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Apley and Solomon’s
System of
Orthopaedics and
Trauma
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Alan Graham
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Ashley W. Blom MBChB MD PhD FRCS FRCS (Tr&Orth)
Head of Translational Health Sciences
Bristol Medical School
University of Bristol
Bristol, UK
CRC Press
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Names: Blom, Ashley, editor. | Warwick, David, 1962- editor. | Whitehouse, Michael (Michael R.), editor. | Preceded by
(work): Solomon, Louis. Apley’s system of orthopaedics and fractures.
Title: Apley & Solomon’s system of orthopaedics and trauma / [edited by] Ashley Blom, David Warwick, Michael
Whitehouse. Other titles: Apley and Solomon’s system of orthopaedics and trauma | System of orthopaedics and
trauma. Description: Tenth edition. | Boca Raton : CRC Press, [2017] | Preceded by Apley’s system of orthopaedics and
fractures / Louis Solomon, David Warwick, Selvadurai Nayagam. 9th ed. 2010.
Identifiers: LCCN 2016059350 (print) | LCCN 2016059955 (ebook) | ISBN 9781498751674 (hardback bundle : alk.
paper) | ISBN 9781498751773 (pbk. : alk. paper) | ISBN 9781498751711 (eBook VitalSource) | ISBN 9781498751704
(eBook PDF). Subjects: | MESH: Orthopedic Procedures | Musculoskeletal System--injuries | Fracture Fixation—
methods. Classification: LCC RD731 (print) | LCC RD731 (ebook) | NLM WE 168 | DDC 616.7--dc23
LC record available at https://lccn.loc.gov/2016059350
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DEDICATIO
N To Louis
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CONTENTS
SECTION 3: TRAUMA
22 The management of major injuries 651
David Sutton & Max Jonas
23 Principles of fractures 711
Boyko Gueorguiev, Fintan T. Moriarty, Martin Stoddart,
Yves P. Acklin, R. Geoff Richards & Michael Whitehouse
24 Injuries of the shoulder and upper arm 755
Andrew Cole
25 Injuries of the elbow and forearm 773
Adam Watts & David Warwick
Children’s sections: Mike Uglow, Joanna Thomas
26 Injuries of the wrist 797
David Warwick & Adam Watts
Children’s sections: Joanna Thomas
27 Injuries of the hand 815
David Warwick
28 Injuries of the spine 835
Robert Dunn & Nicholas Kruger
29 Injuries of the pelvis 863
Gorav Datta
30 Injuries of the hip and femur 881
Richard Baker & Michael Whitehouse
31 Injuries of the knee and leg 913
Nick Howells
32 Injuries of the ankle and foot 937
Gavin Bowyer
Index 965
viii
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CONTRIBUTOR
Consultant Knee Surgeon
Nuffield Orthopaedic Centre
Oxford, UK
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Christopher Edwards BSc MBBS MD FRCP I
Southampton, UK
Professor and Consultant Rheumatologist R
Foundation Trust
O
Southampton, UK
x
Michael Fox FRCS(Tr&Orth)
Stephen A. Jones BSc(Hons) MBBCh MRCS(Eng)
Consultant Surgeon in Peripheral Nerve Injury The
MSc(Orth Eng) FRCS(Orth)
Royal National Orthopaedic Hospital
Senior Lecturer in Orthopaedics
Stanmore, UK
Cardiff University
and
Martin Gargan MA(Oxon) FRCS
Consultant Orthopaedic Surgeon
FRCS(Tr&Orth)
Cardiff & Vale University Health Board
Head, Division of Paediatric Orthopaedics
Cardiff, UK
Harold and Bernice Groves Chair in Orthopaedics
Hospital for Sick Children
Dimitrios Kassimos MD MSc
Toronto, Canada
Consultant Rheumatologist
General Military Hospital of Athens
Enrique Gómez-Barrena MD, PhD
Athens, Greece
University Chair of Orthopaedic Surgery
and Traumatology
Ryan Katchky BEng MD, FRCSC
Facultad de Medicina
Clinical Fellow
Universidad Autónoma de Madrid
Hospital for Sick Children
Madrid, Spain
Toronto, Canada
and
Orthopaedic Surgeon
Nicholas Kruger BSc MBChB FRCS(Ed)
Head of the Lower Limb Reconstructive Surgery
FCSOrth(SA)
Unit at Hospital de Traumatología
Consultant Orthopaedic and Spinal Surgeon
La Paz University Hospital
Head of Acute Spinal Cord Injury Unit
Madrid, Spain
University of Cape Town Student Orthopaedic
Training Coordinator
Boyko Gueorguiev PhD
Groote Schuur Hospital
Program Leader Biomedical Development
Cape Town, South Africa
AO Research Institute
Davos, Switzerland
Nuno Lança MD FEBOT
Orthopaedic Surgeon
Nick Howells MSc MD FRCS (T&O) Clinical Assistant of Hospital de Santa Maria
Consultant Trauma and Orthopaedic Surgeon Orthopaedic Department, Spinal Unit
Avon Orthopaedic Centre Clinical Assistant of Hospital CUF Descobertas,
Bristol, UK Orthopaedic Department, Spinal Unit
Lisbon, Portugal
William Jackson FRCS(Orth)
Consultant Knee Surgeon Jason Peter Mansell BSc(Hons) PhD
Nuffield Orthopaedic Centre Senior Lecturer in Bone Biology
Oxford, UK University of the West of England
Bristol, UK
S
Max Jonas MBBS FRCA FFICM
Consultant and Senior Lecturer Jorge Mineiro MD PhD FRCSEd
Orthopaedic Surgeon
R
University Hospital Southampton and University T Professor of Orthopaedics and Traumatology Clinical
of Southampton Director of Hospital CUF Descobertas Head of
Hospital CUF Descobertas Orthopaedic Department
U
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Fintan T. Moriarty PhD Foundation Trust
Senior Scientist Musculoskeletal Infection AO Research Southampton, UK
Institute
Davos, Switzerland Jonathan H. Tobias MA MD PhD FRCP
Musculoskeletal Research Unit
Michael Parry BSc(Hons) MBChB PGCME MD University of Bristol
FRCS(Tr&Orth) Bristol, UK
Consultant Orthopaedic Surgeon
Department of Orthopaedic Oncology Royal Orthopaedic James Turner FRCS (Tr&Orth)
Hospital Consultant Orthopaedic Surgeon
Birmingham, UK CURE Ethiopia Children’s Hospital
Addis Ababa, Ethiopia
Andrew Price DPhil FRCS(Orth)
Professor of Orthopaedic Surgery Michael G. Uglow MBBS FRCS(Eng) FRCS(Glas)
Nuffield Department of Orthopaedics, Rheumatology and FRCS(Tr&Orth)
Musculoskeletal Science Nuffield Orthopaedic Centre Consultant Orthopaedic Surgeon
Oxford, UK University of Southampton and University Hospital
Southampton NHS Foundation Trust
R. Geoff Richards PhD Southampton, UK
Director
AO Research Institute Charles J Wakeley BSc MBBS FRCS FRCSed
Davos, Switzerland FRCR
Consultant Radiologist, Department of Radiology University
H. Srinivasan MB BS FRCS FRCS Ed DSc (Hon) Formerly Hospitals Bristol NHS Foundation Trust Bristol, UK
Senior Orthopaedic Surgeon
Central Leprosy Teaching & Research Institute Chengalpattu David Warwick MD BM FRCS FRCS(Orth)
(Tamil Nadu), India; Eur Dip Hand Surg
Director Central JALMA Institute for Leprosy (ICMR) Honorary Professor and Consultant Hand Surgeon University
Agra (UP), India of Southampton and University Hospital Southampton
and Southampton, UK
Editor, Indian Journal of Leprosy
Adam C. Watts MBBS BSc FRCS(Tr&Orth)
Jonathan Daniel Stevenson MBChB BMedSci Consultant Upper Limb Surgeon
FRCS(Tr&Orth) Wrightington Hospital
Consultant Orthopaedic Surgeon Visiting Professor, University of Manchester
Department of Orthopaedic Oncology Royal Orthopaedic Manchester, UK
Hospital
Birmingham, UK Michael Richard Whitehouse PhD MSc(Orth Eng) BSc(Hons)
PGCert(TLHE) FRCS(Tr&Orth)
Martin Stoddart MPhil PhD FHEA
Principal Scientist Consultant Senior Lecturer in Trauma and
AO Research Institute Orthopaedics
Davos, Switzerland University of Bristol
and
C
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The provision of health care and resources varies
considerably between countries: Greece has 6.3 E
When Alan Apley produced the first edition of his System of Regional Orthopaedics, where we engage with these
Orthopaedics and Fractures 50 years ago he saw it as an aid disorders in specific parts of the body; and thirdly Fractures
to accompany the courses that he conducted for aspiring and Joint Injuries. In a major departure from previous
surgeons who were preparing for the FRCS exams. With editions, we have enlisted the help of colleagues who have
characteristic humour, he called the book ‘a prophylactic particular experience of con
against writer’s cramp’. Pictures were unnecessary: if you ditions with which we as principal authors are less familiar.
had any sense (and were quick enough to get on the heavily Their contributions are gratefully acknowl edged. Even here,
oversubscribed Apley Course), you would be treated to an though, we have sought their per mission to ‘edit’ their
unforgettable display of clinical signs by one of the most material into the Apley mould so that the book still has the
gifted of teachers. sound and ‘feel’ of a single authorial voice.
You also learnt how to elicit those signs by using a For the second edition of the book, in 1963, Apley added a
methodical clinical approach – the Apley System. The new chapter: ‘The Management of Major Accidents’. Typically
Fellowship exam was heavily weighted towards clinical skills. frank, he described the current arrangements for dealing with
Miss an important sign or stumble over how to examine a serious accidents as ‘woefully inadequate’ and offered
knee or a finger and you could fail outright. What Apley suggestions based on the government’s Interim Report on
taught you was how to order the steps in physical Accident Services in Great Britain and Ireland (1961). There
examination in a way that could be applied to every part of has been a vast improvement since then and the num
the musculoskeletal sys ber of road accident deaths today is half of what it was in the
tem. ‘Look, Feel, Move’ was the mantra. He liked to say that 1960s (Department of Transport statistics). So important is
he had a preference for four-letter words. And always in that this subject that the relevant section has now been rewritten
order! Deviate from the System by grasping a patient’s leg by two highly experienced Emergency and Intensive Care
before you look at it minutely, or by testing the movements in Physicians and is by far the longest chapter in the present
a joint before you feel its contours and establish the exact site edition.
of tenderness and you risked becoming an unwilling Elsewhere the text has been brought completely up to date
participant in a theatrical comedy. and new pictures have been added. In most cases the
Much has changed since then. With each new edi tion the illustrations appear as composites – a series of images that
System has been expanded to accommodate new tests and tell a story rather than a single ‘typical’ picture at one moment
physical manoeuvres developed in the tide of super- in the development of some disorder. At the beginning of
specialization. Laboratory investigations have become more each Regional chapter, in a run of pictures we show the
important and imaging techniques have advanced out of all method of examin
recognition. Clinical classi fications have sprung up and ing that region: where to stand, how to confront the patient
attempts are now made to find a numerical slot for every and where to place our hands. For the experi enced reader
imaginable fracture. No medical textbook is complete without this may seem like old hat; but then we have designed this
its ‘basic science’ component, and advances are so rapid that book for orthopaedic surgeons of all ages and all levels of
changes become necessary within the period of writ ing a experience. We all have some thing to learn from each other.
single edition. The present volume is no excep tion: new bits As before, operations are described only in outline,
were still being added right up to the time of proofreading. emphasizing the principles that govern the choice of
For all that, we have retained the familiar structure of the treatment, the indications for surgery, the design of the
Apley System. As in earlier editions, the book is divided into operation, its known complications and the likely outcome.
three sections: General Orthopaedics, Technical procedures are learnt in
covering the main types of musculoskeletal disorder;
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simulation courses and, ultimately, in the operating theatre. Written instructions can only ever be a
guide. Drawings are usually too idealized and ‘in
D
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SN
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DJW
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ACKNOWLEDGEMENTS
This textbook is an iterative process and for this current edition new authors have been asked to revise and
refresh the existing text. The editors and new authors thoroughly acknowledge the contribution of those who
have gone before them, much of whose work remains in this updated text.
Chapter 2, Infection, contains some material from ‘Infection’ material from ‘Neuromuscular disorders’ by Deborah
by Louis Solomon, H. Srinivasan, Surendar Tuli & Eastwood, Thomas Staunton & Louis
Shunmugam Govender. The material has been revised and Solomon. The material has been revised and updated by the
updated by the current author. current author.
Chapter 4, Crystal deposition disorders, contains some Chapter 11, Peripheral nerve disorders, contains some
material from ‘Crystal deposition disorders’ by Louis material from ‘Peripheral nerve injuries’ by David Warwick, H.
Solomon. The material has been revised and updated by the Srinivasan & Louis Solomon. The material has been revised
current authors. and updated by the new contributor Michael Fox.
Chapter 5, Osteoarthritis, contains some material from Chapter 12, Principles of orthopaedic operations, contains
‘Osteoarthritis and related disorders’ by Louis Solomon. The some material from ‘Principles of ortho paedic operations’ by
material has been revised and updated by the current Selvadurai Nyagam & David Warwick. The material has been
authors. revised and updated by the current authors.
Chapter 6, Osteonecrosis and osteochondritis, con tains Chapter 13, The shoulder and pectoral girdle, con tains
some material from ‘Osteonecrosis and osteo chondritis’ by some material from ‘The shoulder and pectoral girdle’ by
Louis Solomon. The material has been revised and updated Andrew Cole & Paul Pavlou. The material has been revised
by the current authors. and updated by Andrew Cole.
Chapter 7, Metabolic and endocrine bone disorders, Chapter 14, The elbow, contains some material from ‘The
contains some material from ‘Metabolic and endo crine bone elbow and forearm’ by David Warwick. The material has been
disorders’ by Louis Solomon. The material has been revised revised and updated by the new contributor Adam Watts.
and updated by the current authors.
Chapter 16, The hand, contains some material from ‘The
Chapter 8, Genetic disorders, skeletal dysplasias and hand’ by David Warwick & Roderick Dunn. The material has
malformations, contains some material from ‘Genetic been revised and updated by the same authors.
disorders, skeletal dysplasias and malformations’ by Louis
Solomon & Deborah Eastwood. The material has been Chapter 17, The neck, contains some material from ‘The
revised and updated by the current authors. neck’ by Stephen Eisenstein & Louis Solomon. The material
has been revised and updated by the cur rent authors.
Chapter 9, Tumours, contains some material from ‘Tumours’
by Will Aston, Timothy Briggs & Louis Solomon. The material Chapter 18, The back, contains some material from ‘The
has been revised and updated by the current authors. back’ by Stephen Eisenstein, Surendar Tuli & Shunmugam
Govender. The material has been revised and updated by the
Chapter 10, Neuromuscular disorders, contains some current authors.
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Chapter 19, The hip, contains some material from ‘The hip’ by updated by the current authors.
Louis Solomon, Reinhold Ganz, Michael Leunig, Fergal
Monsell & Ian Learmonth. The mate rial has been revised and Chapter 20, The knee, contains some material from ‘The knee’
by Louis Solomon & Theo Karachalios. The material has been
M
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current author.
