain cylinder, or threaded ± self-tapping
Diameter and length
Efficiency of drill system
Immediate or delayed loading
Suitability of abutments
supply. With transmucosal systems, soft tissue is sutured
around the implant neck and a good seal is even more
important.
Bone preparation is carried out with the minimum
heat production so that, as far as possible, the osteocytes
near the bone surface remain vital. If there is bone
damage the inflammatory reaction will produce a fibrous
repair resulting in a connective tissue layer between
implant and bone rather than osseointegration.
The requirements that -must be taken into account
when drilling bone to receive an implant are listed in
Table 37.4.
Primary implant stability
The implant bed should be prepared accurately to conform to the shape of the implant, so that there is maximum
contact with healthy bone. This good congruence also
results in primary implant stability, which is essential
during the healing phase.
Screw threads are often used as they increase primary
stability, enhance resistance to occlusal forces and
increase surface area.
Bone quality and quantity
294
Blood supply is essential for bone vitality so the maxilla
might be thought to be better suited for implant
placement. In fact, there is a significantly better success
rate in the mandible, which is likely to have a poorer
blood supply especially in the older edentulous patient. It
seems, therefore, that a firmer bone structure is an
advantage. The cortical plate in the maxilla is often thin
or absent and the cancellous bone is crumbly.
Table 37.4
Bone drilling for osseointegration
Use sharp drills (single or limited use)
Use purpose designed drills
Use drills of smaller diameters first, rather than onestage cutting
Use slow drill speeds (<2000 rpm)
Use cooling with copious chilled saline
Avoid clogging of drill channels - repeated withdrawal
Thread tapping or self-tapping systems are available
Table 37.5 Methods of improving implant
success in the maxilla
Use additional implants to share load
Use connecting bars for bracing
Use maximum length of implant
Consider augmentation of ridge bone
Consider sinus lift to extend available ridge
Reduce occlusal table and eliminate traumatic occlusion
Allow more time for osseointegration
The pattern of bone resorption and anatomical
structures in the maxilla also cause problems. Resorption
causes bone loss from the anterior and crestal surfaces,
often leaving a narrow ridge in a retruded and high
position. Thus there is less bone and the implants have to
be placed in a poor position. The superstructures may
then be placed in a compromised position. The occlusal
load on the implants may therefore be beyond
physiological tolerances.
Implants can still successfully be placed in the
maxilla if allowance is made to avoid exceeding the
above limitations by the methods listed in Table 37.5.
Resorption in the mandible does not alter the anteroposterior implant position but there can be severe loss of
bone height. The alveolar bone has often been completely
resorbed and there is a pencil-thin mandible. Augmentation
is rarely required, even in this situation, and two implants
may be sufficient to stabilise a lower denture. This is
fortunate, as denture instability is more of a problem in
the mandible.
Blood supply may be compromised by radiotherapy
but, although this causes more failures in the mandible,
there is still a reasonable success rate. In the maxilla
there are many more failures after radiotherapy. A course
of preoperative and postoperative hyperbaric oxygen
therapy, if available, may improve success in the maxilla
but is not usually needed in the mandible.
Table 37.6
I
II
III
IV
Classification of bone quality
Cortical bone predominant
Dense cancellous bone and thick cortical bone
Dense cancellous bone and thin cortical bone
Porous cancellous bone and thin cortical bone
The quality of bone available is also important and
this can be assessed using the classification listed in
Table 37.6.
Healing phase
It is a fundamental requirement that undue loading is
avoided until osseointegration has occurred. This is one
of the main differences compared to previous implant
practice where there was immediate loading and osseointegration rarely occurred.
In the mandible, 3 or 4 months are required for
osseointegration, whereas in the maxilla 6 months is
allowed. These rules have been relaxed in the anterior
mandible only. If bone quality is good, depth is adequate
and four or five (or possibly fewer) implants are placed,
the superstructure may be fitted immediately. Theoretically, function encourages bone formation and there is
some evidence that controlled loading could be
beneficial. This is difficult to control in practice at
present.
Indications for implant
treatment
The availability of implants has expanded treatment
options for a number of restorative problems highlighted
in Table 37.7.
Difficult edentulous cases
Poor retention of a mandibular prosthesis not only
interferes with eating but also inhibits social contact, as
patients are afraid that the denture will dislodge in speech
or mastication. The attached mucosal ridge may be little
more than 1 mm wide and the sulcus mucosa is prone to
pain or ulceration. Severe resorption often results in
prominent genial tubercles or exteriorisation of the
mental nerves so that provision of a comfortable denture
is impossible. An implant-supported fixed prosthesis
Table 37.7
Indications for implant treatment
Difficult edentulous cases
Long span bridges
Free end saddles
Single tooth replacement
Special indications
restores function and confidence. An implant-supported
removable denture is a simple, cheaper and effective
option. Two implants with stud attachments or a bar can
be sufficient to stabilise a denture, which is then mainly
tissue borne. Implants are always placed between the
mental foramina in edentulous cases.
Retention problems occur in the maxilla, although
less frequently because the hard palate gives better support and retention for a conventional denture. Resorption
can lead to a flabby ridge and retrusion. Implants placed
in the anterior maxilla will aid retention and stability but
poor bone quality requires placement of as many implants
as possible and a bar may be required for bracing.
Patients who are unable to tolerate a denture, due to
gagging, or who are unwilling to wear a removable
appliance, can benefit from an implant-born bridge,
although the lip will not be as well supported as with a
denture flange. This problem should be explained to the
patient, who may then prefer a conventional denture.
If the patient decides on implant treatment, ridge
augmentation may be necessary, especially in the
maxilla. The available bone can also be increased by a
sinus lift where a bone graft or synthetic material is
placed in the maxillary antrum.
Long span bridges
Implants can be used where the span is too long for a
conventional bridge or when abutment teeth are compromised by bone loss, short roots or extensive
restoration.
In the maxilla, there may be limiting factors such as
inadequate or poor quality bone. Resorption may result
in an unfavourable position or angulation of the implant,
necessitating a long clinical crown or placement of the
restoration well in front of the ridge. These aesthetic
problems are noticeable with a short upper lip. Lip contour may be not be as good as that obtained by a denture
flange. Augmentation should be considered as in
edentulous cases.
295
In the mandible, the pattern of bone resorption is less
of a problem and the main constraint is the proximity of
the inferior alveolar or mental nerves.
Free end saddles
Replacement of mandibular molars is difficult with conventional dentures. There is a risk of mental anaesthesia
when placing implants in the posterior mandible so it is
essential to allow a good safety margin when calculating
implant length. Drill tips do not conform exactly to the
shape of the implant so allowance must be made for
the additional depth of the implant bed. The maxillary
antrum limits implant placement in the posterior maxilla.
Single tooth replacement
It can be simple and cost effective to replace an incisor
tooth with an implant when there is adequate bone. If
there is a diastema, the difficulties in construction of an
adhesive bridge or partial denture are avoided. Also,
preparation of adjacent teeth is avoided and there are no
denture clasps. Unfortunately, the pattern of bone
resorption can result in an unfavourable path of implant
emergence in the maxilla (especially if there is a history
of previous replantation or transplantation of a canine or
incisor). If there is crowding, the nasopalatine canal can
be large enough to prevent implant placement. This can
sometimes be overcome by restoration of ridge form by
bone augmentation.
Special indications
Implants may also be indicated under special
circumstances that are not dental in nature. These are
listed in Table 37.8.
Patient selection
Patient selection is important when planning implant
treatment to avoid a poor outcome and complications.
Table 37.8
treatment
Special indications for implant
Wind instrument players or singers
Denture intolerance due to gagging
Psychological aversion to dentures
Xerostomia, e.g. Sjogren's syndrome
Physical disability (e.g. cerebral palsy, stroke or
myasthenia gravis)
Table 37.9 Medical problems compromising
implant success
Cardiac disease
Haematological disease
Immunological disease
Bone disorders
Other systemic disease
Oral disease
Medical history
A detailed consideration of the patient's medical history
is essential because several conditions can compromise
implant success by interfering with healing, or increasing
the risk of infection (Table 37.9).
Cardiac disease
Severe cardiac problems can present risk but many patients
with mild disease can benefit from implants. Simple
questions about exercise tolerance give an indication of
the patient's ability to withstand a surgical procedure.
Implant failure is more likely in a patient with severe
debilitation. Patients who are at risk of endocarditis may
be suitable but regular monitoring and radiographs are
advisable, and any failing implant should be removed
without delay. Implants are contraindicated in patients
who have had a recent myocardial infarct, a valve replacement, are in cardiac failure or who have had previous
bacterial endocarditis.
Haematological disease
Clinical history and examination
296
The clinical history and examination will reveal the
patient's caries and periodontal disease experience.
Patient compliance can be an important indication of
suitability. It is also important to ascertain the patient's
expectations of treatment.
Treated or mild anaemias should not prevent implant
treatment. Patients with haemophilia and other significant factor deficiencies would not normally be suitable.
Warfarin therapy is a relative contraindication, but
surgery may be possible in selected cases with careful
monitoring of the international normalized ratio (INR).
Immunological problems
Oral disease
Prolonged corticosteroid therapy can present a risk but
the patient can be given steroid cover. Implant survival
may be reduced in patients on corticosteroids and this
should be balanced against the potential benefit to the
patient. Patients on chemotherapy and those with severe
immune deficiency should not be considered. Drug
addiction depresses immune responses and implies poor
compliance. Smoking has an adverse effect on implant
survival and patients should be strongly advised to cease.
Smoking most probably reduces the success rate by
significantly reducing the bony blood supply, especially
to the mandible.
It is important to ensure that the patient has a stable
periodontal condition and low caries rate at the time of
assessment, although many patients require implant
treatment as a result of previous neglect. Mucosal
disorders should be eliminated as far as possible. Bone
quality and availability should be assessed (Table 37.6).
Bone disorders
Most bone diseases are a contraindication. Osteoporosis
is especially common in older females but the jaws are
less affected and implants can still be successfully
placed.
If a patient has undergone radiotherapy there will be a
poor success rate in the maxilla although hyperbaric
oxygen (HBO) has been used with some success. Fewer
problems are encountered in the mandible and HBO is
not essential.
Other systemic diseases
Many other medical conditions, such as renal or liver
disease, can compromise treatment and consultation with
the patient's physician is advisable if in doubt. Individuals with well-controlled diabetes can be accepted,
although they have a greater risk of peri-implant disease.
Patients with psychiatric disorders should be accepted
with caution, especially if they attribute their problems to
dental disorders.
Table 37.10
implants
Treatment planning
Apart from appropriate patient selection, successful
treatment planning requires consideration of the available bone and space within the mouth (Table 37.10) and
the associated anatomical structures (Table 37.11). Treatment planning also needs to be informed by appropriate
radiographic examination and examination of articulated
study casts.
Radiographic examination
Conventional radiography, including an orthpantomograph (OPT) and periapical or lateral views where
relevant, is necessary. The OPT is most useful because it
indicates vertical bone height and the position of all
relevant bone cavities and nerve canals. It is important to
make allowance for distortion and magnification when
using an OPT. Transparent overlays are available but
more accuracy can be obtained by inserting a base plate
with standard metal balls or strips of gutta percha over
the planned implant positions before taking the radiograph. This latter method enables exact calculation of
available bone when implants are to be placed close to
the inferior alveolar nerve or other important structures.
Serial tomograms or computerised tomography (CT)
scans may also be used where detailed mapping of
available bone and anatomical structures is required. CT
scans are not always readily available and they involve a
Available bone and space for
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 superstructure
Depth of bone
Safety margin for inferior alveolar nerve, floor of nose
and maxillary antrum
Undercuts
Sufficient intermaxillary space for superstructure
Table 37.11 Anatomical structures important in
implant treatment planning
Maxilla
floor of nose
maxillary antrum
nasopalatine foramen
Mandible
inferior alveolar nerve
mental nerve
297
much higher radiation dose. Scatter due to metal
restorations can render the image unusable. CT images
can be very helpful but can be disappointing unless the
radiologist is familiar with dental requirements and
software.
Magnetic resonance imaging (MRI) is becoming
more readily available. It has no radiation dose and the
only known hazard is with ferrous metals in the magnetic
field. It is likely to replace CT scanning and - eventually
- most other X-ray investigations. New machines will be
less likely to induce claustrophobia and noise levels are
now significantly reduced.
Study casts
Study casts are invaluable for demonstrating treatment
options. Duplicates can be used for a diagnostic wax-up
so that tooth position can be planned. A template can
then be constructed with indicator holes drilled as an aid
to the surgeon, so that implants are placed in the optimum
position at operation.
Other treatment options
After considering the factors relating to patient selection
and treatment planning, restorative options should be
considered (Table 37.12).
Surgical technique
Bone drilling
Purpose-made sharp drills are essential. Many manufacturers advise single use and supply prepacked sterile
drill kits. It is essential to have an accurate indication of
drill speed so that overheating is avoided by keeping
below 2000 rpm. Thermal damage is also minimised by
incremental drill stages up to the final diameter. Thread
tapping, where required, may be hand driven or by very
slow drilling, preferably using a drill with a torque controller. Copious irrigation with chilled saline solution is
essential. Drills must be withdrawn frequently to allow
cooling and prevent clogging of the drill channels. It is
important to maintain drill direction, or the implant bed
will be inaccurate.
Countersinking is used where the system requires the
cover screw to be buried or where the transmucosal
element is to be submerged to improve aesthetics.
Flap design
Insertion
Mucoperiosteal flaps are usually taken along the crest of
the ridge. Relieving incisions may be short, as it is not
usually necessary to expose all the alveolar bone. If there
are adjacent teeth it may be necessary to release the
interdental papilla. Flaps should be handled carefully as
poor healing could compromise osseointegration.
