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Rheumatology, Orthopaedics and Trauma at a Glance


Rheumatology, Orthopaedics and Trauma at a Glance Catherine Swales MRCP, PhD Clinical Lecturer in Rheumatology Nuffield Orthopaedic Centre Oxford

Christopher Bulstrode MCh, FRCS(Orth) Emeritus Professor in Trauma and Orthopaedics University of Oxford Oxford

Second edition

A John Wiley & Sons, Ltd., Publication


This edition first published 2012 © 2012 by John Wiley & Sons, Ltd Wiley-Blackwell is an imprint of John Wiley & Sons, formed by the merger of Wiley’s global Scientific, Technical and Medical business with Blackwell Publishing. Registered office: John Wiley & Sons, Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK Editorial offices: 9600 Garsington Road, Oxford, OX4 2DQ, UK The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK 111 River Street, Hoboken, NJ 07030-5774, USA For details of our global editorial offices, for customer services and for information about how to apply for permission to reuse the copyright material in this book please see our website at www.wiley.com/ wiley-blackwell. The right of the author to be identified as the author of this work has been asserted in accordance with the UK Copyright, Designs and Patents Act 1988. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior permission of the publisher. Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. This publication is designed to provide accurate and authoritative information in regard to the subject matter covered. It is sold on the understanding that the publisher is not engaged in rendering professional services. If professional advice or other expert assistance is required, the services of a competent professional should be sought. First edition published 2007 Second edition published 2012 Library of Congress Cataloging-in-Publication Data Swales, Catherine. Rheumatology, orthopaedics, and trauma at a glance / Catherine Swales, Christopher Bulstrode. – 2nd ed. p. ; cm. – (At a glance) Rev. ed. of: The musculoskeletal system at a glance / Christopher Bulstrode, Catherine Swales. 2007. Includes bibliographical references and index. ISBN-13: 978-0-470-65470-5 (pbk. : alk. paper) ISBN-10: 0-470-65470-8 (pbk. : alk. paper) 1. Musculoskeletal system. I. Bulstrode, C. J. K. (Christopher J. K.) II. Bulstrode, C. J. K. (Christopher J. K.). Musculoskeletal system at a glance. III. Title. IV. Series: At a glance series (Oxford, England) [DNLM: 1. Musculoskeletal Diseases–Handbooks. 2. Musculoskeletal Physiological Phenomena– Handbooks. 3. Musculoskeletal System–injuries–Handbooks. 4. Orthopedics–methods– Handbooks. 5. Rheumatic Diseases–Handbooks. WE 39] QP301.B8956 2012 616.7–dc23 2011015187 A catalogue record for this book is available from the British Library. 1

2012


Contents Preface 6 Guide to anatomical terminology 7

24 25 26 27 28 29 30 31 32 33 34 35 36 37

Systemic lupus erythematosus 57 Ankylosing spondylitis 60 The spondyloarthropathies 62 Acute joint disease 64 Infection and malignancy 66 Fibromyalgia 68 Osteoporosis 70 Disorders of bone metabolism 72 Vasculitis 1: Giant cell arteritis 74 Vasculitis 2: Medium and small vessel vasculitis 76 Scleroderma 78 Inflammatory muscle diseases 80 The medical management of inflammatory disease 82 Rehabilitation 84

1 2 3 4

Section 1 Introduction Musculoskeletal structure and function 8 Calcium homeostasis and bone metabolism 10 History and examination – an overview 12 Imaging 14

5 6 7 8 9

Section 2 The arm Anatomy of the arm 16 History and examination of the arm 19 Problems presenting in the arm 22 Upper arm trauma 24 Lower arm trauma 26

10 11 12 13

Section 3 The spine Anatomy of the spine 28 History and examination of the spine 30 Problems presenting in the spine 32 Trauma of the spine 34

38 39 40 41

Section 6 Orthopaedics Orthopaedics in children 86 Sports medicine 88 Neurological disorders and orthotics 90 Orthopaedics in the elderly 92

14 15 16 17 18 19 20

Section 4 The leg Anatomy of the leg 36 History and examination of the leg 38 Problems presenting in the hip 40 Joint replacement 42 Problems presenting in the lower leg 44 Upper leg trauma 46 Lower leg trauma 48

42 43 44 45 46 47 48 49

Section 7 Trauma Initial management of the polytraumatised patient 94 Wound management 96 Plastic surgery 97 Burns 98 Peripheral and spinal nerve injuries 100 Head injuries 102 Fractures and dislocations 104 Compartment syndrome 106

Section 5 Rheumatology 21 Rheumatological history and examination 50 22 Pathogenesis of rheumatoid arthritis 52 23 Rheumatoid arthritis 54

Self-assessment case studies: questions 108 Self-assessment case studies: answers 110 Index 113

Contents

5


Preface This is the second edition of a book specially designed for clinical students who are doing their rheumatology, orthopaedics and trauma attachments. It is one of a very successful ‘At a Glance’ series which gives you, the student, the minimum information you need to pass your exams. It is short and very visual, so it should work well as a fast revision text too. It is based on the 8 week course taught at the Oxford Medical School by the two authors. However, it should also be very useful for GP trainees who have such a huge range of subjects to cover, and so need essential information on each subject in a quick and easily digestible form. Each chapter is one page of diagrams combined with one page of text. We have tried to cover the basic science (including anatomy and physiology) right through to practical procedures such as how to examine a joint in a systematic way which will warm the heart of an examiner. The three subjects rheumatology, orthopaedics and trauma complement each other really well. If you are still a little shy with patients

6 Preface

and want to build up your competence and confidence, then the rheumatology ward is for you. The patients are delightful, the diseases a cornucopia of fascinating physical signs, the staff are true problem solvers and the treatments are at the cutting edge of modern science, and they work! Orthopaedics is very logical and has big simple operations which transform a patient’s quality of life. If you need an adrenaline burst, then the trauma room is for you. There, life-saving decisions have to be taken quickly and boldly. No place for the faint-hearted! This book gives you all you need to know to step boldly into any of these three worlds. A short section at the end provides you with some clinical cases to test your teeth on. These are the sort of questions that you will face at finals. Our thanks must go to Jane Fallows and Roger Hulley for illustrations which throw life and clarity onto the concepts we so clumsily describe in the text, and to Elizabeth Bishop and Laura Murphy for steering the project through in a relaxed but timely way. Enjoy!


Guide to anatomical terminology Fingers abducted

Forearm pronated

Elbow flexed Arm abducted and laterally rotated

Arm adducted Elbow extended

Median plane

Sagittal planes

Forearm supinated Coronal plane Valgus

Fingers adducted Lateral side

Proximal

Distal

Varus

Leg laterally rotated Leg medially rotated

Medial side

Foot extended (dorsiflexed)

Evert

Supinate Fore foot

Invert

Hind foot

Foot flexed (plantar flexed)

Pronate Some anatomical terminology

Guide to anatomical terminology

7


1

Musculoskeletal structure and function Structure of bone unit

Osteoclast HCO3– Cl–

ADP + Pi

ATP

Trabecular/ spongy bone

Sealing zone

MMP

H+

Cortical bone

Collection of Haversian (osteon) units

Trabeculae of bone surrounding marrow

Cl–

Bone Resorptive lacunae within ruffled zone Low pH/proteolytic enzymes Bone resorption by osteoclasts

Canaliculi – route through matrix Haversian canal – blood vessels

Structure of long bone Articular cartilage Epiphysis

Lamellae of matrix Lacunae containing osteocytes

Epiphyseal line Spongy bone Metaphysis

Diaphysis

Medullary cavity

Metaphysis Epiphysis

Motor unit

Muscle unit Motor neuron

Sarcomere–contractile unit z disc

m line

z disc

Myosin myofilaments containing globular heads Synapses

Muscle fibre containing myofibril Actin myofilaments

A band

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. © 2012 John Wiley & Sons, Ltd.

8 Published 2012 by John Wiley & Sons, Ltd.


The locomotor system is composed of bone, cartilage, muscle, tendons and ligaments.

Bone Bone is essentially a mineralised connective tissue. It is comprised of two subtypes: 1 Woven bone is formed when bone is laid down rapidly, as in the developing foetus, healing fractures or bone-forming tumours. 2 Lamellar bone is laid down slowly. It is structurally strong and forms the adult skeleton. It is arranged in two forms: • Cortical or compact bone comprises 80% of the skeleton, accounting for most of the shafts of long bones. It is formed by Haversian systems: rings of collagen and matrix containing central blood vessels and lining cells called osteocytes. • Trabecular or medullary bone is found in contact with bone marrow cells between the cortices, at the end of long bones and in vertebral bodies. In trabecular bone the collagen and matrix run as sheets (lamellae) parallel to the bone surface. The three main cell types in bone are: 1 Osteoblasts (‘builders’) are responsible for bone formation by forming organised lamellae of mineralised matrix and collagen. Osteoblasts lie in sheets on the surface of bone trabeculae and their activity is closely coupled to osteoclasts. 2 Osteoclasts (‘cutters’) resorb bone. These giant multinucleated cells migrate across bone, settle on an area to be resorbed and the plasma membrane adjacent to the bone surface becomes a ‘ruffled border ’. Secretion of proteolytic enzymes (e.g. matrix metalloproteinases, MMP) and hydrochloric acid onto the bone surface remove mineral and matrix simultaneously. 3 Osteocytes are mature, relatively inactive osteoblasts that lie in lacunae within bone. Osteoblasts and osteoclasts are coupled into bone remodelling units that keep adult bone mass relatively constant. See Chapter 31 ‘Disorders of Bone Metabolism’ for more details of osteoclast/osteoblast cell biology. Bone is covered in a vascular membrane (the periosteum) which is a major source of blood supply to the bone (the other supply is derived from perforating vessels which then run up in the medulla). The periosteum is helpful when reducing fractures, as it is often partly intact and can be used to guide the broken frgments together. The periosteum is also important in fracture healing, supplying cells which ‘organise the haematoma’ around the fracture site (see below). The protein matrix of bone consists largely of type I collagen. Osteoblasts lay down triple helices of type I collagen into organised lamellae containing unmineralised matrix (osteoid). The tensile strength of bone is increased by covalent bonds between collagen sheets; rigidity is conferred by mineralisation of bone matrix, with deposition of hydroxyapatite crystals between the lamellae. Bone remodelling occurs throughout life to repair damaged bone. Alternating cycles of recruitment, differentiation and activation of osteoclasts and osteoblasts maintain the structural integrity of bone throughout life; with advancing age however, bone loss exceeds formation. Vigorous bone remodelling follows fracture in 5 stages: 1 – Clot or haematoma formation from bleeding vessels within bone. 2 – Organisation and recruitment of new populations of osteoblasts. 3 – Callus formation from new osteoid and woven bone formation. 4 – Modelling by osteoblasts/clasts transforms woven to lamellar bone. 5 – Remodelling strengthens bone in direction of maximal stress.

Movement stimulates this process, so rigid fixing of fractures with plates prevents callus formation, and healing occurs more slowly on the background of standard bone remodelling. Bone is unique in its ability to heal without scar formation. Bone increasese its circumference by the generation of new bone immediately under the periosteum, but length increases at epiphyseal growth plates. These are cartilage plates with their own blood supply which lie between the epiphysis (end of the bone) and the metaphysis, the part of the bone which connects with the diaphysis (shaft of the bone). These epiphyseal plates are weaker than the surrounding bone and therefore fractures in growing skeletons tend to occur at this site. If the fracture affects the blood supply or the anatomy of the growth plate then development may be affected.

Cartilage Cartilage is composed of chondrocytes and chondroblasts, which create a matrix of type II collagen, and proteoglycans to bind water. Adult cartilage consists of four layers – the superficial, middle, deep and calcified zones, which differ in pattern of collagen fibre deposition, and water and cell content. Articular (hyaline) cartilage is an avascular and aneural shock absorber. It covers articular surfaces and allows friction-free movement of joints. Fibrocartilage forms the menisci and intervertebral discs. Cartilage is lost either through mechanical degeneration at points of load-bearing (in osteoarthritis) or through resorption in an inflamed joint (in rheumatoid arthritis) or both. As cartilage contains no blood vessels, it heals slowly if damaged.

Muscle Muscle is formed by fibres that differ according to their twitch rate and fatiguability. • Type 1 muscle fibres are slow twitch (red) fibres that are highly resistant to fatigue. They have abundant mitochondria and are designed to maintain sustained contractions such as needed in posture control. • Type 2 muscle fibres are fast twitch (white) fibres and are designed to produce greater force and rapidity of contraction but fatigue rapidly. Fibres of similar types group together with a lower motor neuron to form a motor unit. Muscle fibres contain myofibrils formed by the contractile myofilaments actin and myosin. The myosin-binding sites on actin are covered by tropomyosin and troponin. However, when an action potential reaches a motor unit, stimulation causes calcium release into the surrounding cytoplasm (sarcoplasm). The calcium binds with troponin sites on tropomyosin, revealing the active binding sites and disinhibiting actin filaments. These cross-link with the globular heads on myosin, causing shortening of the motor unit. The muscle relaxes once calcium levels fall and the cross-links are broken.

Tendons and ligaments Both of these specialised connective tissues are composed of type I collagen. Tendons attach muscle to bone, while ligaments connect bones to one another, supplying support to a joint.

Nerves Nerves are arranged in a segmental fashion, one pair at each level. The sensory nerves enter dorsally, supplying sensory information from a stereotyped strip of skin (dermatome). The motor root exits ventrally; a myotome is the motor equivalent of a dermatome i.e. the muscles served by a single nerve root. Knowledge of the nerve roots is very useful in determining the site and level of injury in the nervous system. Musculoskeletal structure and function Introduction

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2

Calcium homeostasis and bone metabolism Diet

UV light on skin

Cholecalciferol D3 Liver 25(OH)D3

Kidney Renal Ca absorption PO4 excretion

Ca

PO4

Increases renal hydroxylation of vitamin D precursors

Parathyroid hormone

Bone resorption Gut Ca absorption

Ca

PO4

24, 25(OH)2D3 (inactive)

Bone resorption Vitamin D

Suppresses release

Hypercalcaemia

Gut Ca absorption

1, 25(OH)2D3 (active)

Hypocalcaemia

Depression, paraesthesia QT interval

QT interval

Facial twitching when facial nerve tapped – Chvostek's sign

Depression, thirst, abdominal pain, nausea, constipation, renal stones

Flexion wrist and fingers with occlusion of brachial artery – Trousseau's sign

'Bones, stones, groans and moans' Causes Myeloma Malignancy

Bony deposits PTHrP

1°/3° hyper PTH Sarcoidosis Treatment Rehydration, bisphosphonates, frusemide

The basics The skeleton is more than a structural framework. During constant cycles of bone formation and resorption, it plays a vital role in calcium homeostasis. Calcium is the most abundant mineral in the body and 99% of it is contained in bone. Half of plasma calcium is bound to albumin and is therefore inactive. Calcium results must be adjusted to account for albumin levels by adding or subtracting 0.02 mmol/l for each g/l by which the albumin is below or above 40 g/l, respectively. Calcium homeostasis and bone metabolism are principally governed by vitamin D and parathyroid hormone. Bone metabolism is

Causes Hypo PTH Pseudohypo PTH Chronic renal failure Pancreatitis Treatment Ca supplementation

also modulated by calcitonin, glucocorticoids, sex hormones, growth hormone and thyroxine. See Chapter 31 ‘Disorders of bone metabolism’ for a description of osteomalacia, rickets and Paget’s disease; also see Chapter 30 ‘Osteoporosis’.

Vitamin D This fat-soluble vitamin is found in the diet and its precursors are also generated in the skin in response to sunlight. Following renal and hepatic hydroxylation, the active component 1,25-dihydroxy-D3 is released. Its actions are:

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. © 2012 John Wiley & Sons, Ltd.

10 Published 2012 by John Wiley & Sons, Ltd.


• Gut: increases calcium absorption from the small bowel. • Bone: increases mineralisation and resorption.

Parathyroid hormone Parathyroid hormone (PTH) is released in response to low plasma calcium levels. Its overall function is to increase plasma calcium and decrease plasma phosphate levels via actions on the gut, bone and renal tract: • Gut: increases intestinal absorption of calcium. • Bone: increases osteoclastic resorption of bone. • Renal: increases calcium reabsorption and phosphate excretion; increases renal hydroxylation of vitamin D precursors. Vitamin D and PTH levels are interlinked: PTH responds to low levels of vitamin D by increasing renal hydroxylation of vitamin D precursors into the active form; high levels of vitamin D feedback to inhibit PTH release.

hyperplasia may also be responsible. It causes the symptoms of hypercalcaemia as discussed above and biochemical testing reveals a raised calcium, unsuppressed PTH (i.e. normal or high plasma level), reduced phosphate and elevated alkaline phosphatase. There may be radiological evidence of bone resorption (brown tumours, pepper-pot skull). Treatment is surgical. Secondary hyperparathyroidism Appropriate production of PTH in the presence of a low calcium level. The most likely cause is chronic renal failure. Tertiary hyperparathyroidism Inappropriate and autonomous production of PTH following prolonged secondary hyperparathyroidism. Calcium is elevated, and treatment is as for primary disease.

Hypoparathyroidism

Disorders of calcium homeostasis Hypercalcaemia Elevated calcium levels can cause abdominal pain, nausea, constipation, polyuria, depression and renal stones. They shorten the Q-T interval. The most common cause is malignancy (myeloma, bony metastases, PTH-related protein release from some tumours) or primary hyperparathyroidism. Treatment is with rehydration and frusemide or bisphosphonates.

Hypocalcaemia The main symptoms of hypocalcaemia are depression and paraesthesia. Obstruction of the brachial artery causes carpopedal spasm (Trousseau’s sign) and tapping the facial nerve causes the facial muscles to twitch (Chvostek’s sign). The Q-T interval is prolonged. Causes include (pseudo)hypoparathyroidism, chronic renal failure or pancreatitis. Treatment is with calcium supplementation and reversal of the underlying cause.

Primary hypoparathyroidism Reduced PTH secretion due to autoimmune destruction of the parathyroid glands or their surgical removal. It causes symptoms of hypocalcaemia. Calcium is reduced, phosphate elevated and alkaline phosphatase normal. Treatment is with alfacalcidol. Pseudohypoparathyroidism Similar symptoms and treatment to primary condition, but aetiology is due to end-organ resistance to PTH, so hormone levels may rise. Additional features include a round face and short metacarpals/tarsals. Pseudopseudohypoparathyroidism Phenotypic appearance of pseudohypoparathyroidism but normal endocrine and biochemical features.

Hyperparathyroidism Primary hyperparathyroidism Inappropriate production of PTH in the presence of a raised calcium level. Most commonly due to a single adenoma but carcinoma and

Calcium homeostasis and bone metabolism Introduction

11


3

History and examination – an overview

Taking a history Introduction

Introduce self – give your name and say who you are Check patient's name Explain what you want to do Check that the patient is comfortable

Patient's problems Open questions. Explore what is troubling the patient, what they and hopes think is wrong and what they are hoping will be done for them Clarify diagnosis

Closed questions. Try to work out the most likely diagnoses

Systemic enquiry

Questions should be comprehensive but relevant only to fitness for treatment proposed including significant co-morbid conditions, and social issues which may affect recovery and discharge

Closure

Summarise the points. Ask if patient wants any further information

Performing an examination Introduction

Ask patient to 'Point where it is most tender?' Check for other problems/injuries. Wash your hands

Expose

Both limbs. One joint above and below

Use both sides for comparison Skin – redness, scars, wounds Soft-tissues – swelling/wasting Bone – deformity

Look

Check neurovascular status Skin – temperature, sensation, sweating Soft-tissues – tenderness, effusion, pulses Bone – tenderness, osteophytes

Feel

Active – if necessary demonstrate movement to patient Passive – watch patient's face especially when moving beyond active range Resisted and special tests for stability

Move

Closure

Thank patient, check comfort, check for any questions

NB

Determining the underlying aetiology of locomotor disease requires a directed history and examination, but an overall screening system is crucial to ensure that no feature is overlooked. In addition the locomotor history can be employed in the systems review of any general medical or surgical situation. This chapter will focus on a validated screening tool for the locomotor system, the GALS locomotor screen (Doherty et al., 1992, Annals Rheum. Dis. 51:1165–9). Detailed and regional history and examination is covered in subsequent chapters.

The GALS system is an excellent screening tool For detailed examination of the hand in rheumatoid arthritis, see Chapter 21 'Rheumatological history and examination'

‘GALS (gait, arms, legs, spine)’ locomotor screen Screening questions If the answer to the following questions is ‘Yes’, there is unlikely to be major locomotor pathology. • ‘Are you free of pain or stiffness in your muscles, joints or back?’ • ‘Can you dress yourself completely without any difficulty?’ • ‘Can you walk up and down stairs without any difficulty?’

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. © 2012 John Wiley & Sons, Ltd.

12 Published 2012 by John Wiley & Sons, Ltd.


Screening examination The examination is broken down into gait, arms, legs and spine, and any abnormality in appearance or movement is documented and a regional, directed history and examination undertaken. It should be performed with the patient in light underwear, allowing close inspection of each area following a few simple commands.

Gait • Ask the patient to walk a short distance and then turn around: Is the gait smooth and symmetrical? Normal arm swing, stride length, heel strike, stance and toe-off? Able to turn quickly?

Arms Ask the patient to follow these instructions: • ‘Put your arms behind your head’: Assesses the glenohumeral, sternoclavicular and acromioclavicular joints. • ‘Put your arms straight’: Tests full elbow extension. • ‘Put your hands in front’: Any wrist/finger swelling or deformity? Able to extend fingers fully? • ‘Turn your hands over’: Tests supination/pronation (superior and inferior radioulnar joints). Normal palms? No swelling, wasting or erythema? • ‘Make a fist’: Assesses power grip. • ‘Pinch finger to thumb’: Assesses precision pinch/dexterity. • Metacarpal squeeze test: Evidence of tenderness/synovitis?

Legs Inspect while standing • Normal quadriceps bulk/symmetry? • Knee swelling or deformity? • Forefoot/midfoot/arches normal? Examine while lying • Flex the hip with knee flexed: Crepitus? Limitation? • Passively internally rotate each hip in flexion: Pain/restriction? • Press on patella: Patellofemoral tenderness? Knee effusion?

• Metatarsal squeeze test: Evidence of synovitis? • Inspect soles for abnormal callosities: Evidence of abnormal weight bearing?

Spine Inspect whilst standing, from behind • Muscle bulk normal and symmetrical? • Is the spine straight? Inspect whilst standing, from the side • Normal lordosis? • Evidence of kyphosis? • ‘Bend forward to touch toes’: Lumbar spine flexion normal? • Press over midpoint of supraspinatus: Trigger point of fibromyalgia? Observe from front • ‘Tilt head towards shoulders’ Normal lateral neck flexion?

Documentation Clinical findings can be quickly recorded thus: G A L S

√ Appearance √ √ √

Movement √ √ √

A tick denotes a normal finding. If an abnormality is detected, the tick is replaced with a cross and further clinical details are documented under the chart. Motor strength can be graded according to the MRC grading system: 0 – no movement 1 – flicker perceptible in muscle 2 – movement only if gravity eliminated 3 – can move limb against gravity 4 – can move limb against gravity and some external resistance 5 – normal power.

‘Look, feel, move’ system Combining the GALS screen with the more detailed ‘look, feel, move (active, passive and restricted)’ system in regional problems will ensure that every patient with locomotor pathology is comprehensively and adequately assessed.

History and examination – an overview

Introduction

13


Imaging

4

The alignment of the femoral neck is all wrong. That leads your eye to the fracture line

X-ray Request Card Name

Write tidily

Address

Use sticky labels if possible

Imaging

Don't order views. Describe the side, area, and the diagnosis which needs excluding – put 'Please' at the end Give as much useful information as possible Put your name and contact details clearly

Clinical indications

Reading an X-ray 1 Check Name / Date / Side 2 Check margins. What is included, what not 3 Trace skin, soft tissues, fluid levels, looking for swelling or wasting 4 Trace outlines of bones for alignment and cortical discontinuities. Also check joints for thickness of joint space narrowing, sclerosis, cysts, and osteophytes (OA) or osteopaenia and erosions (RA) 5 Check inside of bone for lytic lesions and sclerosis 6 Check other views 7 Compare with any other (older) films for change over time

CT reconstruction of the lumbar spine showing a crush fracture of a vertebral body X-ray of bone tumour. Note the swelling visible within the soft tissues, as well as the change in the cortical margin

Prolapsed intervertebral disc pressing on nerve roots showing clearly on MRI Modalities of imaging Ultrasound Bounces sound off soft tissue interfaces

Use

Disadvantage

Dynamic visualisation of soft tissues

Cannot see through bone

Cheap. Shows bone outline well

Radiation dose. Not good on soft tissues

Enhances X-ray image allowing images of slices of tissue to be created improving detail and definition

Radiation dose Expensive

Shows soft tissues well No radiation

Expensive Claustrophobic

Plain X-ray Shines X-rays through tissues onto screen CT (computerised tomography) Reconstructs X-ray beams from many directions MRI (magnetic resonance imaging) MRI of same tumour confirms extent of tumour in the soft tissues

Strong magnetic field reverses radio signals emitted by tissues analysed

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. Š 2012 John Wiley & Sons, Ltd.

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Introduction A simple system for requesting and reading radiographs should ensure that you do not ever miss abnormalities. Initially X-Rays are hard to read because there are many ‘normal’ variants. Comparing the X-Ray you are studying with a picture of a normal case (these are available in books and on the web) will help distinguish normal from abnormal.

Requesting an X-ray examination Always fill in your forms tidily; remember there is no harm in adding ‘please’ to the request form. The radiographer and radiologist need to know where to find the patient and who to send the report to; they must be able to read these details. When requesting an examination that uses ionising radiation you are responsible for ensuring that the risk is worth the potential clinical benefit. If in doubt ask a radiologist. The radiographer is allowed to perform examinations only when the indications conform with written protocols and standard guidelines; for unusual examinations you will be asked to justify the exposure to a radiologist. As a general rule do not order specific views. It is the radiographer ’s job to decide on the views, based on the disease you want to prove or exclude. For example, if you want to exclude slipped upper femoral epiphysis in a child, the radiographer will perform special views to do this. The more information that you give about the history and examination, the better the report you are likely to get back from the radiologist.

Interpreting an X-ray examination As in all imaging, check the name, side and date. Check to see that there is more than one view and if there are any previous studies. Looking for changes over time is much more sensitive for identifying disease than looking at a single set of images. The following is one system for checking X-rays.

ment of the bones and joints taking into account the position the patient was in during the examination.

Review areas Before you finish, check the parts of the image that are important clinically and look specifically for the diseases that you are worried about. Then review the areas that you have found difficult in the past and those where others commonly make mistakes. Areas behind other structures such as the heart and the very edge of the image are examples, but your experience will create the most useful list.

Asking for help If you do not know what examination to request or how to interpret the images that you receive, take the problem to a radiologist and ask for help. They are often very shrewd clinicians and are invariably keen to help. Read the written reports and compare them with your findings; this provides a safety net and a learning opportunity.

Pros and cons of the different imaging methods Plain radiographs • They are quick and simple to organise. • They show bones well, but soft tissues are poorly seen. • They involve radiation and so should be used with caution.

Ultrasound • Ultrasound is very good at showing soft tissues, and can be used while the patient moves. This can be especially useful in studying sports injuries. • It does not use ionising radiation and is well tolerated by patients. • It does, however, require a highly skilled operator.

Computerised tomography (CT)

First check the margin of the images and decide which structures are included and, more importantly, which are not!

• This uses the highest doses of ionising radiation routinely encountered in diagnostic imaging but is better at showing soft tissue lesions than plain X-rays. • It also gives far better three-dimensional visualisation of structures in the body and shows fine details in cross-section.

Outlines

Magnetic resonance imaging (MRI)

Trace the skin outline and make sure this is normal, not swollen. Trace any lines in the soft tissues, looking for fluid levels and evidence of swelling or wasting of structures. Finally trace the edges of the bone margins, looking for steps or breaks in the cortex.

• MRI is very useful at showing soft tissues, especially oedema which may surround infections or tumours. • However, it cannot obtain a useful signal from healthy bone cortex and fracture lines may be difficult to see. • It does not involve ionising radiation, and gives good three-dimensional imaging. • Some patients cannot tolerate the confined space and others cannot be examined for safety reasons (pacemakers, etc.).

Coverage

Texture Check the bones, looking for lytic areas, coarsening of the trabeculae or loss of cortical/medullary differentiation. Finally, check the align-

Imaging

Introduction

15


Anatomy of the arm

5

Trapezius Pectoralis major (clavicular head)

Muscles Front

Vascular supply

Deltoid Pectoralis major (sternocostal head) Biceps Triceps (medial head) Brachialis

The palmar interossei

Brachioradialis

Back

Biceps tendon The dorsal interossei

Vein at elbow good for venesection

Pronator teres Flexor carpi radialis Palmaris longus

Back

Flexor pollicis longus Flexor carpi ulnaris Flexor digitorum superficialis

Flexor carpi ulnaris Anconeus

Ulnar artery Must be present if radial artery to be used to take blood gases

Extensor digitorum

Radial artery Good for blood gases and for checking pulse Constant vein at lateral side of wrist good for IV infusions

Extensor carpi ulnaris Extensor digiti minimi Extensor carpi radialis longus and brevis Abductor pollicis longus and extensor pollicis brevis Extensor retinaculum Anatomical snuffbox Extensor pollicis longus First dorsal interosseous

Front Palmaris longus Long flexor tendons Flexor carpi ulnaris Flexor retinaculum Flexor digiti minimi Abductor digiti minimi

Flexor pollicis longus Flexor carpi radialis Abductor pollicis longus Opponens pollicis Abductor pollicis brevis Flexor pollicis longus Flexor pollicis brevis Adductor pollicis

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. Š 2012 John Wiley & Sons, Ltd.

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Nerve supply

Bones and joints of the arm Scapular acromion Scapular coracoid process Humeral great tubercle Humeral lesser tubercle

C5 C6 C7 C8 T1 Brachial plexus injured in high-speed accidents when shoulder is forced down, e.g. in a motorcycle crash

Ulnar nerve on bone at back of elbow supplies sensation to little finger and small muscles of the fingers

Humeral head

Axillary nerve

Humeral coronoid fossa Humeral radial fossa Humeral lateral epicondyle Humeral capitulum Radius head

Humeral medial epicondyle Humeral trochlea

Radial nerve supplies extensor muscles Holds wrist steady when fingers flex

Median nerve passes through carpal tunnel at the front of the wrist Supplies sensation to thumb and most fingers and muscles to the thumb

Styloid process Lunate Triquetral

Tubercle of scaphoid Trapezium

Pisiform

Trapezoid Capitate

Hook of hamate Bones of the hand

Pisiform Triquetral Lunate Flexor retinaculum Scaphoid Figure adapted from Faiz, O. & Moffat, D. (2006) Anatomy at a Glance, 2nd Edition. Blackwell Publishing, Oxford

Function One of the great steps forward in human evolution was the freeing up of the forelimbs for using tools. The human hand is now primarily adapted to hold and manipulate objects. The arms have evolved to enable the hands to be accurately placed, and firmly held, in space in as many positions as possible.

median nerve) passes into the hand through the narrow carpal tunnel under the flexor retinaculum where it can be compressed (carpal tunnel syndrome). The other main nerve to the hand, the ulnar nerve, is also at risk for entrapment as it passes through a groove in the bones behind the medial side of the elbow joint. The digital nerves to the fingers are very easily injured by any penetrating wound to the hand or fingers.

Nerves The nerve supply to the upper limb arises from the lower cervical and upper thoracic spine (C3 to T3). The axillary nerve supplies the deltoid muscle and is commonly temporarily damaged following an anterior dislocation of the shoulder. One of the main nerves to the hand (the

Vessels The blood supply of the upper limb passes through the upper arm along a single artery, the brachial artery, so any damage to that artery from external trauma or an embolus will critically compromise the Anatomy of the arm

The arm

17


blood supply to the hand. Both nerves and vessels are easily damaged in the upper limb, but cannot be seen on X-ray, so always check distal neurovascular status whenever examining a limb. In the crease of the elbow (the antecubital fossa) there are large veins (easier to feel than to see), which are excellent for taking blood and for giving fluid in an emergency. At the wrist on the lateral (radial side) there is a large constant vein which is a favourite choice for siting the needle for an intravenous infusion. In the forearm the blood supply passes through a rigid muscle compartment (containing the flexor muscles of the forearm). Swelling in this compartment can produce a compartment syndrome (see Chapter 49. The radial artery can also be felt easily at the wrist as it passes over the front of the radial head. Its position makes it convenient for taking a pulse and for obtaining blood for arterial gas analysis.

The elbow joint allows the hand to bend up close to the shoulder or stretch out to the full length of the arm. It also contributes with the wrist joint to the complex manoeuvre where the radius and ulna bones fold across each other to allow the hand to rotate from pronation into supination. The large muscles controlling both the wrist and fingers arise on either side of the elbow joint, the extensors arising on the lateral side and the flexors from the medial epicondyle. At the wrist the radius has become the dominant bone, circling around the small ulna head to allow pronation and supination of the hand. The wrist joint is very mobile in all planes giving the hand further mobility. It is stabilised by the balanced contraction of the flexors against the extensor muscles.

The hand Movement The shoulder joint moves around on the end of a strut (the collar bone) with the scapula gliding over the muscles of the chest wall around the arc of a circle. The shoulder girdle and shoulder joint work together to produce a very large range of movement. The shoulder joint itself is a very open cup, compared with the hip joint, to allow this great range.

Anatomical relationships and pathology The head of the humerus is stabilised and controlled by a ring of muscles that all converge into a single sleeve of tendon enclosing the shoulder joint itself and inserting into the articular margin of the humerus. Part of this rotator cuff must slide under the acromion as it overhangs the joint. It is here that it is susceptible to rubbing, inflammation and pain. It can even tear, as its blood supply and hence capacity for repair is poor (see page 25). The radial nerve wraps itself closely around the shaft of the humerus as it winds down from the brachial plexus in the axilla to pass in front of the lateral side of the elbow joint. If the humerus is fractured, the nerve is easily damaged, and the patient will have a wrist drop.

18 The arm

Anatomy of the arm

The key to the anatomy of the hand is the thumb, which is able to rotate out of the line of the other fingers and oppose the other fingers. This allows the hand to power grip, manipulate a key or pick things up with the tips of the fingers. This dexterity relies on: • Sensation to the finger tips (to feel where things are). • Power in the muscles controlling the fingers and thumb (allowing them to open and then close around an object). • Proprioception (so that the brain knows where the hand is). • Mobility of the joints of the arms (to enable the hand to be put and then held where it is needed). Opposition of the thumb is controlled by muscles served by the median nerve, so damage to this nerve reduces the key role of the thumb in opposition. The intrinsic muscles of the hand are controlled by the ulnar nerve. These muscles allow the fingers to spread apart and for the fingers to remain straight while they bend at their base, a key requirement for picking things up with the finger tips. Any stiffness in the hand as a result of injury or inflammation or any loss of sensation has a quite disproportionate effect on the function of the hand.


6

History and examination of the arm

Thumb down test

– for impingement of the rotator cuff at the shoulder

Point if it hurts when I push down on your hand

There!

Supination Pronation Measuring pronation and supination with elbows against the side (to prevent shoulder movements)

Apprehension test

– for dislocated shoulder

Does it worry you when I push your arm back?

Uh! Oh! I don't like that!

Measuring extension and flexion of the wrists using the two sides for comparison

Flexor Digitorum Superficialis test Allen’s test A. Pressing firmly on both arteries, ask the patient to clench and unclench their fist several times Classic signs in the rheumatoid hand

B. When the hand opens the fingers should be white

Subluxation of metacarpophalangeal joints (MCPs) Ulnar drift of fingers on hand Radial drift of hand on wrist

C. Release pressure over the ulnar artery, Fingers should pink up if artery is present D. Repeat steps A and B but release pressure over radial artery to test patency

Swan-neck deformity of the fingers

Boutonnière deformity of the fingers

Dropped finger (ruptured extensor tendon)

Figure adapted from Faiz, O. & Moffat, D. (2006) Anatomy at a Glance, 2nd Edition. Blackwell Publishing, Oxford

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. © 2012 John Wiley & Sons, Ltd. Published 2012 by John Wiley & Sons, Ltd.

19


Introduction Problems in the upper limb may arise from nerve entrapment in the neck, so always check the neck when examining the upper limb. Do not forget to use both sides for comparison and to check distal neurovascular status.

History • In trauma a clear description of how the limb was injured will usually give the likely diagnosis. • In chronic problems, check for early morning pain and stiffness (inflammatory joint disease).

Look Shoulder The acromion (the point of the shoulder) is much more prominent when the shoulder has dislocated. Even after relocation the acromion may appear prominent again after some weeks as there is usually wasting of the deltoid muscle over the shoulder due to bruising of the axillary nerve. A prominent lump over the end of the clavicle is the result of injury to the acromioclavicular joint which may subluxate and then become arthritic.

Elbow Hard lumps may form on the back of the elbow (gouty tophi), also a favourite site for psoriasis (silvery scaly skin on the extensor surface). Any injury to the elbow tends to leave it stiff with loss of flexion and extension.

Wrist Swelling around the wrist is common in inflammatory joint disease.

Hand and fingers • Wasting of the base of the thumb occurs if there is damage to the median nerve, especially at the wrist. • Damage to the ulnar nerve produces wasting in the clefts between the fingers. • Inflammatory arthritis affects the hands in particular, producing a number of characteristic deformities (see Chapter 23). • Dupuytren’s contracture commonly affects the little and then the ring finger, curling them into the palm (see page 22).

Feel The clavicle, acromioclavicular joint and shoulder joint are close to the skin and so are easy to feel. Similarly the bones and joints of the elbow, wrist and hand can all be felt through the skin. Lumps and areas of tenderness can be identified and linked to the underlying anatomical structures. The ulnar nerve can be felt in the groove between the olecranon and the medial epicondyle at the back of the elbow. If it is tender and sends shock waves down the arm when pressed or tapped, it may be inflamed because it is getting trapped in the groove. Similarly the median nerve may get trapped at the wrist under the flexor retinaculum (see carpal tunnel syndrome below).

Move • Shoulder. The functional range of the shoulder can be checked by asking the patient to put their hands behind their head, then straight up, straight forward, out to the side and finally bring the hand up the back from below. Use both sides for comparison. 20 The arm

History and examination of the arm

• Elbow. If the arms are then held straight forward, flexion and extension of the elbows can be compared by watching the patient from the side. • Forearm. Finally, with the upper arms by the side and the forearms facing straight forward, pronation and supination of the forearm can be checked without the patient being able to use the shoulder to confuse the measurements. • Wrist. Wrist movements can be checked by asking the patient to get into a prayer position then to raise the elbows as far as possible. The exact opposite manoeuvre (pointing the fingers down) will check wrist flexion. • Finger. Finger movements can be checked quickly by first asking the patient to make a fist, then unroll the hand to a flat palm and then touch each finger tip to the tip of the thumb in turn. A trigger finger can be diagnosed by finding one finger is late in extending and then goes with a jump as the thickened flexor tendon (which can be felt) passes in to the narrow flexor tendon tunnel in the finger.

Resisted movements • The thumb down test is diagnostic of rotator cuff inflammation. The patient should hold the arms out straight with each arm facing 45 degrees forward of straight out sideways. The hand is set so that the thumb is pointing down. If there is a sharp pain in the shoulder when the examiner pushes the hand down against resistance then the test is positive. • The apprehension sign is a feeling of deep unease that patients feel when the shoulder is pushed into extension with the upper arm abducted and the forearm externally rotated. It is strong evidence that the shoulder has been dislocated in the past, and is still unstable. • Getting the patient to grip your fingers tests the power of both flexors and extensors of the wrist (as the fingers cannot flex properly unless the wrist can be held extended). • Testing the patient’s ability to spread their fingers apart checks the power of the intrinsic muscles of the hand (ulnar nerve).

Special tests In the case of suspected nerve damage you will need to plot areas of loss of sensation as well as weakness and wasting of individual muscles. Then, by reference to the distribution of impaired sensation, you should be able to work out which nerve(s) are damaged and at which level. Loss of sensation in the hand is best determined using two point discrimination, using the other side for comparison.

Carpal tunnel syndrome Tapping with your finger tip over the front of the patient’s wrist (where the median nerve passes under the flexor retinaculum) produces ‘electric shocks’ running down into the fingers if the median nerve is being compressed (Tinel’s test). Phalen’s test involves flexing the patient’s wrist while pressing hard on the median nerve at the front of the wrist. After 30 seconds the patient will find their fingers going numb.