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LIST OF
ABBREVIATIONS USED
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eFAST extended focused assessment HR hip resurfacing
D
sonography in trauma HRT hormone replacement therapy IASP
E
eGFR estimated glomerular filtration rate International Association for the Study of
EMG electromyography Pain
S
I
ESR erythrocyte sedimentation rate ETA
V
estimated time of arrival
E
B
Rheumatism
A
Rotation test
FABS flexion, abduction, supination FAI
O
trauma
S
INR international normalized ratio IP(J) MRC Medical Research Council MRA B
MSSA methicillin-sensitive
I
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factor-ќβ ligand SUA serum uric acid
D
REBOA resuscitative endovascular SUFE slipped upper femoral epiphysis
E
RGO reciprocating gait orthoses RICE TARN Trauma Audit and Research
U
O
RR reversal reaction TBS Trabecular Bone Score
RSD reflex sympathetic dystrophy RSI
I
I
rapid sequence induction
V
B
SAMU Services de l’Aide Medical Urgente
A
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TISS therapeutic intervention scoring system
L
interbody fusion
TMT tarsometatarsal O
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Section 1
General
Orthopaedics
1 Diagnosis in orthopaedics 3 2 Infection 31 3
Infammatory rheumatic disorders 65 4 Crystal deposition
disorders 83 5 Osteoarthritis 91 6 Osteonecrosis and
osteochondritis 107 7 Metabolic and endocrine bone
disorders 121 8 Genetic disorders, skeletal dysplasias and
malformations 157 9 Tumours 179 10 Neuromuscular
disorders 229 11 Peripheral nerve disorders 279 12
Orthopaedic operations 317
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orthopaedics 1 Diagnosis in
Louis Solomon & Charles Wakeley
Orthopaedics is concerned with bones, joints, mus cles, and loss of function or inability to do certain things that were
tendons and nerves – the skeletal system and all that makes easily accomplished before.
it move. Conditions that affect these structures fall into seven Each symptom is pursued for more detail: we need to
easily remembered pairs: know when it began, whether suddenly or gradu ally,
spontaneously or after some specific event; how it has
1 Congenital and developmental abnormalities 2
changed or progressed; what makes it worse; what makes it
Infection and inflammation
better.
3 Arthritis and rheumatic disorders
While listening, we consider whether the story fits some
4 Metabolic and endocrine disorders pattern that we recognize, for we are already thinking of a
5 Tumours and lesions that mimic them 6 Neurological diagnosis. Every piece of infor mation should be thought of as
disorders and muscle weakness 7 Injury and part of a larger pic ture which gradually unfolds in our
mechanical derangement understanding. The surgeon-philosopher Wilfred Trotter
Diagnosis in orthopaedics, as in all of medicine, is the (1870– 1939) put it well: ‘Disease reveals itself in casual
identification of disease. It begins from the very first parentheses.’
encounter with the patient and is gradu ally modified and fine-
tuned until we have a picture, not only of a pathological
process but also of the functional loss and the disability that SYMPTOMS
goes with it. Understanding evolves from the systematic gath
ering of information from the history, the physical Pain
examination, tissue and organ imaging and special Pain is the most common symptom in orthopaedics. It is
investigations. Systematic, but never mechanical; behind the usually described in metaphors that range from
enquiring mind there should also be what D. H. Lawrence has inexpressively bland to unbelievably bizarre – descrip tions
called ‘the intelligent heart’. It must never be forgotten that that tell us more about the patient’s state of mind than about
the patient has a unique personality, a job and hobbies, a the physical disorder. Yet there are clearly differences
family and a home; all have a bearing upon, and are in turn between the throbbing pain of an abscess and the aching
affected by, the disorder and its treatment. pain of chronic arthritis, between the ‘burning pain’ of
neuralgia and the ‘stabbing pain’ of a ruptured tendon.
Severity is even more subjective. High and low pain
HISTORY thresholds undoubtedly exist, but pain is as bad as it feels to
the patient, and any system of ‘pain grading’ must take this
‘Taking a history’ is a misnomer. The patient tells a story; it is into account. The main value of estimating severity is in
we the listeners who construct a history. The story may be assessing the prog
maddeningly disorganized; the history has to be systematic. ress of the disorder or the response to treatment. The
Carefully and patiently compiled, it can be every bit as commonest method is to invite the patient to mark the
informative as exam severity on an analogue scale of 1–10, with 1 being mild and
ination or laboratory tests. easily ignored, and 10 being totally unbearable. The problem
As we record it, certain key words and phrases will about this type of grading is that patients who have never
inevitably stand out: injury, pain, stiffness, swelling, deformity, experienced very severe pain simply do not know what 8 or 9
instability, weakness, altered sensibility or
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1 10 would feel like. The following is suggested as a
simpler
system:
Grade I (mild) Pain that can easily be ignored
Grade II (moderate) Pain that cannot be ignored,
interferes with function and needs attention or
But pain can also affect the autonomic nerves that
accompany the peripheral blood vessels and this is
much more vague, more widespread and often associ
ated with vasomotor and trophic changes. It is poorly
understood, often doubted, but nonetheless real.
S
treatment from time to time
C
Grade III (severe) Pain that is present most of the
I
E
Grade IV (excruciating) Totally incapacitating pain
A
O
Identifying the site of pain may be equally vague. Yet
H
its precise location is important, and in orthopaedics
T
R
it is useful to ask the patient to point to – rather than
O
to say – where it hurts. Even then, do not assume
R
ogy; ‘referred’ pain and ‘autonomic’ pain can be very
E
N
deceptive.
E
Swelling
Swelling may be in the soft tissues, the joint or the
bone; to the patient they are all the same. It is important
to establish whether it followed an injury, whether it
appeared rapidly (think of a haematoma or a
haemarthrosis) or slowly (due to inflammation, a joint
effusion, infection or a tumour), whether it is painful
(suggestive of acute inflammation, infection or a
tumour), whether it is constant or comes and goes, and
whether it is increasing in size.
Deformity
The common deformities are described by patients in
terms such as round shoulders, spinal curvature, knock
knees, bow legs, pigeon toes and flat feet. Deformity of
a single bone or joint is less easily described and the
patient may simply declare that the limb is ‘crooked’.
Some ‘deformities’ are merely variations of the normal
(e.g. short stature or wide hips); others dis appear
spontaneously with growth (e.g. flat feet or
(2) progressive, or if it affects only one side of the body while the
bandy legs in an infant). However, if the deformity is opposite joint or limb is normal, it may be serious (Figure 1.2).
(4)
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(e.g. a prolapsed intervertebral disc), local about musculoskeletal disorders in the
ischaemia (e.g. nerve entrapment in a patient’s family may help with both
fibro-osseous tunnel) or a peripheral diagnosis and counselling. When dealing
neuropathy. It is important to establish its with a suspected case of bone or joint
exact distribution; from this we can tell infection, ask about communicable
whether the fault lies in a peripheral nerve diseases, such as tuberculosis or sexually
or in a nerve root. We should also ask transmitted disease, in other members of
what makes it worse or better; a change the family.
in posture might be the trigger, thus
focusing attention on a particular site.
SOCIAL BACKGROUND
Loss of function No history is complete without enquiry
Functional disability is more than the sum about the patient’s background. There are
of individ ual symptoms and its expression the obvious things such as the level of
depends upon the needs of that particular care and nutrition in children; dietary
patient. The patient may say, ‘I can’t constraints which may cause specific
stand for long’ rather than ‘I have deficien
backache’; cies; and, in certain cases, questions
or ‘I can’t put my socks on’ rather than ‘My about smoking habits, alcohol
hip is stiff.’ Moreover, what to one patient consumption and drug abuse, all of which
is merely incon venient may, to another, call for a special degree of tact and non
be incapacitating. Thus a lawyer or a judgemental enquiry.
teacher may readily tolerate a stiff knee Find out details about the patient’s work
provided it is painless, but to a plumber or practices, travel and recreation: could the
a parson the same disorder might spell disorder be due to
economic or spiritual disaster. One
question should elicit the important 1
information: ‘What can’t you do now that
you used to be able to do?’
Figure 1.2 Deformity This young girl
complained of a prominent right hip; the real
deformity was scoliosis.
PAST HISTORY
D
one limb or to a single muscle group – is present complaint. They should be asked
s
sometimes say that the limb is ‘dead’ ‘twisted ankle’ many years ago may be
when it is actually weak, and this can be a the clue to the onset of osteoarthri
o
source of con t
discover pre cisely which movements are which in the patient’s mind has nothing to
p
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When we proceed to the structured examination,
1 a particular repetitive activity in the home, at work the patient must be suitably undressed; no mere roll
ing up of a trouser leg is sufficient. If one limb is
or on the sports field? Is the patient subject to any
unusual occupational strain? Has he or she affected, both must be exposed so that they can be
travelled to another country where tuberculosis is compared.
common? We examine the good limb (for comparison), then
Finally, it is important to assess the patient’s the bad. There is a great temptation to rush in with
home circumstances and the level of support by both hands – a temptation that must be resisted.
family and Only by proceeding in a purposeful, orderly way can
we avoid missing important signs.
routine, inspection, palpation, manipulation, was Alan Apley, who developed and taught the system
replaced by look, feel, move. With time, his teaching used here, shied away from using long words where short
has been extended and we now add test, to include the ones would do the job. (He also used to say, ‘I’m neither an
special manoeuvres we employ in assessing neurologi inspector nor a manipulator, and I am 6
cal integrity and complex functional attributes. definitely not a palpator.’) Thus the traditional clinical
Look
friends. This will help to answer the question: ‘What S
E
regain?’ mistakes.
A
H
body or the entire person who is being examined. Is the
EXAMINATION patient unusually thin or obese? Does the overall
posture look normal? Is the spine straight or unusu
T
O
ally curved? Are the shoulders level? Are the limbs
normally positioned? It is important to look for defor mity
In A Case of Identity, Sherlock Holmes has the fol L
in three planes, and always compare the affected part
with the normal side. In many joint disorders and in
lowing conversation with Dr Watson.
A
E
[your client] which was quite invisible to me. there a definite lump?
G
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1 must also look further afield. The patient complains
degree of mobility and whether it is painful or not.
Feel
Feeling is exploring, not groping aimlessly. Know your
anatomy and you will know where to feel for the
landmarks; find the landmarks and you can construct a
virtual anatomical picture in your mind’s eye.
The skin Is it warm or cold; moist or dry; and is
(a) (b)
sensation normal?
The soft tissues Can you feel a lump; if so, what are its
characteristics? Are the pulses normal?
The bones and joints Are the outlines normal? Is the Figure 1.4 Feeling for tenderness (a) The wrong way – there
synovium thickened? Is there excessive joint fluid? is no need to look at your fngers, you should know where they
are. (b) It is much more informative to look at the patient’s
Tenderness Once you have a clear idea of the struc tural face!
features in the affected area, feel gently for ten derness Active movement is also used to assess muscle power.
(Figure 1.4). Keep your eyes on the patient’s face; a
grimace will tell you as much as a grunt. Try to localize Passive movement Here it is the examiner who
any tenderness to a particular structure; if you know moves the joint in each anatomical plane. Note
precisely where the trouble is, you are halfway to whether there is any difference between the range of
knowing what it is. active and passive movement. D
‘Movement’ covers several different activities: active ing from zero which, by convention, is the neutral or
movement, passive movement, abnormal or unstable
n
movement, and provocative movement (see Figures 1.5 anatomical position of the joint, and finishing where
and 1.6). s
Active movement Ask the patient to move with out your movement stops, due either to pain or to anatomical
assistance. This will give you an idea of the
i
d
the range of flexion is from zero (the knee absolutely movement, thus demonstrating that the joint is
unstable. Such abnormal movement may be obvi
i
straight) through an arc of 140 degrees (the leg mak ous (e.g. a wobbly knee); often, though, you have to
ing an acute angle with the thigh). Similarly, ‘knee use special manoeuvres to pick up minor degrees of
flexion 20–90 degrees’ means that flexion begins at instability.
20 degrees (i.e. the joint cannot extend fully) and
continues only to 90 degrees. Provocative movement One of the most telling clues
For accuracy you can measure the range of move to diagnosis is reproducing the patient’s symp toms
ment with a goniometer, but with practice you will by applying a specific, provocative movement.
learn to estimate the angles by eye. Normal ranges Shoulder pain due to impingement of the subacromial
of movement are shown in chapters dealing with structures may be ‘provoked’ by moving the joint in a
individual joints. What is important is always to way that is calculated to produce such impinge ment;
compare the symptomatic with the asymptomatic or the patient recognizes the similarity between this
normal side. pain and his or her daily symptoms. Likewise, a
While testing movement, feel for crepitus. Joint patient who has had a previous dislocation or sublux
crepitus is usually coarse and fairly diffuse; tenosy ation can be vividly reminded of that event by stress
novial crepitus is fine and precisely localized to the ing the joint in such a way that it again threatens to
affected tendon sheath. dislocate; indeed, merely starting the movement may
be so distressing that the patient goes rigid with anx
Unstable movement This is movement which is iety at the anticipated result – this is aptly called the
inherently unphysiological. You may be able to shift apprehension test.
or angulate a joint out of its normal plane of 7
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1
A
(a) (b) (c)
P
Figure 1.5 Testing for movement (a) Flexion, (b) extension, (c) rotation, (d) abduction, (e) adduction. The range of
movement can be estimated by eye or measured accurately using a goniometer (f).
(a) (b)
(c) (d)
Figure 1.6 Move (a) Active movement – the patient moves the joint. The right shoulder is normal; the left has restricted
active movement. (b) Passive movement – the examiner moves the joint. (c) Unstable movement – the joint can be moved across
the normal planes of action, in this case demonstrating valgus instability of the right knee. (d) Provocative movement – the
examiner moves (or manipulates) the joint so as to provoke the symp toms of impending pain or dislocation. Here he is reproducing
the position in which an unstable shoulder is 8
likely to dislocate.
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TERMINOLOGY
1 terms is somewhat confusing when it comes to the
Colloquial terms such as front, back, upper, lower, inner FIgure 1.7 Planes The principal planes of the body, as viewed
aspect, outer aspect, bow legs, knock knees have the in the anatomical position: sagittal, coronal and transverse.
advantage of familiarity but are not applicable to every foot: here the upper surface is called the dorsum
situation. Universally acceptable anatomical definitions and the sole is called the plantar surface.
are therefore necessary in describing phys Medial means facing towards the median plane or midline of
ical attributes. the body, and lateral away from the median plane. These
Bodily surfaces, planes and positions are always terms are usually applied to a D
described in relation to the anatomical position – as if limb, the clavicle or one half of the pelvis. Thus the i
together with the knees pointing directly for inner aspect of the thigh lies on the medial side of the g
wards, and arms held by the sides with the palms fac n
ing forwards. limb and the outer part of the thigh lies on the lateral o
named sagittal, coronal and transverse; they define side. We could also say that the little finger lies on the i
viewed in any description. Sagittal planes, parallel to medial or ulnar side of the hand and the thumb on
each other, pass vertically through the body from front to i
into right and left halves. Coronal planes are also the lateral or radial side of the hand.
orientated vertically, cor
responding to a frontal view, at right angles to the o
sagittal planes; transverse planes pass horizontally Proximal and distal are used mainly for parts of
across the body.
t
Anterior signifies the frontal aspect and posterior the the limbs, meaning respectively the upper end and the
rear aspect of the body or a body part. The terms
o
ventral and dorsal are also used for the front and the lower end as they appear in the anatomical position.
back respectively. Note, though, that the use of these
a
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1 Circumduction is a composite movement made up
E
T4
A
T6
O
NEUROLOGICAL EXAMINATION
H
C6 C6 T8
If the symptoms include weakness or incoordination R
T10
or a change in sensibility, or if they point to any dis C5 C5 T1
L1
T12
A
order of the neck or back, a complete neurological
T1
examination of the related part is mandatory. Once
E
R
C7 C7 S3
S5
L1
N
again we follow a systematic routine, first looking at
the general appearance, then assessing motor func C6
E
C6 S2 S4
C8 L3
Table 1.1 Nerve root supply and actions of main
G
L4 L4
S1 S1
L5
L5
FIgure 1.8
Examination
Dermatomes
supplied by the
spinal nerve roots.