With two-stage implants where the implant is buried,
it used to be common practice to keep the incision away
Decontaminated and sterilised implants are individually
packed in vials. Titanium forceps are used if handling of
the implant is required, but this is not normally necessary
due to the design of manufacturer's delivery system. A
fixture mount may be included in the package or attached
by the operator.
The implant should be placed with as little contamination as possible. Good flap retraction will reduce
contamination by saliva and epithelial surfaces. The
method of insertion varies but most implants are screwed
in either by hand or using a drill with a torque controller.
Irrigation is used to prevent overheating. Excessive force
should not be used because heat will be generated, and
there is also a danger of damage to the implant or cold
welding it onto the fixture mount.
A cover screw is placed and the soft tissues are sutured
over or around the fixture according to the system in use.
Table 37.12
298
from the crest so that the suture line was not directly over
the implant. This was technically more difficult and is
now less popular because of the risk of haematoma
formation or flap necrosis.
When augmentation procedures are planned, a bevelled
flap is taken so that mucosal cover of the membrane or
graft is achieved. A bevelled flap taken from the palatal
aspect can also be used to improve the bulk of buccal
interdental papilla when uncovering a buried implant at
the second stage.
Treatment options
Removable partial denture
Fixed bridge
Complete denture
Implant-supported denture
Implant-supported bridge
No prosthesis
With two-stage systems, where the implant and cover
screw are covered by mucosa, it is important to ensure
that the cover screw is seated properly, as soft tissue or
bone formation below the cover screw can be difficult to
remove from the implant face at the second stage.
Abutment connection
Two-stage implants have to be uncovered to allow abutment placement. This is done through a small incision on
the crest of the ridge or by removing a circle of mucosa
using a punch. Bone may have grown over the cover
screw and this is removed using the manufacturer's bone
mill. Instruments are also available to remove any bone
that has formed on the implant face because of a loose
cover screw. The implant face must not be damaged
during bone removal as the junction with the abutment
is accurately machined. A portal of entry for microorganisms would cause problems with infection later.
A suitable abutment is chosen and screwed in, taking
care that it is seated correctly and avoiding crossed
threads. Selection of a suitable abutment at this stage can
be difficult because the soft tissue level will vary as the
mucosal cuff matures. Alternatively, a healing abutment
can be placed and the final abutment is selected once the
soft tissues have healed.
Augmentation of bone
When there is insufficient width or height of bone it may
be possible to gain additional bone either before or at the
time of implant placement.
Various methods of bone augmentation can be used,
including onlay grafts, guided bone regeneration, sinus
lift procedures or ridge expansion. Bone graft materials
may 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 or
intraoral
Allograft: human donor (not used due to risk of crossinfection)
Xenograft: calcified matrix derived from biological
material, e.g. bovine bone or coral (no risk of crossinfection due to removal of protein?)
Synthetic material: e.g. hydroxyapatite, tricalcium
phosphate, glass
Onlay grafts
Blocks of bone may be used for extensive defects.
Cortical bone taken from the patient's iliac crest or
calvarium is preferred but harvest involves major surgery
and the risk of donor site morbidity. Implants are placed
some months later when the graft has taken.
Immediate placement is also advocated, as early
loading may reduce resorption and the patient is spared a
second operation. However, there may be an increased
risk of loss of fixtures and bone due to infection.
A reliable substitute for autologous block bone is still
awaited.
Guided bone regeneration
Healing by osteoblasts produces bone but, when a blood
clot is organised by fibroblasts, collagen formation is
predominant and scar tissue is formed. When a suitable
membrane is placed over bone, however, fibroblasts are
excluded and angiogenesis and osteogenesis occur in the
cavity below. This is the basis of guided bone
regeneration.
Membranes can be non-resorbable (e.g. polytetrafluorethylene) or resorbable (e.g. collagen). The shape of
the cavity can be maintained by using a reinforced membrane. Alternatively, the membrane can be supported
with bone, bone substitute or a mixture of both. Small
steel posts may also be used as supports. The periphery
of the membrane is stabilised by screws or pins, which
can also be resorbable. Recent developments with the use
of bone morphogenic proteins may revolutionise bone
augmentation in the future.
Sinus lift procedure
There is often insufficient bone height in the posterior
maxilla due to bone resorption and the presence of the
maxillary antrum. Onlay bone grafts are prone to failure
and may be unsuitable due to lack of intermaxillary
space. The sinus lift procedure creates additional alveolar
bone height within the antral space.
The antral lining is exposed by removing a window of
bone on the buccal aspect via a buccal mucoperiosteal
flap. The antral lining is carefully elevated intact and is
supported by bone-grafting material. It is also possible to
leave the bony window attached to the antral lining and
support both with graft material or implants. Immediate
implant placement is only advised if there is sufficient
bone for primary implant stability (about 6 mm in height).
299
An alternative is to approach the antral floor using
osteotomes to enlarge a bur hole on the crest of the ridge.
The antral lining can then be lifted and supported by
bone graft material. When there is sufficient bone for
primary implant stability the lining can be lifted through
an implant preparation. If the preparation is stopped just
short of the antral floor the cortical plate can be tapped
upwards with the lining. The cortical plate and the
implant then provide support for the lining.
Ridge expansion
Where there is sufficient bone depth but the ridge is too
narrow, the implant bed may be prepared by bone
expansion, provided that there is a cancellous layer
between the cortical plates. The crest of the ridge is
exposed leaving the rest of the alveolar bone attached to
mucoperiosteum. The ridge is widened by D-shaped and
round osteotomes between the cortical plates prior to
drilling.
Success rates
The patient's appreciation is a very good indicator of
success but objective criteria are required to monitor the
effectiveness of osseointegrated implants (Table 37.14).
Various criteria have been suggested but the most reliable
way to obtain comparable data is to record removal rates.
Cumulative survival rates are based on an actuarial
calculation that allows for the fact that implants in a
series will have been present for differing times. It is
reasonable to expect that, in the maxilla, 90% of implants
will survive for 10 years. In the mandible a 95% 10-year
survival is expected.
A number of adverse events may complicate implant
placement (Table 37.15). Avoidance of these complications can only be achieved by careful planning and an
exacting surgical technique based on sound training and
experience.
300
Table 37.14
Criteria for evaluation of success
Patient satisfaction
Survival
Suitable position
Mobility
Amount of bone loss
Health of adjacent soft tissues - pocketing and
inflammation
Infections or radiographic evidence of peri-implant bone
pathology
Operative complications e.g. damage to nerves or
adjacent teeth
Table 37.15
Complications of implant treatment
Intraoperative
implant in poor position
damage to mucosa and adjacent teeth
bone damage, i.e. lateral perforation, fracture of
alveolar bone or mandibular fracture
perforation into adjacent areas, e.g. lower border of
mandible, nasal cavity or maxillary antrum
nerve damage, e.g. inferior alveolar nerve
loose implant due to incorrect drilling
contamination of implant or bone
implant damage, e.g. crossed thread or surface defect
primary haemorrhage - especially floor of mouth,
possible airway compromise
Postoperative
pain
swelling
reactionary or secondary haemorrhage
infection of peri-implant soft tissue or bone
exposed or loose cover screws
Late
mucosal recession
bone resorption
mobility
implant fracture
38
Cryosurgery
laser surgeryand
Introduction
Conventional surgery has used the scalpel to cut or excise
tissue during surgical procedures. The scalpel, however,
has limitations as a surgical tool. When an area of tissue
is excised haemorrhage may be difficult to control and a
skin graft or flap may be needed to cover the defect or
prevent scarring. Cutting or coagulating diathermy cause
damage to the adjacent tissues. The physical effects of
cold and lasers offer alternative methods of removing or
devitalising tissue. They work in different ways and they
will be considered in turn.
Cryosurgery
Cryosurgery relies on the fact that rapid freezing and
thawing of tissues cause cell death and necrosis. Cryosurgery is thought to cause ice crystals in and around
cells, causing disruption of cell membranes and contents.
These effects are enhanced by rapid freeze and thaw
cycles. Blood flow to the area is reduced so that a larger
and colder 'iceball' is achieved at the next application.
Vascular damage also results in ischaemic necrosis.
Immune mechanisms may be altered with beneficial or
adverse effects.
Oral lesions are often surrounded by abnormal
mucosa. The operator must therefore consider the effects
of cryosurgery at the edges of treated area. If there is
epithelial dysplasia it is possible that cryosurgery could
potentiate malignant change.
Uses of cryosurgery
Cryosurgery can be used in a number of conditions and
in several is the treatment of choice (Table 38.1).
Freezing can be used to treat surface lesions such as
warts or small tumours. It is particularly suitable for
Table 38.1
Uses of cryosurgery
Ablation of warts and small tumours
Ablation of haemangiomas
Treatment of bony cavities
Blocking of nerves
haemangiomas around the mouth. Several applications
may be required but cryosurgery has the advantage that
there is no haemorrhage and the surface may be left
intact. Viral warts necrose and vascular lesions regress.
There is often significant oedema but postoperative pain
is unusual. With a deeper freeze the mucosa or skin may
necrose, but re-epithelialisation occurs as the lesion
sloughs away and healing is usually good with minimal
scarring.
Bone cavities may be treated to reduce recurrence of
lesions such as odontogenic keratocysts or central giant
cell granulomata. The bone is devitalised but still remains
functional until it is replaced by vital tissue. In the
mandible the inferior alveolar nerve may be spared as
nerves regenerate surprisingly well after freezing.
Cryosurgery is also used to treat painful nerve lesions
because nerves can be blocked without causing the
secondary neuralgia that often follows nerve section,
avulsion or alcohol blocks. Pain relief lasts for several
months but repeat treatments are often required. The
evidence-base for this application of cryosurgery is
lacking but it has a place when conventional treatments
are ineffective. Infraorbital, mental or inferior alveolar
nerves can be treated after surgical exposure. An intraoral
approach is used. The most common condition treated in
this way is trigeminal neuralgia that no longer responds
to therapy with drugs such as carbamazepine, or when
drug side-effects are severe. Neurosurgical options should
always be kept in mind. The surgical management of
trigeminal neuralgia is discussed in Chapter 19.
301
Cryosurgery has been advocated for ablation of
malignant tumours either as a curative procedure or for
palliation. Incomplete ablation of the lesion is unacceptable and could easily occur, as it is not possible to predict
accurately the extent of tissue destruction. Moreover,
case reports of accelerated tumour growth following
incomplete treatment raise the possibility that host
immune response is compromised. Malignant and
premalignant lesions are therefore better treated by other
methods.
Table 38.2 Refrigerant properties of liquid
cryoprobe systems
Boiling point
Surface
temperature
-196°C
-89°C
-78°C
-196°C
-150°C
-75°C
-50°C
-196°C
Type
Liquid nitrogen probe
Nitrous oxide probe
Carbon dioxide probe
Liquid nitrogen spray
Cryoprobes
Dermatologists apply liquid nitrogen to skin lesions
using a stick but a more precise method is needed for the
mouth. A cryoprobe is a surgical instrument with a cold
tip. The temperature is determined by the boiling point
of the refrigerant liquid. The freezing effect may be
achieved by evaporation at normal pressure, as with
liquid nitrogen applied directly with a stick or spray, or
within the probe tip. Other probe tips rely on the Joule
Thompson effect, where a pressurised gas is forced
through a small orifice. The refrigerant properties of the
various liquid systems are listed in Table 38.2.
Nitrous oxide units are commonly available in hospitals and are suitable for most oral applications. They
work from a nitrous oxide cylinder so they are always
ready for use. Liquid nitrogen machines are much more
powerful but must be filled with liquid nitrogen on each
occasion. This can be inconvenient for routine use and
handling a liquid at –196°C is hazardous.
Probe tips come in a variety of shapes and sizes. Flat
or dome-shaped tips from 3 to 10 mm are useful in the
mouth (Fig. 38.1). Long, narrow, insulated probes are
available for freezing nerves.
Cryosurgery techniques
302
Under local anaesthesia the probe is applied to the lesion
and switched on. The probe is held firmly onto the lesion
until an ice-ball forms and freezing is continued. The time
of application will usually be about 1 min. The probe
should not be pulled away because it will be adherent to
the lesion. For vascular lesions, the effect is enhanced by
compressing the lesion with the probe, which decreases
blood flow. On turning the machine off there should be a
rapid thaw and the probe is released.
One or two further applications are made after 1 min
to allow a complete thaw. Experience is necessary to
Fig. 38.1
A variety of shapes and sizes of cryoprobe tips.
judge the amount of treatment and the extent of the
freeze. The size of the ice-ball produced in a glass of
water gives an indication of the effects on tissue temperature but the blood supply will modify this effect in
living tissue.
If necessary, a specimen can be obtained for histopathology while the lesion is frozen. Haemostasis would
then be required and, of course, there would be a surface
defect. Freezing fixes the tissue temporarily before transfer
to formal saline so that good sections are possible.
Some liquid nitrogen units have the option of probe or
spray freezing. The latter is a very effective tool for use
on wide areas or uneven surfaces. It produces a very
rapid deep freeze and is more effective than the probe for
freezing 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 the
bone surface and, in this situation, a liquid nitrogen unit
Table 38.3 Advantages and disadvantages of
cryosurgery
Advantages
no haemorrhage
minimal postoperative pain
good recovery of nerve function
minimal scarring
bone structure maintained
blood vessel recovery
adjacent normal tissues recover
excellent for haemangiomas
possible treatment of painful nerve lesions
Disadvantages
cannot be used to cut tissues
difficulty in assessing extent of treatment
excessive swelling (could endanger airway)
effects at the periphery (dysplastic changes can be
potentiated)
whole lesion not available for pathology
tumour growth may be accelerated
not effective for lymphangiomas
would be necessary to provide an adequate effect. A
liquid nitrogen spray would be preferable because it
produces a much faster and deeper freeze.
