Musculoskeletal
Injections and
Alternative Options
A practical guide to
‘what, when, and how?’
Musculoskeletal
Injections and
Alternative Options
A practical guide to
‘what, when, and how?’
Edited by
Maneesh Bhatia
Consultant Orthopaedic Foot and Ankle Surgeon
University Hospitals of Leicester, UK
Video Editor
Kethesparan Paramesparan
CRC Press
Taylor & Francis Group
6000 Broken Sound Parkway NW, Suite 300
Boca Raton, FL 33487-2742
© 2019 by Taylor & Francis Group, LLC
CRC Press is an imprint of Taylor & Francis Group, an Informa business
No claim to original U.S. Government works
Printed on acid-free paper
International Standard Book Number-13: 978-0-8153-5557-1 (Hardback)
978-0-8153-5554-0 (Paperback)
This book contains information obtained from authentic and highly regarded sources. While all reasonable
efforts have been made to publish reliable data and information, neither the author[s] nor the publisher can
accept any legal responsibility or liability for any errors or omissions that may be made. The publishers wish
to make clear that any views or opinions expressed in this book by individual editors, authors or contributors
are personal to them and do not necessarily reflect the views/opinions of the publishers. The information or
guidance contained in this book is intended for use by medical, scientific or health-care professionals and is
provided strictly as a supplement to the medical or other professional’s own judgement, their knowledge of the
patient’s medical history, relevant manufacturer’s instructions and the appropriate best practice guidelines.
Because of the rapid advances in medical science, any information or advice on dosages, procedures or diag-
noses should be independently verified. The reader is strongly urged to consult the drug companies’ printed
instructions, and their websites, before administering any of the drugs recommended in this book. This book
does not indicate whether a particular treatment is appropriate or suitable for a particular individual. Ulti-
mately it is the sole responsibility of the medical professional to make his or her own professional judgements,
so as to advise and treat patients appropriately. The authors and publishers have also attempted to trace the
copyright holders of all material reproduced in this publication and apologize to copyright holders if permis-
sion to publish in this form has not been obtained. If any copyright material has not been acknowledged please
write and let us know so we may rectify in any future reprint.
Except as permitted under U.S. Copyright Law, no part of this book may be reprinted, reproduced, transmit-
ted, or utilized in any form by any electronic, mechanical, or other means, now known or hereafter invented,
including photocopying, microfilming, and recording, or in any information storage or retrieval system, with-
out written permission from the publishers.
For permission to photocopy or use material electronically from this work, please access www.copyright.com
(http://www.copyright.com/) or contact the Copyright Clearance Center, Inc. (CCC), 222 Rosewood Drive,
Danvers, MA 01923, 978-750-8400. CCC is a not-for-profit organization that provides licenses and registra-
tion for a variety of users. For organizations that have been granted a photocopy license by the CCC, a separate
system of payment has been arranged.
Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used
only for identification and explanation without intent to infringe.
Library of Congress Cataloging-in-Publication Data
Names: Bhatia, Maneesh, editor.
Title: Musculoskeletal injections and alternative options :
a practical guide to ‘what, when and how?’ / [edited by] Maneesh Bhatia.
Description: Boca Raton : CRC Press, [2019] | Includes bibliographical references and index.
Identifiers: LCCN 2018060148| ISBN 9780815355540 (paperback : alk. paper) | ISBN
9780815355571 (hardback : alk. paper)
Subjects: | MESH: Musculoskeletal Pain--drug therapy | Injections--methods |
Nerve Block--methods | Treatment Outcome
Classification: LCC RM170 | NLM WE 140 | DDC 615/.6--dc23
LC record available at https://lccn.loc.gov/2018060148
Visit the Taylor & Francis Web site at
http://www.taylorandfrancis.com
and the CRC Press Web site at
http://www.crcpress.com
I would like to dedicate this book to my dearest wife, Sulaxni, and my
adorable kids, Yash and Juhi, for their endless love and support.
Contents
List of videos xiii
e-Resources xv
Foreword by Nicola Maffulli xvii
Foreword by Bill Ribbans xix
Review and endorsements xxi
Editor xxiii
Editor’s Note xxv
Contributors xxvii
1 Musculoskeletal injections in general 1
Devendra Mahadevan and Euan Stirling
Introduction 1
What are corticosteroids? 1
How do steroid injections work? 2
What are the indications and contraindications of
corticosteroid injections? 2
What is the evidence for the use of corticosteroid
injections for musculoskeletal pain? 4
What are examples of injectable corticosteroid agents? 7
How do you select an appropriate corticosteroid
preparation for a specific joint or soft tissue injection? 8
Should corticosteroids be combined with local
anaesthetics when giving injections? 8
Which local anaesthetic agents are appropriate to use
with corticosteroid? 9
What equipment is needed for corticosteroid injection? 9
Which joints can be injected without image guidance? 11
How often can you inject a joint? 12
Should corticosteroids be used around tendons? 13
vii
viii Contents
Do all patients respond to corticosteroid injections? 13
What are the potential side effects and complications of
corticosteroid injections? 14
What adjuncts are available for steroid injection? 15
What are the alternatives to steroid injection? 16
References 18
2 Shoulder and elbow injections 23
Helen Tunnicliffe and Harvinder Pal Singh
Introduction 23
How to differentiate shoulder pain? 24
What is the role of physiotherapy in shoulder
disorders? 25
What is the role of steroid injections for shoulder disorders? 26
Osteoarthritis 27
Impingement/subacromial bursitis/tendinopathy 27
Frozen shoulder/joint stiffness 30
Degenerative rotator cuff tears 30
Calcific tendinitis 31
Diagnostic injection 31
What are the contraindications for injection of
the shoulder? 32
What are the risks? 33
Which drugs to use? 33
How to inject the glenohumeral joint? 34
Anterior approach to the glenohumeral joint? 36
How to inject the acromioclavicular joint? 37
How to inject the subacromial space? 38
How to inject the elbow joint? 40
How to inject for tennis elbow? 40
How to inject for golfer’s elbow? 42
References 44
3 Hand and wrist injections 47
Sunil Garg
Introduction 47
Carpal tunnel syndrome 47
De Quervain’s tenosynovitis 52
First carpometacarpal joint osteoarthritis 54
Contents ix
Trigger finger 57
References 60
4 Hip and knee injections 63
Ashwin Kulkarni and Kimberly Lammin
Introduction 63
Injections around the hip joint 63
What are the indications and contraindications for
lateral soft tissue hip injection? 65
How to prepare and what is the technique for GTPS
injection? 66
What are the injection contents? 68
What is the efficacy of injections for GTPS? 69
What are the treatment options for GTPS? 69
Intra-articular hip injections: Introduction 70
What are the indications and contraindications for
intra-articular hip injections in adults? 71
Preparation and technique for intra-articular hip
injection (in adults) 72
What is the efficacy of hip injections? 74
Injections around the knee joint: Introduction 74
What are the indications and contraindications for
intra-articular knee joint injection? 75
Preparations and technique for knee injection 76
Suprapatellar approach 77
Approaches adjacent to the patellar tendon 78
What are the knee injection contents? 80
What is the efficacy of knee injections? 80
What are various treatment options for osteoarthritis of
the knee? 80
What are the potential complications and risks of all
injections around and into the hip and knee? 81
References 83
5 Foot and ankle injections 85
Bobby Mobbassar Siddiqui, Annette Jones,
and Maneesh Bhatia
Introduction 85
What are the important anatomical considerations? 86
What are the techniques of injection? 90
x Contents
What drugs are used commonly for foot and ankle
injections? 90
What is the role of imaging for foot and ankle injections? 91
Interdigital (Morton’s) neuroma 91
Plantar fasciitis 94
First metatarsophalangeal joint 97
Ankle (tibiotalar) joint 100
Sinus tarsi syndrome 107
Tarsometatarsal joints 108
References 112
6 Image-guided injections in orthopaedics 117
Sangoh Lee and Raj Bhatt
Introduction 117
What and when to perform image-guided injections? 118
How to perform image-guided Injections? 123
References 138
7 Platelet-rich plasma injections 141
Kevin Ilo and Fazal Ali
Introduction 141
What is platelet-rich plasma? 142
Classification of PRP 143
Which PRP preparation is best? 144
What can PRP be utilised for? 145
Does PRP have any contraindications? 148
PRP injection protocol 149
References 159
8 Visco-supplementation injections 163
Zaid Abual-Rub and Sanjeev Anand
Introduction 163
What is the structure of HA? 164
How does HA work? 164
What are the indications for usage? 165
What is the recommended dose for high molecular
weight HA? 166
Is HA clinically effective? 167
Is HA cost-effective? 172
Contents xi
What are the recommendations of national/
international guidelines? 173
References 175
9 Practical prolotherapy 179
Roger Oldham
What is prolotherapy? 179
History 179