Appearance
Some neurological
disorders result in
postures that are
so characteristic as
to be diagnostic at
a glance: the claw
hand of an ulnar
nerve lesion; ‘drop
wrist’ following
radial nerve palsy
(Figure 1.9); or the
‘wait
er’s tip’ deformity of
the arm in brachial
plexus injury.
Usually, however, it
Ankle dorsifexion L4, 5
is when the patient moves that we can best appreciate
plantarfexion S1, 2
inversion L4, 5
the type and extent of motor disorder: the dangling arm
eversion L5, S1 following a brachial plexus injury; the flail lower limb of
poliomyelitis; the sym
Toe extension L5 metrical paralysis of spinal cord lesions; the charac
fexion S1 teristic drop-foot gait following sciatic or peroneal nerve
abduction S1, 2 damage; and the jerky, ‘spastic’ movements of cerebral
palsy.
Concentrating on the affected part, we look for
trophic changes that signify loss of sensibility: the
10 smooth, hairless skin that seems to be stretched too
tight; atrophy of the fingertips and the nails; scars
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resist any attempt to change that position. ankle clonus: a sharp upward jerk on the
The normal limb is examined first, then foot (dorsi flexion) causes a repetitive,
the affected limb, and the two are ‘clonic’ movement of the foot; similarly, a
compared. Finer muscle actions, such as sharp downward push on the patella may
those of the thumb and fingers, may be elicit patellar clonus.
reproduced by first demonstrating the
movement yourself, then testing it in the
unaffected limb, and then in the affected
1
one.
Muscle power is usually graded on the
Medical Research Council scale:
D
Grade 0 No movement i
This patient’s ‘drop wrist’ – typical of a radial disorders the weakness is usually more
t
on the right. e
Tendon reflexes i
that refuse to heal. Muscle wasting is A deep tendon reflex is elicited by rapidly
important: if localized and asymmetrical, it stretching the tendon near its insertion. A
may suggest dysfunction of a specific sharp tap with the tendon hammer does
motor nerve. this well; but all too often this is performed
with a flourish and with such force that the
finer gradations of response are missed. It
Muscle tone is better to employ a series of taps,
starting with the most force
Tone in individual muscle groups is tested
ful and reducing the force with each
by mov ing the nearby joint to stretch the
successive tap until there is no response.
muscle. Increased tone (spasticity) is
Comparing the two sides in this way, we
characteristic of upper motor neu ron
can pick up fine differences showing that
disorders such as cerebral palsy and
a reflex is ‘diminished’ rather than ‘absent’.
stroke. It must not be confused with
In the upper limb we test biceps, triceps
rigidity (the ‘lead-pipe’ or ‘cogwheel’
and brachiora
effect) which is seen in Parkinson’s
dialis; and in the lower limb the patellar
disease. Decreased tone (flaccidity) is
and Achilles tendons.
found in lower motor neuron lesions; for
The tendon reflexes are monosynaptic
example, poliomyelitis. Muscle power is
segmen tal reflexes; that is, the reflex
diminished in all three states; it is
pathway takes a ‘short cut’ through the
important to recognize that a ‘spastic’
spinal cord at the segmental level.
muscle may still be weak.
Depression or absence of the reflex
signifies inter ruption of the pathway at the
Power posterior nerve root, the anterior horn cell,
the motor nerve root or the peripheral
Motor function is tested by having the nerve. It is a reliable pointer to the seg
patient per form movements that are mental level of dysfunction: thus, a
normally activated by spe cific nerves. We depressed biceps jerk suggests pressure
may learn even more about composite on the fifth or sixth cervical (C5 or C6)
movements by asking the patient to nerve roots while a depressed ankle jerk
perform specific tasks, such as holding a signifies a similar abnormality at the first
pen, gripping a rod, doing up a button or sacral level (S1). An unusually brisk
picking up a pin. reflex, on the other hand, is characteristic
Testing for power is not as easy as it of an upper motor neuron disorder (e.g.
sounds; the dif ficulty is making ourselves cerebral palsy, a stroke or injury to the
understood. The simplest way is to place spinal cord); the lower motor neuron is
the limb in the ‘test’ position, then ask the released from the normal central inhibition
patient to hold it there as firmly as possible and there is an exaggerated response to
and tendon stimulation. This may manifest as
11
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discrimination (the ability to recognize two touch
1 Superficial reflexes points a few millimetres apart) are also used in the
assessment of peripheral nerve injuries.
The superficial reflexes are elicited by stroking the
Deep sensibility can be examined in several
skin at various sites to produce a specific muscle contrac tion;
ways. In the vibration test a sounded tuning fork is placed over
the best known are the abdominal (T7–T12), cremasteric (L1,
a peripheral bony point (e.g. the medial mal leolus or the head
2) and anal (S4, 5) reflexes. These are corticospinal (upper
of the ulna); the patient is asked if he or she can feel the
motor neuron) reflexes. Absence
vibrations and to say when they disappear. By comparing the
S
‘up’ or ‘down’. Stereognosis, the ability to recognize two sides, differ ences can be noted. Position sense is tested by
shape and texture by feel alone, is tested by giving the asking the patient to find certain points on the body with the
patient (again with eyes closed) a variety of familiar eyes closed – for example, touching the tip of the nose with the
objects to hold and asking him or her to name each forefinger. The sense of joint posture is tested by grasping the
object. big toe and placing it in dif ferent positions of flexion and
The pathways for deep sensibility run in the pos extension. The patient 12
terior columns of the spinal cord. Disturbances are (whose eyes are closed) is asked to say whether it is
of the reflex indicates an upper motor neuron lesion
C
I
therefore found in peripheral neuropathies and in spinal
(usually in the spinal cord) above that level. cord lesions such as posterior column injuries or tabes
D
sign).
H
A
in flexion) is characteristic of upper motor neuron dis
R
N
reflex which is present in young infants and normally
E
G
disappears after the age of 18 months. Paediatric practice requires special skills. You may
have no first-hand account of the symptoms; a baby
Sensibility screaming with pain will tell you very little, and over
anxious parents will probably tell you too much. When
Sensibility to touch and to pinprick may be examining the child, be flexible. If he or she is moving a
increased (hyperaesthesia) or unpleasant particular joint, take your opportunity to examine
(dysaesthesia) in cer tain irritative nerve lesions. movement then and there. You will learn much more by
More often, though, it is diminished (hypoaesthesia) adopting methods of play than by applying a rigid
or absent (anaesthesia), signifying pressure on or system of examination. And leave any test for tender
interruption of a peripheral nerve, a nerve root or ness until last!
the sensory pathways in the spi nal cord. The area
of sensory change can be mapped out on the skin Infants and small children
and compared with the known seg mental or
dermatomal pattern of innervation. If the The baby should be undressed, in a warm room, and
abnormality is well defined, it is an easy matter to placed on the examining couch. Look carefully for
establish the level of the lesion, even if the precise birthmarks, deformities and abnormal movements – or
cause remains unknown. absence of movement. If there is no urgency or
Brisk percussion along the course of an injured distress, take time to examine the head and neck,
nerve may elicit a tingling sensation in the distal including facial features which may be characteristic of
distribution of the nerve (Tinel’s sign). The point of specific dysplastic syndromes. The back and limbs are
hypersensitivity marks the site of abnormal nerve then examined for abnormalities of position or shape.
sprouting: if it progresses distally at successive Examining for joint movement can be difficult. Active
visits, this signifies regeneration; if it remains movements can often be stimulated by gently stroking
unchanged, this suggests a local neuroma. the limb. When testing for passive mobility, be careful to
Tests for temperature recognition and two-point avoid frightening or hurting the child. In the neonate,
and throughout the first two years of life, examination of
the hips is mandatory, even if the child appears to be ing the subtle signs of developmental dysplasia of the
normal. This is to avoid miss hips (DDH) at the early stage when treatment is most
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Table 1.2 Normal developmental milestones than those of most adults, allowing them what at one point of time might have been
Age to adopt
Normal developmental milestone(s) postures that would be seen as a deformity could over the ages
impossible for their parents. An unusual have turned out to be so advantageous as
Newborn Grasp refex present degree of joint mobility can also be to become essential for survival. So too in
Morrow refex present attained by adults willing to submit to humans. The word ‘deformity’ is derived
rigorous exercise and practice, as witness from the Latin for ‘misshapen’, but the
3–6 months Holds head up unsupported the performances of professional dancers range of ‘normal shape’ is so wide that
and athletes, but in most cases, when the varia tions should not automatically be
6–9 months Able to sit up
exercises stop, mobility gradually reverts designated as defor mities, and some
9–12 months Crawling to the normal range. undoubted ‘deformities’ are not
Standing up Persistent generalized joint hypermobility necessarily pathological; for example, the
occurs in about 5% of the population and generally accepted cut-off points for
9–18 months Walking is inherited as a sim ple Mendelian ‘abnormal’ shortness or tallness are
dominant (Figure 1.10). Those affected arbitrary and people who in one popula
18–24 months Running tion might be considered abnormally short
or abnor mally tall could, in other
populations, be seen as quite ordinary.
However, if one leg is short and the other
effective. It is also important to assess the long, no one would quibble with the use of
child’s gen eral development by testing for the word ‘deformity’!
the normal milestones which are Specific terms are used to describe the
expected to appear during the first two ‘position’ and ‘shape’ of the bones and
years of life (Table 1.2). FIgure 1.10 Tests for joint hypermobility
joints. Whether, in any particular case,
Hyperextension of knees and elbows;
metacarpopha langeal joints extending to 90 these amount to ‘deformity’ will be
Older children degrees’; thumb able to touch forearm. determined by additional factors such as
Most children can be examined in the the extent
same way as adults, though with different
emphasis on particular physical features.
describe themselves as being ‘double-
jointed’: they can hyperextend their
1
Posture and gait are very import ant;
metacarpophalangeal joints beyond a
subtle deviations from the norm may
right angle, hyperextend their elbows and
herald the appearance of serious
knees and bend over with knees straight
abnormalities such as scolio sis or
to place their hands flat on the ground; D
similarly with mild degrees of ‘flat feet’ and should be considered ‘abnormal’.
s
posture and gait patterns, when the child shown that they do have a greater than
usual tendency to recurrent dislocation
i
inwards (medially rotated) or out wards (e.g. of the shoulder or patella). Some
(laterally rotated) are usually due to experience recurrent epi o
antever sion or retroversion of the femoral sodes of aching around the larger joints;
r
osteoarthritis.
a
anything be done about this; the condition Generalized hypermobility is not usually
d
usually improves as the child approaches associ ated with any obvious disease, but
i
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hyperlordosis). Colloquially speaking, excessive tho
1 to which they deviate from the norm, symptoms to racic kyphosis is referred to as ‘round-shouldered’.
which they give rise, the presence or absence of Scoliosis Seen from behind, the spine is straight.
insta bility and the degree to which they interfere Any curvature in the coronal plane is called scoliosis.
with function. The position and direction of the curve are specified
Varus and valgus It seems pedantic to replace by terms such as thoracic scoliosis, lumbar scoliosis,
‘bow legs’ and ‘knock knees’ with ‘genu varum’ and ‘genu S
convex to the right, concave to the left, etc.
Structural deformity A deformity which results from a Postural deformity A postural deformity is one which
permanent change in anatomical structure cannot be the patient can, if properly instructed, correct
voluntarily corrected. It is important to distinguish voluntarily: e.g. thoracic ‘kyphosis’ due to slumped
postural scoliosis from structural (fixed) scoliosis. The shoulders. Postural deformity may also be caused by
former is non-progressive and benign; the latter is temporary muscle spasm.
usually progressive and may require treatment.
valgum’, but comparable colloquialisms are not avail ‘Fixed deformity’ This term is ambiguous. It seems to
mean that a joint is deformed and unable to move but
C
D
able for deformities of the elbow, hip or big toe; and, this is not so. It means that one particular move ment
E
besides, the formality is justified by the need for clar cannot be completed. Thus the knee may be able to flex
A
fully but not extend fully – at the limit of its extension it is
ity and consistency. Varus means that the part dis P
still ‘fixed’ in a certain amount of flex ion. This would be
O
hand.
in the cervical and lumbar regions (lordosis).
Excessive Muscle contracture Fibrosis and contracture of muscles
that cross a joint will cause a fixed deformity of the joint.
N
(a) (b)
(c)
FIgure 1.11 Varus and valgus (a) Valgus knees in a patient with rheumatoid arthritis. The toe joints are also valgus.
(b) Varus knees due to osteoarthritis. (c) Another varus knee? No – the deformity here is in the left tibia 14
due to Paget’s disease.
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1 Muscle imbalance Unbalanced muscle weakness
Size A large lump attached to bone, or a lump that
highly informative (for example, see Figure multiple exostosis and in Ollier’s disease.
s
1.12).
s
JOINT STIFFNESS
i
d
15
i
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1 DIAGNOSTIC IMAGING radiographic image
X-rays are produced by firing electrons at high
The map is not the territory speed onto a rotating anode. The resulting beam of
X-rays is attenuated by the patient’s soft tissues
Alfred Korzybski
and bones, casting what are effectively ‘shadows’
The more dense and impenetrable the tissue, the which are dis
greater the X-ray attenuation and therefore the more played as images on an appropriately sensitized
blank, or white, the image that is captured. Thus, a plate or stored as digital information which is then
metal implant appears intensely white, bone less so available to be transferred throughout the local
and soft tissues in varying shades of grey depend information technology (IT) network. See Figure
ing on their ‘density’. Cartilage, which causes little 1.13.
S
PLAIN FILM RADIOGRAPHY Articular
C
I
cartilage
Epiphysis
Plain film X-ray examination is over 100 years
D
Physis
E
(growth plate)
old. Notwithstanding the extraordinary technical A
P
Metaphysis
advances of the last few decades, it remains the Apophysis
most O
H
useful method of diagnostic imaging. Whereas other
T
Diaphysis
O
ture more accurately, or may reveal some localized
Cortex
L
Medulla
tissue change, the plain film provides information A
N
and bone architecture – characteristics which, taken
together, will usually suggest a diagnosis, or at least
Physis
a E
G
Epiphysis
range of possible diagnoses.
FIgure 1.13 The radiographic image X-ray of an ana
The tomical specimen to show the appearance of various 16
parts of the bone in the X-ray image.
attenuation, appears as a dark area between adjacent
bone ends; this ‘gap’ is usually called the joint space,
though of course it is not a space at all, merely a radio
lucent zone filled with cartilage. Other ‘radiolucent’
areas are produced by fluid-filled cysts in bone. One
bone overlying another (e.g. the femoral head inside
the acetabular socket) produces superimposed images;
any abnormality seen in the resulting com bined image
could be in either bone, so it is important to obtain
several images from different projections in order to
separate the anatomical outlines. Similarly, the bright
image of a metallic foreign body superim posed upon
that of, say, the femoral condyles could mean that the
foreign body is in front of, inside or behind the bone. A
second projection, at right angles to the first, will give
the answer.