Care must be taken to retract and protect mucosal
flaps and adjacent soft tissues, especially with liquid
nitrogen machines.
It is also possible to freeze a resected portion of
mandibular bone after tumour ablation and replace it to
restore continuity without the need to use a bone graft.
The bone section is placed in a container of liquid
nitrogen. This method is not often used because it is
possible that some cells from the original lesion could
survive. The most common reason for removal of full
thickness mandible is squamous cell carcinoma, and such
a risk would not be acceptable.
Advantages and disadvantages of cryosurgery
Cryosurgery is the preferred treatment for some conditions but it has certain drawbacks. The advantages and
disadvantages of cryosurgery are listed in Table 38.3.
Lasers
'Laser' is an acronym for 'Light Amplification by
Stimulated Emission of Radiation'. The properties of
laser light depend on wavelength. A CO2 laser at 10.6 µm
wavelength produces invisible light that is absorbed by
water and biological tissues and destroys them on
contact. An argon laser produces visible light at around
0.5 µm; this passes through water but is absorbed by
pigments such as melanin or haemoglobin. It may be
used in eye surgery because it will not damage the lens or
eye contents but acts on the retinal surface in treating
conditions such as diabetic retinopathy or a detached
retina. Surgical lasers are usually designed for cutting,
coagulation and ablation of tissue. When a CO2 laser
beam meets the target tissue its energy is converted into
heat. Cell structure is destroyed by expansion as water
boils. Denaturation of proteins also occurs but the laser
lesion deepens mainly as a result of cell disintegration at
its surface. The result is a very narrow layer of tissue
damage below the treated area and better healing.
Light waves from a normal source do not produce a
powerful cutting beam because they emerge randomly at
various wavelengths. Laser light, however, is spatially
and temporally coherent. This means that the waves are
all of the same wavelength (monochromatic) and are in
parallel, so that none of the energy from the light source
is lost by interference. Compare a 60-watt light bulb
producing light and heat with a 60-watt laser beam that
would cut through steel.
Laser light has many similar properties to ordinary
light. It is reflected by mirror surfaces. At some wavelengths it will travel along an optic fibre or be refracted
in a lens or prism. These effects are used to deliver the
light to the probe tip or operating microscope and to
focus it on the object. Alternatively, a fibre delivers the
energy by contact or proximity with the target. When the
beam is invisible, as with the CO2 laser, a red aiming beam
is often provided.
Output may be in a continuous wave or pulsed. Pulses
are single or repeated typically with a duration of 0.1 s or
less. Pulses of less than 1 µs are produced in Q-switched
lasers, which deliver very high energy without generating
excessive heat.
Tissue effects may be photoablative (molecular
disruption), photothermal (cutting or coagulation),
photomechanical (tissue disruption) or photochemical
(photodynamic therapy). Low power lasers have been
used to enhance healing, promote blood clotting and
relieve pain, although these effects still require controlled
clinical trials to exclude a placebo effect.
If a laser beam strikes a shiny surface it may be
reflected and burn healthy tissue, the operator or others
nearby. Laser beams travel without loss of intensity, so
even if the beam is focused it may cause damage at a
303
Table 38.4
lasers
Precautions required when using
Non-reflective instruments (achieved by sand blasting)
Protective goggles
Wet swabs to protect tissues
Restricted access to laser area, warning lights and
notices
Training and certification of users
Armoured or reflective endotraccheal tubes (+ inflation
of cuffs with water)
Avoidance of inflammable skin prepping solutions
Smoke evacuation (+ face mask)
lesions need a deeper excision and it is then advisable to
use the laser as a knife so that the whole lesion can be
sent for histopathology.
Erosive lichen planus
Erosive lichen planus that does not respond to any other
treatment is occasionally treated by laser with some
success, but this is best considered as a last resort kept for
patients with severe symptoms.
Denture-induced hyperplasia
distance. Moreover, it will continue to cut deeper into the
wound as long as it is applied An anaesthetic tube can
easily be pierced, resulting in ignition of anaesthetic
gases within the lungs, which is usually fatal.
There is also concern about the potential effects of
plume or surgical smoke produced by electrosurgery and
lasers. Toxic chemicals are produced when tissue is burned.
Blood aerosols and viruses such as human papilloma
virus in the laser plume are thought to be capable of
transmitting disease. A surgeon's mask alone does not
provide adequate protection. High-volume aspiration
(similar to that on dental units but with special filters) is
recommended.
In view of these hazards to patient and operator special
precautions are needed and these are listed in Table 38.4.
Oral surgical applications
The CO2 laser is most useful and is readily available in
general hospitals. At present, the most frequent indications are soft tissue lesions where the extent of the
excision prevents primary closure, and where skin
grafting was previously required to prevent scarring.
White patches and premalignant lesions
Biopsy is essential to determine the diagnosis and degree
of epithelial dysplasia. Nutritional deficiencies such as
iron or vitamin B12 should be treated. Patients must be
strongly advised to give up smoking. If lesions do not
respond and excision is required, the CO2 laser is a good
option.
Erythroplakia and premalignant leukoplakia
304
These are treated similarly. Mildly dysplastic superficial
lesions can be treated by ablation. Severely dysplastic
This is a common condition that is very suitable for laser
treatment, especially if it is extensive. The denture should
be adjusted and left out as much as possible for several
weeks so that extent of surgery can be decided.
Squamous cell carcinoma
The CO2 laser is used in the resection of malignant
tumours, such as squamous cell carcinoma. Small
tumours in the floor of mouth can be completely resected
with a wide margin.
Other lesions
The submandibular ducts can be divided with little
chance of postoperative salivary obstruction. Small
tongue lesions can be excised with the laser alone, except
that larger blood vessels can be troublesome. When
excising large tumours the laser can be used selectively
for dividing tongue or treating areas of field change
beyond the excision margin.
Types of laser
Several types of laser are available (Table 38.5). These
will be discussed below.
Carbon dioxide
The CO2 laser has ideal properties for soft tissue surgery.
It removes lesions with minimal damage to underlying
tissue. There is less inflammation and oedema and little
scarring, so that wide areas can be treated without the
need 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
Argon (continuous wave)
0.488 µm blue and 0.515 µm green
KTP (pulsed) (fibreoptic delivery)
0.532 µm green
Tuneable dye laser (continuous wave
or pulsed)
0.504 - 0.632 µm variable
Helium-neon (continuous wave)
0.633 µm red
Diode lasers (pulsed)
NeodymiurrvYAG (continuous wave,
pulsed or Q-switched)
0.650-950
µm
1.06 µm invisible infrared
Holmium:YAG (pulsed)
(fibreoptic delivery)
2.100 µm invisible infrared
Erbium:YAG (pulsed)
2.94 µm invisible infrared
Carbon dioxide (continuous wave,
pulsed or Q-switched )
10.6 µm invisible infrared
Skin lesions, corneal surgery, angioplasty,
tooth surface conditioning
Vascular lesions, intraocular surgery, blood
coagulation, middle ear lesions, composite
curing
Telangiectasia and coagulation of larger
vessels, tonsillectomy, urethral strictures,
bladder surgery, salivary duct strictures
Vascular lesions, tattoo removal,
photodynamic therapy, ?dentine sensitivity
and other dental uses
Aiming beams and pointers, laser Doppler
flowmetry, caries diagnosis, stimulation of
wound healing
Pain relief, biostimulation, tooth whitening
Tumour removal in oral surgery,
gynaecology, bleeding peptic ulcers,
fissure sealing, caries, dentine
hypersensitivity, dentine, enamel and bone
cutting, varicose veins (long pulse),
analgesia (low power laser)
Ureter and bladder surgery, lithotripsy,
myocardial revascularisation,
dacrocystorhinostomy
Skin resurfacing, caries removal, enamel,
dentine and ?bone cutting
Tumour removal in gynaecology, ENT and
oral surgery, denture-induced hyperplasia,
skin resurfacing, gingival surgery, implant
exposure, fissure sealing, caries, scaling of
root surfaces, ?dentine, enamel and bone
cutting
required. Unlike cryosurgery, no potentiation of malignant change has been observed. Scanning technology
enables a focused beam to adopt a pattern for resurfacing
procedures such as wrinkle removal where it is claimed
that tissue is vaporised before any thermal damage or
carbonisation occurs.
The specific advantages of a CO2 laser are listed in
Table 38.6.
Simple procedures can be quickly carried out under
local anaesthesia. The lasered area is left raw and haemostasis is rarely needed. Carbonisation during treatment
leaves black particles on the surface. A greyish layer
about 2 mm thick forms on the surface due to coagulation
of exudate. This eschar is lost as re-epithelialisation proceeds beneath. The surface is restored after 1 or 2 weeks
and further improvement continues in succeeding months.
Table 38.6
laser
Advantages of the carbon dioxide
Excision of wide areas with minimal scarring
Haemostasis, i.e. bloodless field
No significant swelling (airway not compromised)
Moderate postoperative pain
Safe on malignant and pre-malignant lesions
Extent of excision visible
Skin graft not needed
Neodymium: YAG
The neodymium:YAG (or Nd:YAG) laser units are also
used 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. When
different settings are used, however, deeper penetration is
possible (e.g. in the treatment of endometriosis).
Argon
The argon laser produces visible light that is absorbed by
pigments such as melanin. It is suitable for retinal surgery and is particularly effective in diabetic retinopathy.
It may also be used for vascular lesions such as port-wine
naevus, 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 useful
pointers in the lecture theatre.
Dye lasers
Dye lasers can be tuned to selected wavelengths for
treatment of various types of vascular naevus according
to their colour. They are used similarly in tattoo removal,
306
although removal of green pigment is not achieved by
this, or any other, laser. In photodynamic therapy they
may be used to switch on a cytotoxic drug at the site of a
malignant tumour.
KTP lasers
KTP lasers produce a green light that is used for treating
telangiectasia and pigmented lesions; they are used for
bladder surgery and urethral strictures. In ENT surgery,
KTP lasers are used for tonsillectomy, sinus surgery and
tear-duct surgery. Their versatility is partly due to the
delivery system, which uses optic fibres of 1 mm or less
in diameter. KTP lasers have the potential for treating
parotid or submandibular duct strictures.
Other lasers
A laser may be set to produce a continuous wave or a
pulsed output. Very short pulses allow high energy levels
to be achieved without generation of excessive heat.
Wider surgical applications are then possible. Carbon
dioxide and erbium:YAG lasers are being developed to
cut enamel dentine and bone.
Index
Page numbers in italics refer to figures
and tables. Entries are arranged in wordby-word alphabetical order.
abdominal wounds
dehiscence 10, 57
incisional hernia 10, 58
ABO blood groups 43
mismatch 44
abscesses see brain abscess; dental
abscess; periodontal abscess
achondroplasia 279, 280
acid-base balance 33
abnormalities 33
vomiting 29
compensation 33-34
monitoring in anaesthesia 79
acidosis 33
acinic cell tumour, salivary gland 118
actinomycosis see cervicofacial
actinomyosis
activated partial thromboplastin time
(APTT) 40
and heparin infusion 20
acute submandibular staphylococcal
lymphadenitis 269
adenocarcinoma, salivary gland 119
adenoid cystic tumour, salivary gland
118-119
adenoidal hypertrophy 150
adenoidectomy 150
adenoiditis 150
adenolymphoma 118
parotid gland see Warthin's tumour
adenomatoid odontogenic tumour 288
ADH see antidiuretic hormone
adrenaline (epinephrine) 44
interactions
halothane 75
potassium 275
in oral surgery 201, 202-203, 217, 239
adult respiratory distress syndrome
(ARDS) 22
aerocoeles, cranial 101
aesthetic assessment 103-104
AF see atrial fibrillation
age factors
bone remodelling 63
dental extraction 211
falls 89
general anaesthesia 71
hypovolaemic shock 15
wound healing 9
see also children; elderly patients
agitation, postoperative 80
air-borne spread of infection 46–47
air-filtering systems 56
airway maintenance 74-75, 80
clefts of the lip and palate 134–135
airway obstruction
emergency management 147–149
inhalational induction 72
albumin 27, 30
solution 44
alcohol
drug interactions 82, 86
facial fractures 89
history taking 6, 182-183
laryngeal cancer 154
oral cancer 141, 143
sialadenosis 115
withdrawal 70
alcoholic hand rubs 46
aldehydes 49
aldosterone 28
antagonists 32
alfentanil 77
alkalosis 33
allergies
blood transfusion 44
history taking 6, 70
inferior dental blocks 205
metal 90
alloplasts 177
alveolar clefting 133
repair 137-138
alveolar plate fracture 213
alveolectomy/alveolotomy 247
ameloblastomas 286-287
clinical features 286-287
cystic 232, 287
differential diagnosis 231, 232, 233
treatment 287
American Society of Anesthetists (ASA)
69, 70, 82
amnesia, conscious sedation 82
amoxicillin 198, 267, 271–272
amylase 112
anabolic state 34
anaemia 23, 42–43
complication of blood transfusion 45
oral surgery 274
anaesthesia see general anaesthesia; local
anaesthesia; nerve damage
analgesia
agents 77-78
fracture management 63
postoperative 80
oral surgery 196-198
stage of anaesthesia 73, 84, 85
see also pain relief
anaphylaxis
complication of blood transfusion 44
history taking 6, 70
aneurysms
bone cyst 279, 280
carotid 159-160
subarachnoid haemorrhage 168-169
angiography 20, 166
angiotensin I & II 28
angulation, fractures 62
ankylosis
dental 254
implants see osseointegration
facial fractures 93-94, 102
TMJ
trauma 175
treatment 177, 178
anosmia 99, 162
anthrography 174
antibiotic prophylaxis
excessive use 56, 227
mandibular fractures 92
maxillary fractures 99
open fractures 65
oral surgery 198, 227, 275
oroantral fistula (OAF) 213–214
perioperative 52, 56, 57
postoperative 58
preoperative 71
UTI 23
antibiotic resistance (MRSA) 48, 49, 198
antibiotic therapy
acute sialadentitis 271–272
cervicofacial actinomyosis 268–269
dental abscess 266–267
non-union of fractures 67
307
308
antibiotic therapy—(cont'd)
respiratory tract infections 22
tonsilitis 150
anticholinergics 71–72
anticoagulants 6
contraindications 70
intravenous see heparin
oral see warfarin
anticonvulsants 76–77, 171, 277
antidiuretic hormone (ADH) 28
increased secretion 34
lack of response to 31
antiemetics 13
premedication 72
antihistamines 44, 72
antiseptic packs/dressings 58
antithrombin III 37
antrostomy 101
anxiety
assessment 82
control 71, 72, 81, 82, 84, 85
Apert syndrome 108, 170
apicectomy see periradicular surgery
apnoea monitoring 134–135
APTT see activated partial thromboplastin
time
aqueduct stenosis 171
ARDS see adult respiratory distress
syndrome
argon lasers 306
Arnold–Chiari malformation 170
arterial blood gas analysis 20, 21, 79
artery forceps 266
arthrocentesis 175
arthroscopy 175
ASA see American Society of
Anesthetists
Asche's forceps 98
Ash pattern elevator 191
aspiration
from pathological lesions 257-258
see also fine-needle aspiration
of gastric contents 22, 72-73
aspirin 19, 40, 274
see also non-steroidal antiinflammatory drugs (NSAIDs)
assistance, oral surgery 190
asthma
conscious sedation 84, 85
history taking 6, 70, 82
non-steroidal anti-inflammatory drugs
278
oral surgery 278
astringents 222
ataxia 171
atelectasis 21
ATPase exchange pump 27
atracurium 78
atrial fibrillation (AF) 17
embolus formation 19, 20
atrial naturetic factor 28
atropine71–72, 78, 80
audit, sepsis rate 57
autoclaving 48–49
autoimmune thrombocytopenic purpura 39
AV boots 18
avascular necrosis 67
azidothymidine (AZT) 51
bacteria see infection; skin flora; wound
sepsis; specific organisms
bacterial meningitis 170
Bacteroides 56
barium swallow 151
Battle's sign 167
benzodiazepines
alcohol interaction 70
conscious sedation 81–82, 83, 85-86.