What are the indications and contraindications? 180
What are the advantages, disadvantages and
side effects? 184
What is the current evidence? 185
Getting started 185
Preparation and needle technique 187
Tips from 25 years’ experience 190
Acknowledgement 196
References 196
10 Extracorporeal shock wave therapy 199
Randeep S. Aujla and Philippa Turner
Introduction 199
What is it? 199
How does it work? 200
What are the evidence-based indications? 201
What are the contraindications? 201
What are the side effects/risks? 202
Clinical applications and evidence 202
Shoulder 202
Elbow 203
Hip 204
Knee 206
Foot and ankle 207
References 209
11 Novel treatments for the management of chronic shoulder,
knee and hip joint pain 213
Sadiq Bhayani
Introduction 213
Shoulder joint 213
Knee joint 217
xii Contents
Hip joint 220
Cryotherapy 222
Capsaicin cream and patch 223
Lidocaine plasters 223
References 224
Index 229
List of videos
CHAPTER 1
1.1 An introduction to musculoskeletal injections. 17
(https://youtu.be/An5CRYPuO28)
CHAPTER 2
2.1 Physiotherapy for frozen or stiff shoulder. 44
(https://youtu.be/_3ojJMPvxhY)
2.2 Physiotherapy for painful shoulder. 44
(https://youtu.be/2NsgqaSt4lE)
2.3 Shoulder exercises (strengthening and late rehab). 44
(https://youtu.be/3OhD-xq6ivI)
2.4 How to perform injection for subacromial impingement. 44
(https://youtu.be/rDc61zXwwEE)
CHAPTER 3
3.1 How to perform injection for CTS. 60
(https://youtu.be/lyxKisHEABM)
3.2 How to perform injection for De Quervain’s tenosynovitis. 60
(https://youtu.be/4IJUXMcOQOE)
3.3 How to perform injection for 1st CMCJ OA. 60
(https://youtu.be/AqZxP3wQ7k8)
3.4 How to perform injection for trigger finger. 60
(https://youtu.be/nxUbSuceroM)
CHAPTER 4
4.1 How to perform injection for trochanteric pain syndrome. 82
(https://youtu.be/9uRrjjg2PAo)
4.2 Physiotherapy for trochanteric pain syndrome. 82
(https://youtu.be/F20xnQNFDJ8)
xiii
xiv List of videos
4.3 How to perform injection for knee joint. 83
(https://youtu.be/K7C2tFnkDBY)
CHAPTER 5
5.1 How to perform injection for Morton’s neuroma. 111
(https://youtu.be/vKSr3dnOSCc)
5.2 How to do exercises for plantar fasciitis. 111
(https://youtu.be/iNYNhnBJ7-0)
5.3 How to perform injection for plantar fasciitis. 111
(https://youtu.be/7ZLX2i0tE5I)
5.4 How to perform injection for arthritis of big toe (hallux rigidus). 111
(https://youtu.be/K2DLvAPpWwg)
5.5 How to perform injection for ankle joint using anteromedial
approach. 112
(https://youtu.be/Hxy6nZ4CGDU)
5.6 How to perform injection for ankle joint using anterolateral
approach. 112
(https://youtu.be/_ZGxeNoTMGQ)
CHAPTER 6
6.1 How to perform ultrasound-guided subacromial injection. 138
(https://youtu.be/8Soe89QPJc8)
6.2 How to perform ultrasound-guided hip injection. 138
(https://youtu.be/gw4okfmael8)
6.3 How to perform ultrasound-guided injection for
Morton’s neuroma. 138
(https://youtu.be/YZSpHfWqO0w)
CHAPTER 7
7.1 How to perform PRP injection for tennis elbow. 159
(https://youtu.be/Epw6bNOVNYM)
7.2 How to perform PRP injection for Achilles tendinopathy. 159
(https://youtu.be/nT_VkS2EdnQ)
e-Resources
Both the print and eBook editions of this book are supplemented by video
clips and an information leaflet that can be shared with patients.
You can access the video clips by visiting the links provided at the ends
of chapters and the patient information leaflet by visiting www.crcpress.
com/9780815355571. The patient information leaflet can also be found as a
supplement at the end of the eBook.
Together, these materials bring additional utility to this beautifully
prepared and presented book. We hope you will find them useful.
xv
Foreword by Nicola Maffulli
Ailments of the musculoskeletal system are increasingly prevalent and do not
involve just athletes. We are ageing, and our musculoskeletal system has to
bear the brunt on longer active lives, where we are on the one hand prompted
to continue to undertake exercise for health purposes, but our bones, muscles,
joints, ligaments and tendons are not quite as able to recover as fast and as well.
The economic and social costs of musculoskeletal diseases are ever increasing,
and a multilateral approach to their management is necessary.
In this respect, we are at crossroads: Do we wish to just take away the
pain, or to heal and regenerate? A straightforward answer is impossible to
give, as priorities change according to each individual, and their age, activity,
expectations, sport, stage of their lives.
Musculoskeletal Injections and Alternative Options gives a simple yet well
pondered vision of what, when and how in this field. There are no easy or
difficult undertakings: If one knows how, then a procedure can be done! The
approach used in this book is simple and straightforward, and is not limited
to injections. For a surgeon, clinical anatomy comes as second nature, but it
still needs to be mastered and made more relevant to our patients’ care. The
hints and tips given are invaluable. The fact that other non-injection-based
modalities are outlined makes the book unique, offering a balanced vision
to cherish.
Keep the book in your white-coat pocket, not on a library shelf, and have
fun!
Nicola Maffulli MD MS PhD FRCP FRCS(Orth)
Professor of Trauma and Orthopaedic Surgery
Consultant Trauma and Orthopaedic Surgeon
xvii
Foreword by Bill Ribbans
Maneesh Bhatia and his fellow authors are to be congratulated on the
production of Musculoskeletal Injections and Alternative Options: A Practical
Guide to ‘What, When and How’. Safe and effective injections for a range
of musculoskeletal conditions are an important part of the armamentarium
of clinicians in many disciplines and the allied professions. The book has
been neatly divided into general comments, anatomical locations, and more
specialised treatments and delivery modalities.
Wherever possible the book delivers evidence-based opinions and is
extensively referenced. The chapters deal with pharmacology, side effects and
complications. It carefully examines the indications for each form of injection
and valuable advice upon their delivery.
The book should be an excellent reference for clinicians to guide the
implementation of injection therapy for a range of common conditions. It will
answer many of the questions raised by enquiring patients and help structure
patient information leaflets for pre- and post-injection advice.
The number of alternative forms and types of injectable drugs and modes
of delivery increases every year. Clinicians need to be confident upon the
indications for injections and be able to explain their purposes both diagnostic
and therapeutic. Additionally, the clinician needs to be able to walk a patient
through the post-injection journey with advice on expected response times.
Patients need to be clear about the potential outcomes of any injection –
successful long-term relief of symptoms, short-term relief followed by return
of symptoms, or no relief of symptoms. Each of these provides valuable
information to guide future management. The clinician needs to be clear on
their response to such patient-reported outcomes.
This book will deliver many of the answers to these questions and provide an
excellent resource for the busy clinician in both outpatient and inpatient settings.
Bill Ribbans PhD FRCS(Orth) FFSEM(UK)
Professor of Sports Medicine and Consultant Orthopaedic Surgeon
University of Northampton, United Kingdom
xix
Review and endorsements
As a practising general practitioner, I know just how common
musculoskeletal presentations are in primary care. Moreover I am also
aware of the pain and suffering experienced by patients who can also face
treatment delays. This book and the innovative accompanying video guide
are therefore very welcomed. They offer practical, evidence-based information
on the effective management of musculoskeletal disorders using injection
therapy.
I learnt a lot from reading this book. In an area which is rapidly evolving
with the advent of novel therapies, this book offers a clear guide for use in daily
practice. The book has an easy-to-follow format and helpfully clarifies the
most appropriate settings of care. I like the review of evidence that makes clear
where there is strong evidence of benefit or where more research is needed.
This is a powerful book and an important contribution to the literature
on musculoskeletal injections. The advice contained in this book should be
widely and quickly adopted to improve outcomes for patients and deliver
better value for health services. I believe that a high-quality, safe and accessible
joint injection service is an essential component of modern healthcare. This
book will support commissioners to achieve this objective.
Mayur Lakhani CBE PRCGP SFFMLM
President of The Royal College of General Practitioners
Chair of West Leicestershire Clinical Commissioning Group
xxi
xxii Review and endorsements
This book is an excellent resource for the current evidence and techniques
for commonly performed musculoskeletal injections. One unique feature of
this book is that it has expanded on injectable and non-injectable alternatives
to steroid injections. I am sure that this book would benefit a wide range of
health professionals including doctors in primary care as well as orthopaedic
trainees. I am pleased to endorse Musculoskeletal Injections and Alternative
Options: A Practical Guide to ‘What, When and How’ and would like to
congratulate the team for their innovative efforts and hard work.