Picture Archiving and Communication System (PACS)
This is the system whereby all digitally coded images
are filed, stored and retrieved to enable the images to
be sent to work stations throughout the hospital, to
other hospitals or to the Consultant’s per THE PATIENT
sonal computer. Make sure that the name on the film is that of your
patient; mistaken identity is a potent source of error.
The clinical details are important; it is surprising how
Radiographic interpretation much more you can see on the X-ray when you know
Although radiograph is the correct word for the plain the background. Similarly, when requesting an X-ray
image which we address, in the present book we have examination, give the radiologist enough information
chosen to retain the old-fashioned term ‘X-ray’, which from the patient’s history and the clinical findings to
has become entrenched by long usage. The process of help in guiding his or her thoughts towards the diag
interpreting this image should be as methodical as nostic possibilities and options. For example, when
clinical examination. It is seductively easy to be led considering a malignant bone lesion, simply know ing
astray by some flagrant anomaly; systematic study is the patient’s age may provide an important clue: under
the only safeguard. A convenient sequence for exam the age of 10 it is most likely to be a Ewing’s sarcoma;
ination is: the patient – the soft tissues – the bones – between 10 and 20 years it is more likely to
the joints.
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1 be an osteosarcoma; and over the age of 50 years it is
polyostotic lesions, think of metastases (including
THE SOFT TISSUES describing the abnormality from the centre and move a
may reveal wasting or swelling. Bulging outlines around outwards. Determine the lesion’s size, site, shape, n
soft-tissue swelling around interphalangeal joints may density and margins, as well as adjacent periosteal s
Tumours tend to displace fascial planes, whereas changes and any surrounding soft tissue changes.
infection tends to obliterate them.
i
opaque foreign body? defined with sclerotic margins (Figure 1.15b) and a r
(f)
FIgure 1.14 X-rays – bent bones (a) Malunited fracture; (b) Paget’s disease; (c) dyschondroplasia; (d) congenital 17
pseudarthrosis; (e) syphilitic sabre tibia; (f) osteogenesis imperfecta.
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1
L
(a) (b) (c) (d) (e)
A
FIgure 1.15 X-rays – important features to look for (a) General shape and appearance, in this case the cortices E
are thickened and the bone is bent (Paget’s disease). (b,c) Interior density, a vacant area may represent a true N
cyst (b), or radiolucent material infltrating the bone, like the metastatic tumour in (c). (d) Periosteal reaction,
G
typically seen in healing fractures, bone infection and malignant bone tumours – as in this example of Ewing’s
sarcoma. Compare this with the smooth periosteal new bone formation shown in (e).
abnormal with the normal opposite side. Then look exposed to joint fluid). In gout the erosions are
for narrowing or asymmetry of the joint ‘space’: nar further away from the articular surfaces and are
rowing signifies loss of hyaline cartilage and is described as juxta-articular. Rheumatoid arthritis is
typical of infection, inflammatory arthropathies and classically symmetrical and predominantly involves
osteoar thritis. Further stages of joint destruction are the metacarpophalangeal and proximal
revealed by irregularity of the radiographically interphalangeal joints in both hands. The erosions
visible bone ends and radiolucent cysts in the in psoriasis are usually more feathery with ill-
subchondral bone. Bony excrescences at the joint defined new bone at their margins. Ill-defined ero
margins (osteophytes) are typical of osteoarthritis. sions suggest active synovitis whereas corticated
ero
Erosions Look for associated bone erosions. The
sions indicate healing and chronicity.
position of erosions and symmetry help to define
various types of arthropathy. In rheumatoid arthritis
and psoriasis the erosions are periarticular (at the Diagnostic associations
bare area where the hyaline cartilage covering the However carefully the individual X-ray features are
joint has ended and the intracapsular bone is observed, the diagnosis will not leap ready-made off
the X-ray plate. Even a fracture is not always Limitations of conventional radiography
obvious. It is the pattern of abnormalities that
counts: if you see one feature that is suggestive, Conventional radiography involves exposure of the
look for others that are commonly associated. patient to ionizing radiation, which under certain cir
cumstances can lead to radiation-induced cancer. The
• Narrowing of the joint space + subchondral Ionizing Radiation Medical Exposure Regulations
sclerosis 18 (IRMER) 2000 are embedded in European Law,
and cysts + osteophytes = osteoarthritis (Figure 1.16). requiring all clinicians to justify any exposure of the
• Narrowing of the joint space + osteoporosis + peri patient to ionizing radiation. It is a criminal offence to
articular erosions = inflammatory arthritis. Add to this breach these regulations. Ionizing radiation can also
the typical distribution, more or less symmet rically in damage a developing fetus, especially in the first
the proximal joints of both hands, and you must think trimester.
of rheumatoid arthritis. As a diagnostic tool, conventional radiography
• Bone destruction + periosteal new bone for mation = provides poor soft-tissue contrast: for example, it
infection or malignancy until proven otherwise. cannot distinguish between muscles, tendons, liga
• Remember: the next best investigation is either the ments and hyaline cartilage. Ultrasound (US), com
previous radiograph or the subsequent follow-up puted tomography (CT) and magnetic resonance
radiograph. Sequential films demonstrate either imaging (MRI) are now employed to complement plain
progression of changes in active pathology or sta X-ray examination. However, in parts of the world
tus quo in long-standing conditions. where these techniques are not available, some
modifications of plain radiography still have a useful
role.
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1
Figure 1.16 Plain X-rays of the hip Stages in the development of osteoarthritis (OA). (a) Normal hip: ana p
tomical shape and position, with joint ‘space’ (articular cartilage) fully preserved. (b) Early OA, showing joint e
space slightly decreased and a subarticular cyst in the femoral head. (c) Advanced OA: joint space markedly d
decreased; osteophytes at the joint margin. (d) Hip replacement: the cup is radiolucent but its position is shown s
by a circumferential wire marker. Note the differing image ‘densities’: (1) the metal femoral implant; (2) the
polyethylene cup (radiolucent); (3) acrylic cement impacted into the adjacent bone.
(b) (c)
Figure 1.17 Contrast radiography (a) Myelography shows the outline of the spinal theca. Where facilities are available,
myelography has been largely replaced by CT and MRI. (b) Discography is sometimes useful: note the difference between a
normal intervertebral disc (upper level) and a degenerate disc (lower level). (c) Contrast 19
arthrography of the knee shows a small popliteal herniation.
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Myelography was used extensively in the past for
1 Arthrography the diagnosis of disc prolapse and other spinal
canal lesions. It has been largely replaced by non-
Arthrography is a particularly useful form of
contrast radiography. Intra-articular loose bodies invasive methods such as CT and MRI. However, it
will produce filling defects in the opaque contrast still has a place in the investigation of nerve root
medium. In the knee, torn menisci, ligament tears lesions and as an adjunct to other methods in
and capsular ruptures can be shown. In children’s patients with back pain.
hips, arthrogra The oily media are no longer used, and even with
S
be strictly observed.
Metrizamide has low neurotoxicity and at working
E
raphy may show up torn flaps of cartilage. After hip concentrations it is more or less isotonic with cere
P
contrast radiography can be used to diagnose disc images on either side of the pivotal plane are deliberately
R
degeneration (discography) and abnormalities of studied, lesions obscured in conventional X-rays may
the E A useful procedure in former years, conventional
small facet joints (facetography). tomography has been largely supplanted by CT and
MRI.
G
Myelography
COMPUTED TOMOGRAPHY (CT)
Like plain tomography, CT produces sectional images Clinical applications
through selected tissue planes – but with much greater
resolution (Figure 1.18). A further advance over Because CT achieves excellent contrast resolution and
conventional tomography is that the images are trans- spatial localization, it is able to display the size, shape
axial (like transverse anatomical sections), thus and position of bone and soft-tissue masses in
exposing anatomical planes that are never viewed in transverse planes. Image acquisition is extremely fast.
plain film X-rays. A general (or ‘localization’) view is The technique is therefore ideal for evaluating acute
obtained, the region of interest is selected and a series trauma to the head, spine, chest, abdomen and pelvis.
of cross-sectional images is produced and digi It is better than MRI for demonstrat
tally recorded. ‘Slices’ through the larger joints or tis sue ing fine bone detail and soft-tissue calcification or
masses may be 3–5 mm apart; those through the small ossification.
joints or intervertebral discs have to be much thinner. Computed tomography is also an invaluable tool for
New multislice CT scanners provide images of high assisting with preoperative planning in second ary
quality from which multiplanar reconstruc tions in all fracture management. It is routinely used for assessing
three orthogonal planes can be produced. Three- injuries of the vertebrae, acetabulum, prox imal tibial
dimensional surface rendered reconstructions and plateau, ankle and foot – indeed com plex fractures and
volume rendered reconstructions may help in fracture-dislocations at any site (Figure 1.19).
demonstrating anatomical contours, but fine detail is It is also useful in the assessment of bone tumour
lost in this process. size and spread, even if it is unable to characterize the
tumour type. It can be employed for guiding soft tissue
and bone biopsies.
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1
(a)
i
(c) (d) o
Figure 1.18 Computed tomography (CT) The plain X-ray (a) shows a fracture c
of the vertebral body but one cannot tell precisely how the bone fragments
are displaced. The CT (b) shows clearly that they are dangerously close to the
cauda equina. (c) Congenital hip dislocation, defned more clearly by (d) three
dimensional CT reconstruction.
(b)
(a)
(b) (c)
Figure 1.19 CT for complex fractures (a) A plain X-ray shows a fracture of the calcaneum but the details are
obscure. CT sagittal and axial views (b,c) give a much clearer idea of the seriousness of this fracture.
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rates.
1 external magnetic field. The protons are spinning
make it ideal for non-invasive imaging of the mus
and can be further excited by radiofrequency culoskeletal system (Figures 1.20 and 1.21). The
pulses, rather like whipping a spinning top. These multiplanar capability provides accurate cross-sec tional
spinning positive charges will not only induce a information and the axial images in particu lar will
small magnetic field of their own, but will produce reveal detailed limb compartmental anatomy. The
a signal as they relax (slow down) at different excellent soft-tissue contrast allows identification
22 seven unpaired electrons and work by
S
A proton density map is recorded from creating local magnetic field disturbances
I
(time to echo, or TE) will yield anatomical intravenously will be secreted through
pictures with varying ‘weight ing’ and joint synovium into joint effusions
O
provide good ana tomical-looking pictures. of the joint, which limits its effect.
A
E
T2 weighted (T2W) images give more
N
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1 modality. In the knee, MRI is as accurate as arthros
copy in diagnosing meniscal tears and cruciate liga
Unlike X-rays, the image does not depend on tissue
density but rather on reflective surfaces and soft- tissue
ment injuries. Bone and soft-tissue strength was commonly between 0.5 and
tumours should be routinely examined by 1.5 Tesla. More recently, scanners using
DIAGNOSTIC ULTRASOUND
MRI as the intraosseous and 3 Tesla have started being introduced. High-frequency sound waves, generated
extraosseous extent and spread of The increased field strength yields by a trans ducer, can penetrate several
disease, as well as the compartmental improved contrast and definition, centimetres into the soft tissues; as they
anatomy, can be accurately assessed. but it is also more susceptible to artefacts. pass through the tissue interfaces, some
Additional use of fat-suppression Dedicated small-part scanners are also of these waves are reflected back (like
sequences determines the extent of being introduced to assess limbs, for echoes) to the transducer, where they are
perilesional oedema and intravenous example for occult scaphoid fractures in registered as elec trical signals and
contrast will demonstrate the active part the Emergency Department. Upright displayed as images on a screen.
of the tumour. scanners have been developed to assess interfaces. This is the same principle as
Intravenous contrast is used to distinguish pathology that is apparent only when the applies in sonar detection for ships or
vascu larized from avascular tissue (e.g. patient is weight-bearing. submarines.
following a scaphoid fracture) or in Depending on their structure, different
defining active necrotic areas of tumour, Limitations tissues are referred to as highly
or in demonstrating areas of active echogenic, mildly echogenic or echo-free.
inflammation. Despite its undoubted value, MRI (like all Fluid-filled cysts are echo-free; fat is highly
Direct MRI arthrography is used to distend singular methods of investigation) has its echogenic; and semi-solid organs
the joint capsule and outline labral tears limitations and it must be seen as one of manifest varying degrees of
in the shoul der and the hip. In the ankle, it a group of imaging modal ities, none of ‘echogenicity’, which makes it possible to
provides the way to demonstrate which by itself is appropriate in every differentiate between them.
anterolateral impingement and assess the situation. Conventional radiographs and Real-time display on a monitor gives a
integrity of the capsular ligaments. CT are more sensitive to soft-tissue dynamic image, which is more useful than
calcification and ossifi cation, changes the usual static images. A big advantage
which can easily be easily overlooked on of this technique is that the equipment is
New generation MRI scanners
MRI. Conventional radiographs should simple and portable and can be used
Many new scanners are being developed therefore be used in combination with almost anywhere; another is that it is
in the clin ical setting using more powerful MRI to prevent such errors. entirely harmless.
magnetic fields. Previously, the field
Clinical applications Doppler ultrasound 23
Because of the marked echogenic Blood flow can be detected by using the
contrast between cystic and solid principle of a change in frequency of
masses, ultrasonography is particu larly sound when material is mov ing towards
useful for identifying hidden ‘cystic’ lesions or away from the ultrasound transducer.
such as haematomas, abscesses, This is the same principle as the change in
popliteal cysts and arterial aneurysms. It frequency of the noise from a passing fire
is also capable of detecting intra-articu lar engine when travelling towards and then
fluid and may be used to diagnose a away from an observer. Abnormal
synovial effu increased blood flow can be observed in
sion or to monitor the progress of an areas of inflammation or in aggressive
‘irritable hip’. Ultrasound is commonly tumours. Different flow rates can be
used for assessing ten dons and shown by different colour representations
diagnosing conditions such as tendinitis (‘colour Doppler’).
and partial or complete tears. The rotator
cuff, patellar lig ament, quadriceps tendon,
Achilles tendon, flexor ten dons and
peroneal tendons are typical examples. D
normal or abnormal. o
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RADIONUCLIDE IMAGING radiopharmaceutical used for
1 Changes in radioactivity are most significant when
they are localized or asymmetrical. The following four
Photon emission by radionuclides taken up in
specific tissues can be recorded by a gamma types of abnormality are seen.
camera to pro duce an image which reflects Increased activity in the perfusion phase This is due to
physiological activity in that tissue or organ. The increased soft-tissue blood flow, suggesting
24 centrated in bone. The low background
S
radionuclide imaging has two components: radioactivity means that any site of
I
a chemical compound that is chosen for increased uptake is readily visi ble (Figure
D
Isotope bone scans at two stages: (1) the early per fusion
phase, shortly after injection, while the iso
O
For bone imaging, the ideal isotope is tope is still in the blood stream or the
L
R
blood flow difference; and (2) the delayed
E gamma camera imaging, it has a relatively bone phase, 3 hours later, when the
N
short half-life (6 hours) and it is rapidly isotope has been taken up in bone tissue.
excreted in the urine. A bone-seeking Normally, in the early perfusion phase the
E
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1 Other radionuclide compounds PET is useful in oncology to identify occult malig
Gallium-67 (67Ga) Gallium-67 concentrates SINGLE-PHOTON EMISSION processes. Positron-emitting iso topes
in inflammatory cells and has been used with short half-lives are produced on site
to identify sites of hidden infection: for
COMPUTED TOMOGRAPHY at specialist centres using a cyclotron.
example, in the investiga tion of prosthetic (SPECT) Various radio pharmaceuticals can be
loosening after joint replacement. Single-photon emission computed employed, but currently the most
However, it is arguable whether it gives commonly used is 18-fluoro-2-deoxy-D-
tomography (SPECT) is essentially a
any more reli able information than the glucose (18FDG). The 18FDG is
99m bone scan in which images are recorded
Tc bone scan. accumulated in different parts of the body
and displayed in all three orthogonal
Indium-111-labelled leucocytes (111I) The planes. Coronal, sagittal and axial images where it can effectively measure the rate
patient’s own white blood cells are at multiple levels make spatial localization of consumption of glucose. Malignant
tumours metabolize glucose at a faster
removed and labelled with indium-111 of pathology possible: for example,
rate than benign tumours and PET
before being re-injected into the patient’s activity in one side of a lumbar vertebra
scanners are extremely useful in looking
bloodstream. Preferential uptake in areas on the planar images can be further
of infec localized to the body, pedicle or lamina of for occult sites of disease around the body
on this basis.
tion is expected, thereby hoping to the vertebra on the SPECT images.