87
general anaesthesia 78
premedication 71
respiratory depression 87
reversal 78, 87
beta-blockers 15, 70, 275
bicarbonate (HCOO 33
renal retention 33-34
bile salts 41
biliary disease 41
biopsy 257
bone 286
lymph nodes 145-146, 158-159
oral premalignant lesions 142, 304
salivary glands 113–114, 273
techniques
excision 258
incision 258
punch 258
bleeding tendency, increased 39–42
block anaesthesia, oral surgery 203-207
blood clotting 36-39
abnormal 39-42
disollution 37–38
fracture healing 62, 63
initiation 36–37
limitation 37
prevention 38-39
stabilisation 37
wound healing 7
blood cultures, intravascular lines 22
blood disorders
increased bleeding tendency 39–42
increased clotting tendency 42
oral surgery 274-275
dental implants 296
see also anaemia
blood gas analysis 20, 21, 79
blood glucose monitoring 18, 70
blood loss monitoring 79
blood pressure
monitoring 72, 78, 86
see also hypertension; hypotension
blood products 43–44
blood samples 257
blood serum 257
blood supply, wound healing 8
blood tests
donor screening 41, 45
LRTI 21
blood transfusion 23, 43–45
complications 44–45
massive 42
products 43–44
blood warmers 45
blood-borne viruses 48
see also specific viruses
blunt dissection 266, 272, 273
body osteotomy 106
Bohr effect 43
bone augmentation, dental implants
299-300
bone cavities, cryosurgery 300, 302-303
bone diseases
aetiology 280
see also specific diseases
bone drilling, dental implants 294, 298
bone grafts
alveolar 137
chin deformities 107
dental implants 299-300
facial fractures 92, 93, 97, 102
iliac crest 92, 93
rib 93, 178
TMJ 178
bone morphogenic protein 102
bone necrosis 62
bone plates 106
resorbable 102
bone removal
oral surgery 192
periradicular surgery 240
wisdom tooth extraction 226
bone ronguers 192, 193
bone surgery 247-249
alveolectomy/alveolotomy 247
bony exostoses and bone undercuts
247
genial tubercles 249
ridge augmentation 249
sharp bony ridges 247-248
sharp mylohyoid ridge 249
torus mandibularis 248–249
torus palatinus 248
vestibuloplasty 249
bone undercuts 247
bonewax 216
bony exostoses 247
boots, DVT prevention 18–19
bovine spongiform encephalopathy (BSE)
53
bowel see abdominal wounds;
gastrointestinal system
brachial plexus 14
brachy therapy 144
brain abscess 170
brain damage 167–168
brainstem signs 162
branchial cleft anomalies 120
branchial cyst 120, 159
Bristow elevator 96
bronchodilator therapy 71
Brown's syndrome 101
bruising 24, 39
floor of the mouth 90
fractures 60, 90
mastoid process 167
BSE see bovine spongiform
encephalopathy
buccal advancement flap 193–194, 214,
218
buccal expansion 210
buccal injection 204–205
buccal retraction 191–192
buccal sulcus
abscess 264, 265
ecchymosis 96
bupivacaine 201, 206
buprenorphine 77
calcifying epithelial odontogenic tumour
287
calcium 37
binding 42
defective metabolism 291
calcium gluconate 31
callus
hypertrophic/hypotrophic 67
provisional 63
Candida 245
canines 252
conservative management 252
reimplantation 253
surgical exposure 252–253
buccal 256
palatal 255–256
surgical removal 253
cannulae
arterial, monitoring 78
insertion 86
intravenous induction 70
removal 86
capnography see carbon dioxide (CO2),
expired
carbamazepine 171, 277
carbon dioxide (CO2) 33, 34
expired (ETCO,) 72, 75, 79
lasers 303, 304–305
carbonic acid 33
carbonic anhydrase 33
carcinoma expleomorphic, salivary gland
119
cardiac arrhythmias
atrial fibrillation (AF) 17, 19, 20
halothane 75
potassium levels 31, 32
cardiac catheterisation 17
cardiac disease see endocarditis;
ischaemic heart disease;
myocardial infarction (MI);
valvular disease
cardiac function
dysrhythmias 17
LVF 17
obstructive shock 15
septic shock 23
cardiac pacemaker, and use of diathermy
14
cardiogenic shock 16–17
cardiorespiratory monitoring in
anaesthesia 78–79
cardiorespiratory problems 42–43, 70
cardiovascular reserve
age 15
anaemia 23
pain 18
caries, untreatable 220
carotid aneurysms 159–160
catabolic state 34
caval filter 20
cavernous sinus thrombosis 267
cellulitis 55, 57, 58, 265
cemento–ossifying dysplasia 280, 282
cemento–ossifying fibroma 280, 282
cementoma 288
central giant–cell granuloma 279, 280
Central Sterile Supply Unit (CSSU) 48
central venous lines
pneumothorax 15
pressure monitoring 15, 16, 17, 29, 79
TPN 35
cephalograms 104–105
ceramic dental implants 293
cerebellar pontine angle tumours 172
cerebellar signs 162
cerebral function monitors (CFM) 79
cerebral perfusion 163
cerebrospinal fluid (CSF)
lumbar puncture (LP) 165
obstructed flow 162, 163, 170. 171
otorrhoea 100–101
persistent leak 98, 101, 109, 167
rhinorrhoea 97, 98, 101
shunt 171
cervical facial flap 126
cervical spine, imaging 60, 99, 100, 166
cervicofacial actinomyosis 268–269
aetiology 268
clinical features 268
diagnosis 268
management 268–269
postextraction 218
CFM see cerebral function monitors
chemical pneumonitis 22
chemical sterilising agents 49
cherubism 279, 280, 281–282
chest examination 21
chest physiotherapy 21, 22
chest sepsis 54
children
adenoiditis 150
airway obstruction 148
branchial cleft anomalies/cysts 120, 159
conscious sedation 82, 84, 86
consent 186–187
epistaxis 158
foreign bodies, nasal 156
fractures
craniofacial 102
mandibular 90, 91–92, 93–94
general anaesthesia 72, 74
pyogenic dental infections 268, 269
see also age factors
chin deformities 105, 107
chisels 192
Coupland's 193, 227
chlorhexidine
handwash 8, 56
irrigation 222
mouthwash 93, 198–199
skin preparation 57
chloride (Cl~) 27
cholinesterase abnormalities 70
Christmas disease 41
chronic subdural haematoma (CSDH) 168
cirrhosis 30
citrate 42, 43
CJD see Creutzfeldt–Jakob disease (CJD)
clean contaminated wounds 55, 56, 58
clean wounds 55, 56
cleaning instruments 48
cleft team 134
clefts of the lip and palate 131–139
classification 132
embryology 131–132
patient management 134–135
airways 134–135
feeding 135
philosophy 139
structural abnormalities 132–134
surgical treatment 135–139
Le Fort III osteotomy 108, 109
primary 136–138
secondary 138–139
cleidocranial dysostosis 252, 280, 281
coagulation disorders 40–41
acquired 41–42
inherited 40–41
investigations 40
coagulation factors 37, 40, 41
concentrates 44
transfused blood 42
coagulation pathway 37, 38
common 37
extrinsic 37
intrinsic 37
codeine 198
collagen 7, 8, 9
fracture healing 63
platelet adhesion 37
colloid osmotic pressure 27
colloid solution 32–33
commensals 56
communication, conscious sedation 84, 86
compartment syndrome 66
plaster casts 64
Volkmann's contractures 67
complications of surgery 13–25
early–stage 13–18, 24
general 13
intermediate–stage 18–24
late–stage 24, 25
local 24–25
specific 24
see also specific procedures
composite grafts 126–127
computerised tomography (CT)
dental implants 297–298
fractures 61
mandibular condyle 91–92
maxillary 99
zygomatic (malar) 96
309
310
computerised tomography (CT)—(cont'd)
neurological 166, 169, 170, 171
oral cancer 143, 144
pulmonary angiogram 20
salivary glands 112–113, 117
TMJ 174–175
condylectomy 177
condylotomy 177
confusion 168, 169
postoperative 80
coning 163, 165
conscious level, reduced
Glasgow Coma Scale 163–164, 765
signs and symptoms 163
conscious sedation 81–87
agents 81–82
assessment 82
definition 81
methods 82–87
inhalational 83–85
intravenous 85–86
oral 83
monitoring 86–87
treatment planning 82
consent 82, 84
children 186–187
competence to give 186
mental capacity 187
oral surgery 185–187
general anaesthesia 187, 189–190
unconscious patients 187
contaminated wounds 55, 56, 58
contour lines
facial 123
see also Langer's lines
contractures 10–11
surgical treatment 11
corticosteroids 6, 9, 24, 40, 70
adverse effects 276–277
complications of blood transfusion 44
dental implants 297
inhalers 278
local injection
in scarring 10, 125
TMJ 175
Coupland's chisels 193, 227
cow–horn forceps 208, 210
cranial nerve
palsy 162
vascular compression syndromes
171–172
craniofacial fractures 100–102
complications 101–102
examination 100–101
craniosynostosis 170
craniotomy 166
crepitus, mandibular fractures 90
Creutzfeldt–Jakob disease (CJD) 52–53
healthcare workers 51
tonsillar tissue 151
use of disposables 49
cricoid pressure 72–73
cricopharyngeal spasm 151
cricothyroidotomy 149
cross–infection
extent of the problem 46
routes of transmission 46–47
universal infection control 47—50
see also infection
Crouzon's syndrome 108, 170
crush syndrome 66
Cryer's elevators 193
cryoprobes 302
cryosurgery 300–303
advantages and disadvantages 303
techniques 302–303
uses 262, 300–302
crystalloid solutions 32
CSDH see chronic subdural haematoma
CSF see cerebrospinal fluid
CSSU see Central Sterile Supply Unit
CT see computerised tomography
currettage, periradicular surgery 240
cyclosporin 252
cystic ameloblastomas 232, 287
cystic change, wisdom teeth extraction
220
cystic lesions, aspiration 258
cysts
branchial 120, 159
dermoid 159
extravasation 272, 273
salivary gland 120
thyroglossal 159
tonsillar inclusion 152
see also jaw cysts
Dautrey procedure 176
debridement, oral surgery 193
deep vein thrombosis (DVT) 18–19
clinical features 19
investigation 19, 37
predisposing factors 18, 42, 65
prophylaxis 18–19, 65
treatment 19
dehiscence 10, 57
dehydration, causes and mechanisms
29–30
deltopectoral flap 128
dental abscess 263–267
apical 263
clinical features 263–264
complications 267
management 265–267
antibiotic therapy 266–267
drainage 265–266
removal of source of infection
266
periapical 263
spread of infection 264–265
tooth transplantation 251
dental casts
dental implants 298
feeding plates 135
orthognathic surgery 104
dental complications of craniofacial
fractures 101–102
dental extraction 208–211
abscess management 265, 266
complications 212–218
immediate 212–214
postextraction 215–218
equipment 208
marsupialisation of radicular cysts 232
non–surgical 250–251
preoperative assessment 211
preprosthetic surgery 243–244
supernumerary teeth 255
technique 208–210
application 208–210
consolidation 210
displacement 210
postdelivery 210
unerupted teeth 244, 251
see also wisdom teeth
dental forceps 208, 209
application 210
complications of extraction 212, 213
placement difficulties 211
dental implants 292–300
bone augmentation 299–300
guided bone regeneration 299
materials 299
onlay grafts 299
ridge expansion 300
sinus lift procedure 299–300
bone quality and quantity 294–295
complications 300
healing phase 295
indication for treatment 295–296
materials 292–293
patient selection 296–297
clinical history and examination
296
medical history 296–297
primary stability 294
success rates 300
surgical principles 293–294
surgical technique 298–299
abutment connection 299
bone drilling 298
flap design 298
insertion 298–299
systems 293, 294
treatment planning 297–298
radiographic examination 297–298
study casts 298
types 292
wisdom teeth extraction 221
see also preprosthetic surgery
dental infection see dental abscess;
infection, dental
dental luxators 193, 208
dental malocclusions 101–102
dental tweezers 196
dentigerous cysts 232–233
clinical features 232
diagnosis 232
radiolucencies 232
treatment 233
dentistry
guidelines on general anaesthesia 187
intravenous sedation 85
dentofacial deformities see orthognathic
surgery
denture(s)
design, wisdom teeth extraction 221
–induced hyperplasia 244–245
laser therapy 304
modified, fixation 92
stomatitis 245
dermoid cysts 159
desferrioxamine 45
desflurane 76
dexmedetomidine 78
dextrose solution 32
diabetes insipidus (DI) 31
diabetes mellitus 17–18
delayed wound healing 9
history taking 70
and oral surgery 276
postoperative status 80
diabetic ketoacidosis 33
diabetic nephropathy 30
diarrhoea 29
diathermy 12
–related injuries 14
operating technique 57
diazepam 83, 85
see also benzodiazepines
DIC see disseminated intravascular
coagulation
diclofen 78
diet see nutrition
diethyl ether 75
diffusional hypoxia 85
digoxin 15
diplopia 95, 98, 100, 101, 108–109
dirty wounds 55, 56
disease susceptibility, history taking 6
disposable instruments 49, 53
disseminated intravascular coagulation
(DIC) 39, 42, 44