Ananda Nanu MBBS MS(Orth) FRCS MCh(Orth) FRCS(Orth)
President of British Orthopaedic Association
Editor
Maneesh Bhatia was appointed as consultant
orthopaedic foot and ankle surgeon at
University Hospitals of Leicester in 2009.
Following training in South East Thames
Rotation, he did one-year Fellowship in Foot
and Ankle Surgery at Cambridge. He was
awarded the European Travelling Foot and
Ankle Fellowship to USA in 2009. He is the
Editor of An Orthopaedics Guide for Today’s
GP and has written chapters in books
including one on forefoot disorders in The
Oxford Textbook of Trauma and Orthopaedics. He is actively involved in GP
education and runs a very popular Joint Injection Course. He has published
in a number of peer-reviewed journals. He is the Chief Investigator for a
couple of RCTs and the Principal Investigator for AIM Trial and PATH2
study. He is on the editorial board of a couple of scientific journals and an
Examiner for the Royal College of Surgeons. He was a Specialist Advisor to
NICE regarding non-surgical treatment of Achilles ruptures. He is a member
of advisory panel of NIHR. He is a member of Scientific Committee of
British Orthopaedic Foot Ankle Society. He is currently the Education
Secretary of British Indian Orthopaedic Society.
xxiii
Editor’s Note
Although steroid injections are frequently performed for arthritis,
tenosynovitis, bursitis, overuse injuries and various other musculoskeletal
ailments, evidence-based guidance for the use of these injections is lacking.
In recent years, the role of steroid injections has been questioned. Moreover,
there is a surge in both injectable and non-injectable alternatives to steroid
injections including platelet-rich plasma injections, visco supplementation
and shockwave therapy.
One of the main objectives of this book is to provide the readers the
current evidence and guidelines regarding musculoskeletal injections and
alternative options. As the title suggests, this book is a very useful practical
and information guide to ‘what, when and how?’ regarding these techniques.
The chapters are written by experts in their respective fields who have
shared their vast experience and have provided a number of practical tips.
Coloured illustrations related to anatomy, landmarks and technique and
the accompanying videos make this book truly unique and will serve as
an excellent tool to help clinicians and allied health professionals in their
day-to-day practice.
In addition to indications and contraindications, this book also provides
guidance to the setting where a particular injection should be used and
the role of image guidance for injections. This book will therefore serve a
number of disciplines including allied health professionals and doctors from
specialities including Primary care, Orthopaedics, Rheumatology, Sports
medicine and Radiology. Although I have been practising orthopaedics for
25 years, during the editing process I have learned a lot from this book. I am
confident that the sincere efforts of the team for this book would help the
readers to augment their knowledge and skills.
xxv
Contributors
Zaid Abual-Rub is currently enrolled in the
National Higher Surgical Training program as a
specialty registrar in trauma and orthopaedics to
qualify as a consultant. He graduated in 2008
with an MBBS in medicine and surgery, and has
since become a Member of the Royal College of
Surgeons in Edinburgh in 2013. He has gained
clinical experience in trauma and orthopaedics
through working in various posts in Major
Trauma Centres of Newcastle, Cambridge and
Leeds in the United Kingdom. During this time,
he successfully completed and was awarded a Post-Graduate Diploma in Sports
Medicine from the International Olympic Committee educational program.
Fazal Ali has a special interest in sports injuries
to the knee. He works at Chesterfield Royal
Hospital and the Sheffield Children’s Hospital.
He trained in Sheffield with a Knee Fellowship
in Newcastle and a short Trauma Fellowship in
New York. He is a former Training Program
Director for South Yorkshire and is presently
the Academic Secretary of BOSTAA. He is Head
of the Question Writing Committee of the
Intercollegiate Board.
He has published his work, written
chapters, and given invited lectures on training issues and knee surgery both
nationally and internationally. He has co-edited ‘Examination Techniques in
Orthopaedics’ which is a best-selling orthopaedic text and is presently being
launched in Chinese. He founded the largest clinical examination course
worldwide in 2007: The Chesterfield and Sheffield FRCS Clinical course.
xxvii
xxviii Contributors
Fazal has been voted as ‘South Yorkshire Orthopaedic Trainer of the Year’
five times. He was given a lifetime award for training by the South Yorkshire
training scheme in 2012. He was twice shortlisted by BOTA as one of the
top trainers in the United Kingdom. In 2018, he was again a voted Trainer of
the Year by East Midlands. In 2017, he was honored by the South Yorkshire
Orthopaedic Training Rotation by the creation of an annual award: The ‘Fazal
Ali Award for Academic Excellence’.
He serves as a Senior Examiner for the Intercollegiate Board in the FRCS
(Tr&Orth) examinations. In 2017, he was elected to the panel of international
examiners. Ali also serves on the board of examiners in other countries
with the view that this would help advance the standard of orthopaedic
training worldwide.
Sanjeev Anand is a consultant orthopaedic
surgeon working at the Leeds Teaching
Hospitals NHS Trust, Leeds, United Kingdom.
He specialises in knee surgery and sports
injuries of the knee joint. He has an extensive
practice in complex knee injuries. He has been
involved in developing national guidelines for
arthroscopic knee surgery and the management
of ACL injuries. He is a trainer for arthroscopic
knee surgery and organises cadaveric surgical
courses on advanced knee reconstructive
techniques. He has published extensively on knee pathologies and is an editor
for the Journal of Arthroscopy and Joint Surgery.
Randeep S. Aujla received his medical degree
from the University of Leicester and completed
his Masters in Surgery from the University of
Edinburgh. He is currently a final year trauma
and orthopaedic surgery trainee and has
planned a Sports Surgery sub-speciality
Fellowship in Perth, Australia for one year. He
has a keen interest in lower limb sports injuries
and pathologies.
Randeep also works in professional sports
as team physician in both football and cricket.
Contributors xxix
He has also attended as an athlete doctor at large sporting events such as the
European Games, British University and College Games and the prestigious
UK School Games. He has Diplomas in Sports and Exercise Medicine and
Football Medicine to supports these activities. He advocates the use of
nonsurgical methods of treatment to all patients and understands that often
surgery is a last resort.
Raj Bhatt works as a consultant MSK
radiologist at University Hospitals of Leicester
since 2001. He practise all aspects of MSK
radiology including spinal imaging. He also
perform Ultrasound, Fluoroscopy and
CT-guided MSK and spinal interventions. His
special interest is Sports Medicine imaging. He
has presented and published in various
European and International meetings and
publications.
Sadiq Bhayani is a consultant in pain medicine
and anesthesia. He graduated from India in
2001 and completed his training in anesthesia
and received his Fellowship in Anaesthesia
from Royal College of Anaesthetists, United
Kingdom. He then completed his advance pain
training with specialist qualification in pain
management from Faculty of Pain Medicine,
Royal College of Anaesthetists, United Kingdom
and passed his Fellowship of Faculty of Pain
Medicine examination (FFPMRCA). To
enhance his experience in interventional pain medicine, he completed
fellowship program from the University Health Network, University of
Toronto, Canada.
He has special interest in pain arising from degenerative joint diseases
including shoulder osteoarthritis, rheumatoid arthritis knee and hip
osteoarthritis. Bhayani specialized in the radiofrequency treatment of
genicular nerves to reduce the pain arising from the painful joints.
He is the Chairman (UK Chapter) and director of media and public relations
and of World Academy of Pain Medicine Ultrasonography (WAPMU).
xxx Contributors
He is the member of World institute of Pain (WIP), Spine Intervention
Society (SIS) and European Society of Regional Anaesthesia (ESRA). He
teaches on national and international courses.
He is the first doctor in the United Kingdom to qualify, Certified
interventional pain sonologist examination (CIPS) conducted by The
World Institute of Pain. He is also a Fellow of Interventional Pain Practice
(FIPP).
In addition to his many qualifications, Bhayani also authored journal
articles, book chapters and abstracts for numerous national, international
lectures.
He is actively involved in educating trainee doctors and pain physicians
from across the world by teaching them ultrasound applications in regional
anesthesia, pain medicine and musculoskeletal medicine.
Sunil Garg works as a consultant orthopaedic
surgeon at the James Paget University Hospital
Foundation NHS Trust, Great Yarmouth,
with special interest in shoulder and upper
limb surgery. He is active in promoting
orthopaedic education and research in the
United Kingdom.
Kevin Ilo is an orthopaedic registrar in the
East Midlands deanery, United Kingdom.
His interests are medical education, sports
medicine and knee surgery.
Contributors xxxi
Annette Jones is a MSK clinical specialist
physiotherapist based at University Hospitals of
Leicester (UHL) NHS Trust, with a special
interest in lower limb injuries and rehabilitation.