PET/CT is a hybrid examination
distinguish sites of active infection from performing both PET and CT on the
chronic inflammation. For example, white patient in order to superimpose the two
cell uptake is more likely to be seen with POSITRON EMISSION images produced. The combination of
an infected total hip replacement as
opposed to mechanical loosening. TOMOGRAPHY (PET) these two techniques uses the sensitivity
of PET for func
However, as this technique is expensive Positron emission tomography (PET) is an tional tissue changes and the cross-
and still not completely specific, it is advanced nuclear medicine technique sectional anatomy detail of CT to localize
seldom performed. that allows functional imaging of disease the position of this activity.
nant tumours and metastases and more matched popu
d
accurately ‘stage’ the disease. lation (Z score) and also to the peak adult bone
c
Furthermore, activity levels at known sites mass (T score). The T score in particular
of disease can be used to assess allows calculation of relative fracture risk.
treatment and distinguish ‘active’ residual Individual values for both the lumbar spine
tumour or tumour recurrence from and hips are obtained as there is often a
‘inactive’ post-surgical scarring and discrepancy between these two sites and the
necrotic tumour. fracture risk is more directly related to the
value at the target area. By World Health
Organization (WHO) criteria, T scores of <
BONE MINERAL DENSITOMETRY −1.0 indicate ‘osteopenia’ and T scores of <
−2.5 indicate ‘osteoporosis’.
Bone mineral density (BMD) measurement
is now widely used in identifying patients
with osteoporo sis and an increased risk of
osteoporotic fractures. Various BLOOD TESTS
techniques have been developed,
including radiographic absorptiometry Non-specific blood tests
(RA), quantitative com puted tomography
Non-specific blood abnormalities are
(QCT) and quantitative ultra sonometry
common in bone and joint disorders; their
(QUS). However, the most widely used
interpretation hinges on the clinical and X-
technique is dual energy X-ray
ray findings.
absorptiometry (DXA) (Figure 1.23).
RA uses conventional radiographic Hypochromic anaemia This is usual in
equipment and measures bone density in rheuma toid arthritis, but it may also be a
the phalanges. QCT mea sures trabecular consequence of
bone density in vertebral bodies, but is
not widely available and involves a higher
dose of ionizing radiation than DXA. QUS
assesses bone mineral density in the
peripheral skeleton (e.g. the wrist and
calcaneus) by measuring both the attenua
D
a
25
e
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1
O
DXA Results Summary:
A
(cm2) (g) (g/cm2)
Neck 5.37 3.62 0.675 –1.6 79 –0.5
93
Troch 12.48 7.10 0.569 –1.3 81 –0.6
R
90
E
Inter 20.07 18.92 0.943 –1.0 86 –0.5 92
N
Total 37.92 29.64 0.782 –1.3 83 –0.6 92
E
Ward’s 1.03 0.54 0.527 –1.8 72 0.0 100
G
(a) (b)
Figure 1.23 Measurement of bone mass (a) X-ray of the lumbar spine shows a compression fracture of L2. The
general loss of bone density accentuates the cortical outlines of the vertebral body end-plates. These features are
characteristic of diminished bone mass, which can be measured accurately by dual energy X-ray absorpti ometry. (b)
DXA scan from another woman who attended for monitoring at the onset of the menopause.
Laboratory tests
Acute joint swelling after injury The distinction between s
Acute atraumatic synovitis in adults Synovial fluid If enough fluid is available, it is sent for full laboratory
analysis may be the only way to distinguish between
infection, gout and pseudogout. Characteristic crys tals o
can be identified on polarized light microscopy. investigation (cells, biochemistry and bacteriological t
investigations may provide the answer, but they take culture; see Table 1.3). A simultaneous blood speci o
and is only one of many diagnostic procedures in the concentration; a marked reduction of synovial glucose
investigation of suspected tuberculosis or atypi cal d
organisms. Remember, though, that negative findings histological proof of acute inflammation but also
bacteriological typing of the organism and tests for
i
antibiotic sensitivity.
27
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1 The investigation of metabolic bone disease some
processed. If infection is suspected, the material should go into
times calls a culture tube and be sent to the laboratory as soon as
for a tetracycline-labelled bone biopsy to show: (a) the type of possible. A smear may also be useful. Whole tissue is
abnormality (osteoporosis, osteo malacia, transferred to a jar con
hyperparathyroidism), and (b) the severity of the disorder. taining formalin, without damaging the specimen or losing any
material. Aspirated blood should be
28 proves to be necessary.
S
drawbacks:
H
• The biopsy incision may jeopardize cular tumours may bleed profusely and the
subsequent wide excision of the lesion. means to control haemorrhage should be
E
• The more inaccessible lesions (e.g. a readily to hand. More than one surgeon
tumour of the acetabular floor) can be has set out to aspirate an ‘abscess’ only
reached only by dissecting widely through to plunge a wide-bore needle into an
healthy tissue. aneurysm!
• Clear instructions should be given to
A carefully performed ‘closed’ biopsy, ensure that the tissue obtained at the
using a needle or trephine of appropriate biopsy is suitably
size to ensure the removal of an allowed to clot and can then be preserved
adequate sample of tissue, is the in for malin for later paraffin embedding
procedure of choice except when the and sectioning. Tissue thought to contain
lesion cannot be accurately localized or crystals should not be placed in formalin
when the tissue consistency is such that a as this may destroy the crystals; it should
sufficient sample cannot be obtained. be either kept unaltered for immediate
Solid or semi examination or stored in saline.
solid tissue is removed intact by the • No matter how careful the biopsy, there
cutting needle or trephine; fluid material is always the risk that the tissue will be
can be aspirated through the biopsy too scanty or too unrepresentative for
needle. accurate diagnosis. Close consultation
with the radiologist and pathologist
beforehand will minimize this possibility. In
Precautions the best hands, needle biopsy has an
• The biopsy site and approach should be accuracy rate of over 95%.
carefully planned with the aid of X-rays or
other imaging techniques.
• If there is any possibility of the lesion DIAGNOSTIC ARTHROSCOPY
being malig nant, the approach should be
sited so that the wound and biopsy track Arthroscopy is performed for both
can be excised if later rad ical surgery
diagnostic and therapeutic reasons. The instrument is basically a rigid manipulation and opening of the joint com
Almost any joint can be reached but the telescope fitted with fibreoptic partments. The joint is distended with fluid
procedure is most usefully employed in illumination. Tube diameter ranges from and the arthroscope is introduced
the knee, shoulder, wrist, ankle and hip. If about 2 mm (for small joints) to 4–5 mm percutaneously. Various instruments
the suspect lesion is amenable to (for the knee). It carries a lens system (probes, curettes and forceps) can be
surgery, it can often be dealt with at the that gives a magnified image. The inserted through other skin portals; they
same sitting without the need for an open eyepiece allows direct viewing by the are used to help expose the less
operation. However, arthroscopy is an arthroscopist, but it is far more convenient accessible parts of the joint, or to obtain
invasive pro to fit a small, sterilizable solid-state biopsies for further examination. Guided
cedure and its mastery requires skill and television camera which produces a by the image on the monitor, the
practice; it should not be used simply as picture of the joint interior on a television arthroscopist explores the joint in a
an alternative to clinical examination and monitor. systematic fashion, manipulating the
imaging. The procedure is best carried out under arthroscope with one hand and the probe
general anaesthesia; this gives good or forceps
Technique muscle relaxation and permits
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1 with the other. At the end of the procedure the joint
Arthroscopy of the hip is becoming more common
is washed out and the small skin wounds Diagnostic arthroscopy is safe but not 29
are sutured. The patient is usually able to entirely free of complications, the
return home later the same day. commonest of which are haemar thosis,
thrombophlebitis, infection and joint
Diagnosis stiffness (particularly contracture of the
anterior capsule). There is also a
The knee is the most accessible joint. The significant incidence of algodystrophy
appear ance of the synovium and the following arthroscopy.
articular surfaces usu ally allows
differentiation between inflammatory and
non-inflammatory, destructive and non-
destructive lesions. Meniscal tears can be FURTHER READING
diagnosed and treated immediately by
repair or removal of partially detached Apley AG, Solomon L. Physical Examination
segments. Cruciate ligament deficiency, in Orthopaedics. Oxford: Butterworth
osteocartilag inous fractures, cartilaginous Heinemann, 1997.
loose bodies and syno
vial ‘tumours’ are also readily visualized.
Arthroscopy of the shoulder is more
difficult, but the articular surfaces and
glenoid labrum can be adequately
explored. Rotator cuff lesions can often
D
of over 50%. p
Complications i
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br.com
Infection
2 Enrique Gómez-Barrena
Infection – as distinct from mere residence of microor ganisms musculoskeletal infection need the leadership of the
– is a condition in which pathogenic microor ganisms multiply orthopaedic surgeon to ensure timely diagnosis and
and spread within the body tissues. Microorganisms may treatment of the patient with mus culoskeletal symptoms and
reach the musculoskeletal tis sues by: signs that suggest infection.
• direct introduction through the skin (a pinprick, an injection,
a stab wound, a laceration, an open fracture or an GENERAL ASPECTS OF INFECTION
operation, particularly when bioma terials are implanted),
• direct spread from a contiguous focus of infection, or • Infection usually gives rise to an acute or chronic
indirect spread via the bloodstream from a distant site such inflammatory reaction, which is the body’s way of combating
as the nose or mouth, the respiratory tract, the bowel or the the invaders by destroying them, or at least immobilizing and
genitourinary tract. confining them to a restricted area.
Depending on the type of invader, the site of infection and the The classical signs of inflammation are frequently present
host response, the result may be a pyogenic osteomyelitis, a (redness, swelling, heat, pain and loss of func tion) and offer
septic arthritis, a chronic granulo matous reaction (classically clinical clues about the infection and the patient’s reaction.
seen in tuberculosis of either bone or joint), or an indolent Bone infection differs from soft-tissue infection since bone
response to a less aggressive organism (as in low-grade consists of a collection of rigid compart ments. Bone is thus
periprosthetic infections) or to an unusual organism (e.g. a more susceptible than soft tissues to vascular damage and
fungal infection). Soft-tissue infections range from super ficial cell death due to pressure in acute inflammation. Unless it is
wound sepsis to widespread cellulitis and life threatening rapidly suppressed, bone infection will inevitably lead to
necrotizing fasciitis. Parasitic lesions such as hydatid disease necrosis. Osteomyelitis is infection of bone and frequently
also are considered in this chapter, although these are seeds in trabecular areas affecting both bone and bone
infestations rather than infections. marrow. Soft-tissue infection depends on the main affected
Clinical aspects of infection will be particularly devel oped in tissue, but of special interest to the orthopae dic surgeon is
this chapter. The team approach, including microbiologists, joint infection or infectious arthritis, whether septic arthritis or
infectious disease and internal medicine doctors, is certainly granulomatous arthritis. All these forms of infection will be
the basis for success in infection. However, many cases of addressed below.
Host susceptibility to infection is increased by (a) local factors Malnutrition and general debility
such as trauma, scar tissue, poor cir culation, diminished Diabetes mellitus
sensibility, chronic bone or joint disease and the presence of Corticosteroid administration
foreign bodies including implants, as well as (b) systemic
Immune deficiency
factors such as malnu trition, general illness, debility,
diabetes, rheumatoid disease, corticosteroid administration Immunosuppressive drugs
and all forms of immunosuppression, either acquired or Venous stasis in the limb
induced. Peripheral vascular disease
Loss of sensibility
Iatrogenic invasive measures
BOX 2.1 FACTORS PREDISPOSING TO
Trauma
BONE INFECTION
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implants, protected from both
1 Resistance is also diminished in the very young and
2 Provide analgesia and general supportive measures,
the very old. including rest of the affected part or splintage of the
Bacterial colonization and resistance to affected joint.
antibiotics is enhanced by the ability of certain 3 Release pus as soon as it is detected.
microorganisms (including Staphylococcus) to 4 Eradicate avascular and necrotic tissue. 5 Stabilize
adhere to avascular bone surfaces and foreign the bone if it has fractured and restore
32 necrotic tissue. Purulent material
S
or biofilm). Biofilm formation aids the healed wound. Factors which predispose
development of a complex bacterial to this outcome are the presence of
P
maturation with microorganism release diminished local blood supply and a weak
further expands this colonization, and host response. Resistance is likely to be
O
E
Thus, bacterial adherence to biomaterials diseases such as diabetes and leukaemia.
N
and biofilm formation are crucial aspects Chronic non-pyogenic infection may result
to consider when treating musculoskel from inva sion by organisms that produce
E
etal infections in the presence of implants. a cellular reaction lead ing to the formation
Acute pyogenic bone infections are of granulomas consisting largely of
characterized by the formation of pus – a lymphocytes, modified macrophages and
concentrate of defunct leucocytes, dead multinucle ated giant cells; this type of
and dying bacteria and tissue debris – granulomatous infection is seen most
which is often localized in an abscess. typically in tuberculosis. Systemic effects
Pressure builds up within the abscess are less acute but may ultimately be very
and infection may then extend into a con debilitating, with lymphadenopathy,
tiguous joint or through the cortex and splenomegaly and tissue wasting.
along adjacent tissue planes. It may also
spread further afield via lym phatics Treatment
(causing lymphangitis and
lymphadenopathy) or via the bloodstream 1 Identify the infecting organism and
(bacteraemia and septicaemia). An administer effective antibiotic treatment or
accompanying systemic reaction varies chemotherapy.
from a vague feel ing of lassitude with mild continuity if there is a gap in the bone.
pyrexia to severe illness, fever, toxaemia 6 Maintain or regain soft-tissue and skin
and shock. The generalized effects are cover.
due to the release of bacterial enzymes
If treated early with effective antibiotics,
and endotoxins as well as cellular
acute infec tions can usually be cured.
breakdown products from the host tissues.
Once there is pus and bone necrosis,
Chronic pyogenic infection may follow
operative drainage will be needed.
unresolved acute infection and is
When treating patients with bone or joint
characterized by persistence of the
infec tion, it is wise to maintain continuous
infecting organism (or, more frequently,
collaboration with a specialist in
mul tiple microorganisms) in pockets of
microbiology.