Ulnar neuritis The ulnar nerve frequently gets trapped in the groove on the medial side of the elbow as it passes round the back of the joint. Pressure or tapping on the irritated nerve will produce electric shocks down the arm into the ulnar side of the hand. The most problematic of the carpal bones is the scaphoid whose blood supply enters the distal pole and tracks proximally. If a young person falls hard onto the outstetched hand the scaphoid can fracture


across its middle (the waist) compromising the blood supply to the proximal pole (see Chapter 9). The blood supply to the hand is usually via two arteries (the radial and the ulnar) which anastomose through a proximal and distal palmar arch. Arterial puncture for blood gas analysis can be performed from the radial artery, but first Allen’s test must be performed to check that the ulnar artery is functioning. Otherwise damage to the radial artery might compromise blood supply to the hand. The main nerves of sensation to the hand are the median nerve which supplies the radial three and one half fingers while the ulnar nerve supplies the little finger and half of the ring finger. The motor supply within the hand is mainly the ulnar nerve while the median nerve supplies the thenar eminence of the thumb (especially opponens). The flexor tendons travel up the fingers in sheaths. Inflammation can narrow the mouth of these flexor sheaths and lead to thickening of the flexor tendons (see trigger finger, Chapter 7).

The structures are so tightly packed in the hand that as a general rule if a flexor tendon to finger is cut it is very likely that the digital nerve has been cut too. It can be difficult to diagnose an isolated superficial tendon injury because the deep tendon travels right to insert in the distal phalanx. However flexor digitorum profundus is a mass action muscle, so its action can be blocked by holding the other fingers extended.

TIPS • The best veins at the elbow for taking blood are felt and not seen • The vein on the lateral side of the wrist is good for siting drips • Nerves and vessels lie close to bones and joints in the arm and are prone to injury • Stiffness in the hand produces severe disability • Always check distal neurovascular status

History and examination of the arm The arm

21


7

Problems presenting in the arm

Acromioclavicular joint arthritis

Rotator cuff impingement under acromion

Rotator cuff tear following trauma

Anterior dislocation of shoulder (tear of capsule) 'Frozen shoulder' Adhesive capsulitis

Ulnar nerve entrapment behind medial side of elbow Nerve is tender to palpation and percussion

Tennis elbow Inflammation of the insertion of the extensor muscles of the wrist

Flexor retinaculum

Vein

Trigger finger Thickening of the flexor tendon as it enters its sheath

Carpal tunnel contains median nerve and flexor tendons

Dupuytren's contracture Contracture of palmar fascia

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. Š 2012 John Wiley & Sons, Ltd.

22 Published 2012 by John Wiley & Sons, Ltd.


Shoulder Function Loss of shoulder movement severely compromises the function of the upper limb. A patient with limited mobility in the shoulder should, if possible, be able to put their hand behind the head to brush their hair, behind the back to wipe their bottom, and flex forward to bring their hand to the mouth to eat. Scars on the shoulder can be very disfiguring if they form keloid.

Presentation • Rotator cuff impingement. Several of the muscles around the shoulder insert into a cuff around the head of the humerus. This rotator cuff has a poor blood supply and its superior part (from supraspinatus) must pass through the narrow cleft between the head of the humerus and the acromion. The underside of the acromion becomes more beaked with age, and so the supraspinatus tendon may rub on the underside of the acromion producing a painful arc of movement. This can produce weakness as well as pain. The acromion can be trimmed back arthroscopically. Major tears in the rotator cuff can be repaired but as the blood supply is poor, unfortunately healing is not always good. • Frozen shoulder. Strenuous use of the shoulder (such as painting a ceiling) or injury to a shoulder can lead to the gradual onset of a frozen shoulder. Over a period of days and weeks the shoulder becomes stiffer and more painful until the pain dominates the patient’s sleeping and waking hours. The natural history of the condition is that over a period of months the pain and stiffness gradually improve until near full function is restored. There appears to be no treatment that can cure the condition or even hasten its recovery. • Arthritis of the shoulder (glenohumeral joint) is common and painful. Fusion of the joint leaves a fairly good range of movement because the scapula is so mobile on the thorax. A shoulder replacement should give pain relief and even better movement, but it will wear out in time.

Arthritis of the acromioclavicular joint The acromioclavicular joint is commonly injured following a fall onto the point of the shoulder, but the pain from this injury usually settles spontaneously in time. If the joint is then unstable, it may develop arthritis and produce a painful lump on the point of the shoulder. This interferes with rucksack straps. The joint can be excised without loss of function. This should relieve the pain.

Elbow Function The movements of the elbow are flexion, extension, and pronation and supination. If flexion is lost, the patient may not be able to bring the hand to their mouth. If extension is lost, they may not be able to reach things with the hand. Pronation and supination are crucial in positioning the hand, and loss of this movement significantly reduces the function of the upper limb. Cosmesis is a problem in the elbow if there is a growth abnormality and the elbow is left with a major varus or valgus deformity.

Presentation • Ulnar nerve entrapment. The ulnar nerve can become trapped in the cubital tunnel postero-medial to the elbow joint. If this occurs,

there may be numbness and wasting on the ulnar one and a half fingers of the hand and wasting of the interosseous muscles. The nerve can be released surgically. • Tennis elbow. A common problem, which produces pain in the elbow whenever the patient grips something, pronates their forearm or fully flexes the wrist. Each of these manoeuvres puts strain on the common extensor tendon origin on the lateral epicondyle of the elbow. A similar problem over the common flexor origin (medial epicondyle) is called Golfer’s elbow. Physiotherapy or local steroid injection sometimes helps. • Arthritis in the elbow is not uncommon, particularly in rheumatoid arthritis. If it is the radial head that is particularly painful, this can be removed, but elbow replacements are becoming increasingly successful and can produce a painless, strong and mobile elbow joint.

Wrist and hands Presentation • Arthritis in the wrist commonly follows trauma or inflammatory arthritis. Fusion of the wrist can be useful because it relieves pain, stabilises the joint and improves the strength of grip. • Carpal tunnel syndrome. Most common in middle-aged females and during pregnancy, the patients describe hanging their hand out of bed at night to relieve the pain and numbness. They also notice that they are clumsy, dropping things all the time. On examination there is wasting of the muscles at the base of the thumb, and loss of feeling in the thumb and first two fingers. Nerve conduction studies show the median nerve trapped at the wrist. Steroid injections and splinting may help but surgical decompression of the carpal tunnel will relieve symptoms more reliably.

Dupuytren’s contracture A contracture in the fascia in the palm of the hand draws the fingers into flexion (usually the little and ring finger). The condition runs in families. If caught early the tightening fascia can be removed surgically and function is returned to the hand. If it is left late, amputation of the obstructing fingers may be the only option.

Trigger finger Repeated trauma to the palm of the hand may lead to thickening of the flexor tendons to the fingers. They may then not be able to run freely in and out of the narrow mouth of the tunnels through which they pass from the palm into the finger. If this happens the finger jams (triggers), flexing with a click, then refusing to extend until helped when once again it triggers. Steroid injection may help. Surgical treatment merely involves opening the mouth of the tendon tunnel slightly.

TIPS • The shoulder frequently gets an impingement problem • The ulnar nerve (‘funny bone’) runs close behind the medial epicodyle of the elbow, where it is susceptible to injury • The median nerve can get trapped at the wrist—carpal tunnel syndrome • Trigger fingers look normal until the patient tries to move them

Problems presenting in the arm

The arm

23


8

Upper arm trauma

Injuries to the musculoskeletal system are commonly associated with injuries to nerve and blood supply, so always check distal neurovascular status

Most skeletal injuries are associated with a soft tissue injury—check for it

Injury: Anterior dislocation of shoulder Associated injury: Axillary nerve palsy and deltoid palsy

Injury: Supra-condylar fracture of humerus Associated injury: Tear of brachial artery, loss of circulation to lower arm and compartment sydrome

Injury: Fractured clavicle Associated injury: Tear of subclavian vein and haemothorax

Injury: Torn rotator cuff

Injury: Brachial plexus avulsion with paralysis of arm

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. Š 2012 John Wiley & Sons, Ltd.

24 Published 2012 by John Wiley & Sons, Ltd.


Introduction

Torn rotator cuff

The arm is most commonly injured in a fall when it is used to protect the head and face as well as cushion the fall. Never forget to check ABC (see page 94) for injuries elsewhere in the body, and distal neurovascular status. In high energy accidents (such as falls from a motorcycle) the brachial plexus may be torn. This is a devastating injury often leaving a useless arm and very severe causalgia-type pain. Conversely the clavicle is only a thin strut holding the shoulder complex out and away from the midline. It is therefore easy to break. However, it also heals quickly and has great powers of remodelling if there is a malunion. The joints at each end, especially the acromioclavicular joint, can also be subluxed or even dislocated.

A sudden force on the shoulder, such as a slip from a ladder, may put a large load through the muscles around the shoulder or on their common insertion into the rotator cuff. This will produce weakness in the power of abduction of the arm. In young patients these tears can be repaired surgically. However, in the elderly the poor blood supply and the weakening of the cuff may make a repair impossible to perform, so the patient may have to accept the disability.

Dislocation of the shoulder The shoulder joint itself allows a large range of movement and as a result is prone to dislocation. This is almost always anterior. The patient has frequently had the problem before and will tell you exactly what the diagnosis is, and even how it can be reduced quickly. Reduction is relatively simple immediately after the injury (the arm just needs to be pulled straight). Later, once muscle spasm has set in, strong analgesia or even an anaesthetic may be needed to get the shoulder back into joint. Treatment is then gentle mobilisation while waiting for the torn tissues around the shoulder joint to heal. If dislocations are repeated, surgery to repair the soft tissues around the shoulder may be needed. Any patient who has had a dislocation of the shoulder is liable to another. If the arm is put into the position in which the dislocation can occur (above their head and forced backwards) they will become very worried about what might happen next. This is known as an ‘apprehension sign’ (see page 19). Posterior dislocations are much rarer but are also easy to miss, since to the inexperienced eye the anteroposterior radiograph of the shoulder appears normal, and a lateral view may be difficult to obtain. However, the history is very characteristic as posterior dislocations are classically caused by epileptic fits, electric shocks and forced restraint in violent or psychotic patients. Once an index of suspicion is raised by the unusual history, the diagnosis on examination and investigation should be easier to make.

Fracture of the shaft of the humerus The radial nerve wraps closely around the shaft of the humerus in the spiral groove, so a displaced fracture of this part of the bone is likely to bruise or tear this nerve. Care also needs to be taken if it is decided to plate the fracture as this could trap and damage the nerve.

Elbow A fall on the outstretched arm can fracture the bones of the elbow. In children a fall out of a tree or off a swing can produce a greenstick fracture of the distal radius. But it can also fracture the proximal end of the radius where the bone is driven onto the end of the humerus. The blood in the elbow joint produces a tense painful effusion which can easily be relieved by aspiration and injection of some local anaesthetic. If the radial head is too badly crushed for repair it may need removing, and can be replaced with an artificial one. A more sinister fracture after the same type of fall occurs in the humerus just above the elbow joint. This is a supracondylar fracture of the humerus, common in children. The brachial artery lies immediately in front of the bone at this point so this can be damaged by a spike of bone. Bleeding can also track down into the forearm muscles raising the pressure in this compartment. When the fracture is reduced, it is best held in plaster with the elbow flexed up as much as possible. If there is any more bleeding, then either the dressing or the fascia of the forearm muscle itself can produce a compartment syndrome (see Chapter 49). The circulation to the hand, and the ease with which the fingers can be extended, needs to be carefully monitored for at least 12 hours. If there is any suggestion of circulatory compromise then the plaster must be removed, and if that does not lead to a rapid improvement, an urgent fasciotomy will be needed.

Fractured head and neck of the humerus This injury is commonest in the elderly who have osteoporosis. If the fragments have lost their blood supply or cannot be reduced to create a useful joint surface, a shoulder joint replacement may be the best treatment. A similar explosive fracture can occur at the lower end of the humerus in the elbow joint. The same treatment principles apply. The axillary nerve is close and once again may be injured.

Forearm The radius and ulna can be broken by a twisting fall. As the two bones work together to produce pronation and supination, it is important to obtain an accurate reduction and fixation if full movement is to return. This is best obtained with open reduction and internal fixation.

Upper arm trauma The arm

25


Lower arm trauma

9

Injury Fracture of scaphoid bone Complication Avascular necrosis of scaphoid as a result of damage to blood supply

Injury Fracture of distal radius (Colles' fracture) Associated occasional soft tissue injury: Acute compression of median nerve (carpal tunnel syndrome) Avascular rupture of extensor tendon of thumb

Injury Fractures of phalanges need careful reduction and rehabilitation to prevent deformity and stiffness compromising dexterity Associated occasional soft tissue injury: Stiffness

Injury Cut flexor tendon of finger Associated occasional soft tissue injury: Damage to digital nerve, artery and vein

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. Š 2012 John Wiley & Sons, Ltd.

26 Published 2012 by John Wiley & Sons, Ltd.


Introduction Trauma to the hand is common but also important because it can cause cosmetic and functional damage out of all proportion to the severity of the initial injury.

History and examination Both will be important in determining the structures likely to have been injured. A stabbing injury may damage a nerve, while a crushing injury could lead to a compartment syndrome in the intrinsic muscles. Distal neurovascular status must always be tested as nerve damage is easy to miss.

Falls on the hand These can injure structures all the way down the arm (see Chapter 8) but most commonly affect the writst. Fractures of the distal radius are very common, especially in the elderly with osteoporosis. The fracture produces a classic ‘dinner fork’-type deformity (the Colles’ fracture). Because the bones are crushed together, the fracture is stable. So, if it is decided to leave the fracture as it is rather than reduce it, a soft removable splint for comfort may be all that is needed. This will be much easier for the patient to cope with than the heavy plaster that is needed for many weeks if the fracture is reduced and so made unstable. A distal radial fracture in the non-elderly is a very different injury and should not be called a Colles’ fracture. It is a high velocity injury in hard bone where the fracture enters the joint and is unstable. This fracture almost certainly needs open reduction with internal fixation using a moulded plate if stiffness and arthritis in the joint are to be avoided. Falls may also damage the carpal bones. The commonest of these results in tenderness over the base of the thumb, and is the result of a scaphoid fracture. The diagnosis is important because a fracture across the waist of this bone may lead to avascular necrosis of the proximal pole. Unfortunately the fracture is not always visible on the initial X-rays, so treatment may need to be started on the basis of suspicion rather than proof. If the bone is still tender after a week to 10 days of immobilisation, then a further set of X-rays at this time will be much more reliable, because if there is a fracture the cleft will now be more open. Even if the scaphoid is not broken, the ligaments between the carpal bones can be torn and the bones themselves subluxed or dislocated. The X-rays can be tricky to interpret so if there is severe pain and swelling in the wrist and no obvious fracture, an expert opinion should be sought.

Cuts Cuts in the hand can easily damage nerves, vessels and tendons. They can also leave foreign bodies in the hand that can be difficult to see by eye or on X-ray. The pain, swelling and bleeding can make examination very difficult. Very careful examination is needed to exclude digital nerve damage. If there is any possibility of a retained foreign body or damage to tendons, end vessels or nerves, formal exploration will need to be

undertaken with a tourniquet to control bleeding, a regional or general anaesthetic and time to perform any repairs. This will be best performed in an operating theatre, where a clear view can be obtained. Nerves will need repairing under a microscope and tendons will need moving as soon as possible after repair to avoid adhesions. Extensor tendons are much easier to repair than flexor tendons and tend to move better afterwards. Flexor tendons run in fibrous tunnels into the fingers. If a cut tendon is repaired where it runs in these tunnels the join tends to jam in the narrow tunnel and scar tissue forms preventing all movement. Tendon grafts are needed to move the site of the repair out of the danger zones and into the palm where mobilisation is possible.

Fractures of the metacarpals and phalanges Carpal dislocations. These are caused by high energy falls on the outstretched wrist, and disrupt the ligaments holding the arches of the carpal bones. Most commonly the lunate bone pops out of the line. The wrist is always very swollen and the X-rays are not easily interpreted so the injury is often missed. Reduction of the displaced bones is vital if hand function is to be restored. Metacarpal head fractures caused by punching can usually be left unreduced as they are stable and cause no functional problem. However, spiral phalangeal fractures need careful reduction and holding. The fracture is unstable, and the fingers will tangle in flexion if malunion occurs.

Swelling and stiffness These are the two enemies of rehabilitation of hand injuries: swelling leads to stiffness and stiffness prevents swelling from being pumped away, so they work together. Elevation is used to reduce swelling as quickly as possible, and movement is also started as soon as safe. A lively (dynamic) splint is useful in flexor tendon repairs as it uses an elastic band to flex the finger against the extensor tendon, in place of the repaired tendon. This allows the finger to be kept moving without any force being put through the freshly repaired flexor tendon.

Amputations Traumatic amputations of fingers and even hands can be repaired, but only if the amputation occurred with a clean sharp cut, and the amputated parts can be put back quickly. Even then, it may be better to tidy up an amputation stump and concentrate on getting the individual back to work quickly rather than going through the months of rehabilitation needed for a re-implanted limb when the outcome may be uncertain. The exception to this rule is the thumb where every effort must be made to preserve as much length as possible because of its vital role in hand function.

Rehabilitation Swelling of the hand as a result of trauma (especially crushing) can lead to stiffness and poor function of the hand. Early aggressive rehabilitation needs to be started to reduce swelling as quickly as possible and avoid the onset of stiffness in the joints of the hand.

Lower arm trauma The arm

27


10

Anatomy of the spine

Curves

Typical vertebral units from the side and in transverse section

Cervical lordosis

Facet joint

Thoracic kyphosis

Disc Annular ligament

Damage here produces upper motor neuron presentation (flaccidity followed by spasticity)

Spinal cord stops at L1 Lumbar lordosis

Intervertebral foramen (nerve root)

Nerve roots only (cauda equina) Damage here produces lower motor neuron signs only

Non-skeletal causes of backache Brain – psychiatric disorder Oesophageal tumour or injury Pleurisy and pulmonary embolus Mesothelioma Dissecting aortic aneurysm

Spine

Vertebral body

Facet joint

Pedicle

Musculo-skeletal causes

Dermatomes

Muscle strain/spasm Prolapsed disc Infected disc (discitis) Myeloma Metastases Shingles

C2 C2 C4 T2

Stomach cancer C5 T1

Perforating ulcer Shingles Pancreatitis

T3 T4 T5 T6 T7 T8 T9 T10 T11 T12 L1

C4

T3 T4 T5 T6 T7 T8 T9 T10 T11 S1 T12 L1 S3 S4 S5

Myocardial infarct

Renal infection or stones

C3

C3

C6 C7 C8

Ovarian problems

T2 C5 T1 C6 C7

L2 C8

L2

Pelvic inflammatory disease Testicular problems L3

L3

S2

L4

L5

S1

L5

L4

S1 L5

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. Š 2012 John Wiley & Sons, Ltd.

28 Published 2012 by John Wiley & Sons, Ltd.


Function The spine is the axial skeleton. It supports the head and the upper limbs, acts as a posterior strut for the thorax and abdomen and at its base locks into the pelvic girdle. It also acts as the conduit for nerve fibres travelling to and from the brain to the rest of the body.

Upper and lower motor neuron lesions The upper part of the spine (above the first lumbar vertebra) also contains the spinal cord (not just roots) and so is an extension of the central nervous system. Problems in this part of the spine may produce upper motor neuron signs with up-going plantar reflexes and spasticity. Below the first lumbar vertebra, obstruction of the spinal canal can only produce lower motor neuron signs, weakness and wasting combined with sensory loss.

Curves The healthy spine has three natural curves: 1 The cervical spine is concave (hollow) when looked at from behind. The lowest cervical vertebra has a prominent spine which can be clearly felt and seen on X-ray. 2 The thoracic spine is convex. 3 The lumbar spine is once again hollow. The transition between the thoracic and lumbar spine is more difficult to localise. These curves are in part a result of the shape of the bones making up the spine, but are also maintained by the tone of the muscles around the spine. Loss of, or indeed exaggeration of, these curves is suggestive of an underlying disease process.

Vertebrae The spine is made of seven cervical, 12 thoracic and normally five lumbar vertebrae. The front part of each vertebra is solid (the body) and is the load-bearing part of the structure. Immediately behind the bodies of the vertebrae there is a hollow canal that contains the spinal cord (in the upper spine), but only nerve roots (the cauda equina) in the lumbar spine. The back wall of the canal is a thin layer of bone (the laminae) with a prominent crest in the midline (the spinous process) to which the powerful muscles running down the back of the spine are attached. At the sides, between the vertebral body and the laminae, there are struts connecting the vertebral bodies to the lamellae. Arising from these pedicles are facet joints which are also joints connecting the vertebrae. Right beside these facet joints at each level there are gaps (foramina) through which nerves pass out of the spinal canal. The nerves are named by the level at which they leave and are found to supply quite constant areas of skin (dermatomes) and muscles (sclerotomes).

Between the main vertebral bodies there are intervertebral discs – an outer strong fibrous ring (annulus fibrosus) enclosing a gel-filled dural sack (nucleus pulposus) to create a shock absorber which, combined with the facet joints, allows a little bending and twisting between each vertebral body. When the little movement between each vertebral body is summed over all the vertebrae, the flexibility of the spine in some parts is large. In the cervical spine the neck can flex and rotate. The thoracic spine is relatively rigid, while the lumbar spine flexes but does not allow rotation. The proximity of the spinal nerve roots in their dural sacs to the intervertebral disc, and the proximity of individual nerve roots leaving the spinal canal to the facet joint at that level, makes nerve roots vulnerable to compression if either of these structures are damaged or diseased (see Chapter 12).

Trauma to the spinal cord Significant trauma to the neck or spine usually requires quite high energy. If the displacement of the vertebrae is small, then the only injury may be tears of the ligaments, or fractures and even dislocation of the facet joints. But if the displacement is greater in the upper part of the spine, then the spinal cord may be injured or even transected. Nerves in the central nervous system have a very limited power of healing and so injuries tend to be irreversible. However, things are not always as bad as they first seem, as the initial trauma to the spinal cord is accompanied by spinal shock (the equivalent of concussion) which wears off after 24–48 hours. It is only then that the first clue to the likely severity of the permanent damage can be obtained. The first clue that the prognosis may be good is sacral sparing (preservation of the function of the sacral roots which supply the skin around the anus and the anal sphincter).

Backache Backache is common, indeed it is probably true to say that everyone has backache at some time in their lives. The problem is that it is not just the spine which can cause backache. Pancreatitis, pleurisy, a dissecting aortic aneurysm, pyelonephritis, psychiatric disorders, ovarian cysts and testicular tumours can all present with back pain, to name but a few. To make the situation even more complicated, pathology in the back may produce pain referred to the legs or arms, or even frank neurology far from the spine in the case of nerve root entrapment. As a simple rule, always check the neck if there appears to be a problem in the upper limbs and the lumbar spine if the patient presents with problems in the legs.

Anatomy of the spine

The spine

29


11

History and examination of the spine

Measuring movements of the spine

Lateral deviation

Rotation

Flexion

“Bend forward and try to touch your toes. Don't go further than is comfortable”

“Now slide your hand down the side of your leg, as far as it will go”

“Keep your hips still and now twist your shoulders around as far as they will go”

Straight leg test 1. Flex up the leg – checks movement of hip joint

1b. Now straighten the knee letting the hip extend as little as possible

2. Check pain from tight hamstrings

3. Dorsiflexion of ankle now pulls on sciatic nerve alone

2b. Now let the hip extend 10 degrees more to relieve pain caused by tight hamstrings

3b. Pain down the leg as the foot is dorsiflexed by the examining doctor means the test is positive

Red flags in back ache (warnings of possible severe pathology) For fracture, infection or malignancy History High energy trauma Minor injuries in people known to have osteoporosis New episode of back pain in someone over 50 years old or under 20 Previous cancer Generally unwell, e.g. fever, chills, unexplained weight loss Recent infection especially urinary tract Intravenous drug abuse Immunosuppressed Night pain. Pain that is worse when lying flat. Pain in the thoracic spine

Yellow flags (significant psychological component in back ache) Belief that backache is harmful and/or potentially disabling Fear/avoidance behaviour and reduced activity levels Low mood and withdrawal from social interaction Passivity in approach to treatment Keep from away surgeons

Needs early referral to surgeons

Examination Deformity For cauda equina syndrome or rapidly progressing neurological deficit History Saddle anaesthesia (numbness on the inside of the thighs and around the perineum) Recent onset of problems passing urine (e.g. urine retention, increased frequency, overflow incontinence, and inability to feel urine passing) Recent onset of faecal incontinence Examination

Cauda equina

Immediate referral to surgeons

Severe or progressive loss of sensation in the lower limbs (often both) Unexpected laxity of the anal sphincter when a rectal examination is performed Perianal/perineal sensory loss Major motor weakness: knee extension, ankle plantar eversion, foot dorsiflexion

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30 Published 2012 by John Wiley & Sons, Ltd.


History All patients must have had backache at some time in their lives. Check with them how this episode differs from any others, as this may reveal signs of sinister causes such as infection, fracture, tumour or critical nerve damage. The warning signs in the history and examination are called ‘red flags’ and are designed to alert you to sinister pathology. ‘Yellow flags’ are features that suggest that a psychological approach to the management of the backache will be more useful than a standard organic one (see figure opposite).

Examination Exposure The cervical spine can only be seen if the patient’s hair is well out of the way. The bottom of the spine can be hidden by the top of the trousers. In trauma it is critical that the whole spine is examined, but the patient must be turned carefully (log-rolled) to avoid causing any further damage to the spinal cord in patients who may have an unstable fracture dislocation of the spine.

Look Check for the normal curves of the spine and that there are no lateral curves. A hairy dimple at the base of the spine (hidden by the top of the pants) may indicate a partial failure of closure of the spinal canal (spina bifida occulta) which can trap nerve roots. If there is a lateral curve of the spine and it vanishes when the patient sits on the couch, then the curve is probably caused by unequal leg lengths. If the curve gets worse as the patient bends forward (producing a rib-hump) then it is likely to be an idiopathic scoliosis.

Feel The spine can be felt through its length posteriorly. A full abdominal examination is important because back pain can be the presenting sign of many non-orthopaedic problems. Sensory loss as a result of a spine problem will be most likely in the legs or in the perineum (see section on central discs, page 33).

Move Examination of spinal movement is best performed with the patient standing whenever possible. • Flexion of the spine can be checked by asking the patient to touch their toes. The examiner should have the tip of their thumb on the top

of the lumbar spine and the index finger on the lumbosacral junction, so that the actual movement of the spine (not just flexion of the hips) can be recorded. • Lateral deviation can be tested by asking the patient to slide the flats of their hands down their thighs. • Rotation can be checked by holding the patient’s pelvis still and then asking them to bend and look over their shoulders.

Straight leg raise test Pain in the back commonly radiates down the leg and so can be difficult to distinguish from pain arising from the hip and knee. The straight leg raise test is designed to do this. • The patient lies on their back and first the hip is flexed up with the knee flexed too. If there is no pain during this manoeuvre then it is unlikely that any pain is arising from the hip or knee. • The knee is then straightened and most patients will then experience pain in the back of the thigh as the hamstring muscles tighten. • The leg is then gently extended until the hamstrings are relaxed and the patient is again pain-free. At this point the ankle is firmly dorsiflexed. If this reproduces the back pain running down the leg, it is assumed that the sciatic nerve roots are trapped as they leave the spinal canal, and the test is recorded as positive.

Reflexes and muscle power The decision as to whether a nerve root is trapped is a critical one to the success of spine surgery. Sensory and motor loss at the same nerve level, confirmed by imaging evidence of entrapment of that root as it exits the spinal canal, is a very good prognosticator for the success of surgery. The knee reflex is mainly served by the L4 nerve root, while the muscle extensor hallucis longus is exclusively supplied by the L5 nerve root. The ankle reflex is mainly mediated through the S1 nerve root. These tests are therefore useful for defining the level of a lesion. TIPS • Every one gets backache – most get better spontaneously • Backache can arise from a multitude of different sources • Symptoms in the arms can arise from problems in the neck • Symptoms in the legs can arise from problems in the lumbar spine • The spinal cord only extends down to L1 so problems in the spine below this level only produce lower motor neuron signs

History and examination of the spine

The spine

31


Problems presenting in the spine

12

Central disc

Sinister backache Myeloma deposits or secondaries from prostate, kidney or breast ± collapse Infection in the disc possibly from urinary tract Deep and unremitting pain keeps patient awake at night ± Low grade fever Indications for surgery of prolapsed disc

i. Saddle anaesthesia Sudden onset in young people Numbness in the perineum and inside of thigh Loss of anal tone

e.g. L5

THIS IS AN EMERGENCY

ii. Views of spinal canal with central disc pressing on nerve roots MRI shows complete occlusion of the spinal cord by a large central disc Treatment is urgent decompression, otherwise permanent incontinence will result

1. Sensory loss over a dermatome e.g. L5 weak extensor hallucis longus

Persistent backache after exercise

– spondylolisthesis – stress fracture of spinal pedicle

2. Motor loss on same side and at same level

Facet joint Normal nerve root leaves through spinal foramen

L5 root crushed by disc protrusion as it exits through spinal canal

3. Imaging confirms disc pressing on nerve root at same level and on same side

Neck Function The neck is highly mobile. It is highly susceptible to injury because the weight of the head creates large forces in high energy accidents.

Presentation • Cervical spondylosis (arthritis) presents with stiffness and painful spasm in the neck muscles. However, there can also be numbness and

Spondylolisthesis can be likened to the collar or broken neck of an illusionary 'scotty dog' as seen on oblique X-rays

pain running down the arm. If the cause is shown to be nerve roots trapped by osteophytes, and the symptoms are disabling, surgery may need to be considered. Whenever you see a patient with a problem in the upper limb, examine the neck as this may give you a key to the origin of the problem. • Rheumatoid arthritis. In rheumatoid arthritis, the facet joints may be eroded away to such an extent that the neck becomes unstable. When a patient is being intubated, the spinal cord may be damaged

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by excessive extension. It is therefore important to always inform an anaesthetist of a patient with rheumatoid arthritis so that they can ensure that suitable precautions are taken.

Thoracic spine Function The thoracic spine is a support for the neck and upper limbs. It moves very little apart from allowing the ribs to move and the lungs to expand during inspiration.

• Spondylolisthesis. In this condition, a fracture occurs in the pedicles of the L5 vertebra, allowing it to slip forward on the sacrum. On examination a step is palpable at the base of the spine. It produces backache and, if the slip is severe, there may even be sciatica with nerve root compression. Treatment is difficult as the slip cannot be reduced easily. If surgery is considered the goal is limited to fusing the vertebrae so that the slip does not proceed further.

Cauda equina syndrome or central prolapse of the disc

Presentation

History

• Crush fractures can occur in osteoporotic patients after a fall. Myeloma and secondaries can produce lytic lesions, which may also collapse. • Shingles. Herpes zoster (shingles) may cause severe pain in the dermatome of an intercostal nerve. • Ankylosing spondylitis may produce severe stiffness of the spine, which restricts vital capacity and may also cause a progressive flexion deformity (see Chapter 25). • Scoliosis is commonly a growth abnormality of the spine, which develops during adolescence in children of tall parents, who are growing fast. It leads to rotation and then curvature of the spine, which produces a characteristic hunchback. It is much more noticeable as soon as the patient bends forward to touch their toes. If the curvature looks as if it is going to become severe, surgery may be needed to straighten and fuse the spine, so limiting the deformity.

In young people (especially women just after having children), an intervertebral disc may rupture quite suddenly and without warning. It may then extrude all its contents into the spinal canal in one catastrophic event. There may be no pain, because there is no time for the nerve roots to become inflamed, so the presentation may not be like other types of prolapsed intervertebral discs. Instead, the patient experiences numbness down the inside of both legs (the sensory distribution of the sacral nerve roots) and may have the peculiar feeling of not knowing when they are passing urine or opening their bowels, as well as being frankly incontinent (see section on red flags, Chapter 11). There may or may not be pain, and there may or may not be urinary and bowel symptoms.

Causes of backache • Simple mechanical low back pain. Low back pain or lumbago is a vicious circle of muscle spasm creating pain, which in turn creates more muscle spasm. Most backache will get better whatever you do, but alternative medicine is useful because it seems to be good at breaking this pain cycle. • Sciatica. If pain only radiates as far as the knee, then it is usually assumed that this is referred pain (the origin is in the back). If, however, the pain goes right down into the foot, then it is likely that this is nerve root irritation, possibly caused by a prolapsed intervertebral disc. The differential diagnosis however is of tumour, and infection, although both are much rarer. • Sinister backache. Backache that keeps patients awake at night may be due to an infection (discitis) or a tumour (myeloma or a secondary). It is usually associated with a low grade fever, and the patient feels generally unwell. • Prolapsed intervertebral disc. If the contents of the disc, the nucleus pulposus, prolapse through a rupture in the annulus (the tough ring enclosing the pulposus), then there may be pressure and rubbing of the nerve roots and an inflammatory reaction may be set up. This causes sciatica. In over 90% of cases the inflammation dies down in time. Therefore, the condition should be allowed to take its natural course if possible. The patient will need pain relief – any measure that might help with the muscle spasm such as osteopathy, acupuncture, aromatherapy etc. can be used. The straight leg raise test will be positive (as the nerve roots are irritated). If a patient has sensory loss or motor weakness in the distribution of a lumbar root, then they need urgent referral to an orthopaedic surgeon, where a decision can be made about whether decompression is appropriate to save the compressed nerve. The commonest nerve roots to be affected are L5 and S1.

Examination On examination the patient will have numbness around the perineum and the inside of the thigh (saddle anaesthesia). Anal tone may be absent on rectal examination, so the patient is not able to contract the anal sphincter onto the examiner ’s finger. Straight leg raise may be reduced and if it is, then it is bilateral. Indeed one of the cardinal signs of a possible central disc prolapse is bilateral signs.

Investigation and treatment If in doubt, then you should assume that a central disc is possible. The best investigation is an MRI followed by surgical decompression if the diagnosis is confirmed. The operation involves removing the disc which is pressing on the nerve roots. This is a surgical emergency and, even if decompression is undertaken within hours, the patient may be left permanently incontinent. Immediate surgery is needed to relieve the pressure on the nerve roots. The sooner the pressure is relieved, the better the chance of a good recovery being made.

TIPS • Rheumatoid patients with neck involvement need care when being intubated • Most simple mechanical backache gets better on its own • Evidence of nerve root compression requires investigation • Backache at night may be due to an infection or tumour • Alternative medicine relieves the pain cycle caused by muscle spasm • Central disc prolapse is a true surgical emergency • Saddle anaesthesia and loss of anal tone are diagnostic of central disc prolapse • Urgent imaging and decompression offer the only hope of recovery from central disc prolapse

Problems presenting in the spine The spine

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13

Trauma of the spine

Patients with a suspected broken back must only be moved on a spine board to prevent bending or twisting so avoiding the risk of further damage to the spinal cord (high) or nerve roots (low)

Sepsis from infected catheter

Injured person immobilised on a spine board

Bed sores Patients with neurological damage to the spine need catheterising and turning regularly. Ascending urinary tract infection and infection from bed sores are an avoidable cause of morbidity and mortality in spinal injuries

Whiplash

Spinal injury

Whiplash (neck hyperextended then flexed)

Upper motor neurone lesions – spasticity

High cervical lesion C3, 4, 5 will paralyse the diaphragm so the patient will need assistance with breathing Urinary catheter needed for loss of bladder control but is a route for urinary tract infection which may lead to pyelonephritis and death

T12–L1

Migraine – late symptoms in eye

Lower motor neurone lesions – flaccid paralysis

Headache Ringing in the ears

Preservation of sensation around the anus is a good prognostic sign

Pain in the jaw when chewing Pain and stiffness in the neck

Introduction • Problems with spine trauma can vary from a back sprained when lifting, through to permanent paralysis as a result of transection of the cord. • Most serious spinal injuries are avoidable. Tougher safety regulations in heavy industries like mining, compulsory seat belts, roll-over bars on tractors and stricter rules in sport have all contributed to a dramatic fall in the number of these injuries in the developed world. • All unconscious patients and any patient involved in a high energy accident should be assumed to have a spinal injury until otherwise

Bedsores leading to infection and septicaemia are a potentially lethal complication of loss of sensation

proven. These cases are therefore best transferred to hospital on a spine board with extra protection for the cervical spine.

Minor injuries Most people will experience backache at least once in their life as a result of trauma. After the initial injury the bulk of the pain is thought to come from muscle spasm, so any method that can break the vicious cycle of spasm causing pain which causes further spasm, will bring symptomatic relief. This could involve physiotherapy and/or the use of simple analgesics such as paracetamol with ibuprofen. Alternative

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medicine such as osteopathy, chiropractic and acupuncture can all help by reducing the pain arising from muscle spasm.

Spinal fractures with significant neurological damage

This is a little understood but very common condition in the neck and back of patients who have suffered spinal trauma. The classic presentation is following a car crash where the patient has been struck from behind and the neck has presumably been first hyperextended and then hyperflexed by the energy of the impact. The condition can be late in onset and may affect the head (giving occipital headaches), the jaw (affecting the temporomandibular joint), the ear (producing tinnitus) and even the eyes (producing migraine-like symptoms). It usually settles over a period of months, but has a poor prognosis if it persists for more than 2 years.

• In the first days great care is taken with turning and moving the patient, at least until the spine is stable, to avoid further nerve damage. • The bladder will not be functioning so the patient will need catheterisation under the most sterile possible conditions, as ascending urinary tract infection is a dangerous complication. • The patient needs to be turned regularly to prevent bed sores from forming. Once they have occurred they are very difficult to heal and are another source of potential infection and septicaemia. • From a psychological point of view the patient needs to be started into a rehabilitation programme as quickly as possible, preparing them to return to as independent a life as possible. • Joints need to be kept mobile to avoid contractures.

Crush fracture of the spine

Outcome of spinal injury involving neurological damage

Whiplash

This usually occurs in elderly osteoporotic patients who slip and land on their bottoms, sending a compressive force up the spine. The vertebrae buckle (commonly in the thoracic zone). The fracture is stable but can cause severe pain while healing and even afterwards.

Initial spinal shock may produce almost complete sensory loss and flaccid paralysis, but perineal sparing suggests good prognosis. Maximum recovery may take several years.

Fractures of the spine in younger people These can be divided into those which are stable and those which are not, and those involving damage to the spinal cord or nerve roots and those where they are spared. The extent of neurological damage can be very difficult to assess in the first instance because spinal shock (the equivalent of concussion) may give the appearance of a complete transection of the cord. However, the first sign of recovery may be some sparing of the sacral nerves, with return of sensation around the perineum. If there is no central sparing, then within a few days flaccid paralysis may be replaced by spasticity, an ominous sign that the spinal reflexes are dissociated from the higher centres. If a spinal fracture is unstable it is now commonly felt that the spine should be stabilised whether there is neurological sparing or not. Rehabilitation will be quicker whatever the neurological outcome if the spine is stable. Stable spinal fractures may be explored if there is neurological compromise and it is felt that decompression of the spinal canal might help recovery.

Level of lesion

Residual deficit if transection is complete

High cervical

If the patient survives, they will need a ventilator to breathe Spastic paralysis of the upper and lower limbs = quadriplegia

Low cervical

Breathing is spared Some use of the arms but the hands are worse affected

Thoracic

Upper limbs are spared but there is spastic paralysis of the legs May not be able to sit unaided

Lumbar

Should be able to sit Flaccid paralysis in the lower limbs

Trauma of the spine

The spine

35


Anatomy of the leg

14

Muscles

Front

Back

Nerve supply Gluteal buttock muscles: ideal for injections

Quadriceps muscles: wastes after a knee injury Rectus femoris Vastus intermedius Vastus lateralis Vastus medialis

Femoral nerve Useful site for nerve blocks for knee and front of knee

Hamstring muscles: tear in sportsmen Semimembranosus muscle Semitendinosus muscle Biceps femoris muscle

Distribution of femoral nerve

Tibialis anterior: gets inflamed after heavy exercise Extensor hallucis longus: supplied solely by the L5 nerve root

Common peroneal nerve can be damaged by pressure on operating table

Front

Back

S1 root prolapsed into vertebral disc leads to weak big toe and nerve Sciatic nerve runs behind hip joint. Can be damaged by intra-muscular injection, hip dislocation or hip replacement Distribution of sciatic nerve

Lateral popliteal nerve = Common peroneal nerve

Calf muscle – Gastrocnemius: covers deep muscle compartments which are susceptible to compartment syndrome Achilles tendon: ruptures in the middle-aged

Digital nerves can be trapped between the metatarsal heads producing Morton's neuroma

Function The lower limbs are designed to allow a human to move efficiently over rough ground. • The pelvis acts as a platform for the spine and trunk. • The hip joints are clothed in powerful muscles and have restricted movement compared with the shoulder girdle. • The knees have even more restricted mobility to allow the efficient transfer of force from the foot to the body.

• The foot itself is light for energy-efficient movement, but nevertheless is a complex of joints, which allow the sole of the foot to grip and conform to uneven ground.