Annette qualified from Coventry University
with BSc (Hons) Physiotherapy in 1998. She
gained a PG Cert in Manual Therapy from
Sheffield Hallam University in 2002, and has
ambition to complete her Masters in the near
future. Annette’s current scope of practice
covers Physiotherapy rehabilitation within
OPD; work within ED Minor injuries unit involving acute injury management
and a patient Soft Tissue Review follow up service / clinic; development /
management of conservatively managed acute Achilles Tendon rupture
service within Fracture Clinic and working in Elective Foot and Ankle clinic.
Annette also works privately in a specialist Sports injuries clinic.
Research around the conservative management of Achilles Tendon
ruptures has generated a poster presentation at BOFAS conference (2016),
and Annette is co-author of a paper awaiting publication detailing patient
outcomes at 6 and 12 months post-injury. Two further studies are currently
ongoing.
Ashwin Kulkarni after his initial training in
India, he came to the United Kingdom and
completed basic surgical training in
Birmingham and higher surgical training in
orthopaedics in Newcastle upon Tyne. He did a
fellowship with McMinn and Tracey. He also
did a fellowship in Toronto, Canada.
He was appointed as a consultant in
University hospitals of Leicester in 2010.
His specialist interests are hip arthroscopy
and arthroplasty.
His other interests are in research and training. He co-founded and
developed UKITE, an in-training examination for the trainees. He has several
research publications.
His interest outside orthopaedics is motorbikes.
xxxii Contributors
Mayur Lakhani has been a practising GP in
Leicestershire since 1991. He has combined an
active career as a working GP with high-profile
leadership roles in the Royal College of General
Practitioners, National Health Service (NHS)
and in the wider health community. As the
youngest doctor to be appointed Chairman of
Council of the Royal College of General
Practitioners (RCGP) – the largest medical royal
college in the UK and academy of family
medicine in Europe – Professor Lakhani
instituted and led the development of the document, The Future Direction of
General Practice, a Roadmap which was published in 2007. This document first
set out the vision of GP federations.
He graduated from the University of Dundee in 1983. He has been a GP
for 26 years in the same practice in Sileby, near Loughborough. The practice
has won awards for quality, including the 2014 national long-term conditions
team of the year and has a long-standing PPG and is part of a federation. As
the CCG clinical lead, he pioneered a scheme for palliative care which is now
used by over a 100 practices. He was a trustee and Chairman of The National
Council for Palliative Care from 2008 to 2015.
Mayur was elected President in 2017. He was also awarded a senior founding
fellowship of the Faculty of Medical Leadership and Management in October
2017 (by assessment of portfolio).
Appointed CBE in the 2007 Queen’s Birthday Honours list “for playing a
fundamental role in raising the profile of general practice,” Professor Lakhani
has been included in the Top 50 most influential people in the UK health service
by Health Service Journal in 2006 and 2007. In addition, Professor Lakhani has
served on a number of advisory groups, including the Chief Medical Officer’s
Advisory Group on Medical Regulation and Assurance, and Chaired the
Secretary of State’s Inquiry into primary care access for BAME patients.
Contributors xxxiii
Kimberly Lammin is a consultant orthopaedic
and trauma surgeon at University Hospitals of
Leicester, with a subspecialist interest in hip
arthroplasty and knee surgery, including
arthroplasty, arthroscopic surgery and sports
injuries. She has a postgraduate qualification in
sports and exercise medicine.
She has a background in education and
training, both undergraduate and postgraduate,
and regularly teaches on regional and national
courses, including multidisciplinary courses. She has an interest in simulation
training and won the British Orthopaedic Association Innovation in Simulation
prize in 2014.
Sangoh Lee is a senior registrar at the University
Hospitals of Leicester, subspecialising in MSK
imaging. He has gained further specialist
training at Royal National Orthopaedic
Hospital. Sangoh is very keen on medical
education and has organised and taught at
various national radiology courses as well as
developed many local teaching programmes.
Nicola Maffulli graduated from Naples, Italy,
before moving to the United Kingdom, where
he undertook his training in trauma and
orthopaedic medicine. He earned a PhD and a
mastership of surgery from the University of
London, and an MD from the University of
Aberdeen. In 2001, he was appointed to the
Chair of Trauma and Orthopaedic Surgery at
Keele University School of Medicine, and in
2008 he moved to Queen Mary University of
London to become the centre lead and professor
in sports and exercise medicine. He returned to Italy, and he is now full
professor of musculoskeletal disorders and chief of service, trauma and
orthopaedics consultant at the University of Salerno School of Medicine. He
xxxiv Contributors
maintains an Honorary Professorship in Sports and Exercises Medicine at
Queen Mary University of London, and an Honorary Professorship in trauma
and orthopaedic surgery at Keele University School of Medicine.
His main interest field lies in the basic sciences and clinical management
of soft tissues problems, and he has a superspecialist interest in tendon and
tendinopathy. Throughout his career, Maffulli has closely interacted with basic
scientists, establishing close links with the Institute of Science and Technology
in Medicine in 2001. Such links continue to date, and the collaboration has
produced external funding and peer-review articles.
Maffulli has published more than 1000 peer-review articles and holds the
highest Hirsch index (h-index) in orthopaedics in the world.
Devendra Mahadevan is a consultant surgeon
in Reading who specialises in foot and ankle
surgery. He qualified from the University of
Nottingham and completed his specialist
orthopaedic training in the East Midlands
Deanery. He has undertaken an internationally
recognised foot and ankle fellowship at the
renowned Avon Orthopaedic Centre in Bristol.
His major clinical interest is in arthroscopic
and endoscopic (keyhole surgery) treatment
of ankle and foot conditions. He is actively
involved in research and has published and presented internationally. His
particular research interest is on bunion correction, arthritis of the big toe,
interdigital (Morton’s) neuroma and Achilles tendon inflammation. At his
local NHS base, he is dedicated to passing on skills to the next generation
of surgeons. He is both an educational and clinical supervisor of surgical
trainees at The Royal Berkshire Hospital.
Ananda Nanu was the president of the
British Orthopaedic Association for 2017–2018
during the Centenary of the BOA. Nanu is on the
Council of the Royal College of Surgeons of
England. He has been a Council Member of the
British Orthopaedic Association since 2013 and a
member of the Executive since 2015. He has
contributed to several publications and is a chapter
author of the Oxford Textbook of Orthopaedics
(2011 edition). He is a consultant orthopaedic
surgeon at Sunderland Royal Hospital.
Contributors xxxv
Roger Oldham is a graduate of Charing Cross
Hospital, London, worked as a consultant
rheumatologist privately and has been work-
ing in the NHS since 1978. After a course of
prolotherapy cured his chronic back pain, he
began using this mode of treatment exten-
sively in his practice. Since 1995, he has regu-
larly treated professional footballers and rugby
players with sacroiliac dysfunction, tendinop-
athy, ligament injuries and joint instability
from well over one hundred clubs as well as
using prolotherapy in patients of all age groups
and disabilities.
Harvinder Pal Singh is a consultant orthopaedic
surgeon with University Hospitals of Leicester
NHS trust. His interests include shoulder
(osteoarthritis, impingement syndrome, rotator
cuff pathology and unstable shoulder), elbow
(arthritis and instability) and hand and wrist
disorders. He has a PhD in Health Sciences from
the University of Leicester and continue to
participate in research collaborations on local,
national and international levels. He is
committed to continuing development of his
professional and academic career and have
published articles in Journal of Shoulder and Elbow Surgery, Bone and Joint
Journal, Shoulder and Elbow, Journal of Hand Surgery (American) and
Journal of Hand Surgery (European). He has completed collaborative
projects with research units in Netherlands and Australia. He has also
completed a number of visiting travelling fellowships around the world
sponsored by British Elbow and Shoulder Society, Royal College of
Surgeons of England, British Orthopaedic Association, British and European
Hand Society.
xxxvi Contributors
Kethesparan Paramesparan is a senior
specialty clinical radiology trainee at
University Hospitals of Leicester NHS Trust,
United Kingdom. He has taken a special interest
in musculoskeletal radiology and is actively
involved in local training and teaching. He
completed his medical school training at
St.George’s, University of London. He also
intercalated and achieved a BSc (Hons) degree
in aerospace physiology at King’s College
London and published research involved with
the Ministry of Defense, United Kingdom. He subsequently underwent his
foundation year training in the Wessex deanery and thereafter obtained his
training in clinical radiology. He has several educational and poster
publications and is actively involved in ongoing research and projects. Outside
of work, Paramesparan is a keen video editor and has a solid technological
background with editorial and creative direction.
Bill Ribbans is a consultant trauma and
orthopaedic surgeon. He is a Professor of
Sports Medicine at the University of
Northampton. His main surgical interests are
Foot and Ankle and Knee. He undertook
Fellowships in Sheffield and at Harvard before
becoming a Consultant at the Royal Free,
London in 1991. Five years later, he returned
to his home town in Northampton where he
continues to work.