distraction osteogenesis 102, 109
diuresis/diuretics
cause of dehydration 30
in heart failure 15
potassium–losing 275
Down syndrome 252
drills/drilling 192, 226, 294, 298
drooling 120
drug history 6, 70, 182
drug interactions/precautions
DVT prophylaxis 19
gingival overgrowth 252
hyperkalaemia 32
hypovolaemic shock 15
impaired wound healing 9
oral surgery 182, 274–275, 277, 278
pregnancy 277
dry socket 216–217
postextraction 228
predisposing factors 216–217
treatment 201, 217
DVT see deep vein thrombosis
dye lasers 306
dysmorphophobia 103
dysphagia
hypopharyngeal conditions 151, 153
mandibular fractures 90
dysphasia 162
dysphonia 154
ear
facial fractures 89
'glue ear' 150
mandibular fractures 90, 93
pain referred to 151
ear lobe, postoperative numbness 120
early mobilisation 19, 64–65
early–stage complications
of dental extraction 212–214
of fractures 65
of surgery 13–18, 24
EBA see ethoxy benzoic acid cement
ecchymosis
buccal 96
circumorbital 95, 98
postextraction 217
ECF see extracellular fluid
ECG see electrocardiogram
ECHO cardiography 17
edentulous patients
dental implant 295
raising a flap 191
torus mandibularis 249
elderly patients
adverse effects of aspirin 19
blood tests 21
lateral neck swellings 159–160
pressure sores 24
see also age factors
elective patients, preoperative assessment
71
electrocardiogram (ECG) 17, 20
induction/monitoring of anaesthesia
72, 78
electrolytes
abnormalities 31–32
cardiac arrhythmias 17
gastrointestinal ileus 23
fluid compartments and osmolarity 27
homeostatic mechanisms 26, 27–28
intravenous replacement 29
monitoring, blood transfusion 45
electromyography 165
elevators
oral surgery 191, 193, 208, 213
wisdom tooth extraction 226, 227
zygomatic (malar) bone fracture 96
embolectomy 21
emergency management
airway obstruction 147–149
rapid sequence induction 72–73
eminectomy 176
end tidal carbon dioxide concentration
(ETCO2) 72, 79
end tidal volatile anaesthetic
concentrations 79
endocarditis 71, 218, 275, 276, 296
endocrine disorders 275–277
endoscopy 147
bronchus 143
hypopharyngeal 153
laryngeal 154, 155
nasal 151, 157
oesophageal 143
endotracheal intubation 74
assessment 70–71
complication 14
extubation 75
induction 72
enflurane 75
enophthalmos
complication of Le Fort III osteotomy
109
orbital blow–out fractures 95, 100, 101
ENT, examination techniques 147
enteral feeding 34
enterocococci 56
enucleation, jaw cysts 231, 235–236
'envelope' flap, oral surgery 191, 226
EORTC see European Organisation for
Recognition and Treatment of
Cancer
epinephrine see adrenaline (epinephrine)
epistaxis 155, 157–158
adult 158
childhood 158
fractures
maxillary 98
nasal 97
zygomatic (malar) 95
epithelial cell migration and proliferation
7–8
erythroplakia, laser therapy 304
Escherichia coli 56
escorts, post–sedation 82, 85
ethmoid carcinoma 157
ethoxy benzoic acid cement (EBA) 240
etomidate 77
European Organisation for Recognition
and Treatment of Cancer
(EORTC) 146
Eustachian tubes
middle–ear effusions 150
obstruction 152
Eve's sign 86
examination 70–71, 183–185
chest 21
ENT techniques 147
neurological 161–163
oral cavity 184–185, 211
excision
of mucocoele 273
of scarring 10
excision biopsy 258
external fixation 64, 65
extracellular fluid (ECF) 26, 27–28, 31
extradural haematoma 168
extraoral abscess, incision of 266
extravasation cysts 272, 273
extubation 75
eye
closure, dental abscess 264
examination 184
see also ophthalmic injury; orbital
blow–out fractures; visual
disturbances
eyelid reconstruction 126, 127
311
312
facial examination 184
facial expression 110, 122, 123
facial fractures 89–102
aetiology 89
current developments 102
general examination 89
mandibular 89–94
middle third 94–102
facial incisions 123–124
facial lacerations 124
facial muscles 123
facial nerve
anatomical relationships
parotid gland 110, 114, 116, 117,
119
SMAS 123
submandibular gland 111, 119
function 119
mobilisation/removal 117, 118
monitor and stimulator 119
operating microscope 124
facial paralysis/palsy 119, 184
free skin flaps 128
inferior dental block 205
facial reconstruction
wound closure 125–130, 146
see also orthognathic surgery
facial scars, management 124—125
factor(s) see coagulation factors
fainting, inferior dental blocks 205
falls 89
family history 5–6, 70
oral surgery 182
fasciotomy 66
fasting, perioperative
conscious sedation 82
diabetes mellitus 276
fluid/electrolyte balance 29, 31
postponement of surgery 71
fat embolism 65–66
feeding see nutrition
felypressin 202, 277
fenanyl 77
FESS see functional endoscopic sinus
surgery
FFP see fresh–frozen plasma
fibrin degradation products (FDP) 37, 42
fibrinogen 37, 44
fibrinolysis 37–38
fibrinolytic therapy 20–21
fibro–osseous lesions 280, 281–282
fibroblasts 7, 8, 63
fibrocartilage 63
fibronectin 7
fibrous dysplasia 280, 281
clinical appearance 281
diagnosis 281
management 281
fibrous epulis 259
fibrous overgrowth/tuberosities 246,
259–260
Fickling's forceps 193
fine–needle aspiration 258
neck lumps 143, 158–159
salivary glands 113, 117
fissural cysts 235
fistulae
branchial 120
cause of dehydration 29–30
cleft deformities 138
oroantral (OAF) 213–214, 218
salivary 120
'flabby' ridges 246–247
flaps
oral surgery 191–192
buccal advancement 193–194, 214,
218
dental implants 298
'envelope' 191, 226
labial 255
lingual 249
mucoperiosteal 191, 243–244, 247,
298
osteoplastic 244
palatal gingival margin 256
periradicular surgery 240
skin see skin flaps
flotron boots 18–19
fluid compartments 26–27
distribution of crystalloid solutions 32
osmolarity and electrolyte
concentrations 27
fluid and electrolyte balance 26–34
fluid monitoring 30, 31
fluid overload 30–31
complication of blood transfusion 45
fluid replacement
categories of response 16
in dehydration 29, 30
solutions 32–33
flumazenil 78, 87
fluorosis 280, 281
follow–up, oral surgery 199
forceps
artery 266
Asche's 98
Fickling's 193
tissue 194
Walsham's 98
see also dental forceps
foreign bodies 9
airway obstruction 148–149
facial lacerations 124
nasal 156
fractures 59–68
aetiology 59–60
classification 61–62
angulation 62
configuration 61
displacement 62
extent 61
impaction 62
joint involvement 62
overlying skin integrity 61–62
rotation 62
site 61
stability 62
closed 60, 61–62
management 63–66
complications 65–68
delayed union 67
diagnosis 60–61
clinical examination 60
investigations 60–61
early physiological loading/movement
64–65
healing 62–63
inflammatory phase 62–63
remodelling phase 63
reparative phase 63
immobilisation 64
open 60, 61–62
management 65
principles of management 63–65, 65
reduction 63
tooth extraction
alveolar plate 213
crown 212
mandible 213
root 212
see also facial fractures
fraenal attachments 244, 251
fraenectomy 251
free end saddles, dental implant 296
free skin flaps 128–129
fresh–frozen plasma (FFP) 41, 44
Prey's syndrome 120
frusemide 15, 30–31
full thickness skin grafts 125–126
functional endoscopic sinus surgery
(FESS) 157
gamma–amino butyric acid (GABA) 81
gap arthroplasty, TMJ 177, 178
gastrointestinal system
endogenous organisms 56
fluid losses 29
history, oral surgery 182
ileus 23
gelofusin 44
gender
dry socket 217
haemoglobin (Hb) levels 42
haemophilia 40
general anaesthesia 69–80
agents 75–77
inhalational 75–76
intravenous 76–77
supplementary drugs 77–78
airway maintenance 74–75
complications of surgery 13–14
induction 72–73
emergency/rapid sequence
72–73
inhalational 72
intravenous 72
maintenance 73
monitoring 78–79
oral surgery 187–188, 189
consent 187, 189–190
dislocation of TMJ 215
postoperative care 79–80
postponement of surgery 71
premedication 71–72
preoperative assessment 69–72
preoperative assessment—(cont'd)
elective patients 71
history and examination 70–71
preoperative therapy 71
preparation 72
risk
aspiration of gastric contents 22,
72–73
assessment 69
ischaemic heart disease 275
signs and stages 73
General Dental Council
definition, conscious sedation 81
guidelines, general anaesthesia 187
genial tubercles
aetiology and clinical appearance 249
management 249
GFR see glomerular filtration rate
giant cell
epulis 260
granuloma 279, 280
giantism 280, 282
Gigli saw 177
Gillies temporal approach 96
gingival overgrowth 252
gingivitis 222
gingivoperiosteoplasty 137
Glasgow Coma Scale 163–164, 165
gliomas 169
globus pharyngeus syndrome 151
glomerular filtration rate (GFR) 28
reduced 30
glossopharyngeal neuralgia (GPN) 172
glossoptosis 134
gloves 56
glucose test
rhinorrhoea 97
see also blood glucose
'glue ear' 150
glyceryl trinitrate (GTN) 275
glycine 81
glycopyrronium 71, 78
gold chain attachment 255, 256
Gorlin–Goltz syndrome 234
GPN see glossopharyngeal neuralgia
granulation tissue 7, 8, 58
fracture healing 63
granuloma
central giant–cell 279, 280
pyogenic 261
greater auricular nerve 120
GTN see glyceryl trinitrate
Guedel airway 74
Guedel, signs and stage of anaesthesia 73,
83–84
guided bone regeneration, dental implants
299
gun shot wounds 102
Gunning splints 92
Gustillo and Anderson, classification of
open fractures 61–62
gutta percha 245
haemacel 44
haemangioma 260–261
haematological disease see blood
disorders
haematologists 39, 41, 42
haematoma 24
intracranial 167, 168
periorbital 166–167
surgical technique 57
haemoglobin (Hb) 23
hydrogen ion interaction 33
normal levels 42
haemolysis
complication of blood transfusion 44,
45
perioperative precipitation 43
haemophilia A 40–41
haemophilia B 41
haemorrhage
dehydration 29
intracranial 168–169
postoperative
dental extraction 216
oral surgery 199, 210
primary 15–16, 199
secondary 21, 199
subconjuctival 95, 98, 166–167
haemorrhagic vesicles 57
haemosiderosis 45
haemostasis
surgical technique 9, 12
see also blood clotting
hair–bearing skin
preoperative preparation 8, 57
scalp reconstruction 127
halitosis 151, 222
halothane 75
hamartoma 260–261
hammer, oral surgery 192
hand examination 184
hand washing 8, 46, 56
Hb see haemoglobin
head injuries 166–167
headaches 163, 168, 169, 171
postconcussional 101
healthcare workers
immunisation 50
infection risk 46–47, 49, 50–52
theatre personnel 56
training in infection control 50
Heimlich manoeuvre 148–149
helium–neon lasers 306
hemifacial spasm 172
Henderson—Hasselbach equation 33
heparin 19
infusion pump 19
perioperative 41–42
potentiation of antithrombin III 37
prevention of clot/emboli extension
20
hepatitis B
blood donor screening 45
carriers 46–47, 48, 51–52
HBeAg 50, 52
HBsAg 50, 52
healthcare workers 46–47, 49, 50,
51–52
vaccination 50, 51
non–responders 50, 51
hepatitis C
blood donor screening 45
healthcare workers 49, 50–51, 52
patients 52
hepatocytes 41
hereditary haemorrhagic telangiectasis 40
Hilton–type forceps 266
histamine 37
history 5–6, 70
allergies 6, 70
drug 6, 70, 182
family 5–6, 70, 182
medical 5, 48, 70, 82, 181–182, 183
neurosurgery 161–163
oral surgery 181–183
of presenting complaint 5, 181
social 6, 70, 182–183
HIV
blood donor screening 41, 45
family history 70
healthcare workers 50, 51, 52
homeostasis, fluid and electrolyte balance
26–29
hormone–replacement therapy (HRT) 290
hospital–acquired infections (HAI) see
cross–infection
hot air ovens 49
Howarth elevator 191
hydrocephalus 162, 163, 170, 171
active 171
hydrogen ions
concentration 33–34
loss of 29
transfused blood 43
hydroxyapatite 107, 293
hyoscine 71, 80
hypercoagulable state 34
hyperglycaemia 34, 35
hyperkalaemia 31–32, 45
hypernatraemia 31
hyperparathyroidism 280, 282
clinical features 282
diagnosis 282
management 282
hypersplenism 39, 41
hypertension 71, 275
hypertrophic scarring 10
hyperventilation 33
hypoalbuminaemia 30
hypochlorite 49
hypoglossal nerve 111, 119–120
hypokalaemia 32
diuretic therapy 30–31, 70
hyponatraemia 31
hypopharynx
anatomy and physiology 149
benign conditions 151
tumours 153, 160
hypophosphatasia 280, 282–283
hypotension 14–15
secondary brain damage 168
spinal/epidural anaesthetic–induced 15
therapeutic 14–15
313
hypothermia 14, 45
hypovolaemia, in dehydration 29
hypovolaemic shock 15–16
classification 16
secondary bleeding 21
hypoxia
of anaesthesia 43, 79