Nerves The femoral nerve supplies mainly the front of the upper leg; the sciatic nerve supplies the back of the thigh, then the whole of the lower leg and foot. The sciatic nerve is susceptible to injury as it passes

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Vascular supply

Front

The popliteal artery is vulnerable to damage behind the knee due to dislocation of the knee or knee surgery. The long saphenous vein is a constant feature one finger ’s breadth in front of and above the medial malleolus of the ankle, a useful site for venous access.

Back

Hip

Femoral artery at groin. Suitable for obtaining blood gases

The hip joint is a deep ball and socket, which can only develop normally if the femoral head is securely in joint. Otherwise a dysplastic or even a frankly dislocated hip develops. The femoral head relies almost totally for its nourishment on vessels which run up through the femoral neck. If this blood supply is interrupted the femoral head has little or no capacity to recover and dies. A displaced fracture across the upper femoral neck (sub-capital fracture) commonly does this in the elderly.

Knee

Popliteal artery behind the knee can be torn in a dislocation of the knee

Saphenous vein in front of medial malleolus useful for intravenous access using a cut-down

Dorsal pedis artery. Pulse can be felt on front of foot

The knee joint is especially susceptible to injury because of the extreme forces applied to it in modern sport. The knee cap (patella) transmits the forces of the quadriceps muscle over the front of the knee. The patella runs in a shallow groove, which makes it susceptible to dislocation. The cruciate ligaments inside the knee control forward and backward glide of the femur on the tibia. They lack an adequate blood supply to heal themselves. The knee, like the hip, is susceptible to developing osteoarthritis in the elderly, especially on the inside (medial compartment) where most of the load is taken. Pronation and supination in the lower leg has been lost as the lower limb evolved towards being rigid for more efficient energy transmission.

Ankle Posterior tibial artery. Pulse can be felt behind the medial malleolus

The ankle joint works closely with the subtalar joint to allow the foot to conform to uneven ground, and to enable the lower leg to elongate when running by allowing the foot to plantarflex. The powerful Achilles tendon arising from the heel and passing up to the calf muscles is the main driver of this movement. The ankle, like the knee, is susceptible to injury because shoes enable the foot to grip the ground so securely that the forces transmitted through the bones and ligaments of the lower limb are much greater than those for which they evolved. The fibula makes up the lateral wall of the ankle joint and is liable to be broken if powerful twisting or bending forces pass through the ankle, such as occurs when we ‘go over ’ on our ankle.

Foot just behind the hip joint (dislocation and retractors used at joint replacement) and from poorly placed intra-muscular injections. The peroneal nerve can be damaged on the operating table and by obstetric stirrups.

Vessels The blood supply to the leg is mainly supplied through the femoral artery which passes from the groin to the back of the knee where it becomes the popliteal artery and then divides into three branches.

The foot has been in a rapid phase of evolution from a grasping organ (in tree-climbing primates) to a paw (for savannah-running hominids). Abnormal pressure and rubbing from shoes can produce callouses and bone deformities in the foot, which can be both painful and unsightly. When examining the foot do not forget to check the shoes for signs of abnormal pressure and wear. The normal-wear pattern is at the side of the heel at the back (where heel strike occurs), the outside of the shoe (transfer of load to the forefoot) and a circular wear patch under the ball of the big toe (as the forefoot pushes off).

Anatomy of the leg

The leg

37


15

History and examination of the leg

Modified Thomas' test for flexion/extension

Apley's test for ankle and foot mobility Tibio-talar (ankle) movements

Can you roll yourself up into a ball?

Dorsiflexion

Plantarflexion Subtalar movements Inversion Eversion Now hold onto one leg and let the other drop back onto the bed. Now do the same with the other leg

This hand creates the movement

This hand senses the movement Forefoot movements

Fixed flexion deformity

Pronation

Hold rigid Supination

Rotation

Tell me if that hurts

External rotation

Internal rotation

Anterior draw test for cruciate instability. Rupture of either cruciate will produce a positive draw compared with the other side. Draw forward from an abnormal position to normal suggests damage to the posterior cruciate. Abnormal forward laxity from a normal rest position suggests an anterior cruciate lesion Pressure pushing knee into valgus tests medial collateral ligament

Abduction

Pressure pushing knee into varus tests lateral collateral ligament Tell me if this hurts

Hip • Make sure that you have adequate exposure on both sides so that the normal can be compared with the abnormal. Use the system ‘look, feel, move’ (see Chapters 3, 21) and always check distal neurovascular status. • Watch the patient walk, looking for any signs of a limp, which could be caused by pain (antalgic), weakness (Trendelenburg limp) or

Tuck patient's foot firmly into your axilla. Flex the knee very slightly then gently apply a valgus then a varus force testing each collateral ligament in turn

deformity (short). A painful hip is held flexed, adducted and internally rotated so the leg appears short.

Classification of limps L = Long. If one leg is longer than the other the patient’s head bobs up and down as they walk, but the strides are equal in time and length.

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I = Incoordinated. The gait of a neurological disorder is of someone continuously about to fall. No rhythm, and the arms moving in every direction as the patient attempts to keep their balance. M = Muscle weakness. If the patient has a foot-drop they will have a high stepping gait on that side. If the quadriceps muscle is weak then they will press down with their hand onto the front of their thigh at heel strike. If the abductors of the hip are weak then they will sway sideways over onto that hip each time they try to take weight on it. P = Pain. The patient will spend a short time on the painful leg and drop their body down during that short phase. S = Stiff. A stiff ankle or knee requires the leg to be swung out to the side when bringing it forward. With a stiff hip the patient rocks their pelvis and lower body to and fro as they walk to obtain a decent length of stride.

Hip It can be difficult to tell whether pain in the upper leg is coming from the hip, the knee or even the back. In the ‘pastry roll’ test, let the patient relax then roll the leg in and out with the flat of one hand on their thigh and the other on the shin as if you were rolling pastry. If the hip is pain-free the foot will flop to and fro. If there is pain arising from the hip then the patient will resist this rolling. When checking range of movement, lie the patient on their back and then ask them to curl into a ball. Compare the flexion of the hip with the other normal side. Then, get them to use their hands to hold the normal hip in that flexed position (this fixes the position of the pelvis) and gently allow the affected hip to extend as far as is comfortable. If there is fixed flexion deformity the leg will not be able to extend out onto the couch (modified Thomas’ test). When checking the range of rotation, just flex the hip enough to allow you to bend the knee to a right angle. Then use the tibia as a dial indicating the amount of rotation that can be achieved.

Knee Check for wasting of the vastus medialis, bulging just above and inside the knee cap when the patient forces their knee back into hyperextension. It is an early and sensitive sign of knee pathology. An effusion in the knee is best seen by the loss of the dimple on the inside of the knee cap when compared with the other side. The commonest bony deformity is bowing of the knees (varus) caused by osteoarthritis of the medial compartment.

Range of movement Range of movement can be compared by first lifting both heels off the bed to check for loss of extension, then seeing how far up to the buttock the heel can be drawn when the patient is lying on a couch.

splinted and urgent physiotherapy arranged as otherwise they are liable to trip and suffer a secondary injury.

Stability The collateral ligaments are checked by stressing the knee first into varus (inwards), then valgus (outwards), with the knee very slightly bent. The knee needs to be very slightly flexed when performing this test as otherwise the tight posterior structures may mask collateral tenderness (a partial tear) or laxity (a complete tear). Cruciate ligament instability is revealed by finding that the tibia is loose on the femur when pulled forward. Sit on the end of the couch, with the patient’s feet tucked side by side under your thigh to hold them still. First look from the side to see if one tibia has sunk back on the femur (ruptured posterior cruciate). Then with both hands gripping the top of the tibia, gently pull it forward on the femur. • If the distance that it will draw forward is much more than the other side, then a cruciate ligament is probably ruptured. • If the tibia moves from a sagged back position forward to a normal position (compared with the other side) then it is the posterior cruciate ligament that is ruptured. • If the tibia floats forward from a normal to an abnormal position, then the anterior cruciate has failed. Pushing the patella laterally as you bend the knee will be resisted by patients who have had a previous dislocation of the knee cap (patella apprehension sign).

Ankle Range of movement Range of movement in the ankle, the subtalar joint and the forefoot can all be checked by holding the heel in one hand and the forefoot in the other. • Rocking the hands up and down checks plantar and dorsiflexion at the ankle joint. • Tipping both hands in (inversion) and out (eversion) tests mobility in the subtalar joint. • Twisting the hand holding the forefoot in (pronation) and out (supination), while holding the hindfoot still, checks movement in the small joints of the forefoot.

Foot Check the skin all over the forefoot for bunions and corns, and on the sole of the foot for thickened pads over the metatarsal heads. Pathological flat feet are only reliably visible when the patient stands on their toes. A physiological flat foot (part of the normal spectrum) will form a normal arch on tip-toe. In pathological flat foot no arch forms, suggesting that there may be an abnormality in the bones of the foot.

The quadriceps lag test To test the power of the extensor mechanism of the knee the patient should be asked to lift their leg straight until the heel is 20 cm off the bed. They should then be asked to bend the knee until the heel touches the couch then straighten it again. If they cannot straighten it again they have a quadriceps lag. If this is present then the knee must be

TIPS • Always check distal neurovascular status in lower limb problems • Watch patients walking before starting a full examination • Hip problems can present with knee pain. Use the pastry roll test

History and examination of the leg

The leg

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Problems presenting in the hip

Septic arthritis

Developmental dysplasia of hip (DDH)

Premature baby (more rarely at any age) Toxic Doesn't move the affected limb Joint is destroyed if not treated early

Adult hip Normal

Newborn baby Congenital dislocation of the hip. If the hip is not held in joint it will develop badly (dysplastic)

Perthes' disease Limping child (4–10 years) Spontaneous avascular necrosis of the femoral head. Needs protecting while it regrows or it will collapse

Dysplastic

von Rosen splint to correct congenital dislocation of the hip Slipped upper femoral epiphysis Limping child around puberty Foot turns out. Leg shortens. Only clearly visible on lateral X-ray

Painful limp in elderly

Osteoarthritis in the elderly

Cysts Loss of joint space Sclerosis around joint Osteophytes Femoral head slips down and backwards on epiphyseal plate

Frog's leg lateral view

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. Š 2012 John Wiley & Sons, Ltd.

40 Published 2012 by John Wiley & Sons, Ltd.


Introduction Problems with the hip can occur at any age, and for each age group the most likely diagnosis is different.

unknown cause but may be some form of transient post-viral arthritis. The condition settles spontaneously within a few days or weeks.

Perthes’ disease Hip dysplasia The condition is not common, but is most easily treated if it is spotted early. There are many associations such as family history or the child being a first born female, particularly if the delivery is breech. If there is any suspicion from the history or on examination at birth, then the diagnosis should be confirmed or excluded using a dynamic ultrasound examination of both hips. If the hip is abnormal, then if it can be held in the acetabulum, using splints that hold the legs in abduction and internal rotation, the femoral head will then grow within the acetabulum, and the hip joint will develop normally. If this treatment fails (or was never instituted), then the lack of congruence in the hip joint will result in abnormal development, which will require surgical correction later in life.

Late diagnosis of congenital dislocation of the hip When children start walking it may be noted that they are limping and that the buttock creases are asymmetrical. The most likely diagnosis is a congenital dislocation of the hip that was not spotted at birth. After the age of 6 weeks the femoral head has started to ossify, so it is possible to see that the hip is dislocated on X-ray. An ultrasound scan will also confirm the diagnosis. The key to treatment is to get the hip into the joint as soon as possible and to hold it there, so that the acetabulum and femoral head can develop congruently. Splints that hold the hip abducted may be adequate; if not surgery will be needed to clear out any soft tissue blocking reduction.

Septic arthritis In a child too young to speak it may be difficult to work out where they are getting pain, but if the child is watched for a time it will be noticed that, however fretful they are, they do not move the painful limb. The diagnosis that must be considered is septic arthritis of the joint (see Chapter 28).

Irritable hip Young children are frequently referred as emergencies with a limp. It can be very difficult to make the diagnosis, as they may not be able to explain why they will no longer weight bear normally on that leg. Even when they are old enough to talk and explain the problem, they frequently complain of pain in the knee when the problem is in fact in the hip. Any child who is limping should have a careful examination of the whole leg. If the problem is in the hip then there will be painful limitation to movement of internal rotation of the hip (see p. 39). In more severe cases the hip is held flexed, internally rotated and adducted (the position of maximum comfort). Most cases of irritable hip are of

In children aged 4–10 years, Perthes’ disease produces a sustained irritable hip. The underlying pathology is thought to be avascular necrosis of the femoral head for no known reason (idiopathic). The femoral head will revascularise in time but if the segment of dead bone is large or the hip is subjected to a high load before it has had time to repair, then the femoral head collapses and the early onset of arthritis is inevitable. The hip should therefore be protected as much as possible during this period. Operations to protect the vulnerable segment of cartilage are of unproven value.

Slipped upper femoral epiphysis In children around the age of puberty, the ephiphyseal plate seems to be especially weak. Failure of the plate leads to slip of the femoral head downwards and backwards in relation to the femoral neck. The deformity is easy to miss on an anteroposterior X-ray, but is obvious on a lateral or ‘frog’s leg’ view. The child presents with a limp and often pain in the knee (referred pain), so the diagnosis is easy to miss. The foot is often turned outwards compared with the other side. If pins are run across the epiphysis, any further slip can be prevented until the epiphysis has fused at the end of growth. The condition is often bilateral.

Osteoarthritis of the hip This may develop in young people as a result of trauma, inflammatory joint disease or hip dysplasia (an abnormal-shaped hip from birth). However, it is normally a disease of the elderly, causing a limp because of pain, stiffness, weakness or a shortened leg. Hip replacement is the treatment of choice (see Chapter 17), although in younger patients with dysplasia an osteotomy may be used to improve the shape of the hip and so prolong its life.

Avascular necrosis High alcohol intake, steroids and some storage disorders predispose patients to develop avascular necrosis of the hip. The femoral head may take some years to collapse after the initial insult, but once it has collapsed a total hip replacement is the only option for restoring function and relieving pain.

TIPS • Exclude Perthes’ disease and slipped upper femoral epiphysis in a child with a limp • A subluxed or dislocated hip at birth will not develop properly if it is not relocated

Problems presenting in the hip The leg

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Joint replacement

Joint replacements mainly reduce pain and can improve mobility. The chance of the operation being successful and the longevity of the implant varies between joints

Shoulder Useful in end-stage inflammatory arthritis where they reduce pain but may not improve mobility much Hemi-arthroplasties replace a badly fractured humeral head Results variable

Spine Synthetic intervertebral discs are now available Short and long term value is not yet clear

Wrist Fusion gives a strong pain-free wrist. This is a better option than artificial wrist joints Metacarpophalangeal joints Can be replaced in hands damaged by rheumatoid arthritis Improves cosmesis and function

Knee Now as good as hip replacement in terms of reliability (Over 90% successful for more than 10 years) Half-knee (unicompartmental) replacements also available

Ankle Useful for reducing pain and improving function especially in rheumatoid arthritis Reliability not as good as hips and knees

Elbow Good pain relief and mobility improvement in rheumatoid arthritis Results good Artificial radial head can stabilise the elbow if severity of fracture requires removal of patient's radial head

Hip Reliably reduce pain and improve mobility in arthritis Last for 10–15 years and can then be replaced (revised) New materials (ceramics) and new designs (surface replacement) may provide even better results but are not yet proven Probably over 100,000 performed every year in UK alone

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. Š 2012 John Wiley & Sons, Ltd.

42 Published 2012 by John Wiley & Sons, Ltd.


Introduction Damaged joints become stiff, weak and painful. This interferes with activities of daily living and with sleep, and can convert a person who was an outgoing and independent contributor to society into a depressive reliant on society for their needs.

this stage it is normally possible to replace the worn-out joint with a revision implant fitted into the cleaned-out bed of the old implant. This implant does not usually last as long as a primary replacement but may give 10–15 years of useful life. Once the joint can no longer be replaced, it may need removing to reduce pain, leaving a flail but painless joint.

Pathophysiology Joints most commonly fail because of idiopathic osteoarthritis – the collapse of the articular cartilage for no known cause. However, joints can also fail as a result of the destruction caused by destructive arthritis or even fractures into the joint. If the surface of a joint heals with more than a 2 mm step in the surface, the onset of early traumatic arthritis is thought to be almost inevitable. Arthritic pain at night is a deep ache within the bones of the joint, while during the day the joint is stiff and hurts when it is moved.

Complications of major joint replacements

The options to manage the symptoms are painkillers, physiotherapy and aids to ease activities of everyday living, such as splints and home aids. Injections of local anaesthetic and even steroids into the joint give only minimal short-term benefit and run the risk of introducing infection into the joint. Surgically the options are either to fuse the joint, excise it, or replace it. • Fusion removes all movement but should create a strong limb which is pain-free. • Excision should also remove pain but preserves movement although strength is lost because the muscles no longer have a fulcrum across which they can operate. • Replacement should remove pain, improve mobility at least a little, and provide a strong limb. Surprisingly, loss of mobility in the wrist is no great disability, so fusion may be the operation of choice here. Loss of strength and stability in the lateral compartment of the adult elbow is not a problem so excision of the proximal radial head is the treatment of choice in radiohumeral arthritis. In the hip or knee, joint replacement is now the treatment of choice (at least in the elderly). As techniques improve, joint replacement is becoming the treatment of choice in shoulders, elbows and ankles.

• The death rate after joint replacement is less than one per 1000. Most of these deaths are a result of heart attacks and strokes. • Infection and wound breakdown occurs in less than 2% of cases. Infection rates are held down by using prophylactic antibiotics and by using laminar flow theatres where only sterile air is allowed to flow over the patient’s wound. • A hip replacement is prone to dislocation especially in the 6 weeks after surgery before a new capsule has grown around the hip joint. This risk of around 2% can be kept to a minimum by making sure that the patient does not sit on low chairs or cross their legs during this critical period. • A knee replacement is very painful for many weeks and is susceptible to stiffness as a result. If this cannot be overcome by exercises and physiotherapy then a manipulation under anaesthetic may be needed to break down the adhesions. • Both hip and knee replacements can cause damage to nerves that travel close to the joint being replaced. • In hip replacements leg length may be difficult to match with the opposite leg, and a heel raise may be needed in the patient’s shoe to balance the legs up. An infected joint replacement tends to present insidiously, not at all like septic arthritis. The patient has continuing pain after the joint replacement and may have a low grade fever. The wound may also be red and tender. Sometimes the first clue is bone resorption visible on X-ray. The only way to be sure of the diagnosis is to open the joint and take multiple samples. If the joint proves to be infected, and the infection is caught early, it must be washed out and the patient given high doses of intravenous antibiotics for at least 6 weeks. However, if the diagnosis is delayed, as is so often the case, the implant will need removing. A new implant cannot always be put back in, so the patient may be left without a joint.

Problems with artificial joints

Expectations

The problem with artificial joints is first that they do not last long (not nearly as long as manufacturers would have us believe). They are also not as strong as the joint surfaces they replace and are therefore prone to breaking if the patient falls. The materials used for joint replacement are changing as we seek implants that are stronger, have lower friction and produce fewer wear particles. Implants with low friction put less load on their fixation to the bone beneath. Wear particles stimulate an inflammatory response in the joint which leads to bone resorption around the implant and therefore loosening.

• Patients with successful joint replacements can return to a full, painfree life – driving their cars, playing golf and swimming. • Osteoarthritis appears to be a systemic disease and the replacement of one joint often exposes arthritic pain in other joints, so patients who have had one successful joint replacement often return for several more.

Treatment

Prognosis Hip and knee replacements probably give significant pain relief for 15–20 years. Once they start to loosen, pain and instability return. At

Shoulder, elbow, metacarpal and ankle replacements Replacements for all these joints have now been designed and are starting to produce consistently good results. They are especially useful in patients with rheumatoid arthritis for whom every painless functioning joint is a huge bonus.

Joint replacement The leg

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Problems presenting in the lower leg

Bunion operation

Figure of eight test

Narrows the foot Removes the bunion Straightens the toe

This checks fitness to return to contact sport after a lower limb injury. The athlete is asked to run flat out backwards in a figure of 8. If they feel unstable, they are not yet fit

Hammer toes

Claw toes Corns occur when toes rub on shoe

Hyperextension of metatarsal phalangeal and distal interphalangeal joint Hyperflexion of proximal interphalangeal joint

Knee The knee is very susceptible to problems, especially from sports such as football and skiing, where the body turns fast on a fixed foot. The history will give a clue to the structures likely to be damaged. The key to rehabilitation of problems with the knee is physiotherapy, as the quadriceps muscle wastes very quickly if the knee has been injured. Control of knee movements is lost, and the knee is then susceptible to a secondary injury such as a tear of the meniscus. Patients with injured knees should not return to sport until the muscle has recovered. A simple test for this is to ask the athlete to run as fast as they can – backwards – in a figure of eight (‘figure of eight’ test). If the knee feels unstable to the athlete, more work is needed before they are safe to return to sport.

Locking and pseudo-locking • Locking is the sensation that a patient gets when walking along and quite suddenly the knee will not straighten. The patient may end up sitting in the road jiggling the knee until the mechanical block clears from the knee. This is characteristic of a torn meniscus or of a loose body jamming in the knee.

Corns

Hyperextension of metatarsal phalangeal joint Hyperflexion of proximal distal interphalangeal joint

• Pseudo-locking occurs in a knee which is inflamed, when the knee is first moved after a period of stillness. This first movement causes such severe pain that the patient cannot move it further, until the inflamed layers of synovium that have stuck together are freed up. Pseudo-locking occurs commonly in teenage children, especially girls, and is associated with pain in the front of the knee and great difficulty on stairs especially descending. This anterior inflammation of the knee is sometimes called chondromalacia patellae (a beautiful but meaningless name) and usually resolves spontaneously.

Patella apprehension Hypermobile patients are liable to dislocate the knee cap laterally. Once this occurs, any attempt to reproduce the dislocation (by pushing the knee cap laterally, as the knee is flexed) produces an ‘impending sense of doom’ in the patient similar to the shoulder apprehension sign (see Chapter 6).

Anterior cruciate tear The anterior cruciate ligament stops the tibia sliding forward and rotating on the femur. It is torn by a twisting injury on a bent knee. The

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. © 2012 John Wiley & Sons, Ltd.

44 Published 2012 by John Wiley & Sons, Ltd.


ligament has no blood supply and so cannot heal. If the quadriceps cannot be built up enough to control the knee, then the patient will find the knee giving way when they twist or turn on it. The abnormal movement in the knee often leads to a tear of the menisci as well, causing true locking. The torn menisci need repairing or trimming through the arthroscope, and if the patient cannot cope with the instability even after intensive physiotherapy, then a substitute anterior cruciate ligament may need to be inserted, followed by a long course of rebuilding strength and proprioception around the knee.

Foot Hallux valgus/bunions These are very common especially in people with wide feet who try to wear narrow shoes. The big toe bends laterally (hallux valgus) leaving a prominent head of the metatarsal bone which forms a bursa over it while the skin becomes inflamed. Surgery is designed to narrow the foot with an osteotomy through the metatarsal, while at the same time the bunion itself is removed and the toe straightened.

Claw toes, hammer toes and metatarsalgia Arthritis in the knee This is as common in the elderly as arthritis of the hip. The patient gets pain at the end of the day and at night. There may be a lump at the back of the knee (Baker’s cyst) – an outpouching of the excess synovial fluid. Total knee replacements can now give as reliable results as hip replacements, lasting 10–15 years before wearing out and needing changing. Osteoarthritis normally starts in the medial tibiofemoral joint so there are sometimes indications for a unicompartmental knee replacement (just one-half of the joint).

Calf Gastrocnemius tear This sports injury can mimic a deep vein thrombosis (apart from the history of onset) as it profuces a painful red and swollen calf. It heals with conservative management: Painkillers and anti-inflammatories, Rest, Ice, Compression, and Elevation (PRICE).

Ruptured tendo Achilles See Chapter 20.

Ankle Instability

• Inflammatory joint disease in the feet causes dorsal dislocation of the metatarsal phalangeal joints with clawing of the toes. The metatarsal heads become very tender to walk on. Patients often describe a feeling as of walking barefoot over pebbles (metatarsalgia). Operations to straighten the toes and bring a thick pad of tissue over the metatarsal heads, combined with properly padded shoes, can make walking much more comfortable. • Hammer toes result from spasm, then contracture of the intrinsic muscles of the foot. • Patients with rheumatoid arthritis are especially susceptible to problems in the feet because of the disease’s affinity for the small joints in the hand and foot.

Flat feet Some people have a high arch to the foot, others a lower one, but true flat foot is a failure of the foot to form an arch when the patient stands on their toes (the windlass test). It can be caused by congenital tarsal coalition (bones fused from birth) or occurs in patients with inflammatory arthritis where the ligaments supporting the arch have stretched out. Pathological flat feet are difficult to treat either non-operatively with special shoes or surgically with tendon transfers or joint fusion operations.

Chronic instability of the ankle can arise after a torn ligament fails to heal. Surgical repair with a substitute ligament, followed by intensive physiotherapy, should offer reasonable results, but requires a positive input from the patient too. TIPS

Arthritis of the ankle This is common after trauma involving the ankle and in patients with inflammatory joint disease. Ankles are best fused if there is osteoarthritis or arthritis secondary to trauma, as ankle replacements tend not to do well in these conditions. However ankle replacements do well in patients with inflammatory joint disease and are especially useful because other joints around the ankle affected by the same disease are likely to be stiff.

• The figure of eight test is useful for telling when an athlete is ready to return to sport • Locking of the knee suggests a torn cartilage; pseudolocking may be inflammation only • Osteoarthritis of the ankle is best treated with fusion; rheumatoid arthritis with a replacement • Arthritis and deformity in the foot is common and disabling

Problems presenting in the lower leg

The leg

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Upper leg trauma

Trauma of the upper leg

Blood supply to femoral head passes up the neck inside the capsule of the hip joint

Sub-capital fractured neck of femur (blood supply lost)

Hemi-arthroplasty replacing dead head allows early mobilisation

Locked intramedullary nail allows early mobilisation of this unstable fracture

Pre-trochanteric fracture – blood supply preserved

Dynamic hip screw stabilises the fracture allowing early mobilisation

Fracture of the pelvis

Intra-articular fracture needs careful reduction if early arthritis is to be avoided Large pelvic veins may be torn by pelvic fractures

Fractures here may damage the urethra

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. Š 2012 John Wiley & Sons, Ltd.

46 Published 2012 by John Wiley & Sons, Ltd.


Fractures of the femur One of the most common but potentially disastrous fractures of the elderly is a fractured neck of the femur, a result of osteoporosis. Treatment includes the patient’s rehabilitation into the community, not just the surgery itself. Otherwise the fall and the fracture (whichever came first) may be the ‘straw that breaks the camel’s back’, condemning an elderly person living independently to a life in care or even premature death.

Sub-capital and per-trochanteric fractured neck of the femur The blood supply to the head of the femur runs up the neck of the femur from a rim where the capsule of the hip joint attaches to the base of the neck of the femur. If the fracture is a sub-capital fractured neck of the femur, high under the head, then, in the elderly, the blood supply to the head is usually so badly compromised that even if the fracture is reduced, the head will die. The only choice in this case is to replace the femoral head. The acetabulum is not affected, so only one-half of the joint is replaced. This is called a hemi-arthroplasty. However, if the fracture is outside the insertion of the capsule at the base of the neck or even through the greater and lesser trochanter, the blood supply to the femoral head is unaffected. However, the fracture is very unstable, so it is usually fixed with a large screw inserted up the femoral neck, which is then attached to a plate fixed to the outside of the upper femur using screws. This system of fixation is called a dynamic hip screw because the screw impaling the neck and head of the femur can slip down onto the plate fixed to the upper femur allowing the fracture to compress and bed down. This improves the strength of the fixation and encourages early healing. Both methods of fixation for the two types of fracture relieve pain and allow the patient to mobilise at once. This minimises the risk of all the complications of confining an elderly person to bed, such as bedsores, and chest and urinary tract infection. Most importantly it also helps them psychologically by enabling them to get home before they have lost their will for independent existence.

High velocity fractures Fractures of the pelvis and of the shaft of the femur in young people are usually high velocity injuries, so other injuries need to be excluded. There will also inevitably be heavy blood loss which may precipitate hypovolaemic shock. • Pelvic fractures are notorious for catastrophic haemorrhage and for damage to the urinogenital tract. Fixation of unstable fractures of the pelvis is very difficult. • Femoral shaft fractures are best fixed with a plate or an intramedullary nail so that the patient can be discharged and return to normal life as quickly as possible. The same applies to fractures of the femur

through metastases in the elderly, but in this case radiotherapy will also be used to prevent local recurrence.

Knee Injuries to the knee usually involve damage to the soft tissue, tearing of a meniscus or the rupture of a cruciate ligament. The patella can commonly dislocate laterally, but the knee itself rarely dislocates except in severe trauma. If this occurs, the popliteal artery can be damaged. A check of distal neurovascular deficit will identify what is now the real surgical emergency. The patella can be fractured by excessive force on the extensor mechanism (transverse), or by a direct blow which produces a stellate (multifragment) fracture. Fractures of the femoral condyles or of the tibial plateau usually involve high energy trauma. If early post-traumatic arthritis is to be avoided, the joint surface must be reconstructed so that there are no steps of more than 2 mm in the surface. This usually requires complex internal fixation with plates and screws and bone graft to fill the defect in the bone.

Torn meniscus (cartilage) There are two menisci in each knee helping transmit load from the curved medial and lateral femoral condyles to the flat top of the tibia. The menisci have no blood or nerve supply. If they are trapped in an abnormal position they can split, and jam in the joint. The unstable fragment of the meniscus may cause no symptoms for long periods, but from time to time it may jam in the joint, producing locking. This produces a sudden onset of pain in the joint, which locks in one position. The patient may find that after a period of wiggling the knee, the unstable fragment returns to its normal position and the knee then functions normally again. The diagnosis can be made with MRI or at arthroscopy, when the offending fragment can be trimmed back.

Torn cruciate ligament If the body of an athlete turns rapidly on a fixed foot, the loads on the knee are enormous. It is the anterior cruciate ligament which is commonly ruptured. The knee is now potentially unstable especially when turning on a bent knee and is liable to give way. Intensive physiotherapy to build up the muscles controlling the knee can often provide enough control for an athlete to manage without their cruciate ligament. If not, then a substitute anterior cruciate ligament can be inserted, but it is difficult to find any material strong enough to withstand the forces that go through this ligament, so surgery is not always successful.

Rehabilitation The key to recovery of knee function is physiotherapy designed to: • Build up the strength of the muscles around the knee, especially the quadriceps. • Retrain the athlete in control (proprioception) of the knee, so that the muscles can protect the ligaments from excessive load.

Upper leg trauma

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Lower leg trauma

Laceration to front of tibia Trip on stairs, scraped shin. Flap needs plastic surgery, otherwise an ulcer develops

Ruptured tendo Achilles Sudden action in middle age

and signs of ischaemia

Compartment syndrome Bleeding into a closed muscle compartment increases the pressure and strangles the muscle

Sub-ungual haematoma A red hot needle will drill a hole in the nail releasing the pressure and the pain

Crush fracture of calcaneum Fall from a height landing on the heels

Fractured 5th metatarsal an athlete going over on the ankle may avulse the end of the 5th metatarsal as the muscle tries to stabilise the foot

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. Š 2012 John Wiley & Sons, Ltd.

48 Published 2012 by John Wiley & Sons, Ltd.


Introduction Trauma of the lower leg is common, both as a result of sports and because of accidents at work. ‘Going over ’ on the ankle can simply result in a mild ligamentous sprain, but as the energy involved in the injury rises there is a well defined cascade of fractures and ligament tears associated with each mechanism of injury. Dislocation of the ankle is an emergency because the pressure from the displaced talus compromises the blood supply to the foot and the integrity of the skin that is tented over the bone. Immediate reduction, even if a proper anaesthetic is not available, is appropriate because the neurovascular state of the foot is compromised.

High energy injuries These are commonly associated with contact sports, motor vehicle crashes or falls. • Fractures of the tibia are now best treated with internal fixation in most cases, as they are slow to heal without support and may require long periods in plaster. Fractures of the tibia are associated with compartment syndrome in the deep compartments (see Chapter 49). • Ankle fractures need careful reconstruction to ensure that the joint surfaces are congruent, otherwise early arthritis is inevitable. The distal tibia and fibula are held together by a ligament crossing this diastasis. If this ligament is torn the stability of the ankle joint is lost, and unless it is repaired the instability will lead to early arthritis. Even if the ankle joint is internally fixed the repair will need protecting with a below-knee plaster extending to the toes. It is important that this plaster is applied with the ankle dorsiflexed at least to neutral. If the foot is plastered with the toes pointing down, the ankle stiffens in this position and is very difficult to correct later. • Falls from a height can cause a string of fractures through the body, from crush fractures of the vertebrae, through fractures of the pelvis, crush fractures of the tibial plateau at the knee and the tibial plafond (joint surface) at the ankle, and finally fractures of the calcaneum which can extend into the subtalar joint.

Lower energy injuries • On examination of a simple sprain of the ankle there will be swelling and tenderness over the injured ligament but no tenderness over the bone itself. A below-knee plaster is only needed for comfort in the short term, otherwise the injury should be managed using RICE (see Chapter 39). Physiotherapy is also important to retrain proprioception around the ankle joint, otherwise repeated injuries are likely to occur.

• Inversion of the ankle is controlled by the tendons passing down into the lateral side of the foot. The force generated by these tendons can pull off a fragment of bone where they insert. The classic one of these is avulsion of the proximal end of the fifth metatarsal bone. Surprisingly, it heals well without aggressive intervention. • The Achilles tendon is important for transferring energy through the ankle into the ground. In the middle-aged (as collagen starts to degrade) it is liable to sudden rupture during strenuous sport. The patient may still be able to stand on their toes (using other muscles) but physical examination and, if necessary, ultrasound will confirm the diagnosis. Healing is very slow because of the poor blood supply, but surgery is also problematic because it is difficult to make a strong repair. Either way, rehabilitation is a slow and delicate balance between going too slow and risking stiffness, and going too fast and causing re-rupture.

Degloving injuries The foot or leg can be degloved by a run-over injury. Work boots with steel toecaps are now mandatory in any high-risk work area to prevent these injuries. Initially the injury may look minor and X-rays may show no broken bones. However, the skin will have no sensation and capillary filling will be compromised. When all the dead soft tissues are removed (as they must be), the extent of the injury may make immediate amputation the most obvious choice. A less severe but more common injury is a flap lifted from the front of the shin where an elderly person has tripped and barked their shin on the edge of a step. The temptation to stitch the flap back should be resisted. It is usually not viable and the swelling against tight stitches will seal its fate. Immediate plastic surgical treatment with grafting may prevent the formation of a large leg ulcer which may take many months to heal.

Fractured toes These rarely need reducing unless they are also dislocated. Buddy strapping (bandaging to the next uninjured toe) is valuable in treating both fractured toes and simple fractures of the fingers as it provides support while allowing mobility.

Subungual haematoma A bruise forming under a nail can be disproportionately painful. Decompression by making a hole in the nail with a red hot needle is a surprisingly painless procedure, and provides dramatic and immediate pain relief.

Lower leg trauma

The leg

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Rheumatological history and examination

This figure covers the most common clinical manifestations of rheumatological disease Head and neck

Vascular

Alopecia Red/sore/dry eyes Nasal crusting/epistaxis Oral ulcers Dry mouth Hearing loss

Raynaud's phenomenon DVT/CVA/recurrent miscarriage Cardiac Pericarditis

Joint disease Pain and early morning stiffness Duration, distribution of synovitis Schober's index Disability

Respiratory

Rash

Gastrointestinal

Psoriasis, SLE, dermatomyositis Erythema nodosum Circinate balanitis Keratoderma blennorrhagica Vasculitis Livedo reticularis

Diarrhoea Jaundice

Nails Psoriatic nail changes Vasculitis Dermatomyositis Genitourinary

Pleuritis Fibrosis, effusions Pulmonary embolus Pulmonary hypertension

Neurological Mononeuritis multiplex Compression neuropathy Myelopathy Peripheral neuropathy Haematopoietic Anaemia Lymphadenopathy Splenomegaly

Previous STD Vaginal dryness

History The musculoskeletal history has the same basic framework as any medical or surgical history with details of the presenting complaint, history of presenting complaint, etc. There are, however, a number of features that should be highlighted when clerking and presenting a patient with rheumatological disease. • The most crucial element in a musculoskeletal history is to differentiate inflammatory and degenerative joint disease: Inflammatory joint disease such as rheumatoid arthritis (RA) is characterised by the presence of stiffness after periods of immobility that improves with activity; early morning exacerbation of symptoms is classic. Degenerative joint disease may produce a ‘gelling’ sensation on waking but the problem is short-lived and in general the pain is activity-related and improves with rest.

• Joint swelling may occur with either inflammatory or degenerative disease. The detection of swelling, its character and distribution forms the basis of clinical examination. • Extra-articular disease is a frequent phenomenon in inflammatory conditions. Seeking examples of eye, skin and nail, respiratory or bowel symptoms may help not only in determining the underlying diagnosis but also its severity. • Heritability plays a variable role in inflammatory disease and a family history of joint disease, psoriasis or autoimmune disease may be relevant. • A summary of medications past and present is crucial. The efficacy and tolerability of, and patient’s compliance with, anti-inflammatories, disease-modifying antirheumatic drugs (DMARDs), immunosuppressives or biologic therapy is extremely helpful. A full alcohol and drug history is particularly pertinent in the assessment of a patient with gout.

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. © 2012 John Wiley & Sons, Ltd.

50 Published 2012 by John Wiley & Sons, Ltd.


• The degree of disability does not always correlate with the severity of joint deformity, so a full social history with particular attention to reports of work absenteeism and/or ability to self-care is mandatory.

Examination – general points The purpose of joint examination is the detection of joint swelling, differentiation between inflammatory and degenerative joint disease and the assessment of disease activity in an individual patient. • Joint swelling in inflammation (synovitis) is boggy in nature. The joint is often warm, with overlying erythema and there is often pain at the extremes of movement. Swelling due to degenerative disease is bony hard. • Different inflammatory diseases have predilections for different sites. Rheumatoid arthritis, for example, favours the metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints in the hand, with relative sparing of the distal interphalangeal (DIP) joints. However, osteoarthritis in the hand focuses on the first carpometacarpal (CMC) joint, the PIP joints (forming Bouchard’s nodes) and the DIP joints (forming Heberden’s nodes). The classic distribution for each inflammatory joint disease is covered in individual chapters. • Many rheumatological conditions are systemic diseases. Potential extra-articular manifestations of disease must be sought in clinical examination (see figure opposite). The GALS screen and detailed examination of the arm, leg and spine has already been described (see Chapter 3). The rest of this chapter is therefore devoted to examination of the hand, which follows the same paradigm of ‘look, feel, move’. For RA patients, the focus is not only the description of the classic bony deformity but also the detection of active synovitis (swollen and tender joints).

Hand examination Look • Stand back and take an overall view of the patient: Well or not? Stigmata of steroid use? • Ask the patient to roll up their sleeves and show you their elbows: Glimpse of hand function/disability. Check extensor surface for rheumatoid nodules or psoriatic plaques. • Place the patient’s hands palm down on a pillow:

Skin – Stigmata of steroid use? Erythema? Rash? Scars? Vasculitic lesions? Nails – Psoriatic nail changes? Nail bed changes of connective disease? Soft tissue – Swelling? Rheumatoid nodules? Muscle wasting? Bone – Swelling? Classic rheumatoid changes? • Ask the patient to lift their hands, straighten their fingers and turn their hands over: Extensor tendons intact? Evidence of wrist restriction? • Place patient’s hands palm up on a pillow: Thenar eminence wasting? Palmar erythema? Vasculitic lesions?

Feel • Examine each hand in turn and work distally through the rays of bones (i.e. wrist, MCPs, PIPs, then DIPs). • Quickly run your hands over the wrist, MCPs, PIPs and DIPs: Any increased warmth? • Support the patient’s hands with the tips of your fingers. Roll your thumbs over the dorsum of the wrist and MCPs. Pinch the PIPs and DIPs from the sides. Apply enough pressure to blanch your nail. You must aim to detect tenderness but not hurt the patient! Swelling – presence, quality and pattern? Joint tenderness?