He has been involved in the medical care of
elite Sports people since 1981. He is presently the Chief Medical Officer to
Northamptonshire CCC, Honorary Surgeon to Northampton Town FC and
the English National Ballet. Additionally, he has worked for the last quarter of
a century with numerous professional sports organisations and international
teams as both an orthopaedic surgeon and a pitch-side physician.
Bill has over 140 scientific publications and organises conferences and
lectures widely both nationally and internationally. He has an eclectic range of
Contributors xxxvii
research interests including outcomes in foot and ankle surgery, the genetics of
ligament and tendon injury, Vitamin D activity in the musculoskeletal sphere,
cryotherapy in recovery and rehabilitation, the ethics of sports medicine and
sports injury surveillance.
Bobby Mobbassar Siddiqui is a final year
registrar in the East Midlands (South) training
deanery, looking to pursue a career in foot and
ankle surgery. He is a keen medical educator
looking to improve orthopaedic exposure and
teaching at both undergraduate and
postgraduate levels. After completing BSc from
King’s College, London, he moved to the north-
east of England; graduating with an MBBS
(2006) from the University of Newcastle upon
Tyne. After completing his foundation training
and basic surgical training within the north-east, he was awarded a training
number in the East Midlands (South) deanery. Having attained the FRCS
(Orth), he is now looking forward to my fellowship and preparing for life as a
consultant in Foot and Ankle Surgery.
Euan Stirling is a trauma and orthopaedic
registrar in Oxford University Hospitals, on the
Thames Valley training rotation.
He graduated from the University of
Nottingham in 2011 and completed his basic
surgical training in the East Midlands before
moving to Oxford to begin his specialty training.
Stirling has a keen interest in research and has
published numerous articles in peer-reviewed
journals. Outside of his work, Stirling enjoys
sport, both playing and watching, as well as
mountaineering and skiing.
xxxviii Contributors
Helen Tunnicliffe qualified from the University
of Coventry in 2002 and has been working in
Leicester since 2004. She completed a post-
graduate MSc in 2009 and has also completed
post-graduate injection therapy training. She is
also a BAHT accredited therapist.
Helen has a special interest in shoulders and
hands and works closely with the surgeons and
therapists in University Hospitals of Leicester.
She works as an extended scope practitioner in
elective orthopaedic shoulder and hand clinics,
and also treats a complex caseload of shoulder and hand patients. She has a
special interest in the unstable, hypermobile shoulder, postoperative therapy
and complex hands. Helen has a keen interest in research and audit and is
actively involved in local and national trials to develop future practice.
Philippa Turner currently works as a full-time
SEM Consultant at DMRC Stanford Hall,
Stanford on Soar, Loughborough LE12 5QW.
She completed her medical degree at Cardiff
University in 2008. She went on to undertake
my foundation training in South Wales, before
completing a Master’s Degree in Sports
Medicine, Exercise and Health at UCL, London.
She then completed Acute Care Common Stem
training in the East of England before starting
her Specialist training in the East Midlands in 2014. She has completed a Post
Graduate Certificate in Musculoskeletal Ultrasound and She is now a full-
time Sport and Exercise Medicine Consultant working for the Ministry of
Defence at the Defence Medical Rehabilitation Centre, Stanford Hall. She has
also been working as one of the team physicians with the England Women’s
Cricket Pathway since 2015 and she was the Deputy Chief Medical Officer at
the World University Games, 2017.
1
Musculoskeletal injections
in general
DEVENDRA MAHADEVAN AND EUAN STIRLING
INTRODUCTION
Pain from musculoskeletal problems is an increasing cause for poor quality
of life and is putting increased demands on the healthcare system. The
chronicity of symptoms may impact on the physical, psychological and socio-
economic status of patients (Video 1.1).
Management strategies should focus on the individual needs of these patients
(localised versus systemic pain, co-morbidities, physical status and functional
requirements). There are a multitude of treatment options employed by
healthcare providers. These include non-medicinal treatments (self-management
education, physical/exercise therapy, manual therapy and psychosocial
interventions), complementary therapies (acupuncture, ultrasound, TENS
[transcutaneous electrical nerve stimulation]), pharmacological interventions
(analgesics, anti-inflammatories, corticosteroid injections) and surgery. In
order to provide optimal care to patients with musculoskeletal pain and ensure
efficient use of healthcare resources, evidence-based practice is essential.
This chapter discusses the use of corticosteroid injections in the
management of musculoskeletal pain and the practicalities of providing
this treatment. Like all other procedures, the efficacy of this treatment
depends on appropriate use, i.e. correct indication, selecting the appropriate
pharmacological agent and performing the procedure correctly and safely.
WHAT ARE CORTICOSTEROIDS?
Corticosteroids are steroid hormones that are either naturally produced
by the adrenal cortex in vertebrates or synthetically made to mimic the
1
2 Musculoskeletal injections in general
naturally occurring variant. Corticosteroids regulate a wide range of
physiologic processes, including stress and immune responses, regulation
of inflammation, carbohydrate metabolism, protein catabolism, blood
electrolyte levels and behaviour [1].
They can be given topically, orally or by injection, and may produce a
local or systemic response. Examples of synthetic corticosteroids used as
pharmacological agents include betamethasone, prednisone, triamcinolone
and dexamethasone.
HOW DO STEROID INJECTIONS WORK?
Corticosteroids have a combined anti-inflammatory and immunosuppressive
effect. When injected into joints, they reduce synovial blood flow and
vascular permeability [2], and lower leukocyte and inflammatory mediators
including prostaglandins and leukotrienes [3–5]. They also alter local
collagen synthesis [6] and increase the hyaluronic acid concentration
within the joint [3,4]. The mechanism of action is complex: The steroids act
directly on nuclear steroid receptors and interrupt the inflammatory and
immune cascade at several levels. The net effect is reduction in pain and
inflammation locally.
The esterification (reaction between alcohols and carboxylic acids to make
esters) of corticosteroids enhances their pharmacokinetic properties. The
alteration of the parent steroid chemical properties can improve metabolic and
water solubility and lipophilicity, thus potentially increasing bioavailability
and prolonging duration of efficacy [7]. For example, branched esterification
reduces the solubility of the drug and enhances its duration of action, as it
remains longer at the injection site [2].
WHAT ARE THE INDICATIONS AND
CONTRAINDICATIONS OF CORTICOSTEROID
INJECTIONS?
Corticosteroid injections play an important role in the management of
musculoskeletal conditions. They can be used as a definitive treatment
(e.g. trochanteric bursitis, De Quervain’s tenosynovitis); provide a pain-free
window for rehabilitation (e.g. subacromial impingement, epicondylitis,
What are the indications and contraindications of corticosteroid injections? 3
Table 1.1 Indications for corticosteroid injections
Inflammatory arthropathy
• Rheumatoid arthritis
• Seronegative arthritis
• Crystal arthropathy (gout, pseudogout)
Non-inflammatory arthropathy
• Osteoarthritis
Soft tissue conditions
• Bursitis
• Synovitis
• Tenosynovitis
• Epicondylitis
• Plantar fasciitis
• Morton’s neuroma
• Carpal tunnel syndrome
plantar fasciitis); or to provide episodic pain and symptom relief (e.g.
osteoarthritis).
When used appropriately for the correct indication, corticosteroids will
provide good relief (Table 1.1). One must be aware that corticosteroids are
contraindicated in several conditions that produce a ‘painful and swollen’
joint (Table 1.2). Physicians need to be astute in establishing the diagnosis
prior to instilling corticosteroid injections. If the intra-articular diagnosis is
not obvious, a diagnostic aspiration should be performed prior to injecting
the joint with corticosteroids. The aspirated fluid may be visually analysed
(cloudy synovial fluid or haemarthrosis) and if it looks abnormal, should be
sent for microscopy and cultures.
Table 1.2 Contraindications for corticosteroid injections
Allergy or intolerance to drug
Overlying skin infection or broken skin
Fracture
Septic arthritis
Prosthetic jointa
Unstable coagulopathy
a Relative contraindication.
4 Musculoskeletal injections in general
WHAT IS THE EVIDENCE FOR THE USE
OF CORTICOSTEROID INJECTIONS FOR
MUSCULOSKELETAL PAIN?
The National Institute of Health and Care Excellence (NICE) recommends the
use of intra-articular corticosteroid injections to be considered as an adjunct
to core treatments for the relief of moderate to severe pain in people with
osteoarthritis [8].
Hip
In hip arthritis, corticosteroids are more effective than hyaluronic acid and
platelet-rich plasma (PRP) in providing pain relief for up to 12 weeks. Eighty
milligrams of methylprednisolone is more effective than 40 mg in providing
sustained pain relief. However, there is limited evidence to warrant routine use
in the management of labral tears and femoral acetabular impingement [9].
In greater trochanteric pain syndrome (trochanteric bursitis), corticosteroid
injections demonstrated superior pain relief compared to shockwave therapy
and home training for up to 3 months [10].