ACUTE HAEMATOGENOUS confirm a low incidence (less than 1 case diplococcus S. pneumoniae. In children
per 100 000) in most recent periods between 1 and 4 years of age, the Gram-
OSTEOMYELITIS although it is almost certainly much higher negative Haemophilus influenzae used to
among less affluent populations. Also, a be a fairly common pathogen for
Aetiology and pathogenesis decrease in surgical treatment of those osteomyelitis and septic arthritis, but the
Acute haematogenous osteomyelitis is cases has been identified, possibly related introduc tion of H. influenzae type B
mainly a disease of children. When adults to ear lier and more effective antibiotic vaccination in the 1990s has been
are affected, it is usually because their treatment. followed by a much reduced incidence of
resistance is lowered. Trauma may The causal organism in both adults and this infection in many countries. In recent
determine the site of infection, possibly by children is usually Staphylococcus aureus years its place has been taken by the
causing a small haematoma or fluid (found in over 70% of cases), and less increasing presence of Kingella kingae,
collection in a bone, in patients with often one of the other Gram-positive mainly following upper respiratory
concurrent bacteraemia. The incidence of cocci, such as the Group A beta- infection in young children. Other Gram-
acute haematogenous osteomyelitis in haemolytic strep negative organisms (e.g. Escherichia coli,
Western European children is thought to tococcus (Streptococcus pyogenes) which Pseudomonas aerugi nosa, Proteus
have declined in recent years, probably a is found in chronic skin infections, as well mirabilis and the anaerobic Bacteroides
reflection of improving social conditions. as Group B streptococ cus (especially in fragilis) occasionally cause acute bone
Different studies from the United Kingdom newborn babies) or the alphahaemo lytic infection.
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2 Curiously, patients with sickle-cell disease are prone
rapidly, causing intense pain, obstruction to blood
to infection by Salmonella typhi. Anaerobic organisms Acute haematogenous osteomyelitis shows a charac
(particularly Peptococcus magnus) have been found in teristic progression marked by inflammation, suppu
patients with osteomyelitis, usually as part of a mixed ration, bone necrosis, reactive new bone formation and,
infection. Unusual organisms are more likely to be ultimately, resolution and healing or else intractable
found in heroin addicts and as opportunistic patho chronicity. However, the pathological picture varies
gens in patients with compromised immune defence considerably, depending on the patient’s age, the site of
mechanisms. infection, the virulence of the organism and the host
The bloodstream is invaded, perhaps from a minor response.
skin abrasion, treading on a sharp object, an injection
point, a boil, a septic tooth or – in the new born – from ACUTE OSTEOMYELITIS IN CHILDREN
an infected umbilical cord. In adults, the source of The ‘classical’ picture is seen in children between 2 and
infection may be a urethral catheter, an indwelling 6 years. The earliest change in the metaphysis is an
arterial line or a contaminated needle and syringe. In acute inflammatory reaction with vascular conges tion,
children, the infection usually starts in the vascular exudation of fluid and infiltration by polymor phonuclear
metaphysis of a long bone, most often in the proximal leucocytes. The intraosseous pressure rises
tibia or in the distal or proximal ends of the femur. flow and intravascular thrombosis. Even at an early stage, the
Predilection for this site has tradition ally been attributed bone tissue is threatened by impending isch aemia and
to the peculiar arrangement of the blood vessels in that resorption due to a combination of phago cytic activity and the
area: the non-anastomosing terminal branches of the local accumulation of cytokines, growth factors, prostaglandin
nutrient artery twist back in hairpin loops before and bacterial enzymes. I
entering the large network of sinusoidal veins; the By the second or third day, pus forms within the bone
relative vascular stasis and consequent lowered oxygen
n
The structure of the fine vessels in the hypertrophic and forces its way along the Volkmann canals to the c
zone of the physis may more easily allow bacteria to surface where it produces a subperiosteal abscess. This
pass through and adhere to type 1 collagen in that area.
i
Pathology
(a) (b) infection directly from the metaphysis to the epiphysis.
(b) In older children the physis acts as a barrier and the
Figure 2.1 Epiphyseal and metaphyseal blood sup ply (a) developing epiphysis receives a separate blood supply
In newborn infants some metaphyseal arte rioles from from the epiphyseal and peri articular blood vessels.
the nutrient artery penetrate the physis and may carry 33
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compromise the
1 intracapsular blood supply; by the
end of a week there
(e.g. at the hip,
is usually
shoulder or elbow) microscopic evi
pus
may discharge
through the
periosteum into the
joint. The rising
intraosseous
pressure, vascular
sta sis, small-vessel
thrombosis and
periosteal strip ping
increasingly
dence of bone death. Bacterial tex in neglected cases. Another feature of advancing (b)
acute osteomyelitis is new
O
enzymes also may play their Macrophages and lymphocytes area around the
L
Sequestrum
granulation tissue the boundary E
(a)
between living and bination of phagocytosis and Involucrum
A
osteoclastic resorption.
Sinus
N
infected zone is porotic (probably due to pres sure released at an early stage, this dire
hyperaemia and osteoclastic activity) but if the pus progress can be halted. The bone around the zone
is not released, either spontaneously or by surgical of infection becomes increasingly dense; this,
decompression, new bone starts forming on viable together with the periosteal reaction, results in
surfaces in the bone and from the deep layers of thickening of the bone. In some cases the normal
the stripped periosteum. This is typical of pyogenic anatomy may eventually be reconstituted; in others,
infection, and fine streaks of subperiosteal new though healing is sound, the bone is left
bone usually become apparent on X-ray by the end permanently deformed.
of the second week. With time, this new bone If healing does not occur, a nidus of infection
thickens to form a casement, or involu crum, may remain locked inside the bone, causing pus
enclosing the sequestrum and infected tissue. If the and some times bone debris to be discharged
infection persists, pus and tiny sequestrated intermittently through a persistent sinus (or several
spicules of bone may discharge through sinuses). The infection has now lapsed into chronic
perforations (cloacae) in the involucrum and track osteomyelitis, which may last for many years.
by sinuses to the skin surface (Figure 2.2).
If the infection is controlled and intraosseous
ACUTE OSTEOMYELITIS IN INFANTS life, small metaphyseal vessels pene trate the physeal
The early features of acute osteomyelitis in infants cartilage and this may permit the infection to spread
are much the same as those in older children. into the cartilaginous epiphysis, although definitive
However, a significant difference, during the first proof of this mechanism has not been shown. Whatever
year of life, the mechanism, what is indis putable is that
34 osteomyelitis and septic arthritis often go together
during infancy. Another feature in infants is an
Figure 2.2 Acute osteomyelitis (a) Infection in the metaphysis
unusually exuberant periosteal reaction result ing in
may spread towards the surface, to form a subperiosteal
abscess (b). Some of the bone may die and is encased in sometimes bizarre new bone formation along the
periosteal new bone as a seques trum (c). The encasing diaphysis; fortunately, with longitudinal growth and
involucrum is sometimes perforated by sinuses. remodelling, the diaphyseal anatomy is gradually
restored.
is the frequency with which the metaphyseal infec tion ACUTE OSTEOMYELITIS IN ADULTS
spreads to the epiphysis and from there into the
Bone infection in the adult usually follows an open
adjacent joint. In the process, the physeal anlage may
injury, an operation or spread from a contiguous focus
be irreparably damaged, further growth at that site is
of infection (e.g. a neuropathic ulcer or an infected
severely retarded and the joint will be perma nently
diabetic foot) in over 70% of the cases. True hae
deformed. How this comes about is still argued over. It
matogenous osteomyelitis is uncommon and, when it
has long been held that, during the first 6–9 months of
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2 does occur, it usually affects one of the vertebrae (e.g.
catheterization or a site of infection (however mild)
following a pelvic infection), a metaphyseal region of a In children under 1 year old, and especially in the
long bone or a small cuboidal bone. A vertebral infec newborn, the constitutional disturbance can be mis
tion may spread through the end plate and the inter leadingly mild; the baby simply fails to thrive and is
vertebral disc into an adjacent vertebral body. If a long drowsy but irritable. Suspicion should be aroused by a
bone is infected, the abscess is likely to spread within history of birth difficulties, umbilical artery
the medullary cavity, eroding the cortex and extend ing
into the surrounding soft tissues. Periosteal new bone
formation is less obvious than in childhood and the
BOX 2.2 CARDINAL FEATURES OF
weakened cortex may fracture. If the bone end
becomes involved, there is also a risk of the infection ACUTE OSTEOMYELITIS IN CHILDREN
spreading into an adjacent joint.
Pain
Fever
Clinical features Refusal to bear weight
Clinical features differ in the three described groups. Elevated white blood cell count
Elevated ESR
IN CHILDREN Elevated CRP
The patient, usually a child over 4 years, presents with such as an inflamed intravenous infusion point or even a heel
severe pain, malaise and a fever; in neglected cases, puncture. Metaphyseal tenderness and resistance to joint
toxaemia may be marked. The parents will have noticed movement can signify either osteo myelitis or septic arthritis;
that he or she refuses to use one limb or to allow it to indeed, both may be pres ent, so the distinction hardly matters.
be handled or even touched. There may be a recent Look for other I
history of infection: a septic toe, a boil, a sore throat or sites – multiple infection is not uncommon, espe n
a discharge from the ear. Typically the child looks ill and e
f
feverish; the pulse rate is likely to be over 100 and the cially in babies who acquire the infection in hospital. c
tional sites.
groin). Even the gen tlest manipulation is painful and
joint movement is restricted (‘pseudoparalysis’). Local
redness, swell IN ADULTS
ing, warmth and oedema are later signs and signify that A common site for haematogenous infection is the
pus has escaped from the interior of the bone. thoracolumbar spine. There may be a history of
Lymphadenopathy is common but non-specific. It is some urological procedure followed by a mild fever
important to remember that all these features may be and backache. Local tenderness is not very marked
attenuated if antibiotics have been administered. and it may take weeks before X-ray signs appear;
when they do appear, the diagnosis may still need
IN INFANTS
to be confirmed by fine-needle aspiration and week there may be a faint extracortical outline due
bacteriolog to peri osteal new bone formation; this is the classic
ical culture. Other imaging may be required such as X-ray sign of early pyogenic osteomyelitis, but
MRI, CT or SPECT-CT. In particular, deep abscess treatment should not be delayed while waiting for it
will need to be ruled out in case of suspicion, as to appear. Later, the periosteal thickening becomes
surgi cal drainage may be required. Other bones are more obvi ous and there is patchy rarefaction of the
occa sionally involved, especially if there is a metaphy sis; later still, the ragged features of bone
background of diabetes, malnutrition, drug destruction appear (Figure 2.3). An important late
addiction, leukaemia, immunosuppressive therapy sign is the combination of regional osteoporosis
or debility. In the very elderly, and in those with with a localized segment of apparently increased
immune deficiency, systemic features are mild and density. Osteoporosis is a feature of metabolically
the diagnosis is easily missed. active, and thus living, bone; the segment that fails
to become osteoporotic is metabolically inactive
and possibly dead.
Diagnostic imaging
PLAIN X-RAY ULTRASONOGRAPHY
During the first week after the onset of symptoms, Ultrasonography may detect a subperiosteal collec
the plain radiograph shows no abnormality of the tion of fluid in the early stages of osteomyelitis, but
bone. Displacement of the fat planes signifies soft- it cannot distinguish between a haematoma and
tis sue swelling, but this could as well be due to a pus.
hae matoma or soft-tissue infection. By the second 35
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with underlying structural bone
1
CT
Computed (or computerized) tomography alterations, and clear defi nition of infective
offers the advantage of planar bone foci within complex anatomical locations.
definition, including bone destruction and
soft tissue mass, such as an abscess, MAGNETIC RESONANCE IMAGING (MRI)
within or surrounding bone. Magnetic resonance imaging can be
S
Disadvantages include high radiation helpful in cases
C
I
dose. The excellent anatomical defini infection of the axial skeleton. It is also the
D
tion obtained from CT often justifies the best method of demonstrating bone
E
A
higher radi ation exposure. marrow inflamma tion. It is extremely
P
R increased activity in both the perfusion infection and osteomy elitis. However,
O
phase and the bone phase. This is a specificity is too low to exclude other local
highly sensitive investigation, even in the inflammatory lesions.
L
very early stages, but it has relatively low
A
specific
R
E
ity and other inflammatory lesions can Laboratory investigations
N show similar changes. In doubtful cases, The most certain way to confirm the
E
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2 diagnosis, MRI will help to distinguish between bone
• surgical drainage if required
infection and soft-tissue infection. The organism is diagnosis is made by finding other stigmata of the dis
usually a staphylococcus or streptococcus. Mild cases ease, especially enlargement of the spleen and liver.
will respond to high dosage oral antibiotics; severe
cases need intravenous antibiotic treatment. Treatment
Acute suppurative arthritis Tenderness is diffuse, and If osteomyelitis is suspected on clinical grounds, blood
movement at the joint is completely abolished by and fluid samples should be taken for laboratory inves
muscle spasm. In infants, the distinction between tigation and then treatment started immediately with
metaphyseal osteomyelitis and septic arthritis of the out waiting for final confirmation of the diagnosis. There
adjacent joint is somewhat theoretical, as both often are four important aspects to the manage ment of the
coexist. A progressive rise in C-reactive protein values patient:
over 24–48 hours is considered suggestive of concur
rent septic arthritis. • appropriate antimicrobial therapy (first empirical, then
specific)
Streptococcal necrotizing myositis Group A beta- • splintage and rest of the affected part
haemolytic streptococci (the same organisms which are • supportive treatment for pain and dehydration.
responsible for the common ‘sore throat’) occasionally
invade muscles and cause an acute myo
sitis which, in its early stages, may be mistaken for ANTIBIOTICS
cellulitis or osteomyelitis. Although the condition is rare, Blood and aspiration material are sent immediately for I
diagnosis because it may rapidly spiral out of control examination and culture, but the prompt intravenous f
breakdown. Immediate treatment with intrave Initially, the choice of antibiotics is based on the
nous antibiotics is essential. Surgical debridement of findings from direct examination of the pus smear
necrotic tissue – and sometimes even amputation – and the clinician’s experience of local conditions –
may be needed to save a life. in other words, early empirical antibiotic adminis
tration, a ‘best guess’ at the most likely pathogen.
Acute rheumatism The pain is less severe and it tends Staphylococcus aureus is the most common at all
to flit from one joint to another. There may also be signs ages, but treatment should provide cover also for
of carditis, rheumatic nodules or erythema marginatum. other bacteria that are likely to be encountered in
Sickle-cell crisis The patient may present with fea tures each age group; a more appropriate drug which is
indistinguishable from those of acute osteomy elitis. In also capable of good bone penetration can be sub
areas where Salmonella is endemic, it would be wise to stituted, if necessary, once the infecting organism is
treat such patients with suitable antibiotics until infection identified and its antibiotic sensitivity is known.
is definitely excluded. Factors such as the patient’s age, general state of
resistance, renal function, degree of toxaemia and
Gaucher’s disease ‘Pseudo-osteitis’ may occur with previous history of allergy must be taken into
features closely resembling those of osteomyelitis. The account. The following classical recommendations
are offered as a guide. unless it is known for certain that the child has
had an anti-haemophilus vaccination. This is best
• Neonates and infants up to 6 months of age
provided by a combination of intravenous fluclox
Initial antibiotic treatment should be effective
acillin and cefotaxime or cefuroxime.
against penicillin-resistant Staphylococcus aureus,
Group B streptococcus and Gram-negative • Older children and previously fit adults
organisms. Drugs of choice are flucloxacillin The vast majority in this group will have a
plus a third-generation cephalosporin such as staphylococcal infection and can be started on
intravenous flucloxacillin and fusidic acid. Fusidic
cefotaxime. Alternatively, effective empirical
acid is preferred to benzylpenicillin partly because
treatment can be provided by a combination
of the high prevalence of penicillin-resistant
of flucloxacillin (for penicillin-resistant staph
staphylococci and because it is particularly well
ylococci), benzylpenicillin (for Group B strep
concentrated in bone. However, for a known
tococci) and gentamicin (for Gram-negative
streptococcal infection benzylpenicillin is better.
organisms).