Move • Assess wrist extension and flexion actively and passively. • Assess power and pincer grip. • Assess hand function, e.g. ask them to hold a pen or pick a coin off the table. TIPS • Assessment of median and ulnar nerve function is not routinely necessary unless the history is suggestive or there is evidence of thenar or hypothenar wasting • All examiners or physicians will expect you to recognise and describe the obvious features of rheumatoid arthritis. Additional details to include are assessment of disease activity (based on number of swollen and tender joints) and functional capacity

Rheumatological history and examination Rheumatology

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22

Pathogenesis of rheumatoid arthritis

Antigen (e.g. CCP)

Signal 1 TCR

MHC II CD4+

APC TH cell CD86 CD80

CD28 CTLA-4 (inhibitory)

Signal 2

B cell

TH cell numbers and activity ↑

Antibody production

Cell-mediated immunity

Humoral immunity

Synovial fibroblast

Activated T cell IL-1

Matrix metalloproteinases

IL-6

↑RANKL ↓OPG

IL-17

TNFα

↑DKK-1

Cartilage Osteoclast

Osteoblast

Bone

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. © 2012 John Wiley & Sons, Ltd.

52 Published 2012 by John Wiley & Sons, Ltd.


Introduction

Macrophages

Rheumatoid arthritis (RA) is the prototypical inflammatory arthropathy. The primary site of disease is the synovium, which becomes inflamed and proliferates to form pannus: a mass of T cells, B cells, fibroblasts and activated macrophages. The boggy, inflamed pannus invades cartilage and bone, giving rise to the clinical features of pain and stiffness followed by joint swelling, instability and destruction. RA is a classic autoimmune disease, involving both the cellular and humoral components of immunity. This chapter will cover basic details of the key cells, cytokines and mechanisms involved in the pathogenesis of RA.

Macrophages initiate and perpetuate inflammation both in tissue and the circulation by: • Cytokine production, most notably TNFα (see below). • Antigen presentation to T cells. • Promoting adhesion and migration of leucocytes. • Degradation of collagen matrix. • Angiogenesis.

Cells T cells T cells are the basis of cellular immunity and are up-regulated in RA synovial tissue. CD4+ T helper (TH) cells are divided into the subsets TH1, TH2 and TH17, each with a characteristic cytokine-producing profile. TH17 cells are the dominant cell population in RA, producing interleukin-17 (IL-17), which is responsible for cytokine production, osteoclast activation and matrix metalloproteinase (MMP) release. T cell activation depends on antigen-presenting cells (e.g. dendritic cells) and requires two separate signals: • Signal 1: antigen-specific binding between the T cell receptor and MHC II / antigen complexes on the surface of antigen-presenting cells; indeed RA is associated with HLA-DR4 and DR-1 alleles that contain a shared amino acid motif in the MHC II antigen binding site, commonly known as the shared epitope, and • Signal 2: co-stimulatory binding between the T cells CD28 protein with ligands (CD80/86) on antigen-presenting cells. T cells may also express cytotoxic T lymphocyte antigen 4 (CTLA-4) which binds CD80/86 without providing a stimulatory signal and acts as an endogenous inhibitor. Activated T cells are responsible for: • Induction of pro-inflammatory cytokines (e.g. IL-1, IL-6, IL-17 and TNFα) to enlist and coordinate lymphocyte and macrophage recruitment. • Activation of synovial fibroblasts and osteoclasts to erode cartilage and bone. • B cell proliferation and antibody production. Regulatory T cells (Tregs) home into the site of inflammation and may act locally to resolve inflammation, probably through the release of IL-10 and/or transforming growth factor β.

B cells B cells are responsible for • Autoantibody production. • Cytokine release. • Antigen presentation. • Modulation of T cells. The most crucial role for B cells in RA is likely to be the development of antibodies against self-IgG molecules (rheumatoid factor, RF) and cyclic citrullinated peptides (anti-CCP antibodies – see Chapter 23 for their clinical utility). Anti-CCP antibodies may play a role in disease pathogenesis and/or perpetuation, or merely represent byproducts of the inflammatory process. There is increasing evidence of an association between anti-CCP antibodies, the shared epitope and cigarette smoking. Smoking may promote the citrullination of selfpeptides which are subsequently presented to T cells by antigen-presenting cells with the high-risk HLA-DR shared epitope. As a consequence, cell-mediated immunity against citrullinated antigens is enhanced (via T cell activation and expansion) and B cells secrete anti-CCP antibodies.

Fibroblasts Fibroblasts account for the majority of the cells in RA synovial tissue, and their uncontrolled growth is a major factor in pannus formation. RA synovial fibroblasts are quite different from those in normal tissue as they lack the normal control mechanisms that prevent cellular proliferation (such as tumour suppressor genes) and instead express protooncogenes and anti-apoptotic molecules. Synovial fibroblasts produce pro-inflammatory cytokines and chemokines, thereby attracting activated inflammatory cells into the joint. In addition, they produce matrix-degrading enzymes which erode cartilage.

Inflammatory mediators TNFα is probably the dominant cytokine for most patients with RA. It is present in high concentrations in synovial fluid and rheumatoid synovium and is responsible for key pathological processes such as cellular activation and cytokine, MMP and prostaglandin release. In addition it is responsible for the systemic effects and weight loss seen in very active disease. TNFα blockade using monoclonal antibodies has revolutionised the treatment of RA (see Chapters 36 Medical management of inflammatory disease and 23 Rheumatoid arthritis). IL-1, -6 and -17 are also crucial mediators in inflammatory disease and blocking antibodies are either available or in development.

Cartilage and bone loss Inflammation, cartilage and bone loss are closely linked. Cartilage destruction in RA is driven by matrix metalloproteinases (MMPs) from synovial fibroblasts, neutrophil polymorphs and chondrocytes. Bone thinning (osteopaenia) and erosions are caused by activated osteoclasts, cells of monocyte/macrophage lineage that are specifically designed for bone resorption (see also Chapter 31 Disorders of bone metabolism). Osteoclastogenesis requires macrophage colony stimulating factor (M-CSF) and the receptor activator of NFκβ ligand (RANKL) from synovial fibroblasts and activated T cells; its expression is up-regulated by cytokines in inflamed synovial tissue. The non-signalling decoy receptor for RANKL, osteoprotegerin (OPG), diminishes osteoclast activation and bone resorption; as a result the ratio between RANKL and OPG is a crucial determinant of inflammatory bone loss. A monoclonal antibody against RANKL (denosumab) increases bone mineral density in post-menopausal women and may diminish bone erosion in RA. TIPS • T helper 17 (TH17) and T helper 1 (TH1) cells are the dominant T cell subsets in RA synovium • Interleukin-17 regulates many cytokines including TNFα and plays a role in both cartilage and bone loss • TNFα is the most important inflammatory cytokine in RA and TNFαblockade dominates monoclonal antibody (biologic) therapy for the disease • B cells generate anti-CCP antibodies which may play a pathogenic role • The RANKL/OPG axis is a crucial pathway in inflammatory bone loss in RA

Pathogenesis of rheumatoid arthritis Rheumatology

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23

Rheumatoid arthritis

Features Neurological

Ocular

Early rheumatoid hand Fusiform symmetrical MCP + PIP swelling

Episcleritis Scleritis Keratoconjunctiva sicca

Rheumatoid nodules Extensor tenosynovitis Wrist tenderness/swelling Prominent ulnar styloid

Pulmonary Nodules Effusions Basal fibrosis

Late rheumatoid hands

Renal MCP destruction causing subluxation and ulnar deviation of the fingers

Swan-neck deformity of the fingers

Mononeuritis multiplex Cord compression (atlanto-axial subluxation) Sensorimotor neuropathy Cardiac Pericarditis Conduction defects Vasculitis

Splenomegaly

↓ GFR due to NSAIDs Drugs Amyloid

Felty's syndrome

Clinical examination Look

Skin: Scars, palmar erythema, vasculitis, evidence of steroid use Soft tissue: muscle wasting, nodules, synovitis Bone: Ulnar deviation, swan-neck or boutonnière deformities of fingers, Z thumb, prominent ulnar styloid

Feel

Synovitis, tenosynovitis

Move

Active and passive ranges of movement Tendon integrity Hand function and disability

Haematological Thrombocytosis Anaemia: chronic disease, GI blood loss due to NSAID therapy, bone marrow suppression due to DMARDs, pernicious anaemia

Introduction Rheumatoid arthritis (RA) affects 0.5-1% of most populations worldwide. The average age of onset is 55 years but it can occur at any time, even in infancy (juvenile idiopathic arthritis). It is more common in women and smokers. It is a leading cause of disability and risks premature mortality by 5-10 years due to: • Extra-articular involvement of the renal and respiratory tracts. • Opportunistic infections in the presence of immunosuppressive drug therapy. • Accelerated atheroma and subsequent coronary artery disease. The underlying cause is unknown but is likely to encompass genetic factors, sex hormones and an unidentified initiating agent. B-cells, T-cells (particularly TH17 and TH1) and the pro-inflammatory cytokines

Systemic Exhaustion Weight loss Pyrexia

interleukin 1 (IL-1), IL-6, IL-17 and tumour necrosis factor α (TNFα) generate persistent cellular activation, autoimmunity and inflammation of synovial joints and of a number of extra-articular sites. See Chapter 22, Pathogenesis of rheumatoid arthritis, for more details.

Diagnosis The diagnosis of RA rests on a number of clinical and laboratory features. For the original 1987 American College of Rheumatology (ACR) criteria, at least four of the following following criteria must be met to make a diagnosis of RA. There are no exclusion criteria. Note that joint symptoms must be present for at least 6 weeks to differentiate RA from the post-viral arthropathies (e.g. parvovirus), which generally have a shorter time course and more benign prognosis.

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. © 2012 John Wiley & Sons, Ltd.

54 Published 2012 by John Wiley & Sons, Ltd.


Criteria

Comments

Morning stiffness

Duration > 1 hour (for > 6 weeks)

Arthritis of at least three joints

Soft tissue swelling (for > 6 weeks)

Arthritis of hand joints

MCPs, PIPs or wrist (for > 6 weeks)

Symmetrical arthritis

At least one area (for > 6 weeks)

Rheumatoid nodules

Positive rheumatoid factor

Radiographic changes

Periarticular erosions

Other radiographic features include soft tissue swelling, periarticular osteopaenia, and joint fusion or destruction. N.B. Rheumatoid factor (RF) is present in only 70% of patients and up to 15% of the normal population have RF but not RA. Anti-citrullinated protein antibody (ACPA, also known as anti-cyclic citrullinated peptide anti-CCP) is more specific for RA and is only found in 3% of the general population. The presence of either or both are linked to increased disease severity. The presence of rheumatoid nodules on examination indicates seropositivity for RF and thus a worse prognosis. In 2010, new criteria were devised by collaboration between ACR and the European League Against Rheumatism (EULAR) to increase the sensitivity in early disease. The diagnosis of RA is based on the presence of synovitis in at least one joint (for which there is no better alternative diagnosis) and a score of ≥6 out of 10 from the following: • Number and size of joints involved (score 0–5). • Serologic abnormality (score 0–3). • Elevated acute phase response (score 0–1). • Symptom duration (score 0–1).

Clinical features The most common presentation is insidious pain, swelling and stiffness of the small joints of the hands (metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints, with characteristic sparing of the distal interphalangeals (DIPs)), although any synovial joint may be affected. In contrast to osteoarthritis, the symptoms are most marked in the morning, exacerbated by rest and improve with activity. In a minority of cases the disease can present acutely with widespread synovitis, with a migratory arthritis (palindromic RA) or with marked systemic features of pyrexia, fatigue and weight loss. As the disease progresses, joint instability leads to subluxation and persistent deformity. Classic changes include: • Subluxation at the MCP joints with palmar and ulnar deviation of the fingers. • Disease at the PIP joints causes: boutonnière deformity (fixed flexion at the PIP and extension at the DIP); swan-neck deformity (fixed extension at PIP and flexion at DIP); Z thumb. • Subluxation and radial deviation at the wrist causing prominence of the ulnar styloid. Additional musculoskeletal features include: • (Stenosing) tenosynovitis causing trigger finger or finger drop if a tendon body is eroded. The extensor digiti minimi is most vulnerable

in this regard and the presence of a little finger drop on clinical examination is a warning sign of further tendon damage and profound risk to hand function. • Bursitis. RA is a systemic disease and its extra-articular features are outlined in the figure opposite.

Treatment The spectrum of RA requires a multidisciplinary approach involving: • Specialist nurses – patient education and support, self-care groups. • Physiotherapy – exercise and joint protection. • Occupational therapy – adaption, aids and splints. • Pharmacotherapy – pain and disease control. • Surgery – joint replacement, arthrodesis and tendon repair.

Disease assessment Levels of disease activity are generally based on the DAS28 (Disease Activity Score 28) – a composite of the swollen joint count, tender joint count, ESR or CRP and a patient’s global assessment of their health. The 28 joints included are all MCPs and PIPs, plus both wrists, elbows, shoulders and knees. The DAS28 is the basis for assigning biologic therapy and is used widely in clinical trials.

Pharmacotherapy See also Chapter 36, The medical management of inflammatory disease. RA is treated aggressively as early as possible to prevent deformity and disability and the aim of treatment is total remission. Non-steroidal anti-inflammatories (NSAIDs) NSAIDs can be used periodically or continuously. COX-specific inhibitors have a good gastric safety profile but should be avoided in those with heart disease. Disease-modifying antirheumatic drugs (DMARDs) DMARDs aim to halt disease progression. Although well tolerated, they have a number of side effects and patients therefore need close monitoring. A patient with difficult disease may often require combinations of two or three DMARDs. Listed below are the commonest DMARDs, along with their mechanism of action and side effects: • Methotrexate (folic acid antagonist) + folic acid: myelosuppression, pneumonitis, hepatitis. • Hydroxychloroquine (inhibition of cellular enzyme release): macular damage. • Sulfasalazine (mechanism unknown): myelosuppression, rash, hepatitis. • Leflunomide (arrests activated lymphocytes): myelosuppression, hepatitis, diarrhoea. Other effective DMARDs include azathioprine, gold, penicillamine, cyclosporin and cyclophosphamide. Steroids Systemic steroids are effective in active disease or during flare and can be used to control symptoms until DMARDs have taken effect. High-dose systemic administration is reserved for refractory RA Rheumatoid arthritis Rheumatology

55


and extra-articular complications not responding to immunotherapy. Intra-articular steroid injections are useful in acute flares; the dramatic beneficial effect is short-lived and has no impact on eventual outcome. Biological therapy The biologic treatments in most routine use are anti-TNFα and anti-B cell therapy. TNFα blockers are highly effective. They are divided into: • Monoclonal antibodies against TNFα: Infliximab (chimeric human-murine monoclonal antibody against TNFα) Adalimumab (fully humanised monoclonal antibody) Golimumab (fully humanised monoclonal antibody) Certolizumab (PEGylated Fab fragment of humanised monoclonal antibody). • TNFα:Fc fusion protein Etanercept. TNFα blockade risks opportunistic infection and reactivation of latent TB, and therefore all patients are screened with a chest X-ray (and if necessary TB Elispot) prior to biological therapy. The risk and

56 Rheumatology

Rheumatoid arthritis

cost of these drugs have given rise to specific NICE (National Institute of Clinical Excellence) guidelines on their use. TNF blockade is restricted to patients with active disease (DAS28 > 5.1 on at least two occasions) who have failed treatment with at least two DMARDs, of which one must be methotrexate. The clinical improvement only lasts the duration of treatment. Anti-B cell therapy (rituximab) is used in those who have not responded to TNF inhibition and is effective in up to 50% of those patients with refractory disease. TIPS • Not all patients with rheumatoid arthritis have a positive rheumatoid factor, and not all patients with a positive rheumatoid factor have rheumatoid arthritis. ACPA is more specific for RA • Disease-modifying antirheumatic drugs (DMARDs) may halt disease progression but will not reverse damage already done • TNF blockers are effective but carry the risk of susceptibility to infection and reactivation of latent TB • Anti-B cell therapy is reserved for TNF-blockade ‘non-responders’


24

Systemic lupus erythematosus

Dermatological

Neurological*

Non-scarring alopecia Photosensitivity* Malar rash* Discoid rash* Oral ulcers* Urticaria Purpura Vasculitic ulcers

Seizures, psychosis, depression Pulmonary Serositis* (pleuritis) Effusion Fibrosis Vasculitis Pneumonitis

Cardiac Serositis* (pericarditis) Endocarditis

Musculoskeletal Raynaud's phenomenon Non-deforming arthropathy* Aseptic necrosis of the hip Myopathy

Hepatosplenomegaly

Renal disease* Glomerulonephritis * denotes diagnostic criterion

Haematological* ↓ All cell counts

Investigations

Treatment Mild

ANA positive* FBC* ? Anaemia ? Lymphopaenia ? Thrombocytopaenia U+E Urine dip ? renal disease Immunology* ↑ dsDNA levels Autoantibody associations ↓ Complement levels

NSAIDs Hydroxychloroquine Moderate Steroids Azathioprine Methotrexate Severe Cyclophosphamide Mycophenolate mofetil Rituximab

Introduction

ARA diagnostic criteria for SLE

Systemic lupus erythematosus (SLE) is a complex, multisystem, autoimmune condition characterised by autoantibodies directed against nuclear components. It affects approximately 1 in 4000 and is more common in women (ratio 10 female:1 male) and Africans and Afro-Caribbeans. The variety of autoantigens (e.g. histone, ribonucleoprotein (RNP)) is responsible for an array of patterns and severity of disease, which can range from mild to life-threatening in the same patient over time. The variable and multisystem nature of SLE makes it a great mimic of other conditions, and it can be a difficult diagnosis to make. As a result, clinicians have adopted the diagnostic criteria of the American Rheumatological Association (ARA), which were originally created for research and epidemiological purposes.

Four or more of the following must be fulfilled, either simultaneously or sequentially. Malar ‘butterfly’ rash

Non-scarring rash over cheeks and bridge of nose

Discoid rash

Scarring rash commonly in sun-exposed areas

Photosensitivity Oral ulcers Arthralgia

Non-erosive arthropathy

Serositis

Pleuritis, pericarditis

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. © 2012 John Wiley & Sons, Ltd. Published 2012 by John Wiley & Sons, Ltd.

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Renal disease

Proteinuria > 0.5 g per 24 hours or cellular casts

Haematological

Haemolytic anaemia, leucopaenia or lymphopaenia

Neurological

Seizures, psychosis

Antinuclear antibody (ANA)

Raised ANA titre

Immunological disorder

Raised dsDNA or anti-Sm antibody titres Positive antiphospholipid antibodies

Skin disease and arthropathy In addition to the skin symptoms in the diagnostic criteria, patients with cutaneous manifestations of lupus may present with non-scarring alopecia, purpura, urticaria and hyperpigmentation. The musculoskeletal picture is dominated by polyarticular arthralgia, but the disease is more benign than rheumatoid arthritis and overt joint damage occurs in fewer than 10% of patients. Jaccoud’s arthropathy refers to reversible joint instability and subluxation due to tendonitis rather than irreversible destruction due to synovitis. Muscle disease is rare and may be a consequence of drug therapy.

Drug-induced lupus Hydralazine, procainamide, isoniazid, minocycline and sulfasalazine have all been implicated in causing SLE, but drug-induced disease is generally mild, with few renal or neurological features and the disease disappears with cessation of the drug. These medications are not contraindicated in idiopathic SLE.

Serology Autoantibodies Autoantibodies directed against the nucleus are not specific for lupus but they are very sensitive and therefore a raised ANA titre is a useful first step in the diagnosis of SLE. A negative ANA in a patient with suspected SLE is very reassuring, but a raised ANA titre does not always lead to a diagnosis of lupus as elevated levels can be found in a number of other autoimmune conditions such as rheumatoid arthritis or Sjögren’s syndrome. Antibodies directed against native DNA (dsDNA) are more specific for a diagnosis of SLE and the remaining autoantibodies are associated with particular complications as listed below.

Antibody

Prevalence

Association

ANA

>90%

Not specific, but a diagnostic criterion

DsDNA

40–90%

Renal disease

Histone

30–80%

Drug-induced lupus

Sm

30–80%

SLE-specific if found in Afro-Caribbean patients

RNP

20–35%

Renal disease

Ro

25–40%

Sjögren’s syndrome, cutaneous lupus, congenital heart block

La

10–15%

As for Ro

Renal lupus Renal disease is a serious complication and every patient should have their blood pressure checked, electrolytes measured and urine assessed for casts and protein at each clinic visit. SLE causes a range of glomerulonephritidies, which have been classified by the World Health Organisation according to biopsy findings. Although this system may offer some clues to prognosis, renal lupus is generally treated very aggressively.

Respiratory disease Up to two-thirds of patients will complain of pain or pleuritis at some point during their disease, and a third develop pleural effusions. The more unusual complications of interstitial fibrosis, vasculitis and pneumonitis may present with an insidious development of shortness of breath and/or decrease in exercise tolerance. First-line investigations include a chest X-ray and lung function tests, which may indicate a greater extent of disease than is evident clinically. Pulmonary hypertension may occur as a result of fibrosis, vasculopathy or chronic thromboembolic disease, particularly in those with antiphospholipid syndrome (see below).

Haematological system Autoantibodies against red cells, lymphocytes and platelets may reduce all of these cell counts, and an acute thrombocytopaenia can be dramatic and life-threatening. The commonest haematological finding, however, is anaemia of chronic disease, which is present in up to three-quarters of lupus patients. While the ESR is commonly raised in SLE, an elevated CRP (C-reactive protein) is unusual and should prompt a search for concurrent infection.

Raynaud’s phenomenon Although not a diagnostic criterion, Raynaud’s is common in lupus patients and may predate the disease by some years. Treatment is identical to idiopathic Raynaud’s disease with vasodilators. 58 Rheumatology Systemic lupus erythematosus

Complement SLE causes reduced levels of C3 and C4 due to immune complex deposition. In an exacerbation of lupus, the complement levels would be expected to fall, in association with an elevation in dsDNA titre. However, since patients often have persistently abnormal serology in the absence of active disease, results must be assessed in combination with the clinical picture.

Treatment All lupus patients should avoid sun exposure and use high-factor sun creams. Other treatment varies depending on the severity of the disease. • Mild disease. Non-steroidal anti-inflammatory drugs (NSAIDs) are appropriate for intermittent arthralgia, and hydroxychloroquine is excellent for skin and musculoskeletal disease. • Moderate disease. More persistent disease activity or the presence of haematological features would require the use of oral or pulsed intravenous steroids. Azathioprine or methotrexate can be used as steroid-sparing agents once the disease is under control.


• Severe disease. Cyclophosphamide, mycophenolate mofetil and rituximab are reserved for more serious disease, including renal involvement.

Antiphospholipid syndrome Antiphospholipid syndrome is a procoagulant state which may occur as a primary phenomenon, or in association with SLE. The commonest symptoms include: • Venous and arterial thrombosis. • Recurrent miscarriage (≥ 3 before 10 weeks gestation or ≥ 2 after 10 weeks gestation). • Pre-eclampsia/eclampsia. Other symptoms include: • Livedo reticularis. • Thrombocytopaenia. • Valve disease (up to 30% have mitral valve prolapse). • Neurological features: transverse myelitis, migraine, chorea. The diagnosis is confirmed by the combination of the clinical picture and the presence of anticardiolipin antibody or lupus anticoagulant (or both). Treatment is anticoagulation, usually aiming for an INR between 2.0 and 3.0, although occasionally higher. Potentially pro-coagulant medications such as oestrogen-containing contraceptives and hormone replacement therapy are contraindicated.

Sjögren’s syndrome Sjögren’s syndrome is characterised by lymphocytic infiltration into exocrine glands, causing dry eyes and a dry mouth. It may occur as a

primary disease, or in association with SLE and other inflammatory diseases. The characteristic antibody profile is anti-Ro and/or anti-La; if these antibodies are detected in a pregnant woman, congenital heart block is a recognised complication in the foetus. Other features include: • Parotid swelling. • Cutaneous vasculitis. • Peripheral sensory neuropathy or myelopathy. • Anaemia and hypergammaglobulinaemia. The most feared complication is transformation to lymphoma, so persistent changes in parotid glands or changes in immunoglobulin profile with evidence of immune-paresis should be taken seriously. Treatment is symptomatic with artficial tears and saliva or muscarinic agonists (e.g. pilocarpine). Immunosuppression is only required for severe extra-glandular disease.

TIPS • Not all patients with a positive antinuclear factor have SLE • SLE has a wide range of clinical presentations and severity of disease • Renal lupus is the most feared complication and should be identified and treated promptly • Anti-phospholipid syndrome is an important cause of arterio-venous thrombosis and pregnancy morbidity

Systemic lupus erythematosus

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25

Ankylosing spondylitis

Ankylosing spondylitis Articular features

Extra-articular features

Cervical hyperextension

Anterior uveitis

Exaggerated thoracic kyphosis Apical pulmonary fibrosis Loss of lumbar lordosis

Aortic regurgitation S1

S2

S1

S2

Amyloid

Compensatory flexion at knee

Vertebrae Plus – oligoarthritis Squaring and syndesmophytes Fibrosis/ossification of ligaments 'Bamboo spine'

“Question-mark posture”

Rigid ↓ mobility Risk of fracture Schober's test

Treatment Dimples of Venus 10 cm

15 cm

Physiotherapy NSAIDs Sulfasalazine for peripheral disease Anti-TNF

>20 cm

5 cm On forward flexion Plus assess: Lateral flexion Cervical rotation Chest expansion

Mark the skin 10 cm above and 5 cm below the dimples of Venus (posterior superior iliac spines) Ask patient to bend forward with straight legs Distance between marks should increase to >20 cm

Spondyloarthropathies is a collective term for a group of inflammatory joint diseases that may involve the spine. The classic spondyloarthropathy is ankylosing spondylitis in which pelvic and axial disease is the predominant feature, but inflammatory spinal disease may also occur in psoriatic, reactive or enteropathic arthritis. These diseases are covered in the next chapter (Chapter 26, The spondyloarthropathies). All spondyloarthropathies share a number of features that may affect an individual patient at any time during the course of their disease: • Sacroiliac/pelviaxial disease (back or buttock pain). • Peripheral inflammatory arthropathy (any pattern of joint disease). • Enthesopathy (inflammation of tendon insertions, classically Achilles). • Non-musculoskeletal syndromes (e.g. skin or eye disease).

In addition, the spondyloarthropathies share an association with the MHC molecule HLA-B27, and the closeness of this association varies with the clinical subtype. For example, more than 90% of patients with ankylosing spondylitis (AS) are HLA-B27 positive compared with 50% of those with psoriatic or enteropathic arthritis.

Ankylosing spondylitis AS affects up to 1% of the population. It presents classically with insidious inflammatory back pain and morning stiffness that improves with activity and deteriorates with rest. Typically the patients are young (<40 years) and male (ratio 3 male : 1 female), and a family history of spinal disease may be available.

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60 Published 2012 by John Wiley & Sons, Ltd.


Symptoms are caused by fibrosis and ossification of ligaments, tendons and insertions, mainly in the region of the intervertebral discs and the sacroiliac joints, and eventually spinal fusion may occur as a result of syndesmophyte formation (bridging spurs of bone at the corner of adjacent vertebral bodies). Spinal fusion is surprisingly painless until microfractures occur. Chest expansion is reduced by disease at the costovertebral and costochondral junctions. Insertional tendonitis (enthesopathy) and peripheral synovitis (mono- or oligoarticular) occur in a significant proportion of patients. Advanced AS produces a ‘question-mark’ posture, characterised by: • Loss of lumbar lordosis. • Exaggerated thoracic kyphosis. • Cervical hyperextension. • Compensatory flexion at the knee. One brief assessment of AS relies on assessment of chest expansion and spinal mobility. The latter can be determined by measuring both lateral and forward flexion (Schober’s test, see opposite). A number of validated scores called the Bath Ankylosing Indices cover disease activity (BASDAI), metrology (BASMI) and function (BASFI). The BASDAI is calculated from visual analogue scores regarding: fatigue, spinal pain, joint pain/swelling, areas of local tenderness (enthesopathy), morning stiffness and severity. Decisions regarding biologic therapy for patients with severe AS are based on the BASDAI (see below). AS has a number of extra-articular associations: • Anterior uveitis occurs in up to 40% of patients with AS, but its occurrence bears no relation to disease activity in the spine. • Apical pulmonary fibrosis, pleuritis and fusion of thoracic chest wall cause restrictive lung disease and all patients must be advised against smoking. • Aortic incompetence.

Diagnosis Diagnosis hinges on a combination of radiological evidence of sacroiliitis and either a typical history or examination findings. Additional radiological features in AS include: • Romanus lesions ‘shiny corners’ of localised oedema at entheses. • Squaring of vertebrae. • Ossification. • Syndesmophytes. • Facet joint involvement. The inflammatory markers CRP (C-reactive protein) and ESR (erythrocyte sedimentation rate) are not always elevated. HLA-B27 is not helpful diagnostically as it has such a high prevalence in the normal population; a negative HLA-B27 however is very reassuring.

Treatment The mainstay of therapy is patient education, physiotherapy to maintain mobility and non-steroidal anti-inflammatory drugs (NSAIDs) for spinal disease. Peripheral disease may be controlled by sulfasalazine. For those patients with severe disease (BASDAI > 4 and at least 4cm on a visual analogue score of spinal pain) that have failed to respond to two NSAIDs, biologic therapy in the form of anti-TNF agents have proven to be very effective.

TIPS • Virtually all patients with ankylosing spondylitis are HLA-B27 positive, but not all HLA-B27 patients have ankylosing spondylitis • Physiotherapy is crucial in maintaining patient mobility • BASDAI is helpful in assessing disease activity, response to treatment and need for biologic therapy

Ankylosing spondylitis

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The spondyloarthropathies

Ocular

Conjunctivitis, anterior uveitis

AS/IBD/ReA

Oral

Ulcers

IBD

Nails

Pitting, ridging, onycholysis Leuconychia

PsA/IBD

Skin

Psoriasis PsA/IBD/ReA Circinate balanitis, keratoderma blennorrhagica Erythema nodosum, pyoderma gangrenosum

Gastrointestinal

Diarrhoea

= = = =

Ankylosing spondylitis Psoriatic arthritis Enteric arthritis Reactive arthritis

IBD/ReA

Genitourinary

ReA

Joints

AS/PsA/IBD/ReA

Ankylosing spondylitis Classically symmetrical Sacroiliitis Spondylitis

AS PsA IBD ReA

Enteric arthritis Peripheral Type I vs Type II Asymmetric sacroiliitis/spondylitis

Reactive arthritis Psoriatic arthritis Mono/oligo arthritis Mono/oligo arthritis Asymmetric sacroiliitis/spondylitis Arthritis mutilans Asymmetric sacroiliitis/spondylitis Classic PsA (mainly PIPs/DIPs) RA-like (mainly MCPs/PIPs)

Introduction Ankylosing spondylitis is the commonest spondyloathropathy and is covered in detail in Chapter 25. Psoriatic, reactive and enteropathic arthritis are also referred to as spondyloarthropathies if they involve inflammatory spinal pain at some course during their natural history.

Psoriatic arthritis Five to ten percent of patients with psoriasis develop arthritis. The male: female ratio is equivalent, with a peak incidence between 20 and 40 years of age. Clinical patterns vary widely including: • Distal hand disease predominantly affecting the distal interphalangeal (DIP) joints. • Symmetrical polyarthritis similar to rheumatoid arthritis. • Spondyloarthropathy. • Asymmetrical oligoarthritis. • Arthritis mutilans due to osteolysis of the small joints in the hand.

Dactylitis (so-called ‘sausage finger ’), tenosynovitis and enthesitis are also common.

Diagnosis Differentiating rheumatoid arthritis (RA) in a patient with coexistent psoriasis from true psoriatic arthritis (PsA) can be difficult, especially since up to 10% of those with PsA are rheumatoid factor positive. ACPA (anti-CCP) antibodies are generally absent however. Clinically, the presence of disease at the DIP joint and/or psoriatic nail changes such as pitting, ridging, onycholysis, and salmon-pink patches would suggest an underlying diagnosis of PsA rather than RA. Radiological indicators of a diagnosis of PsA rather than RA include: • Absence of juxta-articular osteopaenia. • Whittling of the terminal phalanges (acro-osteolysis). • Pencil-in-cup deformity (erosion of the proximal and expansion of the distal portion of an interphalangeal joint). • Ankylosis.

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Since psoriasis is a high cell turnover state, hyperuricaemia and gout are also possible causes for arthropathy in this population.

B27 is not helpful with diagnosis but B27+ve patients tend to have a more prolonged, severe course to their arthritis.

Treatment

Treatment

• NSAIDs and occasional intra-articular steroid injection can be used as a ‘rescue’. • Methotrexate and/or leflunomide (may also improve skin). • Sulfasalazine, azathioprine, penicillamine, gold and cyclosporin in severe cases. • Avoid use of hydroxychloroquine as it may produce flares of skin disease. • Biologic therapy in the form of anti-TNFα for those with refractory joint disease (≥3 tender and ≥3 swollen joints despite trials of at least two DMARDs) is very effective.

NSAIDs and local corticosteroid injections will suffice for many patients, and the majority are in remission within 2 years. However, persistent disease (particularly a problem in B27+ve patients) may require DMARDs such as sulfasalazine. Antibiotic therapy against the precipitating infection may not have any impact on the arthropathy.

Reactive arthritis/Reiter’s syndrome Any of the spondyloarthropathies are considered ‘reactive’ if a history of urethritis/cervicitis or diarrhoea is present. Urethritis is commonly due to Chlamydia and may be asymptomatic; the diarrhoeal illness has usually occurred within the preceding month and the most likely pathogens are Shigella, Salmonella and Campylobacter. The syndrome may develop acutely with fever, weight loss and polyarticular involvement, but more commonly patients present with a mono- or oligoarthritis and either a low grade or absent fever. Additional features that may be present include: • Painless ulcers on the palate. • Balanitis circinata: painless plaques on the glans or shaft of the penis. • Keratoderma blennorrhagica: a painless papular/pustular rash on the palms or soles of the feet. • Conjunctivitis: may be followed by uveitis. • Enthesitis. Recurrent/repeated infections do not always lead to recurrence of arthritis. Other post-infective arthropathy differentials include HIV, Lyme disease, Behçet’s disease and parvovirus.

Diagnosis The diagnosis relies on a careful history/examination and the combination of raised inflammatory markers, as well as the results of serologic testing, cultures and swabs. Joint aspirate will rule out a septic or crystal arthropathy. There are no classic radiological features. HLA-

Enteric arthropathy Up to 20% of patients with either Crohn’s disease or ulcerative colitis develop an arthropathy. Of those with arthritis, two-thirds have peripheral symptoms and one third develop AS-like disease. • Peripheral disease has a slightly higher incidence in Crohn’s patients. It has been subdivided into: Type I: oligoarticular and asymmetric, it may coincide with the onset of bowel disease and has a close association with GI exacerbations. Type II: polyarticular and symmetric and less closely associated with flares of bowel disease. • Sacroiliitis occurs in both forms of inflammatory bowel disease. It is not clearly associated with either the onset or exacerbations of bowel pathology.

Treatment Therapy relies on NSAIDs if tolerated and intra-articular and/or oral steroids. Sulfasalazine is the disease-modifying treatment of choice as it has a beneficial effect on bowel disease; methotrexate is occasionally used second-line. Biologic therapy for those with refractory arthritis due to Crohn’s disease is very effective.

TIPS • Nail changes are a characteristic feature of those with psoriatic arthritis • Most patients with reactive arthritis are in remission within 2 years; B27 positivity is a poor prognostic factor • Spinal and bowel disease run independent courses in enteric arthropathy

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Acute joint disease

THE ACUTE JOINT

Features Hot Swollen Tender Held immobile

GOUT

Differential diagnosis Septic arthritis Gout Pseudogout Spondyloarthropathy Haemarthrosis Inflammation periarticular structures Consider also – tumour no swelling – fracture

Diagnosis

Causes Production: Alcohol Meat Shellfish Chemotherapy Haematological malignancy Psoriasis Excretion: Diuretics Alcohol Low-dose aspirin Renal insufficiency

Aspirate joint Visualise crystals Rule out sepsis

Complications Skin: tophi Uric acid crystals

Joints: synovitis

Gout

Kidney: stones (radiolucent) nephropathy

Treatment Acute: NSAIDs, colchicine, steroid Chronic/prophylaxis: allopurinol, uricosuric agents

Introduction An acutely painful, swollen or hot joint is septic arthritis until proven otherwise. Joint infection is a medical emergency and is covered in detail in Chapter 28, Infection and malignancy. This chapter is dedicated to the far less dangerous but much more common causes of a painful joint – in particular, the acute crystal arthropathies gout and pseudogout.

Gout Gout is an inflammatory arthropathy generated by uric acid crystal deposition in the joints and peri-articular structures, e.g. bursae. Uric acid is a product of DNA breakdown (purine nucleotides) but is also present in foods and alcohol. Once a biochemical threshold is reached in a susceptible individual, crystals precipitate into joints, skin and kidneys causing a spectrum of disease.

Clinical picture Gout is characterised by acute attacks of joint inflammation separated by asymptomatic periods. The commonest joint to be affected is the

first metatarsophalangeal joint (podagra), but other common sites include the ankle, knee, wrist and fingers. Attacks are usually monoarticular but may become polyarticular if recurrent attacks are left untreated, and indeed this chronic inflammation can generate a destructive arthritis. Hyperuricaemia can be generated by two processes. 1 Overproduction of urate or increased purine synthesis. A number of different things can cause this overproduction: • Alcohol, red meats and seafood contain high levels of urate. • Increased cell turnover states such as psoriasis, haematological malignancies or chemotherapy produce purines via DNA breakdown. • Enzyme defects can also be responsible, but these are relatively rare. 2 Underexcretion of urate. This can be due to renal failure, alcohol, diuretics, low dose aspirin, dehydration or starvation. Frequently an attack of gout is provoked by trauma, surgery or alcohol/dietary excess. Note that biochemical hyperuricaemia may not produce the clinical syndrome of gout.

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Uric acid deposition in the skin produces tophi – well demarcated collections of crystals that may rupture, releasing a chalk-like substance. Classic sites for tophi include the helix of the ear, the olecranon and prepatellar bursae, the ulnar border of the forearm and the tendons. Tophi may break down or ulcerate and occasionally cause diagnostic confusion with rheumatoid nodulosis. Deposition of urate in the renal tract can cause: • Renal stones (remember that uric acid stones are radiolucent). • Urate nephropathy (deposition of urate in renal interstitium or collecting tubules). Thus, gout can both cause and be caused by renal impairment.

presentation is an acutely hot, swollen and tender joint, usually the knee or shoulder, but it can present more insidiously as a ‘pseudorheumatoid’ polyarticular pattern in the hand. Underlying disease states (including haemachromatosis, Wilson’s disease and hyperparathyroidism) may precipitate pseudogout and these should be sought in a young patient with this diagnosis. Diagnosis relies on the identification of positively birefringent rhomboid-shaped crystals in synovial fluid. NSAIDs are the mainstay of treatment, in combination with joint aspiration and intra-articular steroid injection. Low-dose colchicine may play a role in prophylaxis.

Investigations

Differential diagnosis of the acute joint

Urate levels These may be normal (or even fall) during an acute attack in up to 50% of patients. They are used principally to monitor the success or compliance of urate-lowering therapy.

1 An acute joint is septic arthritis until proven otherwise. Although septic arthritis is not the most common final diagnosis, it must be considered in all cases, including those with established inflammatory arthropathy such as RA, as its consequences are dire. 2 Crystal arthropathy (see above). 3 Flare of established inflammatory arthropathy, e.g. rheumatoid, psoriatic or enteric arthropathy, or Reiter ’s syndrome (see relevant chapters for discriminating features of each). 4 Intra-articular bleed (haemarthrosis) in patients with bleeding diathesis or on warfarin therapy. It should also be remembered that inflammation in periarticular structures (e.g. bursitis or tendinopathy) can mimic a hot joint. Ultrasound investigation can prove very helpful in these situations.

X-ray X-rays show soft tissue swelling, and punched-out erosions in persistent disease which may corticate and heal. Osteopaenia is not a feature and joint fusion is rare. Joint fluid Joint fluid shows low viscosity, a high white cell count and the presence of intraneutrophilic urate crystals – characteristically needleshaped and negatively birefringent under polarised microscopy.

Summary Management Acute attack The priority is to relieve pain and inflammation using non-steroidal anti-inflammatory agents (NSAIDs), colchicine or steroids. Prophylaxis Lifestyle modification with stringent avoidance of risk factors should be undertaken and precipitating drug-therapy altered where possible (e.g. reducing frusemide dose). Urate-lowering therapy is commenced under anti-inflammatory cover once the acute attack has settled. Allopurinol (xanthine oxidase inhibitor) is used most commonly. If renal function is impaired, lower doses must be used. Side effects include rashes and a serious drug interaction with azathioprine, risking bone marrow failure. The alternative xanthine oxidase inhibitor, febuxostat, has recently received NICE approval for patients intolerant of allopurinol. Second-line therapy is the uricosuric agent sulfinpyrazone which increases renal excretion of urate. It cannot be used in the presence of renal stones. In gout patients with hypertension and dyslipidaemia, losartan (angiotensin-1 receptor antagonist) and fenofibrate (hypolipidaemic agent) may be used as adjunct therapy as both reduce serum uric acid levels.