diffusional 85
secondary brain damage 168
314
ICF see intracellular fluid
ICP see raised intracranial pressure
idiopathic thrombocytopenic purpura
(ITP) 39
iliac crest bone grafts 92, 93
immobilisation, fractures 64
immunisation
healthcare workers 50, 51
open fracture management 65
immunocompromised patients 48
bone infection 283
immunological complications
blood transfusion 44–45
dental implants 297
incision biopsy 258
incisional hernia 10, 58
incisions 9, 12
abscess 265–266
facial 123–124
oral surgery 190–191
incisors
ankylosis 254
orthodontic management 251–252
surgical exposure 255
indomethacin 78
induction, general anaesthesia 72–73
infection
agents 55–56
bone 283–285
see also jaw, cysts
complication of blood transfusion 45
dental 268–269
dry socket 216
periradicular 238, 239
wisdom teeth 220, 221–222
see also dental abscess
fractures 66
internal/external fixation 64
mandibular 93
open 65
intracranial 163, 169–170
intravascular lines 22, 35
oroantral fistula (OAF) 213–214, 218
oropharynx 150
postoperative 23
prevention, oral surgery 198–199
respiratory tract
laryngitis 154
LRTI21–22
nasopharyngeal 150
salivary gland 115–116
sinusitis 157
urinary tract 22–23, 54
see also cross–infection; wound sepsis
Infection Control Committee 50
Infection Control Nurses 50
infection control policy 50
inferior dental nerve
block 201,203–205
buccal injection 204–205
complications 205
determination of adequate
anaesthesia 204
fractured mandible 213
technique 203–204
damage, postextraction 225, 228
infiltration technique, local anaesthesia
202–203
infraorbital nerve block 201, 206–207
technique 206–207
infratentorial pathology 162
inhalation pneumonitis 22
inhalational agents 75–76
inhalational induction 72
inhalational sedation
clinical application 83–84
disadvantage 84
history 83
procedure 84–85
insensible fluid loss 16, 30
insulin 17–18, 31, 70
TPN solutions 35
insulin resistance 34
internal fixation 62, 64, 65
International Normalised Ratio (INR) 20,
41, 42, 296
intra–articular fractures 62, 63, 67
intracellular fluid (ICF) 26, 27, 31
intracranial haematoma 167, 168
intracranial haemorrhage 168–169
intracranial infection 163, 169–170
intracranial tumours 169
intradural haematoma 168
intraosseous injection 207
intrapulpal injection 207
intravenous agents 76–77
intravenous induction 72
intravenous sedation
assessment 82
clinical application 85–86
contraindications 85–86
history 83, 85
procedure 86
introduction to the patient 181
intubation see endotracheal intubation
inverted L osteotomy 107
iron overload 45
iron therapy 23, 43
ischaemic heart disease 16–17
oral surgery 275
isoflurane 75–76
ITP see idiopathic thrombocytopenic
purpura
jaundice 184
complication of blood transfusion 45
delayed wound healing 9
surgical 41
jaw
assessment 104
central giant–cell granuloma 279, 280
cysts 229–237
aneurysmal bone 279, 280
dentigerous 232–233
features 229
keratocysts 233–234
nasolabial 236
nasopalatine 235–236
radicular 230–232, 239
solitary bone 236
Staphne's idiopathic bone 236–237
tumours 285–286
see also mandible; mandibular;
maxilla; maxillary
joint(s)
deformity 40, 60
intra–articular fractures 62, 63, 67
movement
complications of surgery 14
in examination 60
scar contractures 10–11
see also temporomandibular joint
(TMJ)
Jorgensen technique 85
juvenile nasopharyngeal angiofibroma
(JNA) 151
Kell and Duffy antigens 45
keloid scarring 10
keratinisation 7–8
keratocysts 233–234
aspiration 258
clinical features 233
diagnosis 233
Gorlin–Goltz syndrome 234
radiolucency 233
treatment 233–234
ketamine hydrochloride 77
kidney see entries beginning renal
KTP lasers 306
Kufner osteotomy 108
labial flap 255
labial fraenectomy 251
upper 254–255
lactic acidosis 33
laminar airflow system 47, 56
Langer's lines 8
contractures 10–11
hypertrophic scarring 10
see also contour lines; wrinkle lines
laryngeal mask airway (LMA) 72, 74
propofol 77
laryngeal obstruction, emergency
management 148–149
laryngeal spasm 75, 76
laryngectomy 155
laryngitis
acute 154
chronic 154
laryngoscopes 74, 75
laryngotomy 149
larynx
anatomy and physiology 153–154
benign conditions 154
larynx—(cont'd)
examination techniques 147, 154
malignant tumours 154–155
lasers 303–306
applications 146, 304
precautions 304
types 304–306
late–stage complications
of fractures 66, 67–68
of surgery 24, 25
Le Fort fractures 94
classification 94–95, 98
I 94, 98, 99
II 94–95, 98, 99
III 95, 98, 99
late deformity 102
Le Fort osteotomies
I 105, 107–108, 109
complications 108
II 105, 108
complications 108
III 105, 108–109
complications 109
leaf fibroma 245–246
aetiology and clinical appearance
245–246
management 246
left ventricular failure (LVF) 17
leukoplakia, laser therapy 304
lichen planus 184
laser therapy 304
lidocaine (lignocaine) 201–202, 277
line infection 22
TNP 35
lines of election 123, 124
lingual flap 249
lingual fraenectomy 251
lingual nerve 1 1 1 , 119–120
block 272
damage 225–226, 228
lingual thyroid tumours 152
lip
incisions 124
lower, nerve supply 110, 111
primary closure 146
lip adhesion 136–137
lip deformities 133
lip repair 136–137
at 3 months 137
at 6 months or later 137
lipoma 261
Little's area 158
liver disease
coagulation disorders 41
fluid overload 30
oral surgery 277
LMA see laryngeal mask airway
LMWH see low molecular weight heparin
local anaesthesia 197–198, 200–207
and adrenaline (epinephrine) 201,
202–203, 217
agents 201–202
action 201–202
maximum safe dose 202
cannula insertion 86
difficulty in obtaining 207
and inhalational sedation 85
in ischaemic heart disease 275
non–surgical extractions 250–251
techniques 202–207
block 203–207
deposition 203
infiltration 202–203
needle insertion 203
other 207
uses 200–201
diagnostic 200
perioperative 201
postoperative 201
therapeutic 201
local complications
of fractures 66–67
of surgery 24–25
local skin flaps 726, 127
long bridge spans, dental implant 295–296
loss of function 25, 67
low molecular weight heparin (LMWH)
19, 20
lower respiratory tract infection (LRTI)
21–22
clinical features 21
diagnosis 21
investigation 21–22
treatment 22
Ludwig's angina 265, 267
lumbar puncture (LP) 165
lung infarction 20
LVF see left ventricular failure
lymph node biopsy 145–146, 158–159
lymph node tumours
metastatic 158–159, 160
nasopharyngeal cancer 152
oral cancer 143, 144, 145
parotid tumour, differential diagnosis
116, 117
lymphadentitis, acute submandibular
staphylococcal 269
lymphangioma 260–261
lymphomas 116, 152, 153, 159
lymphoscintigraphy 144, 146
lysosomes 37
McGill laryngoscope 74
Mclntosh laryngoscope 74
macrophages 7, 62
magnetic resonance imaging (MRI)
fractures 61
maxillary 99
zygomatic (malar) 96
neurological 166
oral cancer 143, 144
salivary gland 113
TMJ 175
malar bone fracture see zygomatic (malar)
bone fracture
mandible
atrophic 220–221
cleft deformities 133
dental implant 294, 295, 296
osteomyelitis 217
spread of infection 264
torus mandibularis 248–249
mandibular fractures 89–94
angular 90, 91, 92–93
clinical features 90–91
complications 93–94
condylar 90, 91–92, 93–94
dental extraction
complication 213, 228
criteria 220
displacement 91
radiography 91 –92
treatment 92–93
mandibular processes, embryology 131
mandibular prognathism 105–106
body osteotomy 106
vertical subsigmoid osteotomy
105–106
mandibular retrusion 106–107
inverted L osteotomy 107
saggital split osteotomy 106
segmental osteotomy 107
MAOIs see monoamine oxidase inhibitors
marsupialisation
jaw cysts 231–232, 233, 234
mucocoele 273
masks
anaesthetic 72, 74
oxygen 70
surgical 56
masseter muscles 95, 123, 174, 177
mattress sutures 195
maxilla
cleft deformities 133
complications of dental extraction
213–215
dental implants 294–295
spread of infection 264
maxillary fractures 98–100
clinical features 98–99
radiography 99
soft tissue management 100
surgical access 99–100
treatment 99–100
tuberosity 214–215
maxillary processes, embryology 131
maxillary sinus tumours 124, 157
maxillary surgery see Le Fort
osteotomies
medical history 5, 70
oral surgery 181–182, 183
universal infection control 48
meningiomas 169
meningism 163
meningitis 169–170
meniscal plication 175
meniscectomy 175–176
meniscus replacement 177
mental abscess 264
mental capacity, consent issues 187
mental nerve 191
blocks 201, 205–206
metabolic acidosis 33
compensation 34
metabolic alkalosis 33
315
metabolic bone diseases 280
metabolic complications of surgery 17–18,
34
metal allergy, intermaxiliary fixation 90
metastatic nodal disease 158–159, 160
methicillin resistant Staphylococcus
aureus (MRSA) 48, 49, 198
metoclopramide 72
metronidazole 198, 267
microcysts (satellite cysts) 234
microplate fixation, orbital rim fractures
97, 100
microvascular anastomosis 128, 129
midazolam 83, 85–86, 87
see also benzodiazepines
migratory abscess 222
Mitchell's osteotrimmer 191
mobilisation, early 19, 64–65
MOFS see multiorgan failure syndrome
molars
ankylosis and submerged deciduous
254
complications of extraction 213, 214,
217
first and second permanent 253
third see wisdom teeth
monoamine oxidase inhibitors (MAOIs) 77
monomorphic adenoma, parotid gland see
Warthin's tumour
morphine 77
mortality
general anaesthesia 69
septic shock 23
motor neuron lesions 162
motor response, testing 164
mouthwashes
chlorhexidine 93, 198–199
saline 199, 210, 222
MRI see magnetic resonance imaging
mucocoele/ranula 121, 272–273
aetiology 272
clinical features 272–273
diagnosis 273
management 273
mucoepidermoid tumour, salivary gland
118
mucoperiosteal flap 191, 243–244, 247,
298
multiorgan failure syndrome (MOFS) 22,
23
muscle
complications of anaesthesia 14, 78
complications of fractures 67
muscle relaxants 78
depolarising 78
suxamethonium 5, 14, 70, 72, 78
non–depolarising 78
myeloneuropathy, nitrous oxide exposure
76
myocardial infarction (MI) 16–17
perioperative 17, 43
recent 296
316
nails, examination 184
naloxone 78
nasal complications of craniofacial
fractures 101
nasal deformity 133
nasal intubation 75
nasal masks 74
nasal obstruction 155–156, 157
nasal polyps 156
nasal reconstruction 126, 127, 137
nasal septum displacement 97, 98, 156
nasal/nasoethmoidal fractures 97–98
clinical features 97
radiographs 97
treatment 98
nasogastric feeding 135
nasolabial cysts 236
nasolacrimal damage 97, 98, 101, 109
nasopalatine cysts 235–236
clinical features 235
diagnosis 235
radiographic appearance 235
treatment 235–236
nasopharynx
anatomy and physiology 149
benign conditions 150
examination techniques 147
tumours 151–152
benign 151
malignant 152
nausea see vomiting
neck
anatomy 158
examination 184
lateral swellings 159–160
midline swellings 159
reconstruction 146
treatment 145–146
necrosis
bone 62
osteoradionecrosis 284–285
soft tissue 57
necrotising fasciitis 267
needle holders 11, 194
needle insertion, local anaesthesia 203
needlestick injuries
avoiding 49, 51
management 51
neodymium:YAG laser 305–306
neoplasms see tumours
neostigmine 78
neovascularisation see granulation tissue
nerve conduction studies 165
nerve damage
complications of surgery 14
oral 189, 197–198
dental extraction 215, 225, 228
facial fractures 101
mandibular 90, 94
maxillary fractures 98, 99, 100
zygomatic (malar) 96
fractures 67
salivary gland 119–120
neurogenic sialadenosis 115
neurological assessment, fractures 60
craniofacial 100
neurological conditions 166–172, 277
acquired 166–170
congenital 170–171
non–localising symptoms 163
see also Creutzfeldt–Jakob disease
(CJD)
neurological deficit see nerve damage
neurosurgery
conscious level 163–164, 165
history taking and examination
161–163
anatomic localisation 162, 163
general pathology 162–163
special pathology 163
investigations and procedures 165–166
nitrogen, daily requirement 34
nitrous oxide 72, 76, 81
cryosurgery 302
see also inhalational sedation
non–Hodgkin's lymphoma 116, 152, 153
non–sterile dressings 65
non–steroidal anti–inflammatory drugs
(NSAIDs) 28, 78, 80
caution in asthma 278
caution in diabetes mellitus 276
oral surgery 198
see also aspirin
non–surgical extractions 250–251