Patients who are allergic to penicillin should be
• Children 6 months to 6 years of age
37
Empirical treatment in this age group should
treated with a polypeptide.
include cover against Haemophilus influenzae,
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lihood of the patient needing invasive procedures. The
antibiotic of choice would be a combination
1 • Elderly and previously unfit patients longer. While patients are on oral antibiotics, it is also important
to track the serum antibiotic levels in order to ensure that the
In this group there is a greater than usual risk minimal inhibitory concentration (MIC) is maintained or
of Gram-negative infections, due to respiratory, exceeded. CRP, ESR and WBC values are also checked at
gastrointestinal, or urinary disorders and the like regular intervals and treatment can be discontin
38 history of MRSA infection, or any patient
S
used to be the preferred antibiotic, though and to the antibiotic trough and peak blood
A
there were always worries about the rare levels adjusted for the patient’s kidney
N
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2 Epiphyseal damage and altered bone growth In
periosteal, epiphyseal, and vertebral) suggested by
neonates and infants whose epiphyses are still entirely tated patients and in those with compromised defence
cartilaginous, metaphyseal vessels penetrate the phy sis mechanisms.
and may carry the infection into the epiphysis. If this
happens, the physeal growth plate can be irrevo cably
damaged and the cartilaginous epiphysis may be SUBACUTE HAEMATOGENOUS
destroyed, leading to arrest of growth and shorten ing of OSTEOMYELITIS
the bone. At the hip joint, the proximal end of the femur
may be so badly damaged as to result in a This condition is no longer rare, and in some coun tries
pseudarthrosis. the incidence is equal to that of acute osteomy elitis. Its
Suppurative arthritis This may occur: (1) in very young relative mildness is presumably due to the organism
infants, in whom the growth plate is not an impenetrable being less virulent or the patient more resis tant (or
barrier; (2) where the metaphysis is intra capsular, as in both). Its skeletal distribution is more vari able than in
the upper femur; or (3) from metastatic infection. In acute osteomyelitis, but the distal femur and the
infants, it is so common as almost to be taken for proximal and distal tibia are the frequent sites. The
granted, especially with osteomyelitis of the femoral anatomical classification (metaphyseal with or without
neck. Ultrasound will help to demonstrate an effusion, cortical erosion, diaphyseal cortical or
but the definitive diagnosis is obtained by joint Roberts and colleagues in the 1980s is still helpful.
aspiration.
Metastatic infection This is sometimes seen – gen erally Pathology
in infants – and may involve other bones, joints, serous Typically, there is a well-defined cavity in cancellous I
cavities, the brain or lung. In some cases, the infection bone – usually in the tibial metaphysis – containing
may be multifocal from the outset. Secondary infection
n
complication and to repeatedly examine the child all lined by granulation tissue containing a mixture of i
over.
o
Imaging Diagnosis
The typical radiographic lesion is a circumscribed, The clinical and X-ray appearances may resemble
round or oval radiolucent ‘cavity’ 1–2 cm in those of cystic tuberculosis, eosinophilic granu loma
diameter. Most often it is seen in the tibial or or osteoid osteoma; occasionally they mimic a
femoral metaph ysis, but it may occur in the malignant bone tumour such as Ewing’s sarcoma.
epiphysis or in one of the cuboidal bones (e.g. the Epiphyseal lesions are easily mistaken for chondro
calcaneum). Sometimes the ‘cavity’ is surrounded blastoma. The diagnosis often remains in doubt until
by a halo of sclerosis (the clas sic Brodie’s a biopsy is performed.
abscess); occasionally it is less well defined, If fluid is encountered, it should be sent for bacteri ological
extending into the diaphysis (Figure 2.4). culture; this is positive in about half the cases and the
Metaphyseal lesions cause little or no periosteal organism is almost invariably Staphylococcus 39
reaction; diaphyseal lesions may be associated with aureus.
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acid) intravenously for 4 or 5 days and CRP levels, and an elevated ESR; it
1 then orally for another 6 weeks usually
result in healing, though this may take up
should be remembered, though, that
these inflammatory markers are non-
to 12 months. If the diagnosis is in doubt, specific and may
an open biopsy is needed and the lesion Figure 2.4 Subacute
may be curetted at the same time. osteomyelitis
S
Curettage is also indicated if the X-ray (a,b) The classic
C
shows that there is no healing after Brodie’s abscess
conservative treatment; this is always
I
D
looks like a small
E
(c) Sometimes
H
OSTEOMYELITIS
T
R
rarefaction is more
O
diffuse and
Open fractures are always contaminated there may be cortical
L
and are there fore prone to infection. The erosion and
A
N
bone fragments and an open pathway to
E
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2 Pyogenic wound infection, once it has taken root,
peripheral vascular disease, skin infections, malnu
is difficult to eradicate. The presence of necrotic soft Bacteria covered in a protein–polysaccharide slime (gly
tissue and dead bone, together with a mixed bacte rial cocalyx) that protects them from both the host defences
flora, conspire against effective antibiotic con trol. and antibiotics have the ability to adhere to inert sur
Treatment requires soft tissue management and repeat faces such as bone sequestra and metal implants,
debridement is required if there is evidence of where they multiply and colonize the area. There is also
inadequate debridement or infection. evi dence that bacteria can survive inside osteoblasts
Traditionally it was recommended that stable and
implants (fixation plates and intramedullary nails) should osteocytes and be released when the cells die. These
be left in place until the fracture had united, and this processes are evident in patients who have been
advice is still respected in recognition of the adage that inadequately treated (‘too little too late’), but in any
even worse than an infected fracture is an infected event certain patients are at greater risk than oth ers:
unstable fracture. However, advances in external those who are very old or debilitated, those suf fering
fixation techniques have meant that almost all fractures from substance abuse and those with diabetes,
can, if necessary, be securely fixed by that method, with trition, lupus erythematosus or any type of immune deficiency.
the added advantage that the wound remains The commonest of all predisposing factors is local trauma,
accessible for dressings and superficial debridement. If such as an open fracture or a pro longed bone operation,
these measures fail, the management is essentially that especially if this involves the use of a foreign implant.
of chronic osteomyelitis. Periprosthetic infection may I
CHRONIC OSTEOMYELITIS
e
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low specificity has led to limited use. RNA fragments (the polymerase chain
1 CT and MRI are invaluable in planning
operative treatment: together they will
reaction or PCR) and their subsequent
identification by gel elec
show the extent of bone destruction and Figure 2.5 Chronic
reactive oedema, hidden abscesses and osteomyelitis
sequestra. SPECT/CT may provide Chronic osteomy
S
advantages of sensitivity and local elitis may follow
C
I
definition, and its use may increase in acute. The young
D complex cases. boy (a) presented
E
with draining
sinuses at the site
Investigations
A
of a previous acute
P
H During acute flares the CSR, ESR and infection. The X-ray
T
to open trauma or
sinuses should be tested repeatedly for
operation.
R
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2 compromised that the prognosis is considered to be
Debridement At operation all infected soft tissue
poor. If the lesion is also classified as Stage 4 (e.g. treatment, and/or clear evidence of a sequestrum or
intractable diffuse infection in a non-united fracture), dead bone; for post-traumatic infections, an intracta ble
operative treatment may be contraindicated and the wound and/or an infected ununited fracture; for
best option may be long-term palliative treatment known postoperative infection, similar criteria and evidence of
as suppression treatment. Occasionally one may have bone erosion.
to advise amputation. The presence of a foreign implant may prompt surgi
cal intervention to remove the implant, whether in case
Treatment of internal fixation (plates, screws and intramedullary
nails that may be substituted by external fixation until
ANTIBIOTICS infection control) or substitution, as discussed below.
Chronic infection is seldom eradicated by antibiotics When undertaking operative treatment, collaboration
alone. Yet bactericidal drugs are important (a) to sup with a plastic surgeon is strongly recommended.
press the infection and prevent its spread to healthy and dead or devitalized bone, as well as any infected implant,
bone and (b) to control acute flares. The choice of must be excised. The wound is inspected after 3 or 4 days
antibiotic depends on microbiological studies, but the and, if there are renewed signs of tissue death, the
drug must be capable of penetrating sclerotic bone and debridement may have to be repeated – several times if
should be non-toxic with long-term use. Fusidic acid, necessary. Antibiotic cover is continued I
lin-resistant Staphylococcus aureus infection (MRSA). Dealing with the ‘dead space’ There are several
Antibiotics are administered for 4–6 weeks (starting
i
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The causative microorganism of PJI is most fre quently
1 PERIPROSTHETIC INFECTION Staphylococcus aureus, followed by coag ulase-
negative Staphylococcus. Together, these represent
Periprosthetic joint infection (PJI) is a specific type more than 50% of PJIs. Streptococcus species,
of infection related to joint replacement and a dread ful Enterococcus species, aerobic Gram-negative bacilli,
complication, potentially chronic, with significant clinical and some anaerobic (such as Propionibacterium acnes
relevance for the affected patient, the treating S
in the shoulder) account for 20–30%, while polymi
44 although some of these may not be true
C
arthroplasty, 2–3% in knee arthro plasty, with the surface of the implant,
1–2% in the shoulder and even 3–5% in microorganisms colonize the surface of
O
the elbow, the economic impact may the implant in competition with the host
H
R
represent a 5- to 10-fold cost increase cells, in the so-called ‘race for the surface’.
O
N
perioperative infection at a distant site, formed on surfaces. From the attachment
E
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2
(a) (b)
Figure 2.6 Periprosthetic joint infection Septic loosening surrounding the tibial stem in this case with PJI 3 years after
total knee arthroplasty associated with immunodepression due to chemotherapy in the treatment of severe malignancy
in (a) anteroposterior and (b) lateral radiographic views.
But besides the complex, multidisciplinary treatment of In 1893 Garré described a rare form of non- suppurative
these infections, perioperative and postoperative osteomyelitis which is characterized by marked sclero
prevention of PJI is a major aspect in the control of sis and cortical thickening. There is no abscess, only a
these severe entities. diffuse enlargement of the bone at the affected site –
usually the diaphysis of one of the tubular bones or the
mandible. The patient is typically an adolescent or
GARRÉ’S SCLEROSING young adult with a long history of aching and slight
swelling over the bone. Occasionally there are recur rent
OSTEOMYELITIS
attacks of more acute pain accompanied by mal aise curetted. Bone grafts, bone transport or free bone
and slight fever. transfer may be needed.
X-rays show increased bone density and cortical
thickening; in some cases the marrow cavity is com
pletely obliterated. There is no abscess cavity. MULTIFOCAL NON-SUPPURATIVE
Diagnosis can be difficult. If a small segment of bone
is involved, it may be mistaken for an osteoid OSTEOMYELITIS
osteoma. If there is marked periosteal layering of
new bone, the lesion resembles a Ewing’s This obscure disorder – it is not even certain that it is an
sarcoma. The biopsy will disclose a low-grade infection – was first described in isolated cases in the 1960s
inflammatory lesion with reactive bone formation. and 1970s, and later in a more com prehensive report on 14
Microorganisms are seldom cultured but the patients of mixed age and sex. It is now recognized that: (1) it
condition is usually ascribed to a staphylococcal is not as rare as initially suggested; (2) it comprises several
infection. different syndromes which have certain features in common;
and (3) there is an association with chronic skin infection,
Treatment is by operation: the abnormal area is
especially pustular lesions of the palms 45
excised and the exposed surface thoroughly
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predominantly
1 and soles (palmo-plantar pustulosis) and pustular
As with recurrent multifocal osteomyelitis, there is a
psoriasis. curious association with cutaneous pustulosis. The
In children the condition usually takes the form usual complaint is of pain, swelling and tenderness
of multifocal (often symmetrical), recurrent lesions around the sternoclavicular joints; sometimes there is
in the long-bone metaphyses, clavicles and anterior also a slight fever and the ESR may be elevated.
ribcage; in adults the changes appear Patients with vertebral column involvement may
46 lesions in the metaphysis, usually closely
S
the ver tebrae. In recent years the various ‘cavities’ are surrounded by sclerosis;
D
syndromes have been drawn together others show varying stages of healing.
under the convenient acronym SAPHO – The clavicle may become markedly
P
standing for synovitis, acne, pustulosis, thickened. If the spine is affected, it may
O
R
round cell infiltration. The aetiology is
E
unknown. Despite the local and systemic lesions there is a chronic inflammatory
N
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2
Figure 2.7
Caffey’s
disease This
infant with
Caffey’s
disease devel
oped marked I
thickening of f
the mandi c
bones. The
lesions gradu
ally cleared up,
leaving little
or no trace of
their former
ominous
appearance.
(a) (b) (c) (d)
or arthroscopy; (2) direct spread from an adjacent bone immunosuppressive drug therapy and acquired immune
abscess; or (3) blood spread from a distant site. In deficiency syndrome (AIDS).
infants it is often difficult to tell whether the infec tion
started in the metaphyseal bone and spread to the joint
or vice versa. In practice it hardly matters and in Pathology
advanced cases it should be assumed that the entire The usual trigger is a haematogenous infection which
joint and the adjacent bone ends are involved. The settles in the synovial membrane; there is an acute
causal organism is usually Staphylococcus aureus; inflammatory reaction with a serous or seropurulent
however, in children between 1 and 4 years old, exudate and an increase in synovial fluid. As pus
Haemophilus influenzae is an important pathogen appears in the joint, articular cartilage is eroded and
unless they have been vaccinated against this organism. destroyed, partly by bacterial enzymes and partly by
Occasionally other microbes, such as Streptococcus, proteolytic enzymes released from synovial cells,
Escherichia coli and Proteus, are encountered. inflammatory cells and pus (Figure 2.8). In infants the
Predisposing conditions are rheumatoid arthri tis, entire epiph
chronic debilitating disorders, intravenous drug abuse, ysis, which is still largely cartilaginous, may be severely
damaged; in older children, vascular occlusion may tenderness and resistance to movement. The
lead to necrosis of the epiphyseal bone. In adults the umbilical cord should be exam
effects are usually confined to the articular cartilage, but ined for a source of infection. An inflamed intrave
in late cases there may be extensive erosion due to nous infusion site should always excite suspicion.
synovial proliferation and ingrowth. The baby’s chest, spine and abdomen should be
If the infection goes untreated, it will spread to the carefully examined to exclude other sites of
underlying bone or burst out of the joint to form infection. Special care should be taken not to miss
abscesses and sinuses. a concomitant osteomy elitis in an adjacent bone
With healing there may be: (1) complete resolution end.
and a return to normal; (2) partial loss of articular In children the usual features are acute pain in a sin
cartilage and fibrosis of the joint; (3) loss of articular gle large joint (commonly the hip or the knee) and
cartilage and bony ankylosis; or (4) bone destruction reluc tance to move the limb (‘pseudoparesis’). The
and permanent deformity of the joint. child is ill, with a rapid pulse and a swinging fever.