Pseudogout Pseudogout is an inflammatory arthropathy due to calcium pyrophosphate deposition, and is frequently associated with chondrocalcinosis (calcification of fibrocartilage and hyaline cartilage). The commonest

If a patient presents with an acutely inflamed joint, you are obliged to rule out septic arthritis. Crystal arthropathy or a seronegative spondyloarthropathy are also possible culprits. There are a number of features one should elicit in the history to determine the most likely underlying diagnosis: • Is the patient septic? • Risk factors/history of gout? • Known inflammatory arthropathy, e.g. spondylarthritis? • Rash? Psoriatic arthropathy/Reiter’s syndrome/enteric arthropathy. • Diarrhoea? Reiter ’s syndrome/enteric arthropathy. • Eye disease? Reiter ’s syndrome/enteric arthropathy. • Known sexually transmitted disease or urethral discharge? Reiter ’s syndrome. • Warfarin or bleeding episodes? Haemarthrosis. The single most important investigation is synovial fluid aspiration. The fluid must be sent immediately for microscopy, culture and sensitivity studies to rule out septic arthritis or crystal arthropathy.

TIPS • An acute monoarthritis is septic arthritis until proven otherwise – and joint aspiration is mandatory • Gout would be unusual in a premenopausal woman • Urate levels may be normal during an acute attack of gout

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Infection and malignancy

SEPTIC ARTHRITIS

Presentation Commonly acute monoarthropathy Pain, erythema, ↑ temperature ↓ Range of movement Febrile/systemic features

Risk factors

Organisms

Extremes of age Trauma Immunosuppression Diabetes mellitus Damaged or prosthetic joint

Staphylococcus aureus Group B streptococcus Gram-negative bacilli Gonococcus

Routes of entry

Treatment Prolonged course of antibiotics Surgical wash-out

Haematogenous Direct – penetrating injuries Spread from neighbouring tissues Differential diagnosis Diagnosis

Crystal arthropathy Reactive arthritis First presentation seronegative arthritis Inflammation peri-articular structures Rheumatoid arthritis rarely presents as an acute monoarthropathy

Synovial fluid aspiration microscopy culture and sensitivity Blood cultures

Septic arthritis

Diagnosis

Septic arthritis is a rheumatological emergency. It is associated with considerable morbidity and mortality (up to 15%), so a high index of suspicion should always be maintained.

The diagnosis hinges on joint aspiration and analysis of the synovial fluid. In non-gonococcal bacterial arthritis, the yield from joint cultures is >95%, falling to 50% yield from blood cultures. In high-risk or clear-cut cases it is prudent to commence antibiotic therapy as soon as joint fluid and blood cultures have been taken; antimicrobial therapy can be adjusted once the microbiological results and sensitivities are available. The commonest causative agents are divided into: 1 Non-gonococcal (80% cases): • Staphylococcus aureus • B haemolytic streptococci • Gram-negative bacilli, e.g. Pseudomonas, Escherichia coli and Proteus. In children, Streptococcus and Haemophilus influenzae are the commonest pathogens. 2 Gonococcal arthritis. Occasionally gonococcal arthritis can be clinically differentiated from non-gonococcal disease and this can prevent considerable diagnostic delay – microbiological yield in gonococcal disease is notoriously poor with up to 75% of synovial fluid cultures being negative. In addition, positive blood cultures are exceedingly rare. Gonococcal

Clinical features A septic joint is exquisitely painful and is often held rigid in the most comfortable position. Systemic features of infection such as fever and constitutional upset are typical but occasionally patients may be afebrile and appear deceptively well. Although the classic presentation of bacterial arthritis is an acute monoarthritis, up to a third of cases are polyarticular. Patients at particular risk of developing septic arthritis include: • Patients with abnormal, damaged or prosthetic joints. • The immunocompromised (including diabetics). • The elderly and the very young. Bacteria reach the joint through three major routes: 1 Haematogenous spread during an episode of bacteraemia. 2 Direct inoculation following a penetrating injury, surgery or joint injection. 3 Spread from neighbouring bone (osteomyelitis) or soft tissue (cellulitis).

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septic arthritis tends to occur in younger, healthier patients, the arthritis may adopt a migratory pattern and tenosynovitis and skin lesions are a frequent feature. It is important to remember that the antecedent infection may be asymptomatic, particularly in women.

Treatment The treatment of choice for septic arthritis is prompt and appropriate antibiotic therapy – empiric choices must cover staphylococcal and streptococcal species and most patients receive 6 weeks of antibiotics. Surgical wash-out of a joint (especially prosthetic ones) may be warranted. Septic arthritis in children may damage the growth plate, causing limb shortening on the affected side.

Osteomyelitis Osteomyelitis is infection of bone or bone marrow and usually presents with deep-seated bone pain, with or without septic features. The majority of cases in adults are caused by Staphylococcus aureus, but tuberculosis, salmonella and pseudomonas are also encountered.

Diagnosis Diagnosis relies on appropriate imaging. X rays are unhelpful early on in disease, but ultrasound may demonstrate pus in the subperiosteal region. Bone marrow oedema and periosteal abscess formation can be visualised on MRI, whereas CT is better at demonstrating the development of vascular congestion or thrombosis. Remember that the white cell count and inflammatory response may be normal despite active infection.

Treatment Treatment is similar to that for the infected joint, with prolonged courses of appropriate antibiotics. Occasionally, surgical debridement is required.

Malignant bone tumours Secondary tumours are far more common than primary bone malignancy. The commonest carcinomas to spread to bone are breast, bronchus, thyroid, prostate and kidney and the commonest sites for deposit are the vertebral column, ribs, proximal femur and humerus. • Metastatic deposits tend to erode bone (lytic lesions) and may present with vertebral collapse or pathological fracture. Extensive destruction may cause hypercalcaemia, but more frequently the hypercalcaemia of malignancy is due to the production of parathyroid hormone-related protein by tumour cells. • Prostate and occasionally breast secondaries may induce reactive new bone formation, giving rise to osteosclerotic metastases. These patients will have a high serum alkaline phosphatase. • Bone pain from malignancy is unremitting. Night pain is a classic ‘red flag’ symptom for malignancy. • Treatment centres on management of the hypercalcaemia, surgical stabilisation of deposits at risk of fracture, radiotherapy and pain control. The commonest primary malignant diseases of bone are myeloma and osteosarcoma.

Myeloma • Multiple myeloma is caused by neoplastic proliferation of plasma cells in the bone marrow leading to bone pain and pathological fractures. If the marrow is replaced by tumour cells a pancytopaenia may result. • Radiologically, myeloma causes multiple ‘punched-out’ lesions; if the disease is widespread a diffuse osteoporosis may occur. Bone scans in myeloma are cold and inconclusive. • Classically myeloma patients have a high erythrocyte sedimentation rate (ESR), elevated calcium and alkaline phosphatase. Diagnosis relies on protein electrophoresis, demonstrating a monoclonal protein in the serum (and Bence-Jones immunoglobulin protein in the urine); bone marrow biopsy reveals a plasma cell infiltrate. • Treatment is chemotherapy.

Primary bone tumours These are rare and can arise from any of the cell types involved in the skeleton. Chondrosarcomas arise from cartilage cells, myosarcomas from muscle, liposarcomas from fat and osteosarcomas from bone cells.

Osteosarcoma • Osteosarcoma affects young people, with most cases occurring between 10 and 25 years of age. • Patients typically present with pain and swelling but pathological fracture is relatively unusual. • The majority of osteosarcomas arise in the metaphysis of the long bones. Classic sites include the knee, proximal humerus and femur and distal radius. • Treatment involves chemotherapy and surgery.

Ewing’s sarcoma • Ewing’s sarcoma is the second commonest primary tumour, again affecting children. • Patients present with systemic upset and warm erythematous swelling, commonly at the diaphysis. Chrondrosarcoma may mimic infection or eosinophilic granuloma. • Treatment involves neoadjuvant chemotherapy, radiotherapy and surgery.

Chondrosarcoma Chondrosarcomas affect adults over 40 years of age. They are relatively insensitive to adjuvant therapy and the treatment is surgical.

TIPS • Any patient presenting with an acute monoarthritis should be assumed to have septic arthritis until proven otherwise • Never inject a joint through infected skin or soft tissues • Think of myeloma in an elderly patient with osteoporosis and/or fracture in the presence of an unexplained elevated ESR

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Fibromyalgia

Pain Diffuse No clear localization

Sleep Poor Non-restorative

Mood Depression

The nine pairs of trigger points in fibromyalgia

Low cervical 2nd rib – costochrondral junction

Occiput muscle insertions Trapezius and supraspinatus

Lateral epicondyle Gluteal Greater trochanter Knee medial fat pad

Introduction Fibromyalgia is a non-inflammatory, non-autoimmune diffuse pain syndrome characterised by combinations of hyperalgesia, disordered non-restorative sleep and low mood. It can occur on its own (primary) or in association with chronically painful conditions such as rheumatoid arthritis (secondary). Primary fibromyalgia is considered under the umbrella term of ‘soft-tissue rheumatism’ and the objective absence of (peri-)articular disease is crucial both in terms of diagnosis and management.

Symptoms and signs There are no good epidemiological studies but primary fibromyalgia may affect up to 4% of the population overall. The overwhelming majority of patients are women, and the average age at diagnosis is early middle-age (40–50 years). Indeed, the development of disabling fatigue and pain in older age groups should prompt a considered search for alternative sinister diagnoses such as chronic infection or occult malignancy. The characteristic clinical features of fibromyalgia are chronic diffuse pain in association with combinations of morning stiffness,

fatigue and non-restorative sleep, depression, anxiety and headache. More rarely the presence of parasthesiae or Raynaud’s phenomenon can add to diagnostic difficulty. Examination is normal, except for the presence of classic ‘trigger points’ – evidence of hyperalgesia at specific soft-tissue sites (see below). However, if fibromyalgia occurs as a secondary phenomenon due to another condition such as RA, then the clinical findings are those one would expect from the underlying disease (e.g. synovitis, effusions and joint destruction). • Pain: is characteristically diffuse, with non-inflammatory spinal pain being a common feature. The pain is hard to localise and patients frequently massage their whole arm/leg, describing it as ‘deep inside’. It may not follow the diurnal pattern or relation to exercise of inflammatory or degenerative disease, and patients frequently experience good days and bad days. • Sleep: is non-restorative leading to daytime fatigue, which may be extreme. The sleep disturbance is characterised by alpha-delta sleep, in which delta (restorative, restful and deep) sleep is interrupted by alpha-waves (found early in the approach to sleep). As a result, late and restorative non-REM stage IV sleep is dramatically reduced. This sleep pattern also occurs during times of emotional stress and is found

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in other causes of chronic pain such as RA; the fatigue in inflammatory disease is compounded by circulating cytokines, which are not a feature of primary fibromyalgia. • Depression: the relationship between pain and mood is reciprocal. Low mood is understandably a common component of chronically painful syndromes and mood impacts profoundly on pain perception. Low mood may also engender a sense of helplessness in the patient, reducing their ability or desire to adhere to treatment strategies. Successful rehabilitation is a frequently a significant challenge. • Parathesiae and neurological features: these are classically nondermatomal/anatomical in distribution and are not accompanied by abnormal investigations such as EMG findings. • Raynaud’s phenomenon: occurs in up to 10% of patients with fibromyalgia, but there are no associated systemic features of either SLE or scleroderma.

Trigger points The clinical examination in primary fibromyalgia is essentially normal, with no objective evidence of articular or systemic disease. However, the presence of multiple tender trigger points (see figure opposite) is highly suggestive of fibromyalgia. These are specific areas on the body that are sensitive to applied pressure, even in normal people. In the context of a pain amplification syndrome, such as fibromyalgia, these areas are exquisitely tender when only moderate pressure is applied (i.e. enough to blanch the examiner ’s thumbnail). There are 18 specific points, of which 11, represented in all 4 quadrants of the body, should be tender to consider the diagnosis.

Aetiology The aetiology of fibromyalgia is unknown. Unlike the closely-related chronic fatigue syndrome, in which a precipitating episode (usually viral illness) is frequently clearly identifiable, patients may not identify a particular trigger for fibromyalgia. Where present, common precipitating events include viral illness, emotional stress or minor injury such as whiplash. Withdrawal from medications, particularly glucocorticoids, may also be implicated. The pathogenesis of fibromyalgia is likely to be an abnormality of central processing, manifesting as a problem of pain perception or amplification; abnormalities in the descending analgesia and endog-

enous endorphin systems, alpha-delta sleep disturbance, affective spectrum disorder and somatoform disorder may all play a role in initiation and perpetuation of the condition. MRIs of patients’ brains are normal but functional imaging studies have suggested reduced blood flow to thalamus and caudate nucleus, which has been reported in other causes of chronic pain.

Treatment and prognosis Treatment for fibromyalgia is a combination of: • Patient education. • Physical therapy and aerobic exercise. • Analgesia. • Correction of sleep disturbance. • Treatment of any associated disorders. Patient education is particularly crucial and must be sensitively handled: there should be agreement that the symptoms are both real and disabling, but strong reassurance that the patient has substantial control over the impact, treatment and outcome of the condition. A steadily graded aerobic exercise system is also vital. Medical therapy is based on low dose tricyclic antidepressants (TCAs) to improve sleep quality and alter pain perception: a standard approach would be amitriptyline 10 mg several hours before going to bed (to try to avoid hang-over effect). This can be increased gradually to a maintenance dose of 30–40 mg daily. If TCA side-effects such as dry mouth or constipation prove troublesome, there is some evidence of the efficacy of SSRIs such as venlafaxine. The prognosis is variable and depends profoundly on patient-physician interaction and the patient’s ability to engage with rehabilitation programmes. TIPS • Fibromyalgia is a combination of hyperalgesia, non-restorative sleep and low mood • Secondary forms often co-exist with inflammatory conditions such as rheumatoid arthritis • The presence of trigger points is helpful in diagnosis • Treatment centres on patient education, exercise, analgesia and restoration of normal sleep patterns

Fibromyalgia

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Osteoporosis

Vulnerable fracture sites

Risk factors

dn

Pre

Maternal Hx hip fracture

Neck of femur

Oestrogen deficiency

Distal radius

Corticosteroid therapy

Vertebral bodies 'Dowager's hump'

Thin habitus Osteoporosis

Treatment General Good diet + vitamins

Smoking, alcohol

Weight-bearing exercise Diagnosis

X-RAY

DO NOT ENTER

DEXA scan compare BMD with young normal mean

Consider secondary causes: Malabsorption, e.g. coeliac disease Hyperparathyroidism Hyperthyroidism Cushing’s disease Hypopituitarism Hypogonadism Multiple myeloma

Introduction The World Health Organisation has defined osteoporosis as a ‘systemic skeletal disease characterised by low bone mass and microarchitectural deterioration of bone tissue with a consequent increase in bone fragility and susceptibility to fracture’. Bone mass or mineral density relies on a balance between osteoblastic and osteoclastic activity. Overall bone mass increases until adulthood, plateaus and then declines from 35 years of age onwards, accelerating in women following the menopause.

No alcohol, cigarettes

Pharmacological Bisphosphonates ? Strontium ? Teriparatide

By 60–70 years of age, 30% of women have osteoporosis, rising to 70% in those over 80 years. Although the entire skeleton is affected, the commonest sites for osteoporotic fracture are the neck of the femur, the vertebrae and the distal radius. The morbidity associated with neck of femur fractures is particularly significant, and generates an increasing economic burden.

Risk factors The most important risk factors for osteoporosis are:

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• Maternal family history of hip fracture. • Oestrogen deficiency, e.g. due to premature menopause, prolonged secondary amenorrhoea or primary hypogonadism. • Corticosteroid therapy e.g. prednisolone dose >7.5 mg/day for >6 months. • Low body mass index (BMI) of <19 kg/m2 due to a combination of reduced oestrogen levels and reduction in impact loading. Other risk factors include: • Smoking. • Excess alcohol. • Anorexia nervosa (low weight, menstrual irregularity, low calcium intake). • Endocrine syndromes (hyperparathyroidism, hyperthyroidism, Cushing’s syndrome). • Multiple myeloma. • Inflammatory arthropathy (probably due to increased IL-1 and TNFα levels). • Prolonged immobilisation.

Diagnosis Osteoporosis is diagnosed using a dual energy X-ray absorptiometry or DEXA scan. This allows a measurement of the bone mineral density (BMD) at the lumbar spine and proximal femur for comparison against someone of the same age and gender (Z score) or of the young normal mean – the T score. • Normal: BMD T score >1 standard deviation (SD) below the young normal mean (more than −1). • Osteopaenia: BMD T score 1–2.5 SD below the young normal mean (between −1 and −2.5). • Osteoporosis: BMD T score >2.5 SD below the young normal mean (more than −2.5). • Severe osteoporosis: as above plus previous fragility fracture.

Treatment General measures All patients with osteoporosis must maintain good nutrition with high levels of calcium and vitamin D, by dietary supplementation if necessary. Increased physical activity improves BMD via impact loading and also reduces the overall risk of falls. Patients should also be advised to stop smoking and to avoid alcohol excess, and steroid doses must be reduced or withdrawn wherever possible.

Pharmacological measures Bisphosphonates: risedronate, alendronate, etidronate and zoledronate As a group, the bisphosphonates inhibit the action and function of osteoclasts, thereby reducing skeletal resorption and the subsequent risk of fracture at both vertebral and non-vertebral sites. They are available as daily or weekly preparations, but have variable acceptability and compliance due to gastrointestinal side effects. In order to reduce side effects and to maximise otherwise relatively poor absorption, patients must take their bisphosphonate on an empty stomach, with plenty of water, remain upright for 30 minutes after ingestion and have nothing to eat or drink for a further 30 minutes. Zoledronate is given as an annual intravenous infusion for those for whom oral administration is intolerable or contraindicated (severe oesophagitis, structurally or functionally abnormal oesophagus e.g. achalasia).

Selective oestrogen receptor modulators (SERMs): raloxifene SERMs such as raloxifene have oestrogenic effects on bone, but not breast or endometrium. They have been shown to decrease bone turnover in post-menopausal women with a subsequent increase in BMD and a reduction in vertebral (but not hip) fracture rate. In general they are well-tolerated, but confer an increased risk of deep venous thrombosis. Strontium Although its precise mechanism of action is unclear, strontium appears to uncouple bone remodelling, thereby stimulating bone formation and increasing BMD at the lumbar spine and femoral neck. It has a proven role in reducing vertebral fracture rate and preliminary data from a large clinical trial also suggest a reduction in hip fracture risk. Teriparatide (synthetic parathyroid hormone) Exogenous parathyroid hormone, given intermittently, has been shown to have anabolic effects on bone, increasing BMD and reducing the osteoporotic fracture rate. Currently licensed for the treatment of severe osteoporosis, it is administered as a once-daily subcutaneous injection. However, treatment is limited to 18 months as toxicology studies have suggested an increased risk of osteosarcoma with prolonged use. Hormone replacement therapy (HRT) Although it has been shown to increase BMD and reduce fracture rate, HRT should no longer be prescribed for primary prevention of osteoporosis as the associated risks of venous thromboembolism and breast carcinoma are deemed unacceptably high. The only current indication for HRT is the management of menopausal symptoms; bone protection is simply an additional benefit. Testosterone is used in men when hypogonadism is the underlying aetiology of their osteoporosis. Vertebroplasty Percutaneous vertebroplasty is used in patients with vertebral compression fractures and persistent pain. A needle is introduced into the bone and cement injected, filling the spaces and forming an internal cast. It is generally well-tolerated and reasonably effective.

Corticosteroid-induced osteoporosis Steroid therapy suppresses bone formation, increases osteoblast apoptosis and disrupts calcium homeostasis. For a given BMD, osteoporosis caused by steroids has the highest rate of fracture. There is a strong correlation between the daily dose and the fracture risk, and the risk both increases and declines rapidly on and off treatment. All physicians must be alert to the profound risk of long-term steroid therapy – particularly in the elderly population. The diagnosis and treatment for corticosteroid-induced osteoporosis is identical to that for idiopathic disease. TIPS • Consider the diagnosis of osteoporosis in any patient with low trauma fracture • Any elderly patient on steroids should receive bone protection • Bisphosphonates in combination with vitamin D/calcium supplementation are the first-line treatment in primary and secondary prevention of osteoporosis

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Disorders of bone metabolism

Osteoclast/osteoblast connections

TNFα Increases DKK-1 expression

Increases RANKL expression RANKL > OPG

BMPs CBFA DKK-1

Macrophage fusion and osteoclast activation

Osterix

Wnt

Sclerostin

β catenin accummulation

Expresses OPG

Osteoclast

Osteoblast

Biochemical abnormalities in metabolic bone disease

Ca

PO4

ALP

PTH

1, 25(OH)2 vitamin D

Osteomalacia

Osteoporosis

Normal

Normal

Normal

Normal

Normal

Paget’s disease

Normal unless fracture or osteosarcoma

Normal

↑↑

Normal

Normal

Bone remodelling Bone is generated and remodelled throughout life in cycles of tightly coupled osteoclastic and osteoblastic acivity. The osteoclast is a giant multinucleated cell derived from the monocyte/macrophage population and is responsible for bone resorption. The key signals in monocyte-osteoclast differentiation and activation are macrophage-colony stimulating factor (M-CSF) and receptor activator of NFκβ (RANK) ligand respectively. RANK ligand (RANKL) on stromal cells and osteoblasts bind to RANK on osteoclast precursors causing fusion and, via activation of a number of intracellular signalling pathways such as c-src, leads to differentiation into mature osteoclasts. The RANKL system is controlled by osteoprotegerin (OPG), also produced by osteoblasts, that acts as a decoy receptor and reduces osteoclast activation. The up-regulation of RANKL and reduced OPG expression is, in part, reponsible for the increased osteoclast activation and bone degradation in inflammatory arthritis. Another recently-identified determinant of inflammatory bone loss is dickkopf-1 (DKK-1). DKK-1 is up-regulated in RA synovium in response to TNFα and inhibits wingless (wnt)-signalling. The downstream effects of this inhibition is twofold: 1 osteoblast activity is directly down-regulated and 2 OPG is expression is reduced; this combination tips the balance of remodelling towards resorption.

In health, resorption by osteoclasts is swiftly followed by the creation of new bone by osteoblasts. Osteoblasts are mesenchymal stem cells. They are multipotent so their development into osteoblasts is promoted by a number of signals including bone morphogenic proteins, CBFA1 (core binding alpha factor 1), osterix and Wnt (see above); the activity of such pathways is modified by endogenous inhibitors such as sclerostin and DKK. Activation of Wnt signalling leads to the intracellular accumulation of β-catenin, leading to specific gene transcription and osteoblast formation. Osteoblasts produce bone matrix. Initially they lay down unmineralised osteoid; within 10 days this scaffold becomes calcified to form bone. Osteoblasts are rich in alkaline phosphatase (ALP) and osteocalcin, which can be used as a marker of osteoblastic activity (see below). The osteoclastic/blastic relationship underlying bone remodelling is further controlled by loading mechanics and both local signals (e.g. cytokines) and systemic factors (e.g. parathyroid hormone, vitamin D, thyroid and growth hormones).

Paget’s disease Paget’s disease is the second most common disorder of bone metabolism after osteoporosis. The disease is rare under 40 years, but increases

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with age and affects 5% of those over 55 years. It is characterised by excessive bone resorption, followed by rapid but disorganised new bone formation; the resultant bone is enlarged, deformed and weak. The most common sites are to be affected are the pelvis, lumbar spine and femur. Only 10-30% of patients experience any symptoms, so usually the diagnosis is made incidentally. Clinical features, where present include: • Bone pain. • Fractures. • Compressive neural deafness. Blood tests reveal a raised ALP in the absence of liver disease. Other markers include increased osteocalcin (from osteoblasts, see above) and urinary N telopeptide of type 1 collagen (as a result of excessive bone resorption). The calcium is normal in the absence of fracture or osteosarcoma. X-rays reveal thickened cortical bone and occasionally localised areas of osteoporosis: ‘osteoporosis circumscripta’. Treatment is aimed at bone pain with with bisphosphonates.

Osteomalacia and rickets These disorders of osteoid mineralisation are due to vitamin D deficiency; the bone is soft but of normal density, in contrast to osteoporosis. Rickets occurs before epiphyseal closure, whereas osteomalacia occurs in the mature skeleton. Rickets affects the metaphyses of the long bones most severely, but a variety of clinical features occur: • Soft skull (craniotabes). • Enlarged epiphyses of the wrist. • Costochondral swelling ‘rickety rosary’. • Harrison’s sulcus at the rib cage. • Leg deformities. The clinical features of osteomalacia are more subtle and a high index of suspicion should be maintained, particularly in high-risk individuals (see below). Predominant symptoms are often non-specific

complaints of musculoskeletal pain, but occasionally bone pain and fracture can occur. In addition, a waddling gait due to proximal myopathy may develop. Osteomalacia may mimic (or co-exist with) fibromyalgia, polymyalgia rheumatica, myositis and rheumatoid arthritis. Vitamin D deficiency most frequently occurs due to: • Inadequate sun exposure (full-body covering or living in institutions). • Poor diet. • Malabsorption (e.g. coeliac disease, post-gastrectomy or pancreatic insufficiency). • Renal disease (e.g. hypophosphataemic renal disease, Fanconi’s syndrome, distal renal tubular acidosis and renal osteodystrophy). • Drugs (e.g. carbamazepine, phenytoin). Biochemical testing reveals a reduced vitamin D with mildly reduced or normal calcium and phosphate and an elevated alkaline phosphatase and parathyroid hormone. X-rays demonstrate evidence of defective mineralisation and Looser ’s zones (low density bands of bone extending inwards from the cortex). Treatment is with vitamin D supplementation. Vitamin D-resistant rickets is caused by diminished renal hydroxylation of precursors or end-organ resistance to the active form: these patients require large doses of active vitamin D supplementation.

TIPS • Osteoclasts are ‘cutters’ and resorb bone, osteoblasts are ‘builders’ and create new bone • RANKL and OPG are the major determinants of osteoclast activity and bone resorption • Paget’s disease is often discovered incidentally on X-ray or due to an isolated elevation in ALP

Disorders of bone metabolism

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Vasculitis 1: Giant cell arteritis

Giant cell arteritis

Headache Scalp tenderness Jaw claudication

Visual loss

Associated PMR

Acute ischaemic optic neuropathy. The optic nerve head (disc) in the affected eye is swollen and pale as the nerve fibres are infarcted. Because this is an arterial ischaemic phenomenon, recovery of nerve function is rare, and optic atrophy supervenes. Courtesy of Dr Peggy Frith, Oxford Eye Hospital

Investigations ESR and CRP raised Temporal artery biopsy Beware: skip lesions! Giant cell arteritis. Temporal artery biopsy shows a narrow lumen and swollen arterial wall. There are widespread inflammatory cells throughout the layers of the artery and several multinucleated 'giant cells' within the media. Courtesy of Dr Peggy Frith, Oxford Eye Hospital

Introduction

Large vessel vasculitis

The vasculitides are a heterogenous group of disorders caused by vascular inflammation. As the vessel wall dies, ischaemia and infarction occur distal to the area of necrosis. The easiest system for classifying this group of conditions is therefore by vessel size, which aids in prediction of outcome and/or complications. The small vessel vasculitides are further subdivided according to their association with antineutrophil cytoplasmic antibodies (ANCAs). 1 Large vessel (aorta and largest branches): claudication, loss of pulses, cardiac failure, organ infarction. 2 Medium vessel (medium-sized arteries and smaller vessels): renal failure, hypertension, purpura. 3 Small vessel: renal and skin disease, pulmonary haemorrhage, arthralgia. The vasculitides can occur as idiopathic or secondary phenomena (e.g. complicating rheumatoid arthritis or systemic lupus erythematosis). In clinical practice, the most common vasculitis is giant cell (temporal) arteritis. The medium- and small-vessel vasculitides will be covered in the next chapter.

Giant cell arteritis (GCA) is a granulomatous inflammation of the aorta and large vessels, with a predilection for the extracranial branches of the carotid artery. The characteristic presentation is of rapid onset (1–2 days) of temporal headache, scalp tenderness and jaw claudication. GCA affects both sexes equally and usually only occurs in those over 60 years of age. Although it is relatively uncommon, with only 42 cases per million over 60 years of age, the diagnosis is frequently considered, as headache is a common presenting complaint. The most feared complication is of visual disturbance. Irreversible blindness occurs when the arteries supplying the retina or optic nerve head become involved (central retinal and posterior ciliary arteries); diplopia and ptosis may also occur. Visual loss may be the first symptom of GCA. In addition, 50% patients have a history of polymyalgia rheumatica (PMR) – an inflammatory disease causing classic shoulder and girdle muscular pain and stiffness, in the absence of weakness (which differentiates it from an inflammatory muscle disease).

Giant cell (temporal) arteritis

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The ESR (erythrocyte sedimentation rate) and CRP (C-reactive protein) are generally elevated, although disease in the presence of normal inflammatory markers has been reported. Temporal artery biopsy is notoriously unreliable due to the presence of skip lesions – areas of normal-looking tissue interspersed between areas of granulomatous inflammation – but if positive is diagnostic. Treatment Treatment for both GCA and PMR is corticosteroid therapy. As GCA can cause acute visual loss, steroids should be commenced before a temporal artery biopsy is performed; the abnormal histological features persist for up to 3 weeks after the commencement of steroid therapy and treatment delay may have devastating consequences. GCA requires high-dose steroids (1mg/kg oral prednisolone/day up to a maximum of 60mg, consider i.v. bolus in the presence of visual symptoms), whereas PMR responds to much lower doses (e.g. 15 mg prednisolone/day). The clinical response is dramatic and steroids can be tapered according to the decline in symptoms and inflammatory markers. However, the majority of patients take 2 years or more to stop steroid therapy, so bone protection is mandatory and the use of azathioprine or methotrexate as steroid-sparing agents should be considered. Relapse rates vary from 30–80%.

Takayasu arteritis This rare vasculitis is commonest in women under 50 years of age from the Far East, Central and South America and India. The UK incidence is only 0.1 per million/year. It is known as the ‘pulseless disease’ as large branches of the aorta become successively occluded. Symptoms are principally those of chronic vascular ischaemia: claudication, visual disturbances and strokes, although many experience systemic upset and arthralgia. On clinical examination, absent pulses and bruits are common, and a record of affected arterial territories is helpful in monitoring disease progression. Diagnosis is by arteriography, which reveals vessel narrowing or post-stenotic dilatation and magnetic resonance ateriography (MRA) reveals vessel wall oedema. Treatment requires corticosteroids and immunosuppression. Five-to-ten year survival rates are now 80–90% but approximately half will experience permanent disability. TIPS • The commonest vasculitis is giant cell arteritis (temporal arteritis) • The ESR and CRP may not be raised; the biopsy may be negative due to skip lesions • Investigation should not delay treatment if the clinical suspicion is high

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Vasculitis 2: Medium and small vessel vasculitis

Aorta

Classification of arteritis

Medium branch

Lobar artery

Small artery Capillary

Glomerulus

Microscopic polyangiitis (pANCA) Giant cell arteritis Takayasu’s arteritis Wegener's granulomatosis (cANCA) Churg–Strauss Henoch–Schönlein purpura Leucocytoclastic vasculitis Cryoglobulinaemia PAN (ANCA negative) Kawasaki disease

Ocular

Neurological

Conjunctivitis (Epi)scleritis Uveitis Visual disturbance/loss Retinal changes

Confusion Seizures Stroke Neuropathy Mononeuritis multiplex

Mucous membranes

Cardiovascular

Oral ulcers Genital ulcers

Loss of pulses Bruits Pericarditis Chest pain Cardiac failure

Ear, nose and throat Nasal obstruction/crushing/ discharge Sinus disease Hearing loss Hoarseness

Respiratory

Gastrointestinal Arthritis/ arthralgia

Abdominal pain Bloody diarrhoea Infarction Perforation

Cough +/– haemoptysis Breathlessness Wheeze Pleurisy Nodules Cavities Pleural effusion Pulmonary haemorrhage

Renal ↑BP ↑Cr Proteinuria Haematuria

Systemic Cutaneous Infarcts Ulcers Purpura

Malaise Myalgia Fever Weight loss Headache

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The commonest vasculitides are giant cell arteritis and Kawasaki disease. Despite their rarity, the medium and small vessel vasculitides are important diagnoses to be familiar with: as multi-system diseases they are great mimics, and their consequences may be life-threatening.

Medium vessel vasculitis Polyarteritis nodosa This necrotising vasculitis leads to aneurysm formation and predominantly involves vessels supplying the peripheral nerves, intestinal tract, kidney, skin and joints. Symptoms include constitutional upset, myalgias, orchitis and ischaemia (leading to vasculitic rashes, mononeuritis multiplex, renal failure, abdominal pain and coronary artery disease). It is associated with a marked inflammatory response and there is evidence of previous hepatitis B infection in up to 40% cases. Diagnosis is by angiography, which reveals microaneurysms in the renal arterial tree and occlusions and irregular visceral arteries.

Kawasaki disease This affects children, causing fever, conjunctival injection, fissuring/ crusting of the lips, strawberry tongue, lymphadenopathy, erythema and desquamation of the hands. The vasculitis can affect all organs but the most feared complication is coronary arteritis. The first investigation of choice is therefore echocardiography to rule out cardiac involvement.

Small vessel vasculitis The small vessel vasculitides are subdivided according to their association with anti-neutrophil cytoplasm antibodies. The ANCA-positive vasculitides are further subdivided according to staining patterns: cytoplasmic staining (cANCA) is directed against proteinase 3 and is classically associated with Wegener’s granulomatosis while perinuclear staining (pANCA) is directed against myeloperoxidase and is classically associated with microscopic polyangiitis. The cANCA / pANCA division is not clear-cut and not a consistent rule; in addition, ANCAs on their own do not constitute a diagnosis of vasculitis.

ANCA-positive vasculitis Wegener’s granulomatosis This is a systemic vasculitis with a classic triad of disease: 1 Upper airway (epistaxis, nasal crusting, outer and middle ear disease). 2 Lower airway (tracheobronchial stenosis, pulmonary haemorrhage). 3 Renal disease (glomerulonephritis, renal failure). Additional symptoms include constitutional upset, palpable purpura, livedo reticularis, arthralgia and mononeuritis multiplex. Diagnosis relies on the clinical picture, raised inflammatory markers, positive cANCA, chest X-ray, CT chest ± biopsy and CT sinuses. Microscopic polyangiitis This predominantly causes a severe glomerulonephritis, but may lead to pulmonary haemorrhage, purpura, abdominal pain, arthralgias, peripheral neuropathy and cutaneous vasculitis. Investigations of choice are pANCA and renal biopsy, revealing a necrotising glomerulonephritis (the absence of granulomas differentiates this from Wegener ’s granulomatosis).

ANCA-negative vasculitis Henoch-Schönlein purpura occurs predominantly in children, presenting with purpura, arthritis, abdominal pain, rectal bleeding and haematuria due to IgA nephropathy. It is generally a self-limiting

disease but carries a worse prognosis in the presence of renal disease or with presentation in adulthood. Churg-Strauss syndrome presents with an association of respiratory (asthma, nasal polyps, allergic rhinitis and pulmonary infiltrates) disease, renal disease, cardiac disease, mononeuritis multiplex and peripheral eosinophilia (N.B. 25% of cases are pANCA positive). Cryoglobulinaemia: Cryoglobulins are immunoglobulins or immunoglobulin-containing complexes that precipitate out at low tempertaures. Type I (25%) is a single monoclonal immunoglobulin, type II (25%) mixed group with monoclonal activity against self IgG i.e. rheumatoid factor activity, and type III (50%) mixed polyclonal group. Type II and III are frequently termed ‘mixed essential cryoglobulinaemia’. The commonest symptoms and signs are purpura, arthralgia, urticaria and glomerulonephritis; type II cryoglobulinaemia has a strong association with hepatitis C infection. Miscellaneous causes of small vessel vasculitis include infections, allergies and malignancy. Some drugs (notably cocaine) can generate ANCAs, increasing diagnostic uncertainty.

Diagnosis and assessment A thorough history and examination, keeping all possible features of disease (see opposite) in mind, is vital. To aid diagnosis, key investigations include: Blood tests: full blood count (eosinophilia?), renal function (impairment?), liver function tests and hepatic serology (impairment? hepatitis B or C?), ESR and CRP, autoantibody screen (ANCA, ANA and RF (very high levels in type II cryoglobulonaemia)). Radiology: Chest X ray ± CT chest/abdomen/pelvis; CT sinuses in Wegener ’s granulomatosis; arteriography. Biopsy: a tissue specimen of the affected area is the gold standard for diagnosis. Assessment tools: the Birmingham Vasculitis Activity Score (BVAS) documents features due to currently active disease and guides treatment; the Vasculitis Damage Index (VDI) is a standardised assessment of damage caused by previous active disease.

Treatment Any patient with systemic vasculitis should be referred promptly to rheumatologists with experience in assessing complex multisystem disease and in using immunosuppression. The exact treatment will depend on each patient, their diagnosis, BVAS and co-morbidity. Even with the improving immunosuppressive techniques, some vasculitides remain relatively resistant to therapy and carry a grim prognosis. Therapeutic options include: Mild (skin disease only) – colchicine, dapsone or steroid. Moderate (e.g. GCA, non-renal small vessel vasculitis) – steroids + methotrexate/azathioprine as steroid-sparing agents. Severe (e.g. life or organ-threatening disease) – cyclophosphamide and steroids; intravenous immunoglobulin; plasmapheresis; rituximab. TIPS • Vasculitis is a great mimic and diagnostic delay is not uncommon: be vigilant! • Vasculitis is classified according to vessel size • Small vessel vasculitis is divided into ANCA-positive (cANCA vs. pANCA) and ANCA-negative vasculitis • The level of immunosuppression depends on disease activity, risk to life or internal organs and co-morbidity

Vasculitis 2: Medium and small vessel vasculitis Rheumatology

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Scleroderma

Scleroderma

Thickened, taut skin telangiectasia, beaked nose puckered mouth

Interstitial fibrosis and/or pulmonary vascular disease

Treatment Raynaud's phenomenon Keeping warm, nifedipine, losartan, iv prostacyclin analogues Pulmonary hypertension

Renal hypertensive crisis

Raynaud's phenomenon Pulp atrophy Sclerodactyly Flexion contractures

The basics Scleroderma is a heterogeneous condition characterised by progressive fibrosis, widespread vascular disease and immunological abnormalities. It is divided into limited cutaneous disease (formerly known as CREST syndrome) and diffuse cutaneous disease (or systemic sclerosis).

Limited cutaneous disease A relatively benign form of the disease affects the majority of patients with scleroderma syndromes. It is characterised by limited skin involvement and late appearance (if any) of visceral complications. • Cutaneous manifestations are the result of overproduction of connective tissue, classically collagen. The skin becomes bound-down, taut, crease-free and hairless. The classic changes occur in the fingers (sclerodactyly) with loss of the finger pulp, development of flexion contractures and reduced movement. This type of contiguous skin change does not extend beyond the elbow or knee in the limited form of the disease. Additional patterns of cutaneous disease include small, localised and circumscribed areas (morphoea), linear streaks frequently following a dermatomal distribution, or en coup de sabre, in which the face and scalp are involved. Calcinosis is also a common occurrence. • Vascular abnormalities include Raynaud’s phenomenon, telangiectasia and capillary nail fold abnormalities. Digital ischaemia and ulceration can occur late in the disease. • Gastrointestinal involvement is limited to oesophageal dysmotility leading to dysphagia and reflux. More distal disease is rare. • Pulmonary hypertension occurs as a result of interstitial fibrosis, pulmonary vascular disease or both.

Renal disease ACE inhibitors Gastrointestinal disease Antacids, antibiotics Pulmonary hypertension Warfarin, digoxin, diuretics; immunosuppression if appropriate; iv prostacyclin analogues, endothelin-1 antagonist (bosentan) Skin disease ? Penicillamine

Note that limited cutaneous scleroderma is now preferred to CREST syndrome (Calcinosis, Raynaud’s phenomenon, Esophageal dysmotility, Sclerodactyly and Telangiectasia).

Diffuse cutaneous disease The complications of diffuse disease are universally more severe. • Cutaneous manifestations spread proximally to include the trunk and face and patients develop a characteristic appearance with taut skin, a beaked nose and a tight mouth (microstomia) with restricted opening. • Vascular disease is characterised by a renal obliterative endarteritis, which can precipitate a life-threatening renal hypertensive crisis. • The entire gastrointestinal tract may become involved. The hypomobility generated by increasing fibrosis causes: – Reflux oesophagitis. – Small bowel malabsortion, particularly following bacterial overgrowth. – Constipation and overflow diarrhoea due to colonic/rectal atony. • In addition, the autoimmune condition primary biliary cirrhosis has an association with scleroderma and is a rare cause of diarrhoea. • Pulmonary hypertension is also a feature of diffuse disease, again due to interstitial fibrosis, obliterative vascular disease or both. The majority of patients with diffuse disease will develop some form of interstitial lung disease, but progression to severe restrictive lung disease affects less than 20%. As in the limited form of scleroderma, the interstitial lung disease has an insidious onset, is largely resistant to treatment and is a large cause of mortality in this population.