non–union of fractures 67
nose
anatomy and physiology 155
see also entries beginning nasal
nose–blowing, avoidance 213–214
nutrition
clefts of the lip and palate 135
deficiencies 9
postoperative 34–35
semifluid diet 93
OAF see oroantral fistula
obstructive shock 15
obstructive sialadenitis 271–273
major gland 271–272
aetiology 271
clinical features 271
diagnosis 271
management 271–272
mucocoeles 272–273
Obwegeser osteotomy 106
occupational diseases
carpenters 157
healthcare workers 46–47, 49, 50–52
odontogenic myxoma 288
odontogenic tumours 286–288
odontotomes 288–289
complex 288–289
compound 289
germinated 289
invaginated 288
oedema
fluid overload 30–31
Reinke's 154
wound sepsis 57
oncotic osmotic pressure see colloid
osmotic pressure
ondansetron 72
onlay grafts, dental implants 299
operating microscope 124, 128
operating theatre, prevention of infection
49, 56
operator dentist 187
ophthalmic injury
facial fracture 89, 101
Le Fort HI osteotomy 108–109
maxillary fracture 98
zygomatic bone fracture 95–96
see also orbital blow–out fractures
opioid(s) 77, 80
antagonists 78
post–oral surgery 198
OPT see orthopantomograph
oral cancer 140
aetiology 140–141
'field change' 143
index primary 143, 144
investigation 143–144
clinical 143
imaging 143–144
morbidity 141–142
premalignant lesions 142
quality of life issues 146
signs and symptoms 142
staging 142–143
synchronous primary 143
treatment
multidisciplinary approach 144
planning 144–145
tumour thickness 144–145
oral cavity
examination 184–185
surgical access 124
oral hygiene 93
oral surgery 189–199
consent 185–187
equipment 190
examination 183–185, 211
follow–up 199
history taking 181–183
medically compromised patients
274–278
postoperative care 196–199
preoperative considerations 189–190
techniques 190–196
see also cryosurgery; lasers
orbital blow–out fractures 60, 95
enophthalmos 95, 100, 101
imaging 96, 99, 100
treatment 100
see also ophthalmic injury
orbital floor defects 97
orbital rim fractures 97, 100
orbital wall defects 100
oroantral fistula (OAF) 213–214
chronic 218
orofacial sinus 267
oropharyngeal airway 74
oropharynx
anatomy and physiology 149
benign conditions 150–151
tumours 152–153
benign 152
malignant 143, 144, 152–153
orthodontic assessment 104
orthodontic problems
causes 250
surgical management 251–254
surgical procedures 254–256
treatment options 250–251
orthodontic wire 214
orthognathic surgery 103–109, 139
assessment 103–105
dental casts 104
distraction osteogenesis 109
mandibular 105–107
maxillary (Le Fort osteotomies) 105,
107–109
orthodontic preparation 105
preoperative preparation 105
splint construction 105
treatment planning 104
orthopantomograph (OPT) 90, 91, 297
osmolarity 27
osseointegration, dental implants 292–295
ossification
fracture healing 63
post–traumatic 67
osteitis see dry socket
osteoarthritis 62, 63, 67
osteoclasts 62
osteogenesis imperfecta 280, 290
osteoma 285
osteomyelitis 64
acute 283–284
clinical features 283
management 283–284
radiographic features 283, 284
chronic 284
chronic sclerosing 284
dental abscess 267
mandibular 217
subperiosteal 284
osteopetrosis 280, 290
osteoplastic flaps 244
osteoporosis 280, 290
dental implants 297
fractures 60
risk factors 290
osteoradionecrosis 284–285
osteosarcoma 285–286
clinical appearance 285–286
diagnosis 286
management 286
osteotomies
body 106
inverted L 107
saggital split 106
segmental 107
vertical subsigmoid 105–106
see also Le Fort osteotomies
otitis media 150
oxygen (O2)
dangers 76
extubation 75
induction of anaesthesia 70
monitoring in anaesthesia 79
see also pulse oximetry
postoperative 80, 85, 87
see also inhalational sedation
oxygen saturation alarm 87
oxygen therapy
ischaemic heart disease 275
respiratory conditions 22, 278
oxygen–carrying capacity 42–43
smoking 70
transfused blood 43
Paget's disease 280, 290–291
clinical appearance 290–291
diagnosis 291
management 291
osteosarcoma 285
pain 18
abscess
dental 263
periodontal 268
chronic pain syndromes 24
deep vein thrombosis (DVT) 19
fractures
compartment syndrome 66
facial 90
muscle, anaesthetic–related 14, 78
oral surgery
diagnosis, local anaesthetics 200
presenting complaint 181, 182
pleuritic 21
postextraction 217
pulmonary embolism (PE) 20
referred to the ear 151
TMJ 173, 174
pain relief
cryosurgery 300
see also analgesia
palatal anaesthesia 203
palatal gingival margin flap 256
palatal hyperplasia 245
palatal splint 248
palatal swellings 264, 266
palate clefts 132
primary 133, 138
secondary 133, 138
soft 133–134, 138
surgical treatment 135–136
palpation of fractures 60
facial 89
Pancoast's tumour 160
pancuronium 78
paracetamol 198
paranasal sinuses 156–157
inflammatory conditions 156–157
malignant tumours 157
parasinal tumours 157
parenteral feeding see total parenteral
nutrition (TPN)
parotid duct 270
cysts 120
parotid gland
anatomy 110
saliva production 112
sialadenosis 114–115
sialolithiasis 114, 271
tumours
317
318
parotid gland—(cont'd)
differential diagnosis 116, 117
pleomorphic adenoma 113,
117–118
Warthin's 113, 118, 120
parotidectomy 115, 116, 117–118
branchial cleft anomalies 120
complications 119, 120
incision 114
paroxysmal trigeminal neuralgia (PTN)
see trigeminal neuralgia
patchy vasculitis 9
pathological fractures 59–60
patient discharge 86
escorts 82, 85
patient preparation 8, 57
patient–operator position 210
PE see pulmonary embolism
pectoralis major myocutaneous flap 128
pelvic fractures 60, 63, 65
fat embolism 65–66
penicillin 267, 269, 275
periapical pathology 220
pericoronitis 221–222
spread of infection from 222
treatment 222
wisdom teeth extraction 220
periodontal ligament injection 207
periodontal abscess 263, 268
clinical features 268
management 268
perioperative fasting see fasting,
perioperative
periorbital haematoma 166–167
periradicular surgery 238–242, 266
indications 238–239
endodontic failure 238
pathology 239, 266
post–crowned teeth 239
post perforation 239, 241–242
post perforations
diagnosis 242
management 242
reasons for failure 241
technique 239–241
anaesthesia 239
apex removal 240
bone removal 240
currettage 240
flap design 240
follow–up 241
retrograde root filling 240
wound closure 241
PET see positron emission tomography
petechiae 39, 65–66
pethidine 77
pharyngeal pouch 151, 752
pharyngitis 150
pharyngoplasties 138
pharynx 149–153
anatomy and physiology 149
benign conditions 150–151
endoscopic examination 147
tumours 151–153
phenytoin 252, 277
phosphate (PO42-) 27
photocephalometric assessment 104—105
physical examination 70–71, 183–185
physical violence 89
physiotherapy
fracture management 64–65
jaw 175, 178
preoperative 71
Pierre Robin sequence 134
Pindborg tumour 287
piriform fossa tumours 153
plasmin 37
plaster casts 64
plate fixation 106
platelet activation 37, 38–39
platelet adhesion 36–37
platelet aggregation 37
platelet count, normal 39
platelet disorders 39–40
decreased function 40
decreased numbers 39
platelet plug 37
platelet transfusion 39, 42, 43–44
plates
bone 102, 106
miniplates 91, 92, 93
titanium 90, 92, 101
pleomorphic adenoma 113, 117–118
pleural effusion 21
pneumonia see lower respiratory tract
infection (LRTI)
pneumothorax 15
rib fractures 60
poliomyelitis immunisation 50
porphyria 70, 76–77
positron emission tomography (PET)
143–144
post perforation 239, 241–242
post–crowned teeth, periradicular surgery
239
post–traumatic ossification 67
postcricoid tumours 153
posterior superior alveolar block 206
postoperative care
general anaesthesia 79–80
oral surgery 196–199
see also under specific
conditions/procedures
postponement of surgery 71
potassium (K+)
daily requirement 31
interactions
adrenaline (epinephrine) 275
suxamethonium 78
intracellular concentration 27
red cell concentrate (RCC) 43, 45
regulation 28
abnormalities 31–32, 45
diuretic therapy 30–31, 70
supplementation 32
TPN 35
povidone—iodine 8, 56, 57
preauricular incision 175, 776
prefabrication, flap reconstruction 130
pregnancy
history taking 70
oral surgery 277–278
sialadenosis 115
pregnancy epulis 261
premalignant lesions, oral 142, 304
premedication, general anaesthesia 71–72
premolars
orthodontic management 253
second, extraction 256
preoperative care
oral surgery 189–190
see also specific conditions/
procedures
preprosthetic surgery 243–249
bone 247–249
extraction 243–244
soft tissue 244–247
presenting complaint
history 5
oral surgery 181
pressure sores 23–24
plaster casts 64
prilocaine hydrochloride 201–202, 207,
277
prions see Creutzfeldt–Jacob disease
(CJD)
Prolene 11, 12
propofol 77
proptosis 101
prostaglandins 28, 39
protamine 20
protective workwear see theatre dress
prothrombin time (PT) 40
psychological assessment 103
psychological support 134
psychological complications 24, 25, 66
ptergoid muscles 91, 174, 177
ptergoid plates 95, 174
ptergoid venous plexus 206
pterygomandibular raphe 204
pulmonary artery catheterisation 79
pulmonary embolism (PE) 19–21
aetiology 19
clinical features 20
investigation 20
pathophysiology 19
fractures 65
treatment 20–21
pulp pathology 220
pulp testing 235, 268
pulse
drugs altering 15
recording 16
pulse oximetry (SpO2) 72, 79, 80, 86, 87
punch biopsy 258
pus
aspiration 257–258
dental abscess drainage 265–266
formation 55, 57, 58
pyogenic granuloma 261
pyrexia 21, 23, 34
fat embolism 65–66
insensible fluid loss 16, 30
UTI 23
wound sepsis 57
Quantiflex MDM machine 84
radiation sialadenitis 116
radicular cysts 230–232, 239
clinical features 230
diagnosis 230–231
radiolucencies 230, 231
treatment 231–232
enucleation 231
marsupialisation 231–232
radiographic viewing screens 190
radiography
bone diseases
metabolic 281, 282
neoplasms 285, 286–287
odontomes 288–289
osteomyelitis 283
Paget's disease 291
deep vein thrombosis (DVT) 19
dental extraction 211, 213, 214–215
wisdom teeth 222–225
dental implants 297–298
dental, parallax methods 252–253, 255
fractures 60–61
mandibular 91–92
maxillary 99
nasal/nasoethmoidal 97
zygomatic (malar) bone 96
head and spine 165–166
jaw cysts 230, 231, 232, 233, 235,
236–237, 279
lower respiratory tract infection
(LRTI) 21
obstructive sialadenitis 271
oral cancer 143
orthognathic surgery 104
in pregnancy 277
pulmonary embolism (PE) 20
TMJ 174
radioisotope scanning
bone 61
salivary gland 113
radiotherapy
complications 9, 129, 217, 294, 297
laryngeal cancer 155
nasopharyngeal cancer 152
oral/oropharyngeal cancer 144, 145
salivary gland tumours 118, 119
tonsillar carcinoma 153
raised intracranial pressure (ICP)
in 'active hydrocephalus' 171
signs and symptoms 163
raising a flap 191–192
ranula see mucocoele/ranula
rapid sequence induction 72–73
red cell concentrate (RCC) 43, 45
red patches, oral premaligant lesions 142
referring dentist 187
Reinke's oedema 154
remifentalin 77
renal blood flow 28
renal disease
dehydration 30
fluid overload 30
and oral surgery 278
renal excretion of hydrogen ions 33–34
renal failure
complication of blood transfusion 44
fat embolism 66
hyperkalaemia 32
renin 28
renin–angiotensin–aldosterone system 28
alterations 30, 32
respiratory acidosis 33
compensation 33–34
respiratory alkalosis 33
respiratory complications of surgery
21–22
respiratory depression 81–82, 87
respiratory disease
intravenous sedation contraindicated
86
and oral surgery 278
preoperative preparation 71
theatre staff 56
respiratory fluid losses 30, 31
respiratory system
history 182
monitoring in anaesthesia 79
resuscitation
'ABC' 168
fracture management 63
preoperative 71
see also fluid replacement
retrobulbar haemorrhage 95
Rhesus factor 43, 45
rhinitis 155–156
rhinoplasty 138–139
rhinorrhoea
CSF 97, 98
foul–smelling 156
rib bone grafts 93, 178
rib fractures 60
rickets 280, 291
ridge augmentation/expansion 249, 300
root canal
drainage 265
filling 240
root forceps 208
root resorption, incisors 252, 253, 254
rotation
dental extraction 210
fractures 62
Rowe's elevator 96
saggital split osteotomy 106
SAH see subarachnoid haemorrhage
salbutamol inhalers 278
saline irrigation 241
saline mouthwashes 199, 210, 222