The overlying skin looks red and in a superficial
joint swelling may be obvious. There is local warmth
Clinical features and marked tenderness. All movements are
restricted, and often completely abol ished, by pain
The clinical features differ somewhat according to
and spasm. It is essential to look for a source of
the age of the patient.
infection – a septic toe, a boil or a discharge from
In newborn infants the emphasis is on septicaemia
the ear.
rather than joint pain. The baby is irritable and
In adults it is often a superficial joint (knee, wrist, a
refuses to feed; there is a rapid pulse and
finger, ankle or toe) that is painful, swollen and
sometimes a fever. Infection is often suspected, but
inflamed. There is warmth and marked local ten
it could be anywhere! The joints should be carefully
derness, and movements are restricted. The patient
felt and moved to elicit the local signs of warmth,
47
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1
Figure 2.8 Acute suppurative arthritis – pathology In the early stage (a), there is an acute synovitis with a puru R
lent joint effusion. (b) Soon the articular cartilage is attacked by bacterial and cellular enzymes. If the infection
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is not arrested, the cartilage may be completely destroyed (c). Healing then leads to bony ankylosis (d). E
should be questioned and examined for evidence of the space between capsule and bone of more than
gonococcal infection or drug abuse. Patients with 2 mm is indicative of an effusion, which may be
rheumatoid arthritis, and especially those on cortico echo-free (perhaps a transient synovitis) or
steroid treatment, may develop a ‘silent’ joint infec positively echogenic (more likely septic arthritis).
tion. Suspicion may be aroused by an unexplained X-ray examination is usually normal early on but
deterioration in the patient’s general condition; signs to be watched for are soft-tissue swelling, loss
every joint should be carefully examined. of tissue planes, widening of the radiographic ‘joint
space’ and slight subluxation (because of fluid in the
joint) (Figure 2.9). With some infections there is
Imaging sometimes gas in the joint. Narrowing and irregular
Ultrasonography is the most reliable method for ity of the joint space are late features.
revealing a joint effusion in early cases. Both hips MRI and radionuclide imaging are helpful in diag
should be examined for comparison. Widening of nosing arthritis in obscure sites such as the
sacroiliac and sternoclavicular joints. may be indistinguishable from septic arthritis; often one
must assume that both are present.
Investigations Other types of infection Psoas abscess and local
infection of the pelvis must be kept in mind. Systemic
The white blood cell count, CRP and ESR are
features will obviously be the same as those of septic
raised and blood culture may be positive. However, arthritis.
special investigations take time and it is much
quicker (and usually more reliable) to aspirate the Trauma Traumatic synovitis or haemarthrosis may be
joint and exam associated with acute pain and swelling. A history of
ine the fluid. It may be frankly purulent but beware! injury does not exclude infection. Diagnosis may remain
– in early cases the fluid may look clear. A white cell count and in doubt until the joint is aspirated.
Gram stain should be carried out imme 48
diately: the normal synovial fluid leucocyte count is Irritable joint At the onset the joint is painful and lacks
under 300 per mL; it may be over 10 000 per mL in some movement, but the child is not really ill and there
non-infective inflammatory disorders, but counts of over are no signs of infection. Ultrasonography may help to
50 000 per mL are highly suggestive of sep sis. Gram- distinguish septic arthritis from transient synovitis.
positive cocci are probably Staphylococcus aureus; Haemophilic bleed An acute haemarthrosis closely
Gram-negative cocci are either Haemophilus resembles septic arthritis. The history is usually con
influenzae or Kingella kingae (in children) or clusive, but aspiration will resolve any doubt.
Gonococcus (in adults). Samples of fluid are also sent
for full microbiological examination and tests for Rheumatic fever Typically the pain flits from joint to
antibiotic sensitivity. joint, but at the onset one joint may be misleadingly
inflamed. However, there are no signs of septicaemia.
Differential diagnosis Juvenile rheumatoid arthritis This may start with pain
and swelling of a single joint, but the onset is
Acute osteomyelitis In young children, osteomy elitis
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Treatment
The first priority is to aspirate
the joint and examine the fluid.
Treatment is then started
without further delay and
follows the same lines as for
acute osteomy elitis. Once the and the wound is closed; repeated closed aspiration of protected against
blood and tissue samples have suction–irrigation is continued the joint; however, if there is no staphylococcus and Gram-
been obtained, there is no for another 2 or 3 days. This is improvement within 48 hours, negative streptococci with one
need to wait for detailed resultsthe safest policy and is certainly open drainage will be of the penicil linase-resistant
before giving antibiotics. If theadvisable (1) in very young necessary. penicillins (e.g. flucloxacillin)
aspirate looks puru lent, the infants, (2) when the hip is plus a
joint should be drained without involved, and (3) if the
waiting for laboratory results
(see below).
aspirated pus is very thick. For
the knee, arthroscopic
ANTIBIOTICS
Antibiotic treatment follows the 2
same guidelines as presented
debridement and copious irri
for acute haematogenous
DRAINAGE gation may be equally effective.
osteomyelitis. The initial choice
Older children with early septic
Under anaesthesia the joint is of antibiotics is based on
arthritis (symptoms for less than
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septic arthritis in sexually active adults, especially
1 joint should be held abducted and 30 degrees flexed,
on among poorer populations. Even in affluent commu
nities the incidence of sexually transmitted diseases
traction to prevent dislocation. has increased (probably related to the increased
GENERAL SUPPORTIVE CARE use of non-barrier contraception) and with it the risk
Analgesics are given for pain and intravenous of gonococcal and syphilitic bone and joint
fluids for dehydration. diseases and their sequelae. The infection is
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acquired only by direct mucosal contact with an
hand). Both syndromes may occur in the same patient. infected person – carrying a risk of greater than
There may be a slight pyrexia and the ESR and WBC 50% after a single contact!
count will be raised. If the condition is suspected, the
patient should be questioned about possible contacts Clinical features
during the previous days or weeks and they should be
Two types of clinical disorder are recognized: (a) dis
examined for other signs of genitourinary infection (e.g.
a urethral discharge or cervicitis). seminated gonococcal infection – a triad of polyarthritis,
AFTERCARE tenosynovitis and dermatitis – and (b) septic arthritis of 50
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a single joint (usually the knee, ankle, shoulder, wrist or
Once the patient’s general condition is satisfactory Joint aspiration may reveal a high white blood cell
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damage is unlikely. If articular cartilage has been sal surfaces and tests should be performed for other
pre O
sexually transmitted infections.
served, gentle and gradually increasing active move
Treatment
H
G
Complications effective.
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2 and yaws. Lyme disease, which also originates with a
dies shortly after birth. The ones who survive man
lymph nodes and thence to the bloodstream. The pain, swelling and tenderness of the bones, especially t
the fetal blood stream directly during the latter half of those with little soft-tissue covering, such as the fron n
pregnancy, giving rise to congenital syphilis. tal bones of the skull, the anterior surface of the tibia,
In acquired syphilis a primary ulcerous lesion, or the sternum and the ribs. X-rays may show typical
chancre, appears at the site of inoculation about a fea tures of periostitis and thickening of the cortex in
month after initial infection. This usually heals with out these bones, as well as others that are not
treatment but, a month or more after that, the disease necessarily symp tomatic. Osteitis and septic
enters a secondary phase characterized by the arthritis are less common. Occasionally these
appearance of a maculopapular rash and bone and joint patients develop polyarthralgia or polyarthritis.
changes due to periostitis, osteitis and osteo chondritis. Enquiry may reveal a history of sexually transmitted
After a variable length of time, this phase is followed by disease.
a latent period which may continue for many years. The
term is somewhat deceptive because in about half the Late features The typical late feature, which may
cases pathological lesions continue to appear in various appear only after many years, is the syphilitic
organs and 10–30 years later the patient may present gumma, a dense granulomatous lesion associated
again with tertiary syphilis, which takes various forms with local bone resorption and adjacent areas of
including the appearance of large granulomatous sclerosis. Sometimes this results in a pathological
gummata in bones and joints and neuropathic disorders fracture. X-rays may show thick periosteal new bone
in which the loss of sensibility gives rise to joint formation at other sites, especially the tibia.
breakdown (Charcot joints). The other well-recognized feature of tertiary syphilis
In congenital syphilis, the primary infection may be is a neuropathic arthropathy due to loss of
so severe that the fetus is either stillborn or the infant sensibility in the joint – most characteristically the
knee.
Other neurological disorders, the early signs of
which may only be discovered on careful examina
tion, are tabes dorsalis and
‘general paralysis of the
insane’ (GPI). With modern
treatment, these late
sequelae have become
rare.
Figure 2.10
Syphilis (a–c) Congenital
syphilis, with diffuse
periostitis of many bones.
(b) (d) Acquired syphilitic
periostitis of the tibia.
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1 Clinical features of congenital syphilis Early
den tal malformations (‘Hutchinson’s teeth’), erosion
of the nasal bones, thickening and expansion of the
congenital syphilis Although the infection is present at birth, fin ger phalanges (dactylitis) and painless effusions
bone changes do not usually appear until several weeks in the knees or elbows (‘Clutton’s joints’).
afterwards. The baby is sick and irritable and examination may
show skin lesions, hep atosplenomegaly and anaemia. Treatment
Serological tests are Early lesions will usually respond to intramuscular
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tropical parts of Africa, Asia and South America. injections of benzylpenicillin given weekly for 3 or 4
Though considered – at least in Europe – to be a ‘rare’ doses. Late lesions will require high-dosage intra
disease, several thousand cases a year are reported in venous penicillin for a week or 10 days, but some
Indonesia. forms of tertiary syphilis will not respond at all. An
The infection is contracted by skin-to-skin con tact. A alternative would be treatment with one of the third
knobbly ulcer covered by a scab (the primary or generation cephalosporins.
‘mother’ yaw), usually develops on the face, hands
usually positive in both mother and child.
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Yaws
The first signs of skeletal involvement may be Yaws is a non-venereal spirochaetal infection
joint D
caused by Treponema pertenue. It is seen mainly in the poorer
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swelling and ‘pseudoparalysis’ – the child refuses to
or feet. Secondary skin lesions appear 1–4 months
A
T
ness at the ends or along the shafts of the tubular period, merging into a tertiary stage during which
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sometimes causes joint contractures at any synovial or bursal sheath.
the knee, the ankle or the foot. Predisposing conditions include chronic
Occasionally an invasive squamous cell debil itating disorders, diabetes, drug
carcinoma develops in a chronic ulcer. abuse, prolonged corticosteroid
medication, AIDS and other disorders
Treatment
resulting in reduced defence mechanisms.
‘Prevention is better than cure.’ For people
living or working in the tropics, the chance
of infection can be reduced by wearing
Pathology
shoes and any type of covering for the Mycobacterium tuberculosis (usually
legs. Scratches and abrasions should be human, some times bovine) enters the
cleaned and kept clean until they heal. body via the lung (droplet infection) or the
Early cases of tropical ulcer may respond gut (swallowing infected milk prod ucts) or,
to benzyl penicillin or erythromycin given rarely, through the skin. In contrast to pyo
daily for a week. If this is not effective, a genic infection, it causes a granulomatous
broad-spectrum antibiotic will be needed reaction which is associated with tissue
(
(e.g. a third-generation cephalosporin). necrosis and caseation.
Ulcers should be cleansed every day and
kept covered with moist or non-adherent Primary complex The initial lesion in lung,
dressings. Topical treat ment with phar ynx or gut is a small one with
metronidazole gel is advisable. lymphatic spread to
a) (b)
Late cases of ulceration will require
Figure 2.11 Tropical ulcer (a) What started as a painstaking cleansing and de-sloughing
small ulcer has turned into a large spreading together with broad spectrum antibiotics
2
lesion. (b) The X-ray shows the typical marked
effective against the causative anaerobic
periosteal reaction in the underlying bone.
Gram-negative organisms as well as
second ary infecting microbes cultured I
(Figure 2.11). The ulcer may eventually from swab samples. Soft-tissue and bone
n
bore its way into the soft tissues and the destruction may be severe enough to
e
underlying bone; occa sionally, after many require extensive debridement and skin-
c
best option.
n
squamous-cell carcinoma.
Clinical features
TUBERCULOSIS
What starts as a small inflamed scratch or
cut develops over a few days into a large Once common throughout the world,
pustule. By the time the patient attends tuberculosis showed a steady decline in
for medical treatment, the pustule has its prevalence in developed countries
usually ruptured, leaving a foul-smelling, during the latter half of the twentieth cen
discharging ulcer with hard rolled edges tury, due mainly to the effectiveness of
on the leg, the ankle or foot. In some public health programmes, a general
cases the ulcer has already started to improvement in nutritional status and
spread and after 4–6 weeks it may be advances in chemotherapy. In the last two
several centi decades, however, the annual incidence
metres in diameter! Two or three adjacent (particularly of extrapulmonary
ulcers may join up to form a large tuberculosis) has risen again, a
sloughing mass that erodes tendons, phenomenon which has been attributed
ligaments and the underlying bone. Even if variously to a general increase in the
the bone is not directly involved, X-ray proportion of elderly peo ple, changes in
examination may show a marked population movements, the spread of
periosteal reaction to the over intravenous drug abuse and the
lying infection. With time that segment of emergence of AIDS. The skeletal
the bone may become thickened and manifestations of the disease are seen
sclerotic, or there may be erosion of the chiefly in the spine and the large joints, but
cortex. With healing, soft-tissue scar ring the infec tion may appear in any bone or
53
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1 regional lymph nodes; this combination is the pri
mary
5% of patients with tuberculosis (Figure 2.12). There
is a predilection for the vertebral bodies and the
large synovial joints. Multiple lesions occur in about
complex. Usually the bacilli are fixed in the nodes
and no clinical illness results, but occasionally the one
response is excessive, with enlargement of glands third of patients. In established cases it is difficult to
in the neck or abdomen. tell whether the infection started in the joint and then
Even though there is often no clinical illness, the spread to the adjacent bone or vice versa; synovial
(or ‘tubercle’) – a collection of epithelioid and mul membrane and subchondral bone have a common
tinucleated giant cells surrounding an area of necro sis, blood supply and they may, of course, be infected
with round cells (mainly lymphocytes) around the simultaneously.
periphery (Figure 2.13). Once the bacilli have gained a foothold, they elicit a
Within the affected area, small patches of caseous chronic inflammatory reaction. The characteris tic
necrosis appear. These may coalesce into a larger yel microscopic lesion is the tuberculous granuloma
initial infection has two important sequels: (1) within lowish mass, or the centre may break down to form an
abscess containing pus and fragments of necrotic bone.
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nodes which are apparently healed or even calcified, Bone lesions tend to spread quite rapidly. Epiphyseal
cartilage is no barrier to invasion and soon the infec tion
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response is quite different, the lesion being a destruc
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tive one which spreads by contiguity.
A
Secondary spread If resistance to the original
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N
bloodstream may occur, giving rise to miliary tuber
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Figure 2.12 Tuberculous arthritis – pathology The disease may begin as synovitis (a) or osteomyelitis (b). From
either, it can extend to become a true arthritis (c); not all the cartilage is destroyed, and healing is usually by 54
fbrous ankylosis (d).
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