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Diagnosis and monitoring The diagnosis of scleroderma relies on a thorough history and examination, with particular emphasis on the presence and severity of cutaneous and visceral involvement. Patients are anti-nuclear factor positive and disease-specific autoantibodies have been identified: diffuse/systemic disease is associated with antitopoisomerase-1 (Scl70), limited disease with anticentromere antibodies (ACA). All patients should be monitored with regular outpatient assessment. Clinical evidence of end-organ damage should be sought and renal biochemistry and urinanalysis must be taken. Regular echocardiography and full lung function testing should be performed regularly as a screening tool for cardiopulmonary involvement.

3 Gastrointestinal disease: treatment of reflux disease is identical to that of idiopathic disease: antacids/alginates and proton-pump inhibition. Antibiotics may assist with bacterial overgrowth and bulking agents can help with constipation. Total parenteral nutrition may be necessary if the bowel fails completely. 4 Pulmonary hypertension: all patients should receive warfarin, diuretics and digoxin. Interstitial lung disease (histologically nonspecific interstitial pneumonia) may respond to immunosuppression with corticosteroids and cyclophosphamide. 5 Skin disease: penicillamine and colchicine have been used to prevent progression of cutaneous disease, and there are a number of trials assessing the efficacy of alkylating and immunomodulating agents.

Treatment Scleroderma has no specific or curative treatment. Individual problems are tackled as follows: 1 Raynaud’s phenomenon: keeping warm and using vasodilators such as nifedipine and losartan. Fluoxetine may also prove beneficial. Acute digital ischaemia may respond to ring-block and/or iloprost infusions. 2 Renal disease and hypertension: ACE inhibition remains the treatment of choice. Dialysis may be necessary.

TIPS • Raynaud’s phenomenon can be either primary (idiopathic) or secondary • Common causes of secondary Raynaud’s phenomenon are scleroderma and SLE • All patients with scleroderma should be screened for pulmonary hypertension with echocardiography and pulmonary function tests

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Inflammatory muscle diseases

Polymyositis/dermatomyositis Heliotrope rash Treatment Steroids azathioprine methotrexate Hydroxychloroquine Bone protection

Dysphagia Proximal muscle weakness steroid sparing agents

Interstitial fibrosis Diaphragmatic weakness

Gottron's papules Arthralgia Ragged cuticles Dilated nail fold capillary loops

Introduction The inflammatory muscle diseases polymyositis and dermatomyositis are characterised by an inflammation of striated muscle. As with other conditions in the spectrum of connective tissue disease, they can occur on their own or in association with, for example, SLE. They are rare, with only 5–7 new cases per million per year and affect women more frequently than men. In general they can affect any age, although dermatomyositis has a peak of incidence in childhood and in the elderly; in the latter it may be related to underlying malignancy. Inclusion body myositis has a different clinical, histopathological and prognostic profile (see below). Polymyositis is characterised by insidious muscle weakness and pain that develops over 3–6 months, but acute catastrophic presentations can also occur. Large proximal muscle groups are involved preferentially and patients have difficulty climbing stairs, rising from sitting or raising their arms above their heads. Shortness of breath may also occur as a result of diaphragmatic involvement, aspiration pneumonia (dysphagia caused by upper oesophagus involvement) or interstitial fibrosis. Dermatomyositis refers to polymyositis in the presence of a characteristic rash that frequently precedes the myopathy. Papules develop over the metacarpophalangeal and proximal interphalangeal joints (Gottron’s papules) with areas of linear erythema running the length of the fingers’ dorsal surface; the cuticles become ragged and dilated nail fold capillary loops become visible. Further cutaneous stigmata include a classically heliotrope rash across the eyelids and a macular eruption in a ‘V’ formation at the base of the neck and over the shoulders and back (the ‘shawl’ sign). More unusual manifestations of disease include myocardial involvement, pericardial effusions and arthropathy.

Secondary post-inflammatory fibrosis and scarring lead to longterm weakness and an inability to reach pre-morbid levels of activity. This is particularly problematic in children in whom development of calcinosis also contributes to the formation of flexion contractures. Scarring following inflammatory lung disease leads to pulmonary fibrosis and an irreversible reduction in exercise tolerance.

Diagnosis 1 Blood tests: Patients usually have a mild anaemia of chronic disease and a raised ESR. The creatine kinase (CK) level, a systemic marker of muscle necrosis can rise extremely high; myoglobinuria occurs in the presence of extensive muscle death and may cause acute renal impairment. Many patients are anti-nuclear antibody (ANA) positive and myositis-specific autoantibodies may delineate specific clinical profiles. Anti-Jo-1, for example, is associated with the development of interstitial lung disease. 2 Electromyography: EMG demonstrates myopathic potentials: spontaneous fibrillation at rest and polyphasic potentials on contraction. 3 Muscle biopsy: Histology reveals lymphocytic infiltration and muscle necrosis. In polymyositis, the infiltration tends to occur throughout the muscle, whereas in dermatomyositis it localises to perivascular areas. Biopsy also helps to identify those with inclusion body myositis (see below). An MRI may be used to guide biopsy placement and increase the chances of a positive result.

Treatment Immunosuppression with high-dose oral corticosteroids (1mg/kg) forms the mainstay of treatment. The dose is gradually tapered according to clinical response and CK levels and many patients will need up

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to two years of therapy. Up to a quarter of patients will require additional immunosuppression with azathioprine or methotrexate to obtain disease control. If the skin does not respond to steroid therapy, hydoxychloroquine may be added. Interstitial fibrosis is treated with steroids and cyclophosphamide. Intravenous immunoglobulin may play a role in those with severe or refractory muscle disease. Occasionally longterm steroid treatment is complicated by the development of steroid myopathy which can be hard to differentiate from the underlying inflammatory disease. In general, patients with steroid myopathy have a normal CK. EMG may be also able to distinguish between the two, but occasionally MRI or repeat biopsy may be required.

and insidious development of muscle pain and weakness. Interestingly, inclusion body myositis can also affect distal musculature, particularly early on in disease and asymmetry is not uncommon. The legs, particularly the anterior thigh, are affected more than the arms. Patients may develop a mild peripheral neuropathy but lack the other extramuscular features such as interstitial lung disease. The CK tends to be only modestly elevated (600–800 mg/dL) and is even normal in up to a third of cases. ANA may be present but myositis-specific autoantibodies like Jo-1 are absent. The characteristic biopsy finding is redrimmed vacuoles containing beta-amyloid. Sadly, inclusion body myositis is poorly responsive to immunosuppression and is generally progressive.

Malignancy Data suggest an increased risk of malignancy in those with dermatomyositis (and polymyositis to a lesser degree). The depth of investigation for a possible malignancy is debatable, but a careful history and thorough clinical examination is mandatory. Chest X ray, mammography, abdominal and pelvic ultrasounds would form the bare minimum of specialist investigations.

Inclusion body myositis Inclusion body myositis predominantly affects white males over the age of 50. As for polymyositis and dermatomyositis, its leads to slow

TIPS • The diagnostic triad for the inflammatory myopathies is raised CK, myopathic EMG and abnormal biopsy • Dermatomyositis may be associated with malignancy in the elderly • Steroid-induced myopathy has a normal CK and lack of inflammatory features on MRI and/or biopsy

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The medical management of inflammatory disease Steroids

Routes of administration

Uses

Oral

Intramuscular (thigh or buttock)

Side effects

Long course to control systemic inflammatory disease

Weight gain → Cushingoid appearance

Short course to reduce inflammatory flare

Hypertension

‘Bridge’ until DMARDs take effect

Osteoporosis

Intra-articular injection to reduce localized inflammation

Diabetes

40 35

Intra-articular (knee)

Infliximab

25 20 15 10 5 0 1955

Drug

Dose/route

Side effect

Methotrexate

10–25 mg/week oral or subcutaneous Folic acid adjunct

Bone marrow suppression Hepatitis Pneumonitis Stomatitis

Sulfasalazine

Up to 2 g/day

Bone marrow Hepatitis

Leflunomide

Up to 20 mg/day

Bone marrow Hepatitis Hypertension

Hydroxychloroquine

200–400 mg/day

Maculopathy

Monoclonal antibody against TNFα

30

TNFα receptor fusion protein

Adalimumab Golimumab

TNF

Certolizumab

T cell

Biologics

APC

65

70 75 Year of birth

80

85

1990

Etanercept

Cellular activation Cytokine release MMP, prostaglandin release Osteoclast activation

Anti-TNF

Anti-T cell CTLA-4 Ig fusion protein

60

Antigen presentation Anti-B cell (CD20)

Rituximab B cell

Anti-cytokine

Antibody formation

Abatacept Anakinra

IL-1

Tocilizumab

IL-6

In trial

IL-17

Inflammatory cell proliferation MMP release Angiogenesis Osteoclast activation

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82 Published 2012 by John Wiley & Sons, Ltd.


Introduction Although many of the treatments for inflammatory disease such as RA have been around for several decades, knowledge about the pathogenesis of disease has highlighted several new therapeutic options. This chapter will focus primarily on the treatment of RA, but similar principles apply for psoriatic arthritis; treatment of SLE, vasculitis and crystal arthritis is covered more fully in individual chapters.

Analgesia Standard analgesics with no anti-inflammatory action (paracetamol, opioids) have a role in controlling pain, but are only used as an adjunct to other therapy and have no impact on disease progression.

Non-steroidal anti-inflammatory drugs (NSAIDs) and COX-2 inhibitors NSAIDs inhibit the cyclo-oxygenase (COX) pathway in prostaglandin synthesis. The efficacy of NSAIDs must be balanced against their side effect profile (primarily gastric and renal) due to inhibition of the constitutive COX-1 pathway. The COX-2 isoform of the enzyme is induced at sites of inflammation and the so-called COXIBs (COX-2 inhibitors) target this form more specifically, although all have some residual COX-1 effect. Though they reduce gastric side effects, they are associated with an adverse cardiovascular profile. The persistent use of any NSAID is not only a risk in an aging population with substantial co-morbidity but also should be seen as a marker of treatment failure – escalating DMARD therapy may be a safer option than allowing long-term use of non-steroidal anti-inflammatory agents.

Disease modifying anti-rheumatic drugs (DMARDs) DMARD is an umbrella term for several drugs used to control pain and swelling with evidence of inhibition of disease progression (functionally and/or radiographically). All DMARDs carry some risk of bone marrow suppression and hepatotoxicity; they are initiated in secondary care and require careful monitoring to avoid toxicity. DMARDs should be used as early as possible in active disease, generally with methotrexate as first-line; unfortunately they may take up to three months to reach clinical effect, so patients may require steroids as a ‘bridging’ therapy. Combinations of DMARDs are frequently required to achieve disease control, although this increases the risk of adverse effects.

Biologics The advent of monoclonal antibodies directed against key cells or cytokines in inflammatory disease has revolutionised the treatment of refractory arthritis (see Chapter 22, Pathogenesis of rheumatoid arthritis). TNFα inhibition is indicated in patients with active disease (DAS28 score > 5.1) despite treatment with two or more DMARDs, one of which must be methotrexate. For those who fail to respond to anti-TNF, or in whom its use is contraindicated, anti-B cell therapy may prove beneficial. Antibody therapy directed against T cells, IL-1 and IL-6 are licensed for use in RA but have not yet received NICE approval; clinical trials looking at the efficacy and safety of IL-17 blockade are underway. • TNFα inhibitors. TNFα blockers are highly effective in the majority of patients. The greatest risk of TNF inhibition is infection, both common and opportunistic, and re-activation of latent TB. All patients are therefore carefully screened prior to initiation. TNF blockers are usually given in combination with methotrexate, which may reduce

the patient’s immune responses to antiTNF (particularly against the mouse chimera infliximab). If low-dose methotrexate is not tolerated, etanercept and adalimumab are licensed as monotherapy in RA. • Anti-B cell therapy. Rituximab, the monoclonal antibody directed against CD20 depletes circulating B cells, thereby impacting on a number of key processes in RA (see figure). Terminally differentiated plasma cells are unaffected. Rituximab is given as two intravenous infusions two weeks apart and may be repeated after 6 months; treatment is frequently limited to 3 or 4 cycles due to concerns about long-term hypogammaglobulinaemia.

Steroids Steroids have excellent anti-inflammatory actions, but their long term use is relatively contraindicated due to side effects (e.g. weight gain, peripheral oedema, diabetes and osteoporosis). Steroids may be administered via a number of routes, according to therapeutic demand: • Oral: low dose to control inflammatory arthritis or polymyalgia rheumatic, high dose for GCA and other vasculitides. • Intramuscular: as ‘bridging’ therapy until DMARDs therapy reaches therapeutic effect; to abort a flare of established disease. • Intra-articular: for isolated joint pathology when systemic treatment is not indicated (or to settle a local flare of established disease). Osteoporosis and bone protection. Bone loss starts early with steroid use. Bisphosphonates and vitamin D/calcium supplementation should be considered in all patients on long term steroids, especially in elderly or those with previous fragility fracture. Steroid-sparing agents. If long-term steroid use is unavoidable (e.g. in SLE or vasculitis), a steroid-sparing agent such as methotrexate or azathioprine can be used alongside prednisolone to aid dose reduction.

Special circumstances Many inflammatory diseases will require long-term, if not life-long, treatment. Although patients may go into remission on treatment, subsequent withdrawal of therapy carries the risk of disease flare. There are, however, certain situations in which treatment should be suspended temporarily. • Intercurrent illness/surgery. In general, DMARD and biologic therapy can continue during mild or moderate intercurrent illness, but the threshold is much lower in the presence of infective illness. Some units will also continue with standard DMARD therapy during an elective surgical period, but schedule operative dates between injections/infusions of biologic agents. • Pregnancy/breastfeeding. Many DMARDs are teratogenic and/or contraindicated in breastfeeding; treatment should be stopped preconception with sufficient ‘wash-out’ time. There are few data on the safety of biologic therapy and pregnancy, but increasing reports of successful pregnancies on antiTNFα are reassuring. The decision to continue biologic therapy in pregnancy is often clinician-specific. TIPS • Treatment for RA should be early, aggressive and aim for disease remission • All DMARDs require monitoring and take up to 3 months to reach clinical effect • Methotrexate is the first-line DMARD • Biologic therapy is indicated for those who fail DMARD therapy; re-activation of latent TB is a major concern of anti-TNFα

The medical management of inflammatory disease

Rheumatology

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Rehabilitation

Specialist Nurses Occupational Therapy

Physiotherapy

POOL

Orthotics Multi-disciplinary team

Patient Treatment Support Education

Podiatry

Introduction The majority of rheumatological diseases are long-term chronic conditions, occasionally associated with considerable disability. Even in a stable or slowly progressive disease such as RA, discrete events such as joint surgery may demand sudden physical, mental and occupational adaptation. One of the main principles of rehabilitation is the return, maintenance and protection of a patient’s functionality; a patient’s sense of control – of ‘ownership’ and ability to self-manage can also prove very beneficial psychologically.

Rehabilitation requires a multi-disciplinary team (MDT) approach. Each member of the team has specific but complementary roles; not all patients will require the expertise of all members at any one time.

Physiotherapy The main role of the physiotherapist is the maintenance or improvement of physical function through specific focussed exercises. As part of physical rehabilitation, a thorough assessment of the patient’s physical function is mandatory, in combination with identification of

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contributing factors such as unfavourable biomechanics or poor core stability. The physiotherapist is then able to teach each patient a specific set of stretches and exercises to target problem areas and design a program for escalating either repetitions or resistance as pain/function improves. The most common aims are to rehabilitate post-surgery, to improve muscle strength and balance, relieve tendinopathy and enhance core stability. Hydrotherapy is a crucial component of rehabilitation for inflammatory arthropathy, especially ankylosing spondylitis. Physical therapy may also include the application of heat, cold and transcutaneous electrical nerve stimulation (TENS) to relieve pain and stiffness.

Occupational therapy Occupational therapists (OTs) are invaluable in offering advice and adaptations so that patients are able to realise their full potential both in their home and workplace. Advice and support they offer include: • Equipment. • Housing adaptations (e.g. bathroom alterations, stair-rails). • Seating and wheelchair assessments. • Splinting (especially upper limb). • Energy conservation, task prioritisation and delegation. As part of the MDT, they are particularly important in the postoperative period, facilitating a smooth and successful discharge to a safe environment; frequently home visits for ‘on-site’ assessments of a patient’s needs highlight issues that might have been missed while in hospital. OTs work in close liaison with Social Workers and are very helpful in providing information on workplace-related issues such as worker ’s rights and disability allowance.

aims are to maintain or limit mobility, protect joints or correct malalignment. Orthotics can range in size (e.g. insoles/adaptive footwear up to thoraco-lumbo-sacral orthosis) and are based on a cast of the patient’s limb or trunk for a perfect fit.

Specialist nurses Clinical nurse specialists (CNS) are a major source of information, education and support for patients with arthritis. The days and weeks after a new diagnosis of, for example, rheumatoid arthritis can be a bewildering and frightening time for patients. Many are fearful for the future and anxious about potentially life-long treatment with disease modifying agents; a CNS can dedicate time to individualised patient education which not only alleviates fear but improves concordance and outcome. They also play a role in counselling patients before treatments with risks of specific side-effects, such as reduced fertility with cyclophosphamide or transfusion reactions with rituximab. The increasing use of nurse-led clinics for those with stable disease or emergency helplines for patients who are struggling is proving very successful. The main roles of a nurse specialist encompass: • Patient education regarding diagnosis and treatment. • Emotional support and informal counselling. • Organisation of bloods monitoring. • Teaching subcutaneous injection techniques (e.g. for methotrexate or biologics). • Arranging delivery of subcutaneous drugs, needles and safe disposal systems to patients homes. • Nurse-led clinics. Patients with musculoskeletal pathology need various forms of support at different stages of their disease; the multidisciplinary approach to patient education, support and rehabilitation is central to successful management.

Podiatry Foot disease is frequently overlooked in assessment of arthritis. Pain in the heels, forefeet and toes can make life unbearable for many patients and can be a major restriction in activities of daily living or rehabilitation. Podiatrists’ skills rest in managing foot pathology and, in combination with orthotists (see below), provide advice on footwear. Podiatrists offer: • Callus removal and advice to avoid recurrence. • Skin management to avoid pain and ulceration. • Nail care.

TIPS • All patients with a new diagnosis of inflammatory disease should be offered a multi-disciplinary assessment • Physiotherapists and occupational therapists are particularly valuable in the peri-operative period • The expanding role of clinical nurse specialists has improved patient care tremendously • Rehabilitation takes many forms – all of the multi-disciplinary team have a valuable role to play

Orthotics Orthotists design devices to support or modify skeletal structures with adverse biomechanics due to joint or neuromuscular disease. The main

Rehabilitation

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Orthopaedics in children Diagnosis

Hairy dimple at top of natal cleft suggests spina bifida

Problems

Accessory fingers and toes need removing

Webbed or fused fingers need separating

May cause clawed foot later in life from tethered nerves Cerebral palsy

Asymmetric buttock crease in a limping child suggests late presentation of congenital dislocation of the hip

If the hip is not put back in joint as soon as possible, the hip joint does not develop normally

Wasted calf and foot turned down and inwards suggests 'club foot'

Correction with surgery and/or plaster is needed as soon as possible to get a cosmetically acceptable functional foot Child may initially present as floppy Spasticity may not develop until later

Antenatal and birth checks

Irritable hip

Screening, genetic counselling, the withdrawal of teratogenic drugs and appropriate nutrition have greatly reduced the incidence of spina bifida and other congenital abnormalities in babies in the developed world. However, at birth all babies are checked for the most common abnormalities, which are unstable hips, club foot and abnormalities of the fingers and toes such as webbing, extra or absent digits.

This is a common orthopaedic emergency because of the concern that serious pathology might be missed. The differentials are septic arthritis, Perthes’ disease and slipped upper femoral epiphysis (see Chapter 16).

Developmental dysplasia of the hip (DDH)

See Chapter 16.

Perthes’ disease and slipped upper femoral epiphysis

See Chapter 16.

Knock-knees and bow legs Club foot (talipes equinovarus) When the child is born, the foot is noted to be twisted down (equinus) and inwards (varus). This can either be a result of the position in the uterus (positional) or it can be congenital (failure of proper development of the calf and foot). If the problem is positional, then careful splinting will correct the problem. However, if the problem is anatomical (congenital), then surgical correction will be needed.

Webs, fusions and absent and accessory digits Congenital abnormalities of the hand and foot can vary from slight webbing between two fingers or toes, through to complete absence of the limb. There may also be extra digits. Hands are very important in communication and not just for manipulation of tools, so cosmesis can be an important issue. Functionally in the hand, one of the most important needs is an opposable digit (a thumb). If this is absent then another digit may need to be rotated to take its place. Artificial hands have proved very difficult to design because they require sensory feedback and exquisite control on grip pressure to come anywhere near the functionality of the normal hand.

Children may be referred to the clinic with either knock-knees (valgus) or bow legs (genu varus). The degree of deformity is best measured by getting the child to stand with either their feet together (in the case of bow legs), or with their knees together (in the case of knock-knees). The distance between the medial condyles of the femur (in the case of bow legs) or the medial malleoli of the ankles (in the case of knockknees) can then be measured. Most of these cases are benign and correct with time. All that is required is a regular check that the deformity is indeed improving as the child grows, combined with reassurance to the parents.

Fractures Fractures heal rapidly in children; even if there is some malunion, the bones have great potential for remodelling, so angulation that would be quite unacceptable in an adult can be left in a child to heal itself. Children’s bones are also quite flexible and may only break partially (a greenstick fracture). These tend to be stable and only need protecting for a couple of weeks while they heal. However, there are two issues that need careful consideration:

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. © 2012 John Wiley & Sons, Ltd.

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1 The possibility of non-accidental injury. 2 The problem of fractures through epiphyseal growth plates.

Type 5 is a crush of the epiphyseal plate which superficially looks like a Type 1 fracture but the growth plate is destroyed and growth ceases.

Non-accidental injury Certain fractures such as the spiral fracture of the femur in infants are highly suggestive of non-accidental injury, but there are many other features that may suggest that injuries have been caused deliberately: • In the history there may be an inexplicable delay in presentation. • The description of how the accident occurred does not fit with the nature of the injury (rolling off a sofa onto a carpet does not usually fracture the skull!). • On examination the child is often quiet and watchful. • There may be more bruises than expected, and they are sometimes of different ages suggesting multiple episodes of trauma. • On X-ray there may be evidence of previous healed fractures, again suggesting that there has been more than one episode of trauma. If there is any possibility of non-accidental injury, senior help should be sought.

Epiphyseal injuries Fractures through the epiphyseal plate do not normally damage the blood supply (as the weakest zone is furthest away from the entry of the blood supply). However, if the fracture is displaced or enters the vascular zone the growth of the plate in that area may be arrested. If this is not recognised and corrected quickly the limb may end up deformed. The Salter-Harris classification is the simplest for these fractures. Type 1 is difficult to see on X-Ray as it travels along the epiphyseal growth plate. As it is on the metaphyseal side the blood supply to the growth plate is unaffected so the fracture has a good prognosis. Type 2 is the commonest type. The fracture line travels along the metaphyseal side of the growth plate then angulates off into the metaphysis. This too has a good prognosis. Type 3 angulates towards the joint so has the risk of creating a step in the joint surface as well as damaging the growth plate’s blood supply. Type 4 crosses from epiphysis to metaphysis. If this fracture is displaced then a bone bridge can grow across between the fragments and block further growth. This will need releasing if normal growth is to resume.

Leg lengthening and correction of deformity The invention of the Ilizarov type external fixators (see also Chapter 40) allows distraction or angular correction forces to be applied to epiphyseal plates, so that limbs can be lengthened and indeed straightened. This technique can also be applied in adult bones by first creating a fracture (osteotomy) then drawing the bone ends apart at just the right speed so that neither does the fracture heal solid prematurely, nor is there a non-union created.

Cerebral palsy The cause of cerebral palsy is not always known but can sometimes be a result of brain hypoxia secondary to birth trauma. Initially the child is floppy and then is slow to reach developmental landmarks. Spasticity then starts to develop, affecting variable amounts of the body. However severely affected the child is, it is vital to remember that in many cases intelligence is unaffected, and no false assumptions should be made based on the problems the child has with taking in information or expressing themselves. Spasticity in muscles can cause abnormal bending of the spine and dislocation of joints, especially the hip. Treatment is based on a careful blend of physiotherapy, orthotics and occasionally surgery to try to enable the child to get as much out of life as possible. This might involve fusion of the spine which enables them to sit straight up in a wheelchair, or a brace for a foot to enable them to walk better.

TIPS • If a child has one congenital abnormality, look for more • Never assume that a child with cerebral palsy does not have normal intelligence • Non-accidental injury has specific features in the history and examination • Fractures in children are often partial and heal quickly • Fractures through the growth plate may lead to growth arrest

Orthopaedics in children Orthopaedics

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Sports medicine

39

History of injury Type

Example

Acute extrinsic

Haematoma of thigh following a kick

Acute intrinsic

Anterior cruciate ligament rupture following a twisting injury to the knee when boot studs are caught in the ground

Chronic

Stress fracture of the tibia in a long-distance runner developing over some weeks

Examination Skin Soft tissue Bone

Skin Soft tissue Bone

Feel

Look

Tell me if that hurts

R E S T Athletes cannot/will not rest. Find an alternative activity which uses the same energy but spares the injured area (e.g. swimming, cycling or weights)

I C E Cold reduces swelling and relieves pain

Active Passive Resisted

Move

Don't go further if it hurts

C O M P R E S S I O N A firm compression bandage reduces swelling but should not compromise circulation

E L E V A T I O N The higher the limb the quicker the swelling will reduce. Swelling is the enemy of mobility

Definition

History and examination

Sports medicine is at one end of the spectrum of musculoskeletal disorders in that it relates to individuals who have very high expectations of their bodies, and who also have high motivation to get better as quickly as possible. Luckily, most of the patients are young so the potential for natural healing is also high.

As usual, a good history can be very helpful. Careful listening to the athlete at the start of a consultation may reveal unexpected expectations. The injury may also be serving a purpose for changing training or as an honourable way out of sport altogether. It also allows classification of the injury into clear categories which simplify diagnosis.

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88 Published 2012 by John Wiley & Sons, Ltd.


Classification by presentation In terms of diagnosis there are three types of presentation. 1 Acute extrinsic. The injury is caused by a direct blow and results in a bruise, a laceration or even a break. 2 Acute intrinsic. There is a sudden failure of a structure as a result of excessive load. This results in a tear of a muscle or ligament, a dislocation or a break in a bone. 3 Chronic. There is no single event that can be identified as the cause of the problem, more often there is a gradual onset. The problem may be inflammation of a tendon or its sheath, or a stress fracture.

Sport specificity Injuries tend to be associated with certain sports. The human body is not always well adapted to the loads applied. A few examples are given below.

Sport

Type of injury

Reason

Contact sports, e.g. football and rugby

Tear of the anterior cruciate ligament of the knee

Studded boots lock the foot to the ground imposing huge loads on the knee when athlete turns or is tackled

Weight lifting

Spondylolisthesis of the spine

High repetitive loads to the base of the spine

Running

Stress fracture of the tibia

Repetitive high load from road running

Cricket

Shoulder, elbow and back problems

Repetitive loading especially when fast bowling

Ice hockey

Lacerations and teeth knocked out

High velocity impact. Sharp skates

Boxing

Acute and progressive brain damage

Multiple impacts to skull

Ice applied to injured areas (especially acute extrinsic injuries) appears to reduce inflammation and therefore speed recovery. Ice applied directly to the skin can cause a burn. Bags of frozen peas conform to the contours of a limb nicely. Compression used carefully can also reduce swelling and so speed recovery. Elevation speeds the recovery of swelling and inflammation.

Physiotherapy This is the cornerstone of rapid and safe rehabilitation. Its role is to restore strength and mobility as fast as possible without allowing excessive exercise to cause further damage.

Injections Injections of steroid into painful ligaments and joints can be used to try to reduce inflammation. The effect is usually short term and if more than two or three injections are given the steroid can weaken the tendon itself and cause a rupture. If local anaesthetic is given the injection can be used to try to diagnose the exact source of the pain or tenderness.

Fitness to return to sport Athletes are fit to return to their sport when they are fit enough and confident enough to do so. For lower limb injuries the ‘figure of eight’ test is valuable (see p. 44).

Ligament tears Partial tears can be allowed to heal without surgical intervention. Early movement with minimal loading stimulates healing while minimising pain and stiffness. Controlled exercises, hinged braces and removable splints may all have a role to play. Complete ligament tears may be best treated by surgical repair as this may speed up healing and return to full function.

Ruptured tendons The blood supply to tendons is not good, so healing tends to be slow. However surgical repair is also not easy. This is especially true of the ruptured Achilles tendon which blights the career of so many middleaged squash players.

Examination

Broken bones

This will often include watching the athlete performing their sport live. The purpose is to try to work out exactly what is happening to their body during performance of their sport. The examination will then follow the ‘look, feel, move’ system described in Chapters 3 and 21.

Bones can be broken by direct trauma, or following repeated loading (stress fractures). Each stress fracture is associated with a certain sport. Running tends to produce fractures of the tibia (one cause of shin splints) or of the second metatarsal (the ‘march’ fracture). Weightlifting can cause a fracture of the spine leading to a slip of the vertebral bodies on each other (spondylolisthesis). Stress fractures can be hard to see on X-ray and so may be difficult to diagnose. The gradual onset of symptoms can be confused with a simple strain or very rarely the onset of symptoms in a primary bone tumour.

Imaging Dynamic imaging of the soft tissues is more likely to yield useful information than static imaging of the skeleton, so ultrasound may prove especially useful.

Treament RICE (rest, ice, compression, elevation) Rest is not a meaningful concept for athletes. If one part of the body needs to be rested to allow healing to take place, then an equally strenuous programme of exercise which does not involve that part needs to be part of the prescription. Swimming and gym work can be very useful for runners with injured legs. Cycling can also be very good for unloading injured areas.

TIPS • • • •

Classify sports injuries from the history RICE is useful for initial treatment The ‘figure of eight’ test is valuable for checking fitness Each sport is associated with specific injuries

Sports medicine

Orthopaedics

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40

Neurological disorders and orthotics Hand muscles may need balancing to improve the cosmetic appearance of the hand. The thumb may need to be brought out of the palm of the hand to allow grip and to work as a pillar against which the fingers can work

Scoliosis (curvature of the spine) may need correcting with fusion of the spine if the child is to be able to sit up in a chair or even to breathe properly

Hip adductors + flexors of hip on knee may need releasing (lengthening) to allow more upright walking

Splints and calipers stabilize joints where there is flaccid paralysis (floppy limb)

Spasticity and contractures (tight muscles) need surgical release followed by splinting

Walking sticks

Crutches

Wheel chair

Help balance and increase confidence, especially out-of-doors, but rely on strong wrists. Aids may be needed for washing, shopping and house-work

Improve balance but also compensate for legs too weak to allow walking without extra help. Rely on strong elbows and shoulders. Aids will be needed and modifications to the house, e.g. stair lift, and a modified car may be needed

Requires no strength in the lower limbs (except when transferring in and out of the chair). However, requires strength or stiffness in the spine to be able to sit up straight, and strength and co-ordination in the upper limbs if mobility is to be maintained without help or electric power and controls. Help may be needed around the house and modifications will be needed, ramps, etc.

?

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. Š 2012 John Wiley & Sons, Ltd.

90 Published 2012 by John Wiley & Sons, Ltd.


Neurological disorders There are multitudes of neurological disorders that may present in an orthopaedic clinic. These can vary from polio, which has now almost disappeared from the developed world (but which once dominated orthopaedics), through to rare familial disorders.

When requesting imaging, you would be wise not to tell the radiographer what views you want, just explain the problem. The same rules apply to an orthotist; it is their job to decide what splint is required. It is your job to explain the problem in terms of pain, deformity and disability, so that they can decide on the best way of managing the problem.

Classification Neurological disorders can be divided into simple groups. There are those which are static, such as polio and cerebral palsy, and there are those which are progressive, such as Huntington’s chorea. Secondly, there are those that affect only the motor or sensory modality (polio only affects motor nerves), or they can be mixed motor and sensory. The diagnosis and management is to a large degree based on this simple classification.

Management The principles of management revolve around the same principles as in the rest of orthopaedics – the relief of pain, deformity and disability. In these cases disability is usually the main problem and physiotherapists, occupational therapists and social workers have a very major role to play in enabling these patients to live as full a life as possible.

Cerebral palsy This is a non-progressive condition. The cause is unknown. It used to be thought that it was usually caused by birth trauma. More recently it appears that sometimes the damage may have already occurred in utero. The child is commonly a floppy baby with delayed ‘milestones’, and it is not for some time that the spasm develops that characterises cerebral palsy. These children are frequently of normal intelligence and great care must be taken not to assume that just because they are physically disabled and may have difficulty in communicating, that they are not of normal intelligence. The spasm of muscles reduces the ability of the child to produce powerful, coordinated movements, but also may produce fixed deformities of joints. These need to be avoided wherever possible. Treatment goals in cerebral palsy One of the key skills with a patient with a neurological disorder is to set realistic and useful goals. Devoting every waking hour for 5 years to getting a child to walk may be a triumph for everyone. But if this is achieved at a cost to their development in other ways, and if in a few years they go back off their feet, then this was not an appropriate goal. It might have been better devoting time and effort to developing good seating and training in the use of computers to help communication.

Dilemma of limb reconstruction versus early amputation Severely injured limbs can pose a difficult clinical dilemma. Should a long reconstruction programme be started with an uncertain result, or would a better result be obtained by an early amputation with quick discharge from hospital and return back to normal life? As fast as new techniques are developed for reconstructing severely damaged limbs, new designs of prosthesis are appearing which are strong, cosmetically acceptable and give very good function, especially in the lower limb. Upper limb prostheses are hampered by the fact that no artificial limb can come near to the function of a normal limb that has feeling and which can use that feeling to control grip.

Sensory loss However, if sensory function is unlikely to return because of permanent damage to sensory nerves, then amputation of a lower limb is strongly indicated. This is because if there is no protective sensation, then sores will develop which will ulcerate, and which may even lead to septicaemia. Amputation may also be the most appropriate route if there is no muscle power to stabilise joints, as this too severely reduces the functionality of a limb.

Modern methods of reconstruction Bone transport using the Ilizarov fixator has now made it possible to grow bone across large defects in long bones. Similarly, vascularised flaps allow large soft tissue defects of muscle, as well as skin, to be covered. However, all these procedures are time-consuming and difficult to perform. If they fail, the patient is left depressed and will have been in hospital for so long that their chances of return to normal life have effectively been destroyed. In retrospect an early amputation may have been the best option.

Modern orthotics Below-knee prostheses are now light and strong. They are cosmetically almost indistinguishable from a normal leg and allow the patient to run, dance and take an active part in life. Above-knee amputations are more difficult as the knee hinge is more difficult to manage and the fit that can be obtained onto the thigh may be more difficult than the shin where there is less fat. Even so, a properly fashioned aboveknee prosthesis can prove highly functional.

Orthotics and artificial limbs This is the specialty of producing braces and splints designed to provide patients with support for limbs and artificial limbs. These can be temporary or permanent and may serve to reduce pain, improve function or even improve cosmesis. The traditional materials of leather and steel have been replaced with lightweight plastics, which conform so well in shape and colour that they can be almost invisible. They can be static (providing simple support) or dynamic (reproducing a movement that the patient is not capable of producing themselves).

TIPS • Children with cerebral palsy start floppy then go spastic • Goals need to be chosen appropriate to intelligence and mobility • Artificial limbs are improving as fast as limb reconstruction techniques, so early amputation and rapid rehabilitation must remain a treatment option

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Orthopaedics in the elderly

Common fractures from falls in the elderly Sub-capital

Pertrochanteric

Crush fracture of vertebral body Treatment Pain control and bracing

Blood supply lost, femoral head dead

Treatment Not too aggressive Only reduce if necessary Protect with a splint Mobilise as soon as possible

Treatment

Hemiarthroplasty

Distal radius fracture (dinner fork deformity)

Dynamic hip screw

Introduction The population of the developed world is ageing rapidly. The problems of the elderly have come to dominate orthopaedic and trauma services. There are a number of special problems: • Falls, both because of weakness and loss of balance. • Fractures, because of falls and because bones are weakened by osteoporosis. • Osteoarthritis. • Malignant disease, producing pathological fractures. • Foot problems, causing painful bunions and corns. • The rotator cuff around the shoulder weakens and may tear. • Arthritis in the spine may cause symptoms of nerve root compression. The elderly are much more susceptible to injury because: • Their bones are weakened by osteoporosis. • Their physiological and mental reserves are reduced. • They may be on medication which drops their blood pressure or increases confusion. • Their muscle bulk to weight is reduced. Old people value their independence just like everyone else but rehabilitation after an accident becomes increasingly difficult with age. Accidents need to be prevented if possible, and treated quickly and efficiently when they do, otherwise even a trivial injury can become the ‘straw which breaks the camel’s back’ precipitating an independent patient into one who is in permanent care.

Fractures caused by osteoporosis Bone density falls with age, especially in thin women after the menopause (see Chapter 30). Trivial falls can then lead to major fractures.

The commonest sites of these osteoporotic fractures are the wrist, spine and neck of the femur.

Wrist At the wrist the fracture involves impaction (crushing) and bending backwards of the forearm bones just above the wrist joint, sometimes called the ‘dinner fork’ deformity or Colles’ fracture. The fracture tends to be stable because of the impaction and some surgeons feel that it is best not to reduce the fracture (and so make it unstable), but let it heal quickly in its new position. This offers the best chance of preserving the patient’s independence as they may only need a simple splint for comfort for a couple of weeks if the fracture is left alone, rather than a full plaster for over a month if it is reduced (see Chapter 9).

Spine Crush fractures of the spine are stable and rarely compress nerves, although they can be very painful. Treatment is symptomatic (see Chapter 13).

Neck of the femur Fractures of the neck of the femur are very different. There are two types (see Chapter 19): 1 The high neck fracture interrupts the blood supply to the head, so if it is displaced the head dies and needs to be replaced with a hemiarthroplasty (half a hip joint). 2 If the fracture is low in the neck then the blood supply to the head will remain intact but the fracture will need treating with internal fixation. The device used (a dynamic hip screw) holds the fracture while

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allowing the margins to compress together. This holds the fracture steady and stimulates rapid healing. The great advantage of these two techniques is that they allow the patient to get up and start walking at once, so minimising the chance of the patient losing their independence or developing some other illness associated with prolonged bed rest.

Osteoarthritis The cause of osteoarthritis is not known but once the articular cartilage is damaged, the deterioration can be rapid. The joint becomes stiff and painful and may be fixed in a position that is not ideal for function. For example, both the hip and the knee tend to become fixed in flexion making it difficult for the patient to walk upright. Joint replacement should primarily reduce the pain but can also improve range of movement, converting someone who is housebound, dependent on others and in pain to an outgoing, independent, cheerful person once again. The joints now last for around 10–15 years and can then be changed (revised) to prolong a good quality of life even further.

Metastases Primary tumours of bone are rare but many tumours can metastasise to bone. If the lesions can be spotted early, radiotherapy can be used to prevent further bone destruction. If the bone is so eroded that it is at imminent risk of breaking, or has in fact already broken, fixation with a locked intramedullary nail will reduce the pain and prevent the patient from being confined to bed during the whole of their terminal illness.

Bunions, corns and metatarsalgia The feet become less and less able to cope with pressure and rubbing as patients get older. Deformities that were once correctable may also

become fixed producing even more problems from shoes. The treatment of choice is usually non-surgical by providing insoles and special shoes which reduce excessive pressure. Surgery to correct deformity needs to be embarked on with great care as healing may be slow.

Rotator cuff Extra bone forming on the outer edge of the acromion may rub on the rotator cuff producing pain as the inflamed area passes in under this sharp shelf of bone. If the rotator cuff is overloaded or subject to repeated rubbing from impingement it may tear, making it difficult or even impossible for the patient to lift their arm above their head because the supraspinatus tendon has snapped. Impingement can be treated by trimming the beak of bone, but tears of the rotator cuff are difficult to repair in the elderly because of the poor blood supply.

Spinal stenosis Narrowing of the spinal canal or of the gaps between the facet joint and the disc where the spinal nerve leaves the canal, present with back pain and spinal stenosis. This commonly presents as pain on walking for some distance, especially downhill when the extension of the spine narrows the canal even further. Surgical treatment to open up the narrowed areas is difficult and may not always be successful.