saline solution 32
saliva
drooling 120
production 111–112
salivary duct cysts 120
salivary fistula 120
salivary gland 110–121
anatomy 110–111,270–271
branchial cleft anomalies 120
complications of surgery 119–120
investigation 112–114
biopsy 113–114
fine–needle aspiration 113, 117
radiological 112–113
minor 270–271
biopsy 273
mucocoele/ranula 121, 272–273
obstructive sialadenitis 271–273
physiology 111–112
swellings 114–116
tumours 116–119
benign 117–118
malignant 118–119
sarcoidosis 116
scalp injuries 166
scalp reconstruction 127
scar(s)
delayed eruption of teeth 251, 252
formation 7, 8
hypertrophic 10
keloid 10
management 124–125
neck 184
scavenging systems 72, 84
scrubbing see hand washing
scurvy 280, 291
sealants 240
secondary bleeding 21, 199
sedative agents 81–82
segmental osteotomy 107
seizures/epilepsy 162, 167, 169
enflurane contraindicated 75
inhalational sedation 84
intravenous sedation 85
post–infective 109
post–traumatic 101
sentinel node biopsy 145–146
sepsis see cross–infection; infection;
wound sepsis
septic shock 23
septicaemia 23
sequestra, postextraction 218
sevoflurane 76
sharp bony ridges 247–248
aetiology and clinical appearance 247
management 248
sharp mylohyoid ridge
aetiology and clinical appearance 249
management 249
sharps bins 49, 50
sharps injuries see needlestick injuries
shaving, preoperative 8, 57
shock 15–17
cardiogenic 16–17
hypovolaemic 15–16
obstructive 15
pulmonary embolism (PE) 20
septic 23
shortness of breath 20
history 70
sialadenitis 115–116
acute 115
chronic 115–116
sialadenosis 114–115
sialography 112
319
320
sialolithiasis 114, 271
removal of stones 272
'sick role' 24
sickle–cell disease 43
sinus lift procedure, dental implants
299–300
sinusitis 156–157
acute 157
chronic 156–157
SIRS see systemic inflammatory response
syndrome
Sjogren's syndrome 116, 273
skin
head and neck 122
integrity see fractures, open
preoperative preparation 8, 57
skin allergies 6
skin clips 12
skin flaps
blood supply 8
distant 128
free 128–129
local 726, 127
tissue expansion 127
novel methods 130
wound tension 8
skin flora 8
inpatients 57
line infection 22
skin grafts 125–126, 130, 146
skin rashes 184
skull
fracture 166–167
radiography 165–166
sutures, premature fusion 170
SMAS see superficial muscular and
aponeurotic system
smoking
dental implants 297
dry socket 217
history taking 6, 182–183
laryngeal conditions 154
oral cancer 140–141, 143
oxygen–carrying capacity 70
respiratory complications of surgery
21
snoring 151
social history 6
oral surgery 182–183
sodium
daily requirement 31
extracellular concentration 27
regulation 27–28
abnormalities 31
sodium citrate 72
soft palate deformities 133–134
soft tissue
inflammatory response 263, 265
oral lesions 259–262
preprosthetic surgery 244–247
trauma, tooth extraction complication
213
soft tissue retractor 194
solitary bone cysts 236
sore throat
anaesthetic–related complications 14
theatre staff 56
special needs patients, sedation techniques
83, 85
speech 109
cleft deformities 138
following total laryngectomy 155
spillages
blood/body fluids 49
of organisms 55
spina bifida 170
spinal lesions 162
spinal/epidural anaesthetic–induced
hypotension 15
spine radiography 165–166
splint(s)
construction
fractured tuberosity 214
orthognathic surgery 105
Gunning 92
palatal 248
split bone technique 226
split thickness skin grafts 125, 146
sputum culture 22
squamous cell carcinoma
larynx 154
lymph node 159
oral 140, 142
parasinus 157
salivary gland 119
squamous cell papilloma 261–262
staff see healthcare workers
Staphne's idiopathic bone cysts 236–237
Staphylococcus aureiis 55, 269
methicillin resistant (MRSA) 48, 49,
198
Stenson's duct see parotid duct
sterilisation of instruments 47, 48–49
Steristrips 98
Streptococcus
beta–haemolytic 150
pyogenes 55
streptokinase 20–21
stress fractures 59
stretch receptors 28
subarachnoid haemorrhage (SAH)
168–169
subconjuctival haemorrhage 95, 98,
166–167
subdural empyema 170
sublingual abscess 265, 266
sublingual ducts 270
sublingual gland, anatomy 111
submandibular abscess 264–265, 266
submandibular duct 270
laser therapy 304
surgery 120
submandibular gland
anatomy 111
complications of surgery 119–120
obstructive sialadenitis 271
sialolithiasis 114, 271
submandibular staphylococcal
lymphadenitis, acute 269
submental abscess 264, 265, 266
subperiosteal implants 292
suction, oral surgery 190
Suedeck's atrophy 67–68
superficial muscular and aponeurotic
system (SMAS) 123
superior orbital fissure syndrome 96
supernumerary teeth
extraction 255
incisors 251, 252
supratentorial pathology 162
surgical embolectomy 21
surgical emphysema 95
surgical exposure of teeth 251
surgical implants 25
surgical instruments 190
cleaning 48
contaminated 21, 46–47
disposable 49, 53
sterilisation 47, 48–49
'tagging' 49
see also specific types
surgical technique
dehiscence 10
prevention of wound infection 57
wound healing 9
Surgicel 216
suture breakage 10
suture knot
oral surgery 195, 796
slippage 10
prevention 11
suture materials
classification 11
oral surgery 195
properties 77
selection 11, 57
suture needles 11–12
oral surgery 194
suture removal 9
oral surgery 196
wound sepsis 57, 58
suture technique
oral surgery 193–194, 195–196
wound healing 9
suxamethonium 5, 14, 70, 72, 78
Swann–Morton blades 190–191
sweating, complication of parotidectomy
120
swelling
cervicofacial actinomyosis 268
compartment syndrome 66
dental abscess 263–264
fractures 60, 62
facial 89, 90
neck 159–160
periodontal abscess 268
postextraction 217
salivary gland 114–116
sympathetic activity 34
sympathetic block 68
sympathetic monitoring 79
synostosis 170
syphilis, blood donor screening 45
systemic inflammatory response syndrome
(SIRS) 22, 23
tachycardia
compensatory 15, 70, 82
fat embolism 65–66
wound sepsis 57
Talbot's iodine 222
taste, altered perception 228
TEDS see thromboembolic deterrent
stockings
teeth/tooth
anaesthetic–related complications 14
crowding/impaction see orthodontic
problems
division 192
mandibular fractures 90, 91, 92–93
maxillary fractures 98, 99
mobility, periodontal abscess 268
post perforation 239, 241–242
replacement 296
transplantation 220, 251
vertical fracture 241
see also entries beginning dental;
specific types
temazepam 83
temperature
local, fractures 60
monitoring 79
temporalis muscle 123
flap 177, 178
temporomandibular dysfunction 173
temporomandibular joint (TMJ) 173–178
anatomy 173–174
clicking 173, 174
conditions 173
dislocation 176
complication of tooth extraction
215
examination 174
history 174
reconstruction 177–178
special investigations 174–175
treatment 173, 175–178
tenderness
fractures 60, 63, 67
wound sepsis 57
tendons
complications 67
examination 60
tetanus immunisation
healthcare workers 50
open fracture management 65
TF see tissue factor
theatre dress 49, 56
theatre personnel 56
therapeutic hypotension 14–15
thiopentone sodium 76–77
thrombocytopenia 39, 41
platelet transfusion 39, 44
thromboembolic deterrent stockings
(TEDS) 18
thromboxane (xA2) 37, 39
thyroglossal cyst 159
tissue damage 24
tissue engineering 130
tissue factor (TF) 37
tissue forceps 194
tissue plasminogen activator (TPA) 37
tissue sampling 257–259
disposition 258–259
frozen section 259
titanium dental implants 293
titanium plates 90, 92, 101
TIVA see total intravenous anaesthesia
TMJ see temporomandibular joint
TNM staging, oral cancer 142–143
tobacco see smoking
tongue see entries beginning lingual
tonsillitis 150
tonsillar carcinoma 152–153
tonsillar inclusion cysts 152
tonsillectomy 150–151
indications for 151
tooth see teeth/tooth; entries beginning
dental; orthodontic
torus mandibularis 248–249
torus palatinus 248
total intravenous anaesthesia (TIVA) 77
total parenteral nutrition (TPN) 35
complications 35
constituents 35
zinc deficiency 9
TPA see tissue plasminogen activator
tracheopharyngeal speaking valve 155
traction 64
trauma
metabolic responses to 34
neurological 166–167
Treacher–Collins syndrome 109
trichloracetic acid 222
trigeminal nerve 123
block 172, 201, 206
trigeminal neuralgia 171–172
cryosurgery 300
trismus 102
dental abscess 266–267
fractures
mandibular 90, 93
maxillary 98
zygomatic (malar) 96
inferior dental block 205
oral cancer 142
osteomyelitis 283
postextraction 218
tonsillitis 150
tuberculosis
history taking 70
immunisation 50
occupational risk 51
sialadenitis 116
tuberculous meningitis 170
tubocurarine 78
tumours
cryosurgery 301, 303
endoscopy 124
neurological imaging 166
wisdom tooth extraction 220
see also specific types/regions
tympanic neurectomy 120
ulceration, oral cancer 142
ultrasound
DVT 19
salivary gland 112
unconscious patients
cervical spine radiography 60
consent 187
mandibular fractures 91, 92
universal extraction forceps 209
universal infection control 47–50
key elements 48–50
principles 48
University of Washington Quality of Life
Questionnaire (UW–QOL) 146
unstable fractures 62
uraemia, delayed wound healing 9
urinary catheters 22–23, 80
urinary retention 22–23
urinary tract infection (UTI) 22–23, 54
urine specimen 23
uvulopalatopharyngoplasty (UPPP) 151
vaccination see immunisation
vagal bradycardia 71–72
valvular disease 275
see also endocarditis
vascular compression syndromes 171–172
vascular damage, tooth extraction 215
vascular disorders 40
vascular endothelium 37, 38–39
vascular examination, fractures 60
vascular permeability 33, 34
Vaseline 98
vasoconstriction 36
vCJD see Creutzfeldt–Jakob disease (CJD)
velopharyngeal incompetence 138
venography 19
ventilation/perfusion (V/Q) scan 20, 22
vercuronium 78
Verrill's sign 86
vertical subsigmoid osteotomy 105–106
vessel see entries beginning vascular
vestibular denture–induced hyperplasia
244–245
vestibuloplasty 249
Vicryl 12
viral meningitis 169–170
viral papilloma 152, 154
viral warts 262
cryosurgery 300
Virchow node 160
visual disturbances 84–85
diplopia 95, 98, 100, 101, 108–109
inferior dental block 205
loss of vision 95, 96, 101, 109
vitamin A 9
vitamin B1 70
vitamin B I2 76
vitamin C 9, 291
vitamin D 297
vitamin deficiencies 41, 291
TPN 35
vitamin K 41
vocal cord(s) 153–154
nodules 154
palsy 154
papilloma 154
321
Volkmann's contractures 67
volume receptors 28
vomiting
cause of dehydration 29
complication of anaesthesia 13
neurological disorders 163, 168
von Willebrand's disease 40, 41
Walsham's forceps 98
war injuries 89
warfarin 41–42
in chronic AF 17
contraindication 296
in DVT 19
INR 20, 41, 42, 296
in PE 20
Warthin's tumour 773, 118, 120
Warwick James'elevators 191, 193,
227
waste disposal 50
water regulation 28–29
abnormalities 29–31
Weber Fergusson incision, modified
124
weight 82, 83
Wharton's duct see submandibular duct
white cell count 21
white patches
laser therapy 304
oral premalignant lesions 142
tonsils 151
322
Whitehead's varnish pack 217, 232,
254–255, 256, 259, 260, 285
wisdom teeth 219–228
clinical assessment 222
clinical management 225–227
criteria for removal 219, 220–222,
253–254
curve of Spee 223, 224
extraction techniques 225–227
lower 225–227
upper 227
perioperative complications 227–228
postextraction complications 228
dry socket 217
patient information 225
postoperative care 227
radiographic assessment 222–225
wound classification 55
wound closure 12
head and neck surgery 125–130, 146
periradicular surgery 241
wound healing
classification 7
complications 9–11
factors affecting 8–9
local 8–9
systemic 9
normal sequence 7–8
rate 7, 8
age 9
regulation 8
wound sepsis 8, 54–55
causative organisms 55–56
clinical features 57
definition 55
diagnosis 57
prevention 56–57
risk factors 54
treatment 58
wound swabs 57, 58
wound tension 8, 10, 12
wrinkle lines
facial 123
see also Langer's lines
written information
consciousness sedation 82, 86
oral surgery 189
postoperative 196, 797
preoperative 225
Z–plasty 254
facial scars 125
zinc, role in wound healing 9
zinc oxide pack 217, 240, 244, 245
zygomatic arch 123, 128, 176
zygomatic (malar) bone fracture 95–97
clinical features 95–96
displacement 96
radiography 96
treatment 96–97