Knee
Most trials and reviews conclude that intra-articular steroid injections decrease
short-term pain, make little or no difference in the mid-term, and may have no
effects in the long-term. Corticosteroids were found to be effective in treating
moderate to severe knee pain in the short-term compared to placebo (RR
3.11 [95% CI, 1.61 to 6.01]) [11]. A Cochrane Database of Systematic Reviews
article on intra-articular corticosteroid injections for knee osteoarthritis
found evidence for efficacy on pain and patient global assessment, at 1-week
post injection, continuing to 2 and 3 weeks’ post injection. Thereafter, there
was diminishing evidence for efficacy, partly due to an absence of data. At 4
to 24 weeks post injection, there was a lack of evidence of effect on pain and
function (small studies showed benefits which did not reach statistical or
clinical importance, i.e. less than 20% risk difference). The review concluded
that in cases where there are obvious signs of inflammation, a corticosteroid
preparation may offer relief of inflammation and short-term pain relief
[12]. Whether there are clinically important benefits of intra-articular
corticosteroids after 6 weeks remains unclear in view of the overall quality
What is the evidence for the use of corticosteroid injections for musculoskeletal pain? 5
of the evidence, considerable heterogeneity between trials and evidence of
small-study effects.
A systematic review of treatment options for patella tendinopathy showed
no benefit of corticosteroid injections in treating patellar tendinopathy and
recommended that they should not be used [13].
Foot and ankle
Corticosteroid injections are effective for treating a variety of foot and ankle
conditions and may reduce the need for surgery.
A retrospective review of patients (n = 365) who underwent a corticosteroid
injection of the foot or ankle found that 86% of patients reported a significant
improvement in symptoms [14]. Sixty-six percent reported complete resolution
of their pain, with nearly one-third (29%) remaining asymptomatic at 2-year
follow-up.
Corticosteroid injections were particularly effective for the treatment
of ankle soft tissue impingement with 90% showing significant benefit and
59% benefiting for more than 6 months. Eighty-two percent of patients with
mid- or hind-foot osteoarthritis had significant improvement in pain from
an injection with 32% reported benefit for longer than 6 months, and 12% for
2 years. Corticosteroid injections did not provide significant improvement
in pain for longer than 3 months in conditions such as plantar fasciitis and
hallux rigidus [14].
A Cochrane Review found low-quality evidence that local steroid
injections compared with placebo or no treatment may slightly reduce heel
pain (plantar fasciitis) up to 1 month but not subsequently [15]. An injection
of corticosteroid with local anaesthetic was more effective than anaesthetic
alone for at least 3 months for Morton’s neuroma [16]. The evidence of
corticosteroid injections for foot and ankle tendinopathies is sparse,
heterogeneous and inconclusive.
Shoulder and elbow
The evidence supported short-term benefits of corticosteroid injections
(<4 weeks) for relieving moderate to severe shoulder pain compared to
non-steroidal anti-inflammatory drugs (NSAIDs) (RR 1.43 [95% CI, 0.95
to 2.16]) [11]. Short-term efficacy of corticosteroid injections for rotator-cuff
tendinopathy is not clear from the literature [17].
6 Musculoskeletal injections in general
In patients with subacromial impingement, corticosteroid injections have
been found to be superior to placebo. However, exercise was also found to be
superior to non-exercise controls. It is unclear whether corticosteroid injections
were superior to exercise therapy in these patients [18].
For lateral epicondylitis, corticosteroid injection had a large effect (defined
as SMD > 0.8) on reduction of pain compared with no intervention in the
short term (SMD 1.44%, 95% CI 1.17–1.71, p < 0.0001), but no intervention
was favoured at intermediate term (–0.40, –0.67 to –0.14, p < 0.003) and long
term (–0.31, –0.61 to –0.01, p = 0.05) [17].
Wrist and hand
Moderate evidence was found for the effect of corticosteroid injection on the
very short term for trigger finger and De Quervain’s disease. A Cochrane
Review found two randomised controlled trials on trigger fingers and
both studies showed better short-term effects of corticosteroid injection
combined with lidocaine compared to lidocaine alone. In one study the
effects of corticosteroid injections lasted up to 4 months [19]. The efficacy of
corticosteroid injections for De Quervain’s tenosynovitis has been studied in
only one small controlled clinical trial, which found steroid injections to be
superior to thumb spica splinting [20].
In carpal tunnel syndrome, a Cochrane Review found local corticosteroid
injection provided greater clinical improvement in symptoms 1 month
after injection compared to placebo. Significant symptom relief beyond one
month has not been demonstrated. Local corticosteroid injection provided
significantly greater clinical improvement than oral corticosteroid for up
to 3 months. However, local corticosteroid injection did not significantly
improve clinical outcome compared to either anti-inflammatory treatment
and splinting after 8 weeks. Furthermore, two local corticosteroid
injections do not provide significant added clinical benefit compared to
one injection [21].
Spine
Epidural corticosteroid injections for radiculopathy were associated with
immediate reductions in pain and improvement in function. However,
benefits were small and not sustained, and there was no effect on long-
term requirement for surgical intervention. Limited evidence suggested no
effectiveness for spinal stenosis [22].
What are examples of injectable corticosteroid agents? 7
WHAT ARE EXAMPLES OF INJECTABLE
CORTICOSTEROID AGENTS?
The main injectable corticosteroids listed in the British National Formulary
include methylprednisolone, triamcinolone, hydrocortisone and dexamethasone
(Table 1.3). In the United States, betamethasone injections are also used.
Table 1.3 Properties of commonly used steroid agents
Corticosteroid Medicinal product Solubility Dose
Methylprednisolone Depo-Medrone (Pfizer Intermediate 4–80 mg
acetate Ltd)
Triamcinolone Kenalog (Bristol-Myers Low 5–40 mg
acetonide Squibb Pharmaceuticals 2.5–15 mg
Ltd)
Adcortyl (Bristol-Myers
Squibb Pharmaceuticals
Ltd)
Triamcinolone Non-proprietary Intermediate
hexacetonide
Hydrocortisone Hydrocortistab (AMCo) High 5–50 mg
Dexamethasone Non-proprietary High 0.3–3 mg
Figure 1.1 Examples of commonly used steroid agents.
8 Musculoskeletal injections in general
The most commonly available corticosteroid preparations in the United
Kingdom are methylprednisolone acetate (Depo-Medrone, Pfizer Ltd) and
triamcinolone acetonide (Kenalog, Bristol-Myers Squibb Pharmaceuticals
Ltd) (Figure 1.1).
HOW DO YOU SELECT AN APPROPRIATE
CORTICOSTEROID PREPARATION FOR A
SPECIFIC JOINT OR SOFT TISSUE INJECTION?
There are no specific guidelines for selecting corticosteroid preparations
for injections. As there is little scientific evidence, most recommendations
are based on a combination of personal preference and clinical experience.
A review within the National Health Service (NHS) in 2007 recommended
triamcinolone and methylprednisolone as preferred agents for large joint
injections (e.g. knee and hip). For smaller joints (e.g. finger and toe), either
hydrocortisone or methylprednisolone are recommended [8].
Empirically, many physicians choose corticosteroids with low solubility
(e.g. Kenalog) for intra-articular injections as they have a longer duration of
action. Corticosteroid preparations with higher solubility (e.g. Depo-Medrone)
are chosen for soft tissue injections as they have fewer cutaneous and soft tissue
side effects [23]. Longer-acting preparations have a slightly higher risk of
complications including tendon rupture and tissue atrophy, but these risks
are nevertheless small [24].
SHOULD CORTICOSTEROIDS BE COMBINED
WITH LOCAL ANAESTHETICS WHEN GIVING
INJECTIONS?
Corticosteroids are frequently given mixed in a local anaesthetic (LA) agent.
The main advantage of using local anaesthetic is the rapid onset of pain relief,
as corticosteroids may take up to 2 days to take effect. They also add volume to
the injectate to help distribute the corticosteroid within the joint. As the local
anaesthetic is only short acting, patients may experience transient increase in
pain as the local anaesthetic wears off. The choice of local anaesthetic used is
based on personal preference.
What equipment is needed for corticosteroid injection? 9
Concerns regarding chondrolysis following intra-articular local
anaesthetic have been highlighted in the literature. Current evidence
suggests that prolonged continuous intra-articular administration of higher
concentrations of local anaesthetic, especially bupivacaine results in adverse
clinical effects, whereas a single injection of low-concentration bupivacaine
appears safe [25].
WHICH LOCAL ANAESTHETIC AGENTS
ARE APPROPRIATE TO USE WITH
CORTICOSTEROID?
Commonly used LA agents include lidocaine and bupivacaine. Table 1.4
displays some of the properties of these agents. Combinations of two agents
can be used for their complementary nature of action; lidocaine has rapid
onset of action, with bupivacaine sustaining analgesia for a longer period.