TIPS • Elderly patients need and deserve early treatment of their common orthopaedic problems to preserve independent existence • Healing, especially in the feet, is slow • There are two types of fractured neck of the femur with completely different treatments • Tumours in bones are metastases

Orthopaedics in the elderly

Orthopaedics

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42

Initial management of the polytraumatised patient

AIRWAY

Check conscious state Clear debris from mouth with sucker

History from ambulance crew helps assess nature and severity Hello, what is your name?

Chin lift/jaw thrust lifts tongue forward Cervical spine control Neck collar, sand bags, and head tape

Symptoms and signs of tension pneumothorax ↑ Cyanosis despite clear airway Deviated trachea ↓ Expansion Hyper-resonant, ↓ breath sounds

BREATHING

100% O2 (15 litres/min) Check for air entry to lungs Check for cyanosis

Urgent treatment of likely tension pneumothorax

Exclude tension pneumothorax

Insert needle into 2nd intercostal space mid-clavicular line

CIRCULATION

Check pulse, blood pressure, and conscious state Put up two drips with wide-bore cannulae Take blood for Hb, U+E, cross-match, glucose plus drug screen If shocked, give 2 litres saline stat (in adult) Observe response to fluids

Sustained rise in blood pressure and fall in pulse = RESPONDER

Initial improvement in pulse and blood pressure followed by fall = TRANSIENT RESPONDER

Continue with saline only and observe

Start colloid and/or blood transfusion at once. Investigate for source of bleeding

No improvement in vital signs. Give 'O' negative blood and proceed to the operating theatre to find and control bleeding = NON-RESPONDER

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Introduction Patients involved in serious accidents are becoming rarer and rarer in developed countries, but are more likely than ever to arrive at hospital alive however severe their injuries. This is a result of better communications and improved pre-hospital care. Serious accidents often involve young people with great potential for healing and a long productive life ahead of them. The stakes are high and the first few hours have a profound effect on the long-term outcome. Working to a system allows a team to work quickly and efficiently. This chapter presents a simple system for this initial management.

History The patient may not be able to give a history, but a description from the paramedics of the energy involved in the accident will give a clue to the likely type and severity of the patient’s injuries. As a general rule if there is one significant injury then there are likely to be more, so always do a complete survey in a seriously injured patient.

falls back to normal levels and then they remain stable, the patient is a ‘responder ’. No further aggressive action needs to be taken for the moment, although blood should still be cross-matched. If the patient improves but then starts to deteriorate again, then a plasma expander is needed urgently and further investigations are necessary to find the source of the bleeding. ‘O’-negative or typespecific blood may be ordered to save time on the cross-match. Up to 8 units should be ordered in the first instance. If there is no response to the fluid challenge then the patient needs ‘O’-negative blood at once and surgery to try to stem the haemorrhage at once. The main sites for heavy bleeding are the chest, abdomen and pelvis.

Disability (D) Check and record the patient’s conscious state using the Glasgow coma scale (see Chapter 47). At every stage keep rechecking the ABC, especially if the patient’s condition starts to deteriorate.

Exposure (E)

Initial management The initial approach to a seriously injured patient is given by the acronym ABC followed by D and E.

Airway and neck stabilisation (A)

Remove all clothes and check the patient from top to toe using the ‘look, feel, move’ system (see Chapters 3 and 21). Log-roll the patient to check the back as well, looking all over the body for cuts, bruises and deformity. A rectal and vaginal examination will also be needed, to check for pelvic injuries. A urinary catheter can then be safely inserted and used to monitor the patient’s perfusion.

• Start by asking the patient for their name. If they can answer then you have confirmed that their airway (A), breathing (B) and conscious state are all reasonable. • While this is being done someone should be taking control of the neck with ‘in-line immobilisation’, prior to the neck being stabilised with a stiff collar, sandbags and tape, just in case there is an unstable fracture of the cervical spine. • If the patient does not answer, start by checking the mouth and throat for obstructions, broken teeth and other material. A sucker is safer than a finger, as a semiconscious patient may bite. • A chin lift or jaw thrust will lift the tongue forward from out of the throat if this is the cause of the obstruction.

Every check must be repeated again and again. Patients can ‘go off ’ at any time and if they do it is commonly something simple like their airway, breathing or circulation that is causing the problem and which needs correcting. Investigations like CT scans should only be undertaken once the patient’s condition is stable so a further check of ABC will be needed before the patient is moved.

Breathing (B)

All findings should be clearly recorded with the time when they were observed. It is often a gradual change in an observation which tells you more about what is happening to a patient than a single value.

Start giving 100% oxygen at 15 l/min (full bore). Check for breathing and air entry into the lungs by looking for chest movement and listening to the lungs. If the patient does not appear to be breathing start bagging them with an Ambu-bag and prepare for intubation. If the patient’s colour is not good, check again that the airway is clear, then check for a tension pneumothorax. The most obvious sign will be a deviated trachea. If a tension pneumothorax is suspected then a blue needle needs to be introduced into the second intercostal space in the mid-clavicular line. If the diagnosis is correct the patient’s condition should improve at once, and a chest drain can then be inserted later. If not, little has been lost.

Circulation (C) Two wide-bore cannulae should be introduced, one into each antecubital vein (front of the elbow). Bloods are drawn for cross-match, full blood count, electrolytes, glucose and drug screen. Two litres of Hartmann’s solution can then be given as quickly as they can be transfused (stat) if the patient is in deep shock. This fluid challenge will give a clue to the seriousness of the situation and allow you to plan the next stage. If the patient’s blood pressure rises and their pulse

Repetition

Recording

Check Before the patient leaves the resuscitation room, perform a final check. Every injury however small must have been found, measured and noted, and an appropriate care plan written. Once the patient has been transferred to the ward, it is all too easy for injuries to be missed and what might have been a trivial injury at the start (e.g. a dislocated finger) now may become a major impediment to returning to normal existence. TIPS • Rescue workers can give a good estimate of the energy involved in an accident • Use ABC • A sucker is better than a finger for clearing the mouth • If there is one significant injury then look for more • Working to a system allows the whole team to work quickly and efficiently • Record all your findings clearly, looking for trends • Keep going back to check ABC

Initial management of the polytraumatised patient

Trauma 95


43

Wound management

Everted – good

Inverted – bad

If you cannot completely clean a dirty wound, pack it and leave it open

Your stitch should reach to the floor of the wound and take more tissue deep than superficially Then, when the stitch is tightened, the wound will evert and there will be no dead space

General assessment

History

injury occurred to its position when the examination is performed, it is easy to miss the depth of the wound. For example, it is easy to miss that the knuckle joint has been penetrated in an injury from a punch onto the teeth of an opponent. If the hand is examined with the fingers extended, the skin wound appears to be well away from the knuckle itself.

Try to find out how long ago the wound occurred and whether the object that caused it was likely to have been clean or contaminated, or even whether any noxious chemicals or electrical burn may be involved (see Chapter 45). Clean cuts that occurred recently are managed completely differently from dirty wounds or those that may already be infected.

Damaged nerves, vessels, ligaments and bones should be repaired as soon as possible, but the first priority must be to remove non-viable tissue and then to ensure that there is adequate skin and soft tissue cover to ensure infection-free healing.

Examination

Tetanus

Check distal neurovascular status. The sooner that damage to a vessel or nerve can be identified, the better the chance that a repair can be performed and the function of the limb saved.

Prophylaxis against tetanus must be up to date or tetanus toxoid will be needed. Prophylactic antibiotics may also be given but are no substitute for proper wound cleaning.

Carry out a rapid general assessment of the whole patient to make sure that their airway, breathing and circulation are satisfactory (ABC, then D and E; see Chapter 42) before focusing in on the presenting injury.

Repair

Investigation

Pain relief and rehabilitation

An X-ray is useful to exclude fracture or dislocation. Two views need to be taken at right angles to each other, centred on the injured area. The entry wound can be marked with a paper clip taped to the skin. Ultrasound may be better than an X-ray for finding glass.

Wounds are painful and can lead to wasting and stiffness if no effort is made to ensure that the patient builds up muscle strength and mobility as quickly as possible. This is especially important in the hand where the role of the physiotherapist is crucial.

Cleaning

Stitching

Wounds must not be closed if there is any chance that they might become infected. Copious volumes of saline should be used to wash the wound out – dead and contaminated tissue must be removed. If at the end of your best efforts you cannot be sure that the wound is clean then pack it and review the situation daily until you are sure it is clean. Then, and only then, should you close it.

When stitching a wound make sure the edges are everted.

Exploration Good light is needed to inspect a wound properly. Local or general anaesthesia may also be needed, so wounds are best explored in an operating theatre. If the limb was in a different position when the

TIPS • • • • • •

Check ABC and for other wounds Test distal neurovascular status Ultrasound may be better than an X-ray for finding glass Do not close a wound unless you are sure it is clean Exploration of a wound is best done in an operating theatre Protection against tetanus needs to be checked

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44

Plastic surgery

Superficial skin loss Superficial skin loss will heal well provided there is no dirt left in it and it does not become infected. The donor site of a split skin graft heals in a similar way

Full thickness skin loss If the wound cannot be closed and there is healthy soft tissues in the floor of the wound, a split skin graft can be harvested elsewhere on the body and used to provide cover. The scar does not look good and cannot tolerate heavy use, e.g. sole of the foot

Wide excision of melanoma

Large areas of full thickness loss Skin defect from congenital abnormalities Tissue expanders can slowly stretch the skin to create spare skin for reconstruction

Split skin grafts can be ‘meshed’ to increase the area which each piece can cover. Skin cells can be grown in culture to cover very large areas

Meshed skin graft

Congenital syndactyly Exposed bone A vascular graft of skin and muscle is needed. Sometimes it is possible to rotate a flap locally, covering the donor area with a split skin graft. Otherwise a vascularised free graft will need to be taken from elsewhere on the body (usually the back) and connected into the local blood supply using micro-surgery. The donor site is closed or grafted

Plastic surgery is the craft of moving skin and soft tissues to repair damage or to improve appearance and function. The skin provides a crucial function preventing excess fluid from leaving the body and infection from entering the body. Soft tissues are also necessary to provide a substrate for healthy skin. When skin and soft tissues are lost due to trauma or because diseased tissue has been excised, it may not be possible to simply close the defect. Exposed bone and ligaments will become infected if they are not covered, while soft tissues left to heal of their own accord may leave ugly scars which hamper normal function when they contract as part of the healing process. • Superficial defects (grazes and partial thickness burns). In these cases the skin heals from nests of epithelial cells growing out from hair follicles where they were protected from the original trauma. Healing is reasonable providing the damaged area is cleaned and kept free of infection. • Full thickness defects (complete loss of skin with intact soft tissues beneath). Surgeons use the skin’s ability to heal partial thickness defects to harvest epithelial skin which can then be used as a split skin graft to cover a full thickness defect. The graft can be meshed to cover a larger area and will stimulate rapid healing without contrac-

ture, although the scar is not attractive and the resistance of the graft area to abrasion is poor. For very large defects it is now possible to culture epithelial cells from the patient and use these to ‘seed’ the growth of an epithelial cover. • Complete soft tissue loss (exposed bone). Skin and underlying vascularised muscle will be needed to cover these defects. If it is possible to rotate nearby skin and muscle to cover the defect while maintaining its blood supply, then this pedicle graft will be the best option. Normally it is possible to dissect out an area of skin and underlying muscle from a part of the body where it can be spared. This vascularised graft is then plumbed into its new site, using microsurgery to connect its arterial supply and venous drainage to the local blood supply.

TIPS • • • •

Decide depth of defect and plan treatment accordingly The body needs skin cover to prevent fluid loss and infection If infection is allowed to set in, the wound effectively becomes deeper Don’t close dirty wounds

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Burns

45

Patients with burns may also have many other injuries from explosions or falls. Carry out ABC

% Total Body Surface Area Burn Be clear and accurate, and do not include erythema (Lund and Browder)

A

A 1

1

Rule of 9s for areas of burns 2

9

9% front upper torso 9% front lower torso 9% back upper torso 9% back lower torso 9 9% whole arm 9

9 9

9

9

The area which can be covered by the palm of the hand is 1% of body area

9

9

11/2

Soot around the nostrils or nose suggests that smoke or flames may have been inhaled. Prophylactic intubation may be needed before laryngeal oedema blocks the airway. Check for carbon monoxide poisoning

9% front of leg 9

2 13

11/2

1

11/2

B

11/2

9% back of leg

11/2 21/2 21/2

11/2

B

11/2

B

%

C

C

13/4 13/4

Pain relief Fluid replacement Protect burn from sepsis Graft

11/2

B

Treatment 9

2

2 13

9% head

Area A = 1/2 of head B = 1/2 of one thigh C = 1/2 of one lower leg

PTL REGION Head Neck Ant.trunk Post.trunk Right arm Left arm Buttocks Genitalia Right leg Left leg Total burn Age 0 91/2 23/4 21/2

1 81/2 31/4 21/2

FTL

5 61/2 4 23/4

C

C

13/4 13/4

10 51/2 41/2 3

15 41/2 41/2 31/4

Adult 31/2 43/4 31/2

Adapted from, Hettiaratchy, S. et. al (2004) The ABC of Burns. BMJ Books, Oxford

Partial thickness burns retain sensation to pin prick

Avoidable causes of death Full thickness burns have no sensation

Multi-organ failure, secondary to severe hypovolaemic shock and/or sepsis

History

Initial treatment

If the patient cannot tell you what happened, then the paramedics should be able to advise on whether the burn was caused by heat, chemicals, electric shock or a combination of all of these. They will also be able to warn if other trauma is involved (such as a jump from a burning building).

Move the patient to safety, (taking care not to be injured yourself). For heat or chemical burns apply as much clean water as possible, to prevent further heat damage and to dilute chemicals so that the burning process stops as quickly as possible. Cold water will also reduce pain, and wash out any contamination which may cause infection. Cover the burn with a dressing (cling film will do well) to prevent subsequent contamination and reduce pain. Pain relief will also be needed.

Airway and breathing • If smoke was involved or if there is any sign of soot or burns around the mouth or nose, then damage to the airway from smoke inhalation must be considered. The patient must be put on 100% oxygen and a very careful watch put on their airway and their oxygen saturation. Specific problems which the patient may experience are: • Smoke may contain carbon monoxide. • Toxic fumes in the smoke may also have caused chemical damage to the lungs. This may lead to a rapid onset of pulmonary oedema with a fall in blood gases and the need for assisted ventilation. • If the patient has actually breathed in flames, damage to the lining of the upper airway will lead to swelling of the glottis. Stridor will be the first sign – followed rapidly by complete airway obstruction. It is safest to perform endotracheal intubation early, as it can be almost impossible to find the vocal cords once oedema has set in. Otherwise, an emergency tracheostomy will be needed.

Circulation Patients with burns lose large volumes of fluid by exudation and evaporation. These fluids need to be replaced if circulation is to be maintained and renal failure avoided. A cut-down may be needed to obtain good venous access, for crystalloids, colloids and even blood transfusion. In severe cases a urinary catheter and a central venous line will be needed to monitor the state of the circulation so that the appropriate volume of fluids can be given.

Protection and pain relief Exposed wounds lose fluid, cool the patient by evaporation, are very painful and are at risk of becoming infected. Any foreign material embedded in the wound will need removing, but at this stage it is only important to make sure that noxious chemicals are washed away and

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any smouldering material is cooled down so that the burn does not extend. The burns are best covered with cling-film or some other nonstick conforming dressing covering some kind of antiseptic cream such as silver sulfazine.

The severity of burns is determined by the area involved and the depth of the burns.

• The dead tissue must be removed as it is a focus for infection. Dead tissue is shaved off layer by layer until fresh bleeding is obtained. • Then a decision needs to be made as to how the area is to be covered. Meshed split skin grafts provide a good source of cover, especially for large areas in the first instance. However they tend to give a poor result cosmetically. • Once the patient has recovered from the initial trauma it may be decided to replace the initial grafts with full thickness grafts or even free flaps, especially in areas where appearances are important (e.g. the face), or where heavy wear is likely to ulcerate a split skin graft (e.g. palm of the hand). • Full thickness burns left to heal of their own accord shrink down as they heal, producing contractures that can destroy function and look very ugly.

Area

Sepsis

In the first instance, the area of the body surface that is burnt is estimated using three techniques: 1 The area covered by the hand of the patient is estimated to be 1% of the total body surface area. 2 The rule of 9s is more useful in extensive burns. Nine areas of the body each make up approximately 9% of the total surface area. 3 The Lund and Bowdler chart is the most accurate way of estimating the area.

Sepsis in a superficial burn can convert it to a full thickness lesion, while sepsis in a graft can lead to death of the graft. If the sepsis then spreads, septicaemia may lead to multiorgan failure, the commonest cause of death after burns if the patient survives the first few hours. Full sterile precautions, proper surgical cleaning and prophylactic antibiotics all play a role in trying to prevent infection.

Electrical burns High voltage electric shocks will traverse the patient’s body leaving only a small entry and exit burn visible externally, even when there is extensive internal damage. An electrocardiograph (ECG) will be needed to exclude myocardial damage; compartment syndrome is also a risk in the limbs.

Assessing the severity of the burn

Depth Superficial burns • Superficial burns cause reddening or blistering of the skin. • Sensation is preserved and the prognosis for recovery is good provided sepsis does not set in. • The deepest parts of the dermis – around the pores and hair follicles – are preserved and act as a source of cells from which the rest of the epithelium regenerates. • Fluid loss can be considerable but once healing has occurred scarring is minimal. Full thickness burns • Full thickness burns completely destroy the dermis and the tissues beneath. • They can be distinguished from superficial burns because there is no sensation when the area is tested by pinprick.

Fluid balance Burn patients lose large volumes of fluid and go into renal failure if these fluids are not replaced. Colloid and blood, not just crystalloid, may be needed to maintain the extracellular fluid compartment volume, and prevent shutdown of the kidneys.

Mortality The chance of a patient surviving a burn decreases with the increasing area and depth of the burn and with the age of the patient.

TIPS • Smoke inhalation may need urgent intubation • Burns patients need to be kept well hydrated • Sepsis needs to be avoided if at all possible

Burns

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Peripheral and spinal nerve injuries

Tell me if the two sides feel the same

Operating microscope

Always test distal sensation at every trauma and orthopaedic examination

Even after nerve repair, recovery is slow from proximal to distal. After 2 years further recovery is unlikely

Muscle power and sensation now recovered

If a nerve is cut and the ends have separated, the ends must be brought back together or a graft used to give nerve axons a chance to regrow

Zone of muscle power and paraesthesia creeping distally at 1mm/day Zone where recovery has not yet started or will never occur

Diagnosis

Minor injuries

Nerve injuries are easily missed in the turmoil of major injuries, or if the patient is drunk or upset. Testing should be done by comparing sides, not by asking the patient to close their eyes and then asking if they can feel you touching them. The second method is notoriously unreliable, while the first reliably warns you when a full formal neurological examination may be needed. As a general rule penetrating wounds in the hand have always damaged a nerve until otherwise proven. Similarly, in the neck and spine it is best to assume the worst (there is an unstable fracture with potential for further nerve damage) until this possibility has been actively excluded (see Chapter 42). Some nerves, like the lateral popliteal (foot drop) and the radial nerve (wrist drop), are especially susceptible to injury because of their position close to bone with no soft tissue protection.

Minor compression of a peripheral nerve can lead to loss of function of that nerve for some days or even weeks. The nerve fibres are intact and physiological function returns in time without any need for tissue healing.

Peripheral nerve injuries Chronic injuries Nerves passing through narrow canals are liable to become acutely or chronically compressed if: • The canal is narrowed by new tissue deposition such as osteophytes. • There is local swelling and inflammation of tissues such as synovium in rheumatoid arthritis. • There is generalised oedema such as occurs at menopause. • A tumour in the nerve causes thickening of the nerve. • There is excessive external pressure from the patient’s occupation such as using a pneumatic drill. The common sites for the compression are the median nerve in the carpal tunnel at the wrist, the ulnar nerve on the medial side of the of the elbow joint, as well as spinal nerves as they pass through the intervertebral foramina. There are many others including Bell’s palsy and acoustic neuroma causing deafness.

Severe injuries • Incomplete severing of the nerve. In more severe injuries some of the fibres (axons) in the nerve may be severed but the overall structure of the nerve may remain intact. In these cases the axon proximal and distal to the cut dies (Wallerian degeneration), leaving the tunnel of Schwann cells (if it was a myelinated fibre) through which the fibre originally passed. This tunnel acts as a guide for a new nerve fibre to grow back at around 1 mm/day. The progress of the regrowth can sometimes be traced by tapping your finger over the path of the healing nerve. When you tap over the tip of the new growing fibre, the patient will experience electric shocks running down the arm. • Complete severing of the nerve. An injury that completely separates the ends of the nerve cannot heal unless those nerve ends are brought back into close contact, preferably with the nerve fibre ends correctly aligned with each other. Otherwise there is a danger that the regenerating axon tip will set off down the wrong track thus compromising the function of the nerve. The repair of the nerve is best performed under an operating microscope to obtain accurate opposition; if there is a segment of nerve missing, then a nerve graft may be created from a length of another less important nerve to act as a guide to the regenerating nerve fibres.

Nerve recovery • Nerve recovery tends not to be so good in the elderly, where the nerve fibres are very long, and where the nerve has a mixture of sensory and motor fibres.

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• While waiting for nerves to regrow there is important work to be done by physiotherapists in preventing muscles from wasting, and joints from stiffening up. • If there is also sensory loss then these areas may need to be protected from unnoticed damage, especially burns, which may lead to ulceration. • Recovery of sensation can be tested using hair bristles of differing stiffness (noting the softest that the patient can feel), and by testing two point discrimination (the smallest distance between two pricks that can be distinguished as separate points).

Injuries to the central nervous system The peripheral nervous system extends out from the spinal ganglia (dorsal for sensory, ventral for motor). The rest of the nervous system (pre-ganglionic) consists of the brain and the spinal cord. Injury to these nerves leads initially to a state of spinal shock (concussion) when the nerves fail to work at all. The spinal shock wears off over a period of hours or days and it is only then that the true extent of the damage to the nervous system will become apparent. In spinal cord injuries, the finding that there is sparing of the central sacral roots is the first indication that there may be some recovery of function and that the transection of the cord is not complete. The central nervous system has very little capacity for tissue healing but has an extraordinary ability to reorganise so that damaged tissue is by-passed. This process takes time and this plasticity decreases with age. As the spinal shock wears off, patients may get a false hope of recovery from the fact that their muscles are starting to contract. However, this may be spasticity setting in, a result of complete and irreversible nerve damage.

Repair is likely to be at best a limited success, and is technically very difficult. The patient is unfortunately often left with severe and intractable pain in a useless arm. The pain is very difficult to treat and is not usually helped by amputation. The patient may become suicidal as a result. If a nerve attempts to regrow but the new tissue becomes trapped in scar tissue, then a painful lump (neuroma) may develop which may need excision. Patients who suffer a traumatic or even elective amputation may be left with a strong feeling that the limb is still present. It may then be itchy or even painful (phantom pain). Interestingly placing a mirror so that the patient sees an image of their normal limb where the amputated limb would have been lying allows the patient to scratch their normal limb and obtain relief from ‘phantom itching’ in the missing limb.

Rehabilitation • Long periods of rehabilitation will be needed if a patient who has suffered a significant injury to the brain or spinal cord is to have the best chance of returning to a full independent life. • Head injuries can result in significant behaviour changes, memory loss and problems with concentration, as well as problems with spasticity. • Permanent sensory loss means that the patient must learn to move regularly if bedsores are to be avoided, as once these have started they can be very difficult to treat. Both partial and complete nerve lesions especially in the brachial plexus region can cause severe pain resistant to normal pain killers (causalgia).

TIPS

Brachial plexus injuries If the arm is dragged down by a high energy impact (such as a fall from a high speed motorcycle), there may a tearing injury to the nerves coming from the neck through the brachial plexus into the arm. The injury can be a mixture of: • Pre-ganglionic damage where the nerve roots actually pull out the ganglia. • Post-ganglionic damage where the brachial plexus is torn apart.

• If the tendon is damaged in a finger injury then the digital nerves are also probably injured • Nerve ends need bringing together (if necessary with a graft) if any nerve recovery is to occur • After 2 years there is unlikely to be further nerve recovery • Stiffness and wasting need to be minimised while waiting for nerve recovery

Peripheral nerve lesions Name

Site

Cause

Effect

Treatment

Carpal tunnel syndrome

Median nerve at the wrist

Oedema Trauma Inflammation

Numbness in radial fingers. Wasting and weakness of opposition of thumb

Release of flexor retinavulum to de-roof the carpal tunnel

Ulnar nerve palsy

Ulnar nerve on medial side of elbow

Trauma Arthritis

Numbness in ulna one and a half fingers. Weakness and wasting of intrinsic muscles of hand

Transposition of the ulnar nerve releasing scar tissue

Common peroneal nerve Sciatic nerve

Over the fibula head

Trauma (iatrogenic from obstetric stirrups)

Foot drop and numbness in foot

May recover in time

Behind the hip joint

Dislocated hip from trauma or hip replacement

Foot drop and numbness in foot

May need exploration to drain haematoma. May recover in time

Peripheral and spinal nerve injuries

Trauma

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47

Head injuries

Secondary brain injury Swelling may compromise circulation to brain = Unavoidable

Brain swelling secondary to injury = ↑ Pressure = ↓ Circulation

The concussion and other injuries may compromise Airway, Breathing, Circulation = Avoidable Airway = O2 to lungs

Breathing = O2 to blood

Brains need continuous circulation of oxygenated blood The skull is a rigid box enclosing the brain Brain injury leading to loss of consciousness (concussion) and swelling = Primary brain injury

Circulation = O2 to brain

Extradural haemorrhage

Direct blow – fractures skull

An initial phase of unconsciousness (concussion) soon passes

A lucid interval leads to a secondary loss of consciousness

Introduction The brain is arguably the human’s most precious organ. It is well protected by the skull, but it is large and heavy and so is prone to injury, especially from blows that rapidly accelerate and then decelerate it within the confines of the skull. Significant injuries to the brain lead to a temporary shut-down of higher functions (concussion). However, it must never be forgotten that unconsciousness can also be coma, or a result of stroke, hypoglycaemia, epilepsy or drugs. So, the loss of consciousness may have been the cause of the accident not the result. The key to the management of most head injuries is ensuring that the brain remains well perfused in the post-injury and recovery period. Failure to keep the airway clear, the blood well oxygenated and the brain well perfused may lead to so-called ‘secondary injury’ to the brain. This damage should be avoidable.

Examination shows unequal pupils Scan confirms extradural haemorrhage

Burr hole relieves intra-cranial pressure Allow perfusion of the brain Patient recovers consciousness

any effort to breathe or may have lost their gag reflex. Early endotracheal intubation may be needed to keep the patient well oxygenated, and to protect the airway from inhalation. Assessment of conscious state is initially made using AVPU (see below), but later the Glasgow coma scale should be used which gives marks for the best response in a set of different areas (response to verbal command, response to pain, eye movements). An early measure of the conscious state is valuable because it is any subsequent change in the conscious state, rather than the absolute level that guides further investigation and treatment. If the conscious state starts to deteriorate, always check ABC before looking for neurological causes. A scan of the brain is needed if intracranial bleeding is suspected but the patient must first be made safe to enter the scanner.

Types of head injury Initial management

Cuts on the scalp

As in any serious injury the initial management is ABC (see Chapter 42) followed by an assessment of conscious state and a check for any other injuries. Patients with serious head injuries may not be making

These bleed profusely and can cause hypovolaemic shock. They should always be explored in case they lie over a fracture or even a penetrating wound into the brain itself.

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Fractured skull

Rehabilitation

A fractured skull is of no great significance in itself unless it is depressed and fragments are pressing into the brain. However, it is an indication of the severity of trauma, and if close to a blood vessel may provoke an intracranial bleed. If the fracture is open then blood mixed with cerebrospinal fluid will flow out of the ear, nose or wound and prophylactic antibiotics need to be given to protect against meningitis.

Although the central nervous system is thought to have very limited powers of regeneration, the brain does seem to be able to achieve some recovery by plasticity – recruiting new pathways to perform tasks where the old pathway has been damaged. This appears to occur much more easily in the young than in the old, but either way occurs over a period of many months. During that time the patient will need considerable social and physical support, as their personality can be profoundly altered and their behaviour may become very disruptive.

Extradural haemorrhage Fractures near cranial arteries – especially the middle meningeal artery (running up the side of the skull by the temple) – may tear the artery itself. This produces bleeding between the skull and the dural membrane, which will slowly start to compress the brain over a period of hours. Classically the patient has a short period of unconsciousness (concussion) followed by a recovery of faculties. However, some time later, after this lucid interval, the patient may start to develop localising signs of raised intracranial pressure, with weakness on the side opposite to the lesion and a fixed dilated pupil on the side of the lesion. Rapid recognition of the possibility of an extradural haemorrhage should result in immediate imaging using a CT scan or MRI, followed by surgical decompression using burr holes, followed by raising a flap. The moment that the pressure is relieved the patient miraculously recovers.

Subdural and intracranial haemorrhage following trauma These can be diffuse or localised. Diagnosis is best made by CT or MRI. Treatment in the first instance is to avoid ‘secondary injury’ by making sure that the patient is well perfused and well oxygenated.

Brain injury Direct damage to the brain itself will be made worse by bleeding and swelling secondary to the trauma of the injury. Controlled dehydration, hyperventilation reducing blood carbon dioxide and high-dose steroids are all used to try to minimise the secondary damage caused by the brain swelling inside a rigid container (the skull), but so far there is no conclusive evidence that any of these techniques improve the outcome. However, what does make a difference is making sure that the brain is well perfused and well oxygenated.

TIPS • In head injuries check and recheck ABC, intubating if necessary • Check for other injuries • Remember hypoglycaemia and drugs; coma may have caused the accident, rather than the accident causing concussion • A lucid interval followed by deterioration may indicate an extradural emergency AVPU A = Alert V = responds to Verbal commands P = responds only to Painful stimuli U = Unresponsive to any stimuli Glasgow Coma Score Fully conscious scores 15. Minimum score is 3. A score of less than 8 suggests that the patient needs intubation to protect their airway. When reporting conscious state give the score for each area separately e.g. Eyes 3, Verbal 2, Motor 4. Changes in the GCS are more important in guiding treatment than the absolute score.

Score

Eyes

6 5

Normal oriented conversation

Localises to pain

4

Open Spontaneously

Confused

Withdrawal/ flexion

3

To verbal command

Inappropriate/ words only

Abnormal flexion (decorticate)

2

To painful stimulus

Sounds only

Extension (decerebrate)

1

Do not open

No sounds

No motor response

Raised intracranial pressure In the acute phase of raised intracranial pressure, the patient’s conscious state will be depressed and respiration will be reduced, as will the pulse, although paradoxically blood pressure may go up (the opposite of hypovolaemic shock). If pressure continues to rise, the patient’s conscious state will deteriorate and they will become rigid and spastic (decerebrate). Eventually the brainstem will be driven down into the foramen magnum, leading to coning and death.

Motor Obeys commands

Chronic subdural haemorrhage In the elderly a trivial fall can lead to a small subdural haemorrhage that may continue to expand long after the original trauma has been forgotten. The patient may show a gradual deterioration in mental faculties over a period of weeks or even months. The underlying cause will only be revealed once a scan has been performed.

Verbal

T

Intubated

Head injuries Trauma

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48

Fractures and dislocations History

Examination

Head injury Broken neck Crush fracture of vertebrae Wrist fracture

Shear fracture of pelvis

Fracture of neck of femur The description of the accident will tell you much about the likely sites of injury and the energy involved Warning High-energy injuries break more than one bone

Tibial plateau or femoral condyle fracture

ABC first Get proper exposure Check distal neurovascular status If you find one fracture, check for more Always check the back

Crush fracture of heel (calcaneum)

Investigation X-rays need at least 2 views MRI or CT scan for head injuries Ultrasound for abdominal bleeding

Treatment

1. Pain relief – The only thing needed for some fractures e.g. clavicle

2. Splintage – tape, plaster or fibreglass Protects stable fractures. Will hold simple fractures. No surgery needed

Classification of fractures

Open vs closed Stable vs unstable – unstable fractures need reducing and holding

3 point pressure holds reduction

Crush fractures, especially those which are transverse or undisplaced, are often stable Spiral fractures, especially those which are displaced and have many fragments, tend to be unstable Viable vs avascular – unstable fractures need reducing and holding 3. External fixation – Useful when soft tissue badly damaged

Sub-capital fractured neck of femur

Blood supply lost, femoral head dead

Allows accurate reduction of intra-articular fractures

Allows early mobilisation of an unstable fracture

4. Open reduction and internal fixation (ORIF) – Plates, screws, wires and intramedullary nails

Hemiarthroplasty

Intra-articular vs extra-articular – displaced intra-articular fractures need accurate reduction if early arthritis is to be avoided

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Causes

Growth plate fractures in children

If the load on a limb exceeds the strength of the bone, joint capsule or ligaments, then a fracture, dislocation, or joint sprain will occur. If the load is normal but the bone is weak, then this is a pathological fracture e.g fractured neck of femur in an elderly female. Repetitive loading may cause a stress fracture as in long-distance runners.

Fractures across the growth plates of children’s bones can interfere with the ability of that bone to grow, and need handling with special care. Every effort must be made to prevent the epiphyseal plate from producing a deformity.

Management Shape and direction of injury 1 Shape of the fracture. This is determined by the direction of force applied: • Spiral fractures result from twisting. • Crush fractures result from excess longitudinal load. • Transverse fractures result from bending forces. • Very high impact energies tend to explode the bone. 2 Dislocation. A joint is more susceptible to dislocation if the patient has lax ligaments or if there is damage to the capsule from a previous dislocation.

History The patient will be able to describe what they have felt or heard. Dislocations may relocate spontaneously, so the patient’s description of what happened is valuable.

Examination Do not forget to check distal neurovascular status, then use the ‘look, feel, move’ system to check for: • Wounds on the skin. • Bleeding into the soft tissues. • Deformity of bones and joints. Movement needs to be performed carefully, watching the patient’s face, testing for ruptures of muscles and ligaments, instability of joints and even crepitus in bones. Don’t forget: if there is enough energy for one injury, then there is plenty for more, so check the whole body.

Investigation At least two X-rays will be needed centred on the site of injury, aligned at right angles to each other.

Classification of fractures 1 Open versus closed. Any wound in a limb which is fractured means that we must treat the fracture as if it is open rather than closed. Open fractures are contaminated until otherwise proven. If the wound is not cleaned out at once, then infection will set in. Once infection has established itself in the bone, then it is said that it can never be eradicated – it may always break out again. It is better to prevent osteomyelitis than try to cure it. Photograph the wound then cover it to prevent further contamination, give prophylactic antibiotics, and arrange for urgent surgery to clean the wound and close it if possible, once the fracture has been fixed. 2 Viable versus avascular. If the fracture pattern results in pieces of bone losing their blood supply, they cannot heal. They may then need removing and/or replacing. 3 Stable versus unstable. Some fractures (especially those involving a simple crush) are stable. In other cases fractures are unstable, especially spiral or comminuted (multifragmentary) fractures. 4 Intra-articular versus extra-articular. If displaced intra-articular fractures are not reduced exactly (less than a 2 mm step in the articular surface) then early arthritis in that joint is inevitable.

A displaced fracture needs ‘Reducing’ and then ‘Holding’. 1 Reduction. Paradoxically, the first move is to increase the deformity in the direction of the original damaging force. This allows the joint or fracture fragments to be separated from each other without damaging the capsule or periosteum, which is intact on the inside of the deformity. The intact periosteum is then used as the hinge and the guide to bring the structures back into their correct relationship. 2 Fixation. Once reduced the fracture or dislocation needs to be held to prevent it displacing again. • Sometimes a simple sling will be adequate. • In other cases bone fragments may need to be held exactly in position with a plate and screws. • Plaster of Paris is cheap and simple to use but does not hold fractures very precisely and is a great inconvenience to the patient while they wait for the fracture to heal. However, this method may be ideal for fractures in children, which heal quickly and remodel as they grow. If the fracture is unstable, moulding the plaster using three-point pressure may reduce the risk of the fracture slipping. • In patients with fractures through metastases, quick and strong fixation with an intramedullary nail will allow them to get home as quickly as possible.

Complications Fractures can unite in a bad position (malunion) or heal slowly or even not at all (non-union). Failure to unite can be a result of poor blood supply. In this case the bone ends just wither away. A little movement stimulates bone healing. Too much movement produces exuberant new bone, but a failure to bridge the cleft. Bone grafting and secure fixation of the fracture may be needed to treat delayed union or non-union. Stiffness and weakness can be a problem after fractures or dislocations. Physiotherapy has a key role in rehabilitation.

Osteotomies Bones can be broken deliberately to correct deformity or even to lengthen limbs. External fixator frames can then be used to move fragments of bone, providing the speed is not so high that non-union results or too slow so that the osteotomy unites before adequate movement has been achieved.

TIPS • Check ABC first, then for other injuries • Check distal neurovascular status • Open fractures need cleaning out to prevent osteomyelitis • Fractures into joints need exact reduction • Fractures into the growth plates of children’s bones need special care • Pathological fractures in the elderly need quick fixation to return their mobility

Fractures and dislocations Trauma 105


49

Compartment syndrome

Does that hurt?

Bleeding or swelling into a closed muscle compartment collapses the veins and blocks venous drainage. The pressure rises to arterial pressure preventing circulation of blood

Passive stretching of the affected muscle causes extreme pain N.B. distal pulses may still be intact

Treatment

Result of a missed diagnosis – Volkmann's ischaemia, a withered useless, ugly claw

Pathophysiology If there has been damage to the blood supply of a limb or severe damage to the soft tissues (with or without a fracture), then there may be swelling or haemorrhage of the muscles. Some muscles are enclosed in a rigid fascia. If they swell, the pressure inside that compartment may rise and actually cut off the blood supply to the muscle. Over a period of hours the muscle dies, and is then replaced by fibrous tissue that contracts. The end result is a Volkmann’s ischaemic contracture – a useless, withered, clawed limb. Even those muscles that are not in a fixed fascia can behave in the same way if the limb is encased in a tight dressing or a closed plaster. Ischaemia can therefore be iatrogenic (caused by a doctor), and all dressings and casts should be split if there is any possibility that the limb might continue to swell.

Diagnosis Compartment syndrome is diagnosed by having a ‘high index of suspicion’. There are said to be five Ps – pain, paralysis, pallor, paraesthesia and pulseless – but these are also present in the ischaemic

Remove all dressings and plasters which may be compressing the limb. If there is no improvement the fascia must be split immediately and left open until the swelling is reduced

limb. Not all of these need to be present for a compartment syndrome to be diagnosed. Only pain and paralysis are reliable features. The pulse can still be present as the artery passing through the compartment has stiff walls that may resist the pressure even when the tissues in the compartment are not being perfused. The cardinal sign of compartment syndrome is the finding of extreme pain when the muscles in the compartment are stretched (passively extending the fingers for the flexor compartment of the forearm, flexion and extension of the toes for the compartments of the lower leg). Compartment syndrome can also develop in the small muscles of the hand and of the foot after a severe crush injury. Measurement of the pressure within the compartment (using a wick catheter or a transponder) is difficult to perform and appears to be unreliable in deciding whether decompression is indicated, so the diagnosis is a clinical one. Late or chronic compartment syndrome is rare, so if late pain is a problem, consider deep infection (especially gangrene) and regional pain syndrome (sometimes called Sudek’s atrophy or reflex sympathetic dystrophy).

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Presentation The commonest presentation is being called to see a patient (especially a child) in whom there has been trauma and who is now complaining of severe and increasing pain just at a time when the pain should be settling down. This could be after an elective operation but is usually after trauma. It can be difficult to distinguish between a patient who is anxious and a developing compartment syndrome. It is best to be on the safe side and act on the assumption that it is a compartment syndrome.

Examination A reliable physical sign is to distract the patient and then flex and extend the digits at the end of the limb in question. If the patient cries out in pain (because the ischaemic muscles are being stretched) then the diagnosis has been made.

Treatment The treatment of a compartment syndrome is a surgical emergency. • The first thing to do is to divide the plaster and dressings in case it is these that are constricting the circulation.

• If there is not an immediate improvement, the patient must go to the operating theatre and the compartments in question should be opened up from end to end. If there is no compartment syndrome found, then no great harm has been done, and the wound can be closed the following day. If there is a compartment syndrome the muscle will pout out and if it has been caught early enough the muscle will reperfuse. If it has been left too late and it is literally a matter of a few hours then the muscle will be dead and will need excising. Either way the wound should be left open initially, then a second look taken a day later when it will be clear what is the likely outcome, and the swelling will have gone down.

TIPS • • • • •

Always split a dressing or plaster on a limb which may still swell Have a high index of suspicion for compartment syndrome If stretching the affected muscles causes pain, take action at once First remove all casts and dressings in case they are the cause Urgent fasciotomy is needed if there is not immediate improvement

Compartment syndrome Trauma 107


Self-assessment case studies: questions Case 1: Acute joint disease A 42-year-old man presents to casualty with a painful and swollen right knee, which he attributes to an old football injury ‘flaring up again’. He is otherwise well but is unable to weight-bear. He has insulin-dependent diabetes and psoriasis. He is a businessman and drinks 32 units of alcohol per week. 1 What elements of the history so far are helpful in forming a differential diagnosis and why? Further questioning reveals a history of a red eye. 2 What other rheumatological diagnoses might link this symptom with his arthropathy and what other features would you ask about to confirm or refute these possibilities? The red eye transpires to be a history of subconjunctival haemorrhage and unrelated to his current presentation. 3 What is your first-line investigation in this patient and why? A diagnosis of acute gout is made. 4 How would you treat this patient? What if he suffered recurrent attacks?

Case 2: Initial management of polytrauma A 19-year-old motorcyclist had just bought a 1000 cc super motorcycle. While negotiating a corner, it appears that he lost control and the bike skidded into the path of an oncoming 4 × 4. The rider ’s body hit the vertical front of the vehicle obliquely bouncing across into the ditch. The car driver was uninjured and used a mobile phone to summon assistance. A paramedic was on site within 10 minutes. The helmet was removed and the rider was put onto a spineboard and brought in blue and unresponsive arriving 25 minutes after the 999 call. 1 Describe your initial management. As soon as the leathers and clothing were cut away, it became clear that the left femur was sticking out through the skin of the mid-thigh. 2 What must now be checked? 3 What are the principles of treatment of the broken femur? 4 What options are available for fixing the fracture?

Case 3: Rheumatoid arthritis A 28-year-old woman is referred to the clinic with painful hands. Her symptoms began several months ago and now all of her metacarpophalangeals are affected. Her fingers are stiff for several hours each morning and swollen for most of the day. 1 Does she meet all the ACR (American College of Rheumatology) diagnostic criteria for rheumatoid arthritis? 2 What role would measurement of rheumatoid factor play in this patient? The patient is diagnosed with rheumatoid arthritis and commenced on methotrexate as first-line disease-modifying therapy. 3 What information does she need to be given concerning this treatment? Several months later she presents as an emergency with increasing shortness of breath. 4 What is your differential diagnosis and how would you investigate her further?

After several years of DMARD (disease-modifying antirheumatic drug) therapy her disease remains uncontrolled. Examination reveals classic bony deformities and muscle wasting in her hands. 5 List the causes of small muscle wasting in patients with rheumatoid arthritis. The patient has read about TNF (tumour necrosis factor) blockade on the internet and is keen to try it. 6 What are the current guidelines for use of TNF blockade in patients with rheumatoid arthritis?

Case 4: Septic arthritis A 4-year-old child is brought in by her mother. For 2 days she has been off colour, and is now toxic and generally unwell. The child is crying, wants to be picked up by her mother but screams when her mother tries. There appears to be extreme pain in the left leg and she will not take any weight through that leg. It is difficult to localise the source of the pain – it could be the knee, the hip or even referred from the back. 1 What would you look for on examination? 2 What investigations would you do to confirm/exclude the diagnosis? 3 What is the treatment?

Case 5: Limps in the elderly A 75-year-old presents with increasing pain in the right leg on walking. He also describes stiffness in the left hip, and mentions that the leg now feels shorter than the other side. 1 What is the likely diagnosis? 2 What questions might you ask to determine the severity of symptoms? 3 What four classic features of this condition might you see on X-ray? 4 List four treatment options.

Case 6: Osteoporosis A 72-year-old woman is admitted to Accident and Emergency following a fall. The medical team are concerned that she may have sustained low trauma fractures due to osteoporosis. 1 What are the commonest sites for osteoporotic fracture? 2 List the risk factors for osteoporosis that you would seek in the history. 3 How would you confirm the diagnosis of osteoporosis? 4 What is the first-line treatment for the primary prevention of osteoporosis in this patient? What instructions would you give her on how and when to take this therapy?

Case 7: Problems in the hand A 60-year-old labourer who works with pneumatic drills and erects scaffolding presents with an inability to straighten his little and ring fingers of his dominant hand. It has been coming on for some time. He says his father developed the same problem at the same age. He smokes 20 a day and is a hard drinker too. 1 What is the diagnosis? 2 What is the likely natural history if this is left untreated?

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3 What four features in the history given predispose him to this condition? 4 What is the surgical treatment and postoperative care?

Case 8: More problems in the hand A 45-year-old woman starts noticing that she is becoming increasingly clumsy. She also notices that the index and middle finger of her right dominant hand go numb at night. If she hangs her hand out of bed and shakes it, the symptoms are relieved. 1 What is the likely diagnosis? 2 What might you notice on examination? 3 What investigation might you use to confirm/exclude the diagnosis? 4 What is the surgical treatment?

Case 9: Systemic lupus erythematosis A 24-year-old patient presents with arthropathy and a rash. Her ANA (antinuclear antibody) is positive (1/640) and you are concerned that she has developed systemic lupus erythematosus (SLE). 1 What types of rash are associated with SLE? 2 What questions would you ask in the history to confirm the diagnosis of SLE? The patient meets the diagnostic criteria for lupus. Her immunology reveals positive dsDNA, Ro and La; lupus anticoagulant is also detected. 3 What other symptoms may this patient experience? And if she were pregnant? At a routine clinic visit she complains of swollen ankles. Her blood pressure is elevated and a urine dipstick is positive for protein and blood. 4 How would you proceed?

Case 10: Complications of fractures An 8-year-old child falls from a tree landing on her outstretched arm. She was not knocked out, but complains of pain in the right arm. The right elbow is deformed. 1 What is the likely fracture? 2 What must be checked in that arm? You reduce the fracture, and put the arm into a back-slab plaster with the elbow flexed to hold the fracture reduced. The child is admitted to hospital for observation. Late that night you are called by the nurse to see the child, because the child is in severe pain despite analgesia, and will not settle. The sensation and circulation to the fingers is OK. 3 What is the dangerous diagnosis that must now be excluded?

4 What simple examination/test can you perform that confirms the diagnosis? 5 Describe what you would do first to try to relieve the symptoms, and what you would have to do then if the symptoms did not resolve?

Case 11: Congenital abnormalities A child is born full-term following a breech delivery with one foot bent downwards and inwards. This is the mother â&#x20AC;&#x2122;s first child, and the pregnancy was uncomplicated. 1 What is the likely diagnosis? 2 List two causes and/or associations with this condition. 3 What are the treatment options?

Case 12: Back pain A 25-year-old man was lifting a heavy weight when he felt a sudden pain in his back. He then noticed numbness down the side of his left leg into the side of his foot. When asked he also noticed that his foot was catching on door mats and on steps as he did not seem to be able to lift it properly. He is in very severe pain and seems to be having a little difficulty in passing urine. 1 What is the most likely diagnosis? 2 Why was it a good idea to ask about the patient catching his foot? 3 What might you find on physical examination? 4 What is a less likely diagnosis (it is rare) but which is much more urgent and dangerous? 5 What examination would you perform to exclude this rare but dangerous condition? 6 How would you investigate this case? 7 If your likely diagnosis is correct what is the treatment of choice?

Case 13: Knee replacement A 50-year-old male has severe arthritis in a knee following a motorcycle accident some years before. The knee is painful, and in 10 degrees of varus. Range of movement is from 10 to 80 degrees. He has had to give up his job as a roofer. 1 What treatment would you offer in the first instance? 2 What are your options if your initial management fails? 3 If he were to be offered a total knee replacement, what results could you expect to offer him, in terms of the problems he is experiencing as described above? 4 What early complications do you need to warn him about when you take consent? 5 How long could he expect a well performed knee replacement to last?

Questions

Self-assessment case studies 109


Self-assessment case studies: answers Case 1: Acute joint disease 1 The most crucial piece of information is that the patient is well. The diagnosis to rule out in every case is septic arthritis, and this seems unlikely in this scenario. However, his diabetes is a risk factor for infection, and a careful history of the previous injury might reveal a route of entry for bacteria. Although sports injuries can cause recurrent problems, acute flares of swelling and pain are unusual in the absence of a clear precipitating event. His psoriasis may indicate the development of a large-joint psoriatic arthropathy, but psoriasis is also a risk factor for gout, and his alcohol intake would certainly put him at risk of this. 2 The combination of a painful red eye and arthropathy raises the possibility of anterior uveitis or scleritis in association with one of the following: • Reiter ’s syndrome (check for a history of urethritis or gastrointestinal upset, circinate balanitis, keratoderma blennorrhagica). • Enteropathic arthropathy (history of abdominal pain or bloody diarrhoea, erythema nodosum). • Ankylosing spondylitis (inflammatory back pain). 3 Joint fluid aspiration to rule out septic arthritis and to diagnose gout. 4 First-line treatment for gout is a non-steroidal anti-inflammatory drug (NSAID). If he continues to experience attacks, a urate-lowering therapy such as allopurinol should be considered. All patients with gout should attempt lifestyle modification. In this instance, a reduction in his alcohol intake is crucial. Additional risk factors in his diet would also need to be addressed. See Chapter 27 for further details.

Case 2: Initial management of polytrauma 1 ABC: A Check airway with cervical spine control. B Breathing: give 100% oxygen at 15 l/min; check for pneumothorax. C Circulation: introduce two wide-bore cannulae. Take bloods for cross-match, haemoglobin, glucose, urea and electrolytes, and drug screen. 2 Distal neurovascular status. 3 The fracture is open and potentially contaminated. The wound must therefore be opened and cleaned. All contaminating material should be washed out, and dead tissue excised. If it is not possible to be sure that the wound is clean, then it should not be closed. The wound should be packed and then inspected daily until it is clean. The fracture needs to be reduced, and then held. The operation should be covered by prophylactic antibiotics. The patient should be mobilised as soon as practicable. 4 Options include intramedullary nail with locking screws; plate and screws; external fixator (Ilizarov or conventional); balanced traction; plaster or brace. An intramedullary nail allows secure fixation and early mobilisation but infection is a dangerous complication. A plate with screws needs a much longer incision, but will also give secure fixation. An external fixator is very difficult to apply, especially in the thigh where the soft tissues are deep so the pins rub on the muscle. Traction is safe but takes many weeks with the patient languishing in

a hospital bed. A plaster or brace would be almost impossible to fit to a thigh so that the fracture could be held. See Chapters 42 and 48 for further details.

Case 3: Rheumatoid arthritis 1 No, but enough to make the diagnosis! The diagnostic criteria stipulate at least four of the following: • Morning stiffness: duration > 1 hour (for > 6 weeks). • Arthritis of at least three joints: soft tissue swelling (for > 6 weeks). • Arthritis of hand joints: MCPs, PIPs or wrist (for > 6 weeks). • Symmetrical arthritis: at least one area (for > 6 weeks). • Rheumatoid nodules. • Positive rheumatoid factor. • Radiographic changes: periarticular erosions. 2 Rhematoid factor positivity is associated with more severe disease and a higher incidence of extra-articular manifestations. 3 Methotrexate is effective and generally well tolerated. Side effects include nausea and oral ulcers. Regular blood tests are used to screen for myelosuppression and hepatitis. An idiosyncratic (and reversible) allergic alveolitis/pneumonitis can occur and pre-treatment lung function testing and chest X-ray is advised. Pregnancy is contraindicated as methotrexate is a folic acid antagonist. 4 Differential diagnoses: • Respiratory disease: – Pleural effusion – Pulmonary fibrosis – Allergic alveolitis due to methotrexate therapy – Bronchiolitis obliterans (rare) – Cryptogenic organising pneumonia (rare). Investigations include arterial blood gases, chest X-ray and lung function testing. • Symptomatic anaemia: – Anaemia of chronic disease – Gastrointestinal blood loss due to NSAID use – Myelosuppression due to methotrexate therapy – Associated B12 deficiency (pernicious anaemia). Investigations include haematinics and endoscopy. 5 Causes include: • Disuse atrophy. • Compression neuropathy (median and/or ulnar). • Cervical myelopathy. • Mononeuritis multiplex due to rheumatoid vasculitis. 6 NICE (National Institute for Clinical Excellence) has stipulated that patients must have active disease and have failed two or more DMARDs (disease modifying anti-rheumatic drugs), of which one must be methotrexate. All patients must be screened for TB prior to commencing therapy. See Chapter 23 for further details.

Case 4: Septic arthritis 1 Pyrexia, redness, swelling and pain on moving the affected joint.

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. © 2012 John Wiley & Sons, Ltd.

110 Published 2012 by John Wiley & Sons, Ltd.


2 Ultrasound. If effusion is found, aspirate and send for microscopy, culture and sensitivity. 3 High-dose intravenous antibiotics. Open drainage if not immediate settling. See Chapters 16, 28 and 38 for further details.

Case 8: More problems in the hand 1 2 3 4

Carpal tunnel syndrome. Wasting of the thenar eminence and weakness of opposition. Nerve conduction studies. Decompression of the carpal tunnel roof.

See Chapters 6 and 7 for further details.

Case 5: Limps in the elderly

Case 9: Systemic lupus erythematosus

1 Osteoarthritic hip. 2 Ask about pain – waking at night, need for regular painkillers and use of walking aids. Is there difficulty with getting socks and shoes on, and getting in and out of the bath? 3 Loss of joint space, osteophyte formation, subchondral sclerosis and cysts in the bone below the joint. 4 Painkillers, physiotherapy, home aids and joint replacement.

1 Malar rash, discoid rash and photosensitivity. 2 Ask about the following; • Details of the rash (distribution, scars, exacerbations, etc.). • History of the arthropathy (features of early morning stiffness?). • History of oral ulcers? • Previous episodes of serositis – pericarditis or pleurisy? • Remember that symptoms such as Raynaud’s phenomenon and fatigue, although common in lupus, do not contribute to the diagnostic criteria. 3 dsDNA has a high specificity for SLE and levels may fluctuate with disease activity. The Ro and La antibodies suggest a Sjögren’s syndrome pattern of disease, i.e. dry eyes, dry mouth and vaginal dryness. Fatigue is a particular problem in these patients. Lupus anticoagulant puts her at risk of thromboembolic phenomenon. In the pregnant lupus patient with this Ro/La positivity, neonatal lupus and foetal heart block are a concern; those with lupus anticoagulant are at risk of deep venous thrombosis and/or miscarriage. 4 The patient may have developed renal lupus. The urine should be sent for microscopy to examine for the presence of red cell casts – evidence of glomerular bleeding in glomerulonephritis. A 24-hour collection of urine should be undertaken to quantify the proteinuria. The case must then be discussed with renal physicians for consideration of a renal biopsy. If glomerulonephritis is confirmed, aggressive immunosuppression should be instituted. Meticulous blood pressure control is mandatory.

See Chapters 15, 17 and 41 for further details.

Case 6: Osteoporosis 1 Vertebral body, neck of femur and distal radius. 2 Factors include: • Maternal family history of hip fracture. • Oestrogen deficiency. • Corticosteroid therapy. • Low body mass index (<19 kg/m2). • Smoking and excess alcohol. • Anorexia nervosa (low weight, menstrual irregularity, low calcium intake). • Endocrine syndromes (hyperparathyroidism, hyperthyroidism, Cushing’s syndrome). • Inflammatory arthropathy (probably due to increased IL-1 and TNFα levels). • Prolonged immobilisation. 3 Osteoporosis is diagnosed using a dual energy X-ray absorptiometry (DEXA) scan. This allows a measurement of the bone mineral density (BMD) at the lumbar spine and proximal femur for comparison with that of the young normal mean. The T score in osteoporosis is > 2.5 SD below the young normal mean (i.e. T > –2.5). 4 Bisphosphonate and vitamin D/calcium supplementation is the treatment of choice. In order to improve its poor bioavailability, and reduce gastrointestinal side effects, patients must take their bisphosphonate on an empty stomach, with plenty of water, remain upright for 30 minutes after ingestion and have nothing to eat or drink for a further 30 minutes. See Chapter 30 for further details.

See Chapter 24 for further details.

Case 10: Complications of fractures 1 Supracondylar fracture of the humerus. 2 Distal neurovascular status. 3 Compartment syndrome. 4 Pain on passive stretching of the muscles – stretch the fingers. 5 Split the plaster, then fasciotomy if there is not a resolution of symptoms. See Chapters 5, 8, 48 and 49 for further details.

Case 11: Congenital abnormalities

1 Dupuytren’s contracture. 2 Steady progression to fixed contracture. 3 Alcohol intake, liver disorder, family history and prolonged use of vibrating equipment. 4 Excise the palmar fascia, then physiotherapy to regain mobility.

1 Club foot (talipes equinovarus). 2 Oligohydramnios. Other congenital abnormalities such as spina bifida and congenital dislocation of the hip are associated with this condition. Position in uterus. 3 If the deformity is only a result of bad positioning in the uterus, then serial strapping of the foot can gradually correct the deformity. However, if the deformity is a developmental defect then surgical release of the tight structures will be needed if the foot is to grow as normally as possible.

See Chapter 7 for further details.

See Chapter 38 for further details.

Case 7: Problems in the hand

Answers

Self-assessment case studies 111


Case 12: Back Pain The patient may have just torn a muscle in his back (lumbago), but the numbness down the leg into the foot and the weakness suggests a prolapsed intervertebral disc (sciatica). The problem he is experiencing with passing urine is probably only secondary to the pain that the patient is experiencing, but it may be that there is an element of a central prolapsed disc (a rare but dangerous diagnosis, see page 33). The question about tripping is to find out whether the patient has a foot drop or weakness in extension of the big toe. The sensory loss is in the distribution of the L5 nerve root. The L5 nerve is the exclusive supply to the extensor hallucis longus muscle, so examination might reveal sensory loss in the L5 dermatome (side of the foot), and weakness in the extensor hallucis longus muscle. The examination which would exclude the diagnosis of the central prolapsed disc would be a) test of perineal sensation (there is saddle anaesthesia in central disc prolapse) and b) loss of anal tone on rectal examination. The investigation of choice is either a CT scan or better still an MRI if it is available. If there is any suspicion of a central prolapsed disc then this should be done with the utmost urgency, then followed by surgery to decompress the spinal roots immediately afterwards. However, the most likely diagnosis is a lateral prolapsed intervertebral disc compressing the L5 nerve root. The options for treatment are either to give analgesia and wait for the problems to settle (prolapsed discs frequently resolve spontaneously), or perform surgery to remove the disc and decompress the nerve.

Case 13: Knee replacement This is traumatic arthritis in a youngish patient. The first line of treatment is analgesia, with anti-inflammatories, knee support and physiotherapy. It may also be possible for Occupational Therapists to review the arrangements of his home to improve his ability to continue inde-

112 Self-assessment case studies Answers

pendent existence. Once these options have served their purpose the next stage is to consider surgery. Excision arthroplasty is not an option in the knee, so the alternatives are either a fusion (arthrodesis) of the knee or a knee replacement. Fusion is best for young patients and should give a painless and strong knee but there will be all the problems and frustrations for the patient of a stiff knee. It is contra-indicated if there is any arthritis in nearby joints as they will then be overloaded and fail more rapidly. For older patients, then total knee replacement is the best option. You will be able to say to the patient that they should get almost complete relief of pain. It should also be possible to correct the varus/valgus deformity of the knee. However, they may or may not get an improvement in the range of motion, and you should certainly not assure them that they will. It is a bonus not a promise. This is important because if the patient cannot flex the knee beyond 90 degrees, then they will have difficulty rising from a chair. If they cannot straighten the knee, then walking will be more exhausting because they cannot lock the knee out straight. The patient will also not be able to resume work involving heavy lifting or working in dangerous places so a return to roofing is not a good idea. The other problem is that total knee repacements have a finite life, so the younger patient needs to accept that the knee replacement will wear out and need revision. A primary replacement now lasts 15 to 20 years and the revision will last as nearly as long. The early complications can be divided into general and specific. General complications include heart attack, stroke and pulmonary embolus, and the total risk of early death is less than 1%. There are also risks of infection and excessive bleeding (less than 2%). Specific complications include nerve damage from the use of a tourniquet as well as bone fracture when fitting the implant, and failure to get the implant correctly postitioned, so that the leg is not properly aligned and the implant fails prematurely due to abnormal loading.


Index Page numbers in italics denote figures, those in bold denote tables. abatacept 82 ABCDE system 95 accessory digits 86 acetabulum 41 Achilles tendon 36, 37 rupture 48, 49 acro-osteolysis 62 acromioclavicular joint 20 arthritis 22, 23 subluxation 25 acromion 20 actin 9 action potential 9 adalimumab 56, 82 airway 94, 95 burns patients 98 alendronate 71 alfacalcidol 11 alkaline phosphatase 67 Allen’s test 19, 21 allopurinol 65 American College of Rheumatology diagnostic criteria 54–5 American Rheumatological Association 57 amitriptyline 69 amputation 49, 91 hand 27 anaemia of chronic disease 58 anakinra 82 anal tone loss 32, 33 analgesia 83, 96 burns patients 98–9 ANCA 74 ANCA-positive vasculitis 77 ankle 37 arthritis 45 dislocation 49 examination 39 fracture 49 instability 45 inversion 49 mobility 38 range of movement 39 replacement 42, 43 sprains 49 ankylosing spondylitis 33, 60–1, 60, 62, 62 antalgic gait 38 antecubital fossa 18 antenatal checks 86 anterior draw test 38 anti-B cell therapy 56, 82, 83 anti-citrullinated protein antibody 55 anti-T cell therapy 82 antibiotics 67 antineutrophil cytoplasmic antibodies see ANCA antinuclear antibodies 80 in SLE 58 antiphospholipid syndrome 59 Apley’s test 38

apprehension sign 19, 20, 25 arms anatomy 16–19, 16, 17, 18 blood vessels 16, 17–18 examination 13, 19–21, 19 function 17 lower, trauma of 26–7, 26 movement 19 muscles 16 nerve supply 17, 17 problems of 22–3, 22 upper, trauma of 24–5, 24 see also forearm arthritis acromioclavicular joint 22, 23 ankle 45 cervical 32–3 destructive 43 elbow 23 enteric 60, 62, 63 hip 40, 41 juvenile idiopathic 54 knee 37, 45 mutilans 62 psoriatic 60, 62–3, 62 reactive 60, 62, 63 septic 40, 41, 65, 66–7, 66 traumatic 43 see also osteoarthritis; rheumatoid arthritis artificial limbs 91 athletes see sports medicine autoantibodies in scleroderma 79 in SLE 58 azathioprine 55, 58, 63, 77, 80, 81 B cells 53 backache 28, 29, 31 after exercise 32 causes 33 mechanical 33 minor 34–5 red flags 30, 31 sinister 32, 33 yellow flags 30, 31 Baker’s cyst 45 balanitis circinata 63 Bath Ankylosing Indices 61 bed sores 35 biologics 83 birth checks 86 bisphosphonates 11, 71 blood vessels arm 16, 17–18 leg 37, 37 bone cortical 8, 9 lamellar 9 mass 70 metabolism 10–11, 10, 72–3, 72 remodelling 9, 72 structure 8, 9

trabecular 8, 9 tumours 67 woven 9 see also fractures; osteoporosis bone mineral density 71 Bouchard’s nodes 51 boutonnière deformity 19, 54, 55 bow legs 86 brachial plexus 17 avulsion 24 injuries 101 tear 25 brain injury 102, 103 plasticity 103 breastfeeding 83 breathing 94, 95 bunions 44, 45, 93 burns 98–9, 98 electrical 99 rule of 9s 98 bursitis 55 C-reactive protein 61, 75 calcaneum, crush fracture 48 calcinosis 78 calcium homeostasis 10–11, 10 calcium pyrophosphate deposition 65 calipers 90 callouses 37 carpal bone trauma 27 carpal dislocation 27 carpal tunnel syndrome 17, 20, 23, 26, 101 cartilage 9 destruction of 53 β-catenin 72 cauda equina syndrome 29, 30, 33 cell-mediated immunity 52 cellulitis 66 central nervous system injuries 101 see also brain; spine cerebral palsy 86, 87, 91 certolizumab 56, 82 cervical spondylosis 32 children 86–7, 86 antenatal and birth checks 86 epiphyseal injuries 87 hip problems 40, 41 Kawasaki disease 77 knee pseudolocking 44 non-accidental injury 87 rickets 73 scoliosis 31, 33, 90 chondroblasts 9 chondrocalcinosis 65 chondrocytes 9 chondromalacia patellae 44 chondrosarcoma 67 Churg-Strauss syndrome 77 Chvostek’s sign 10, 11 circulation 94, 95 burns patients 98

Rheumatology, Orthopaedics and Trauma at a Glance, Second Edition. Catherine Swales, Christopher Bulstrode. © 2012 John Wiley & Sons, Ltd. Published 2012 by John Wiley & Sons, Ltd.

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clavicular fracture 24, 25 claw toes 44, 45 clinical nurse specialists 84, 85 club foot 86 colchicine 65, 77 collagen 9 Colles’ fracture 26, 27, 92 common peroneal nerve 36, 101 compartment syndrome 18, 24, 25, 48, 106–7, 106 complement system, in SLE 58 compression 89 computerised tomography (CT) 14, 15 corns 93 corticosteroids see steroids COX-2 inhibitors 83 creatine kinase 80 CREST syndrome 78 Crohn’s disease 63 cruciate ligaments 37 instability 39 rupture 39 tears 39, 44–5 crush fractures calcaneum 48 spine 33, 35, 92 crutches 90 cryoglobulinaemia 77 crystal arthropathies 64, 65 cyclophosphamide 55, 58 cyclosporin 55, 63 dactylitis 61 dapsone 77 decerebrate rigidity 103 degloving injuries 49 denosumab 53 depression 69 dermatomes 9, 28, 29 dermatomyositis 80, 80, 81 developmental dysplasia of hip 40, 41 DEXA scan 71 diaphysis 9 dickkopf-1 72 digital nerve 17, 26, 27 dinner fork deformity 27, 92 disability 95 disease-modifying antirheumatic drugs see DMARDs DMARDs 55, 83 special circumstances 83 dowager’s hump 70 drug therapy 82–3, 82 see also individual drugs Dupuytren’s contracture 20, 22, 23 dynamic hip screw 47, 92–3 elbow 18 arthritis 23 examination 20 movement 20 replacement 42, 43 tennis 22, 23 trauma 25 elderly patients 92–3, 92 electrical burns 99 electromyography 80 enteric arthritis 60, 62, 63 enthesitis 61, 63

114 Index

enthesopathy 60 epiphyseal injuries 87 epiphyseal plate 41 fractures 105 epiphysis 9 erythema 51 erythrocyte sedimentation rate 61, 67, 75 etanercept 56, 82 etidronate 71 European League Against Rheumatism (EULAR) diagnostic criteria 55 Ewing’s sarcoma 67 examination 12–13, 12 exposure 95 extradural haemorrhage 102, 103 facet joints 29 falls, fractures caused by 49 febuxostat 65 femoral artery 37, 37 femoral fracture 37, 47, 92–3 femoral nerve 36, 36 fenofibrate 65 fibroblasts 53 fibromyalgia 68–9, 68 fibula 37 figure of eight test 44, 44, 89 finger drop 19 fingers accessory 86 amputation 27 examination 20 flexor tendon injury 26 movement 20 sausage 61 flat feet 45 flexor digitorum superficialis test 19 fluoxetine 79 foot 36, 37 bunions 44, 45, 93 examination 39 flat 45 mobility 38 foramina 29 forearm movement 20 trauma 25 fractures 104–5, 104 ankle 49 in athletes 89 in children 86, 105 classification 105 clavicle 24, 25 complications 105 crush see crush fractures elderly patients 92–3, 92 femoral 37, 47, 92–3 forearm 25, 26, 26, 27 metacarpal 27 metatarsal 48 osteoporotic 70 pelvis 46, 47 phalangeal 27 scaphoid 26, 27 spinal 34, 35 tibia 49 toes 48, 49

upper leg 46, 47 wrist 92 frozen shoulder 22, 23 frusemide 11 gait 13 GALS screen 12–13, 12, 51 gastrocnemius 36, 45 genu varus 86 giant cell arteritis 74–5, 74 Glasgow Coma Score 103 glenohumeral joint, arthritis 23 gluteal muscles 36 gold 55, 63 golfer’s elbow 23 golimumab 56, 82 Gottron’s papules 80 gout 64–5, 64 gouty tophi 20, 65 greenstick fracture 25, 86 growth plate see epiphyseal plate haemarthrosis 65 haemothorax 24 hallux valgus see bunion hammer toes 44, 45 hamstrings 36 hands 18 amputations 27 anatomy 17 cuts 27 examination 20, 51 falls on 26, 27 problems of 23 rehabilitation 27 swelling/stiffness 27 head 50 injuries 102–3, 102 headache 35 giant cell arteritis 74–5, 74 migraine 35 Heberden’s nodes 51 hemi-arthroplasty 47, 92 Henoch-Schönlein purpura 77 hip 36, 37 avascular necrosis 41 congenital dislocation 41 developmental dysplasia 40, 41 examination 38, 39 fixed flexion deformity 39 irritable 41, 86 osteoarthritis 40, 41 Perthes disease 40, 41 replacement 42 septic arthritis 40, 41 slipped upper femoral epiphysis 40, 41 history taking 12–13, 12 HLA-B27 61 hormone replacement therapy 71 humerus 18 fractures 24, 25 humoral immunity 52 Huntington’s chorea 91 hydralazine, and SLE 58 hydroxychloroquine 55, 58, 80, 82 hypercalcaemia 10, 11, 67 hyperparathyroidism 11 hyperuricaemia 64


hypocalcaemia 10, 11 hypoparathyroidism 11 ibuprofen 34 ice therapy 89 Ilizarov fixator 87, 91 imaging 14, 15 inclusion body myositis 81 infection 66–7, 66 inflammatory mediators 53 inflammatory muscle diseases 80–1, 80 infliximab 56, 82 interleukins 53 interphalangeal joints 55, 62 intervertebral discs 29 prolapse 32, 33 see also cauda equina syndrome replacement 42 intra-articular bleeding 65 intracranial haemorrhage 103 intracranial pressure, raised 103 intramedullary nailing 93 irritable hip 41, 86 isoniazid, and SLE 58 Jaccoud’s arthropathy 58 joint(s) disease 50, 64–5, 64 excision 43 facet 29 failure 43 fusion 43 intra-articular bleeding 65 replacement 42–3, 42, 93 see also individual joints juvenile idiopathic arthritis 54 Kawasaki disease 77 keratoderma blennorrhagica 63 knee 36, 37, 44–5 collateral ligaments 39 effusion 39 examination 39 locking/pseudolocking 44 meniscal tears 47 osteoarthritis 37, 45 quadriceps lag test 39 range of movement 39 rehabilitation 47 replacement 42 stability 39 see also cruciate ligaments; patella knock-knees 86 laminae 29 leflunomide 55, 63, 82 leg lengthening 87 legs anatomy 36–7, 36, 37 blood vessels 37, 37 degloving injuries 49 examination 13, 38–9, 38 length inequality 31 lower 44–5, 44, 45 trauma 48–9, 48 muscles 36 nerve supply 36–7, 36

straight leg raise test 30, 31, 33 upper, trauma 46–7, 46 ligaments 9 tears 89 limbs, artificial 91 limp 38–9 look, feel, move screen 13 lordosis 28, 29 losartan 65, 79 lucid interval 103 Lund and Bowdler chart 99 lupus, drug-induced 58 lytic lesions 67 macrophage colony stimulating factor 53, 72 macrophages 53 magnetic resonance imaging (MRI) 14, 15 malignancy bone tumours 67 dermatomyositis 81 elderly patients 93 secondary tumours 93 march fracture 89 matrix metalloproteinases 52, 53 median nerve 17, 17 metacarpal fractures 27 metacarpophalangeal joint replacement 42, 43 metaphysis 9 metastases 93 metatarsal fracture 48 metatarsalgia 45, 93 methotrexate 55, 58, 63, 77, 80, 81, 82 microscopic polyangiitis 77 migraine, whiplash injury 35 minocycline, and SLE 58 monoclonal antibodies 83 Morton’s neuroma 36 motor neuron lesions 29 motor unit 8, 9 multiorgan failure 99 muscle biopsy 80 muscle unit 8 muscle(s) 9 arm 16 leg 36 motor unit 8, 9 sclerotomes 29 spasticity 35, 101 musculoskeletal system 8, 9 mycophenolate mofetil 58 myeloma 67 myofibrils 9 myosin 9 myotomes 9 nails 50 neck 32–3, 50 cervical spondylosis 32 rheumatoid arthritis 32–3 stabilisation 95 nerve(s) 9 arm 17, 17 dermatomes 9, 28, 29 injuries 100–1, 100 leg 36–7, 36 nerve root compression 89

entrapment 22, 23 see also carpal tunnel syndrome neurological disorders 90–1, 90 nifedipine 79 night pain 67 non-accidental injury 87 non-steroidal anti-inflammatory drugs see NSAIDs NSAIDs 55, 58, 61, 63, 65, 83 occupational therapy 84, 85 orthotics 84, 85, 90–1, 90 osteoarthritis elderly patients 93 hip 40, 41 and joint failure 43 joint replacement 42–3, 42, 93 knee 37, 45 osteoblasts 9, 72 osteoclasts 8, 9, 53, 72 osteocytes 9 osteomalacia 72, 73 osteomyelitis 66, 67 osteopaenia 53 osteoporosis 70–1, 70, 72 Colles’ fracture 26, 27, 92 fractures 92–3 myeloma 67 risk factors 70–1 steroid-induced 71 osteoporosis circumscripta 73 osteoporotic fractures 70 osteoprotegerin 53, 72 osteosarcoma 67 osteosclerotic metastases 67 osteotomy 87, 105 osterix 72 Paget’s disease 72–3, 72 pancytopaenia 67 paracetamol 34 parasthesiae 68, 69 parathyroid hormone 10, 10, 11 pastry roll test 39 patella 37 apprehension sign 39, 44 pelvis 36 fracture 46, 47 pencil-in-cup deformity 62 penicillamine 55, 63 periosteum 9 peroneal nerve 37 Perthes’ disease 40, 41 phalangeal fractures 27 Phalen’s test 20 physiotherapy 84–5, 84 sports injury 89 plastic surgery 97, 97 pleuritis, lupus-associated 58 podiatry 84, 85 polio 91 polyarteritis nodosa 77 polyarticular arthralgia 58 polymyalgia rheumatica 74 polymyositis 80, 80 polytrauma 94–5, 94 popliteal artery 37, 37 pregnancy 83 PRICE regimen 45

Index 115


procainamide, and SLE 58 pronation 19, 23 proprioception 18 proteoglycans 9 pseudogout 64, 65 pseudohypoparathyroidism 11 pseudopseudohypoparathyroidism 11 psoriasis 20 psoriatic arthritis 60, 62–3, 62 pulmonary hypertension 78 pulmonary oedema 98 punched-out lesions 67 quadriceps 36, 37 lag test 39 question-mark posture 60, 61 RA see rheumatoid arthritis radial artery 16, 18 radial nerve 17 radius 18 Colles’ fracture 26, 27, 92 greenstick fracture 25, 86 raloxifene 71 RANKL 53, 72 rash 50 Raynaud’s phenomenon 58, 68, 69 treatment 79 reactive arthritis 60, 62, 63 reflex sympathetic dystrophy 106 reflexes 31 regional pain syndrome 106 rehabilitation 84–97, 84, 101, 103 Reiter’s syndrome 63 renal disease glomerulonephritis 77, 111 lupus 58 scleroderma 78–9, 78 rheumatoid arthritis 54–6, 54 American College of Rheumatology diagnostic criteria 54–5 clinical features 55 European League Against Rheumatism (EULAR) diagnostic criteria 55 joint replacement 42–3, 42 neck 32–3 palindromic 55 pathogenesis 52–3, 52 treatment 55 tumour necrosis factor-alpha blockers 55, 61, 82, 83 rheumatoid factor 53, 55 rheumatoid nodules 54 rheumatological disease 50–1, 50 examination 51 history 50–1 RICE regimen 89 rickets 73 risedronate 71 rituximab 56, 58, 82, 83 Romanus lesions 61 rotator cuff 93 impingement 22, 23 tear 22, 24, 25 rule of 9s 98 sacroiliitis 63 saddle anaesthesia 32, 33

116 Index

Salter-Harris classification 87 saphenous vein 37, 37 sausage finger 61 scaphoid fracture 26, 27 Schober’s test 60, 61 sciatic nerve 36–7, 36 injury 101 sciatica 33 sclerodactyly 78 scleroderma 78–9, 78 sclerotomes 29 scoliosis 33, 90 idiopathic 31 selective oestrogen receptor modulators (SERMs) 71 sensory loss 91 sepsis 99 septic arthritis 65, 66–7, 66 hip 40, 41 shawl sign 80 shin splints 89 shingles 33 shoulder 18 dislocation 24, 25 examination 20 movement 20 problems of 22, 23 replacement 42, 43 Sjögren’s syndrome 59 skin grafts 97, 97 burns patients 99 skull fracture 103 SLE see systemic lupus erythematosus sleep disturbance 68–9 slipped upper femoral epiphysis 40, 41 smoke inhalation 98 soft tissue replacement 97 spasticity 35, 101 spina bifida occulta 31 spinal board 34 spinal cord 29 trauma 29 spinal problems 32–3, 32 spinal shock 29, 35, 101 spine anatomy 28–9, 28 crush fractures 33, 35, 92 curves 28, 29 elderly patients 93 examination 13, 30–1, 30 fractures 34, 35 function 29 history 30–1, 30 motor neuron lesions 29 movement 30, 31 myeloma 67 stenosis 93 trauma 34–5, 34 spinous process 29 splints 90 spondyloarthropathies 60, 62–3, 62 see also individual conditions spondylolisthesis 33, 89 sports medicine 88–9, 88 steroids 55, 65, 75, 77, 80, 83 injections 89 steroid-induced osteoporosis 71 steroid-sparing agents 83

stitching 96 straight leg raise test 30, 31, 33 stress fractures 89 stridor 98 strontium 71 subdural haemorrhage 103 subungual haematoma 48, 49 Sudek’s atrophy 106 sulfasalazine 55, 61, 63, 82 and SLE 58 sulfinpyrazone 65 supination 19, 23 supraspinatus tendon 93 swan-neck deformity 19, 54, 55 syndactyly, repair 97 syndesmophytes 61 synovitis 51 systemic lupus erythematosus 57–9, 57 diagnosis 57–8 treatment 58 T cells 53 regulatory (Tregs) 53 T helper cells 53 Takayasu arteritis 75 talipes equinovarus 86 tarsal coalition 45 temporal arteritis see giant cell arteritis temporomandibular joint 35 tendons 9 rupture 89 tennis elbow 22, 23 tenosynovitis 55, 61 tension pneumothorax 95 teriparatide 71 testosterone 71 tetanus prophylaxis 96 Thomas’ test, modified 38, 39 thoracic spine 33 thrombocytopaenia 58 thumb 18, 86 amputation 27 extensor tendon rupture 26 thumb down test 19, 20 tibia 37 fracture 49 laceration to front of 48 tibialis anterior 36 Tinel’s test 20 tinnitus 35 tocilizumab 82 toes 44, 45 accessory 86 claw 44, 45 fractures 48, 49 hammer 44, 45 webs 86 transcutaneous electrical nerve stimulation (TENS) 85 trauma arms lower 26–7, 26 upper 24–5, 24 initial management 94–5, 94 legs lower 48–9, 48 upper 46–7, 46 polytrauma 94–5, 94


spine 34–5, 34 wound management 96 Trendelenburg gait 38 tricyclic antidepressants 69 trigger finger 20, 22, 23 Trousseau’s sign 10, 11 tumour necrosis factor-alpha 53 tumour necrosis factor-alpha blockers 55, 61, 82, 83 special circumstances 83 two point discrimination test 101 ulnar artery 16 ulnar fracture 25 ulnar nerve 17, 17 entrapment 22, 23 palsy 101 ulnar neuritis 20–1 ultrasound 14, 15

urinary tract infection, in spinal trauma 35 uveitis, anterior 61 valgus deformity 86 van Rosen splint 40 varus deformity 39 vascularised flaps 91 vasculitides large vessel 74–5, 74 medium and small vessel 76–7, 76 see also individual conditions vastus medialis, wasting 39 venlafaxine 69 vertebrae 28, 29 vertebroplasty 71 vitamin D 10–11, 10 Volkmann’s ischaemia 106, 106 walking sticks 90 Wallerian degeneration 100

Wegener’s granulomatosis 77 wheel chairs 90 whiplash injury 34, 35 windlass test 45 Wnt 72 wound management 96, 96 wrist examination 20 fracture 92 movement 20 problems of 23 replacement 42 X-ray 14 interpretation 15 requesting 15 zoledronate 71

Index 117


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