The volume of LA used depends on the target structure. Large joints will
accommodate large volumes of injectate; corticosteroid may be mixed with
10 mL of LA. In smaller joints, there may be only 2–3 mL capacity allowing
only 1–2 mL of LA (Figure 1.2).
WHAT EQUIPMENT IS NEEDED FOR
CORTICOSTEROID INJECTION?
Although many corticosteroid injections can be performed without specialist
equipment, image guidance (fluoroscopy or ultrasound) is usually required for
smaller joints in hands and feet, deep structure (e.g. hip joint) and most soft
tissue injections (specially in proximity to tendon, nerve or vessel). Regardless
Table 1.4 Properties of commonly used local anaesthetic agents
Local Onset Duration Concentration Maximum
anaesthetic of action of action (%) dose
Lidocaine Rapid (2–5 Intermediate 1 3 mg/kg
hydrochloride minutes) (80–120 minutes) 2
Bupivacaine Slow (5–10 Long (180–360 0.25 2 mg/kg
hydrochloride minutes) minutes) 0.5
10 Musculoskeletal injections in general
Figure 1.2 Examples of commonly used local anaesthetic agents.
of indication, all joint and soft tissue injections should be performed with
an aseptic technique. It is advisable to use a sterile pack for musculoskeletal
injections. Needles and syringes should be disposed into a designated sharps
bin immediately after the procedure. Figure 1.3 displays the equipment needed
and a demonstration of the no-touch technique.
The size of needle and syringe used depends on the procedure being
performed, with consideration also given to patient habitus. If an effusion is
present, joint aspiration may be performed prior to corticosteroid injection to
remove excess fluid. This can yield significant volumes, which may be cloudy
or purulent in inflammatory or infective arthritis; larger syringes (20 mL or
50 mL) and larger gauge needles (18G or 21G) should therefore be used for
this. Luer lock syringes can facilitate easier application and removal of the
syringe, allowing multiple aspirations with the needle left in place when a
large effusion is present. If the aspirate suggests an underlying infective process,
samples should be sent urgently for laboratory analysis (gram stain, culture
Which joints can be injected without image guidance? 11
(a) (b)
Figure 1.3 (a) Equipment required for steroid injection and (b) no-touch
technique for drawing up injectate.
and crystals), the planned corticosteroid injection abandoned, and the patient
referred for immediate assessment by orthopaedic or rheumatology teams
according to local protocols.
Most injections can be performed using needles that are 1 to 1½ inches
long. Shorter needles (½ inch) may be advantageous for injection of small
joints of the hand or foot. In larger patients or where the target may be deep
(e.g. trochanteric bursa), a 3-inch spinal needle can be used. Needle gauge
is guided by the size of the target structure and the volume of injectate; as a
general rule 21G are appropriate for large joints, 23G or 25G for medium and
small joints. Syringe choice (2.5–10 mL) is likewise determined by the volume
of injectate.
WHICH JOINTS CAN BE INJECTED WITHOUT
IMAGE GUIDANCE?
The general principles and techniques of musculoskeletal injection are the
same regardless of the target, i.e. to deliver corticosteroid to the affected
structure and reduce inflammation. Some joints and soft tissues are easily
identified and approached using surface landmarks, whilst others may
require assistance with image guidance (x-ray or ultrasound scan) to ensure
accurate administration. Table 1.5 lists examples of structures that are
routinely injected ‘blind’ or unguided using surface landmarks only, as well
12 Musculoskeletal injections in general
Table 1.5 Complications of corticosteroid injections
Soft tissue
Skin atrophy <1%
Skin depigmentation <1%
Tendon rupture <1%
Intra-articular
Post-injection flare 2%–10%
Septic arthritis <0.03%
Systemic
Vasovagal reaction 10%–20%
Facial flushing 1%–12%
Hypersensitivity <1%
BOX 1.1 Example structures amenable to unguided
injection and those requiring image guidance
Blinda X-ray guided Ultrasound guided
Knee Hand/wrist joints Achilles tendon
Shoulder Foot/ankle joints Tibialis posterior tendon
Elbow Hip joint
Trochanteric bursa Facet joint injections
Epidural injections
a Blind or unguided injections should only be performed by appropriately trained per-
sonnel who have knowledge of local anatomy and good clinical skills.
as the imaging modalities commonly used in our practice for specific targets.
However, it is important to note that the evidence remains unclear as to the
importance of accurate intra-articular corticosteroid injection with regard to
treatment response [26] (Box 1.1).
HOW OFTEN CAN YOU INJECT A JOINT?
Too many injections weaken the soft tissue structures including tendons and
ligaments, increase the risk of infection and become ineffective over the period of
time. Rheumatology studies however suggest that multiple steroid injections
can be performed on the same joint [27]. The recommended interval between
Do all patients respond to corticosteroid injections? 13
intra-articular injections is at least 3 months [28]. A reasonable approach is to
limit the frequency of injections to three to four for a single joint per year if the
patient is medically unfit to have joint replacement surgery.
Soft tissue injections should be used more sparingly as they are more
likely to cause local effects. There is no guidance in the literature on this,
but injections within tendon sheaths or plantar fascia have been shown to be
associated with increased risk of rupture.
SHOULD CORTICOSTEROIDS BE USED
AROUND TENDONS?
Corticosteroid injections should be used cautiously around tendons, as rupture
is a concern. Kennedy and Willis [29] found that Achilles tendon in vitro
failing strength decreased by 35% after administration of steroid. Cystic
spaces and collagen necrosis were appreciated in the steroid group and
this continued through to 7 days. However, at 2 and 4 weeks post injection
fibroblast proliferation was noted. In addition, the failing strength returned
to that of control subjects. By 6 weeks, full biomechanical integrity was
re-established as evidenced by reorganisation of collagen into parallel fibres.
They concluded that steroid injection weakens normal tendons for up to 14 days
through collagen necrosis, recommending limited physical activity for the
2 weeks following injection and against repeated injection.
Tendon ruptures are not that common but have been reported following
injections into the carpal tunnel [30], tennis elbow [31], trigger finger [32],
patellar tendon [23] and Achilles tendon [33]. One study described 13 patients
who developed 15 ruptured tendons subsequent to injection of a depository
steroid in or around the tendons injected [34].
In cases of tendinopathies, it is very important to ensure that the drug
is injected into the tendon sheath and not the tendon. Ultrasound-guided
injections are advocated to ensure accurate placement of the needle. A general
rule for tendon sheath injection is to not inject if resistance is met.
DO ALL PATIENTS RESPOND TO
CORTICOSTEROID INJECTIONS?
The degree and duration of pain relief following corticosteroid injection is
unpredictable. There is some evidence that patients with minimal arthritic
14 Musculoskeletal injections in general
changes on plain radiographs benefit more and for a longer duration compared
to those with more severe arthritic changes [35].
In general, if a patient is going to respond to a steroid injection, they tend
to respond after the first injection (assuming the target structure has been
successfully injected). Patients who have gained no symptom relief or functional
benefit from two injections should probably not continue with repeat injections
because the likelihood of improvement is small. If significant benefit is achieved
after the first injection, then an argument can be made for a repeat injection.
WHAT ARE THE POTENTIAL SIDE EFFECTS
AND COMPLICATIONS OF CORTICOSTEROID
INJECTIONS?
Corticosteroid injections are generally safe with low complication rates if
correct techniques are applied. The most common complication following a
corticosteroid injection is post-injection ‘flare’ or inflammation which occurs in
2%–10% of cases [36]. This is caused by the irritant nature of steroid crystals
deposited within the joint. The crystals can cause pain and inflammation that
is worse than the condition being treated, and may mimic symptoms of septic
arthritis. A cortisone flare typically lasts one or two days after the injection
and can be treated with rest, anti-inflammatories and intermittent cold packs.
Septic arthritis usually occurs later than post-injection ‘flare’ and the findings
are more persistent. The risk of septic arthritis from intra-articular injections,
however, is extremely low, estimated to be less than 0.03% [37].
Soft tissue (skin or fat) atrophy is a possible rare adverse effect of any
steroid injection, particularly when given at a superficial site with an
estimated risk of less than 1% [36]. It appears 1 to 4 months after corticosteroid
injection and is usually reversible, spontaneously resolving between 6 and
12 months [38].
Skin depigmentation is another side effect that may occur in less than 1%
of cases and patients with darker skin are more at risk [39]. The risk of soft
tissue complications can be minimised by using corticosteroid preparations
with suitable solubility and potency. More soluble and less potent agents (e.g.
Depo-Medrone) should be used for soft tissue injections. In addition, some have
recommended manual compression over the injection site after pulling out the
needle to prevent steroid leakage along the needle track [40].
A summary of potential complications of corticosteroid injections is listed
in Table 1.5.
What adjuncts are available for steroid injection? 15
WHAT ADJUNCTS ARE AVAILABLE FOR
STEROID INJECTION?
Depending on the indication, there are a number of additional treatments
which can complement the effect of steroid injection. For chronic degenerative
conditions, such as osteoarthritis, many patients may take regular analgesia
such as paracetamol and NSAIDs. These should be continued following steroid
injection. Immediately after the procedure they help to control pain after
LA effects wear off. They also help in managing symptoms in case of steroid
flare. Similarly, for patients receiving treatment for inflammatory conditions,
administration of disease-modifying anti-rheumatic drugs (DMARDs)
should not be stopped.
Orthotics offer a simple and safe treatment strategy and are commonly
employed alongside steroid injection for a number of specific presentations.
Their use is particularly common in foot and ankle pathology, and range
from ‘off-the-shelf’ inserts (such as heel raises for Achilles tendinopathy and
metatarsal pads for Morton’s neuroma), to custom-made ankle foot orthoses
for more complex conditions (e.g. tibialis posterior insufficiency). Figure 1.4
shows a range of devices available for treatment. Following steroid injection
for Achilles or tibialis posterior tendinopathy, it is recommended that an
Figure 1.4 Examples of various orthoses (heel cup, medial arch supports,
ankle foot orthoses).
16 Musculoskeletal injections in general
orthotic brace (e.g. air-cast boot) be used for a period of 2–4 weeks to reduce
the risk of tendon rupture.
For many soft tissue presentations, corticosteroid injections are themselves
adjuncts to other treatment modalities. Physiotherapy is the mainstay of initial
management for a number of conditions (e.g. plantar fasciitis, tendinopathies,
adhesive capsulitis of shoulder), but patients are frequently unable to actively
engage in treatment due to the severity of symptoms in particular pain.
Steroid injections are administered with the primary aim of reducing pain
and inflammation sufficiently to allow active participation with stretching and
strengthening exercises under the supervision of physiotherapists. In most cases
physiotherapy can be started one week following steroid injection.
Longer life expectancy, higher rates of obesity and increasingly sedentary
lifestyles have precipitated a significant increase in the prevalence of
osteoarthritis in the general population. Soft tissue pathology, such as
tendinopathy, has also seen an increase, likely in part due to the latter reason.
Exercise therapies are therefore often recommended both as a treatment
strategy in itself, but also as means to facilitate weight loss and improve overall
cardiovascular fitness. As with physiotherapy, corticosteroid injection may be
required to modulate pain initially prior to activity.
WHAT ARE THE ALTERNATIVES TO STEROID
INJECTION?
Intra-articular injection of viscoelastic agents, such as hyaluronic acid (HA),
has been advocated for the treatment of non-inflammatory arthritis, in
particular for treatment of knee osteoarthritis. HA is a naturally occurring
glycosaminoglycan found in synovial fluid and cartilage matrix. It has anti-
inflammatory, anabolic, analgesic, and chondroprotective effects, and acts
both as a joint lubricant and an elastic shock absorber. However, the clinical
efficacy of HA remains the subject of debate and has not been recommended as
part of routine management of osteoarthritis [8]. Further details regarding HA
injections are covered in Chapter 8.
Platelet-rich plasma (PRP) injections have been used for the treatment
of a number of orthopaedic and rheumatological conditions, including
degenerative joint disease, tendinopathy and tendon rupture. Platelet
concentrate, derived from centrifuged autologous blood, contains high
concentrations of a broad spectrum of growth factors which have anti-
inflammatory, proliferative and remodelling effects. Some studies suggest that
Video 17
PRP appears to provide symptomatic relief in the treatment of osteoarthritis,
but the evidence remains inconclusive for its use and further study is required.
Evidence for PRP injection for rotator cuff tendinopathy, epicondylitis, Achilles
tendinopathy and plantar fasciitis similarly remains uncertain. Further details
regarding PRP injections are covered in Chapter 7.
Prolotherapy, the injection of irritant solution (usually containing a
combination of dextrose, glycerol, phenol and LA) into damaged ligaments,
tendons or joints, has been advocated for use in the treatment of a number of
chronic musculoskeletal conditions. It is thought to work by creating a mild,
controlled injury to the target structure and thereby stimulating the body’s
natural healing mechanisms. Studies have suggested it can be beneficial in the
treatment of tendinopathies, knee and finger joint osteoarthritis, and spinal/
pelvic pain due to ligament dysfunction [41], however it is not part of routine
practice in the United Kingdom. Further details regarding prolotherapy
injections are covered in Chapter 9.
TAKE-HOME MESSAGES
●● Corticosteroid injections are used for a wide variety of
musculoskeletal pathologies. Efficacy of injection is variable and
practitioners should be aware of the evidence to support injection
use for different indications.
●● Different injectable steroids are available; practitioners should
be aware of which preparation should be used for different
indications.
●● As a general rule, a minimum of 3 months should be left between
steroid injections to the same target structure.
●● Steroid injections should be used alongside other therapies to
increase their efficacy.
●● Patients should be warned of the potential complications of
steroid injection, in particular that of steroid flare.
VIDEO
Video 1.1 A
n introduction to musculoskeletal injections.
(https://youtu.be/An5CRYPuO28)
18 Musculoskeletal injections in general
REFERENCES
1. Nussey S, Whitehead SA. Endocrinology: An Integrated Approach.
Oxford: BIOS Scientific Publishers, 2001.
2. Caldwell JR. Intra-articular corticosteroids. Guide to selection and
indications for use. Drugs. 1996 October; 52(4):507–14.
3. Ostergaard M, Halberg P. Intra-articular corticosteroids in arthritic
disease: A guide to treatment. BioDrugs. 1998 February; 9(2):95–103.
4. Creamer P. Intra-articular corticosteroid treatment in osteoarthritis.
Curr Opin Rheumatol. 1999 September; 11(5):417–21.
5. Lavelle W, Lavelle ED, Lavelle L. Intra-articular injections. Med Clin
North Am. 2007 March; 91(2):241–50.
6. Wei S, Callaci JJ, Juknelis D, Marra G, Tonino P, Freedman KB, Wezeman
FH. The effect of corticosteroid on collagen expression in injured rotator
cuff tendon. J Bone Joint Surg Am. 2006 June; 8(6):1331–8.
7. Taylor WN. Anabolic Steroids and the Athlete. Jefferson, NC: McFarland,
2002.
8. NICE. “Osteoarthritis: care and management; Guidance and
guidelines.” February 2014.
9. Chandrasekaran S, Lodhia P, Suarez-Ahedo C, Vemula SP, Martin TJ,
Domb BG. Symposium: Evidence for the use of intra-articular cortisone
or hyaluronic acid injection in the hip. J Hip Preserv Surg. 2016 April;
3(1):5–15.
10. Barratt PA, Brookes N, Newson A. Conservative treatments for greater
trochanteric pain syndrome: A systematic review. Br J Sports Med. 2017
January; 51(2):97–104.
11. Babatunde OO, Jordan JL, Van der Windt DA, Hill JC, Foster NE,
Protheroe J. Effective treatment options for musculoskeletal pain in
primary care: A systematic overview of current evidence. PLOS ONE.
2017; 12(6):e0178621.
12. Bellamy N, Campbell J, Welch V, Gee TL, Bourne R, Wells GA.
Intraarticular corticosteroid for treatment of osteoarthritis of the knee.
Cochrane Database Syst Rev. 2006 April; 9(2):CD005328.
13. Everhart JS, Cole D, Sojka JH, Higgins JD, Magnussen RA, Schmitt
LC, Flanigan DC. Treatment options for patellar tendinopathy:
A systematic review. Arthrosc J Arthrosc Relat Surg. 2017 April;
33(4):861–72.
14. Grice J, Marsland D, Smith G, Calder J. Efficacy of foot and ankle
corticosteroid injections. Foot Ankle Int. 2017 January; 38(1):8–13.
References 19
15. David JA, Sankarapandian V, Christopher PR, Chatterjee A, Macaden,
AS. Injected corticosteroids for treating plantar heel pain in adults.
Cochrane Database Syst Rev. 2017 June; 6:CD009348.
16. Thomson CE, Beggs I, Martin DJ, McMillan D, Edwards R, Russell
D, Yeo ST, Russell IT, Gibson JA. Methylprednisolone injections for
the treatment of Morton neuroma. J Bone Joint Surg Am. 2013 May;
95(9):790–8.
17. Coombes BK, Bisset L, Vicenzino B. Efficacy and safety of corticosteroid
injections and other injections for management of tendinopathy:
A systematic review of randomised controlled trials. Lancet. 2010
November; 376(9754):1751–67.
18. Steuri R, Sattelmayer M, Elsig S, Kolly C, Tal A, Taeymans J, Hilfiker R.
Effectiveness of conservative interventions including exercise, manual
therapy and medical management in adults with shoulder impingement:
A systematic review and meta-analysis of RCTs. Br J Sports Med. 2017
September; 51(18):1340–47.
19. Peters-Veluthamaningal C, van der Windt DA, Winters JC, Meyboom-de
Jong B. Corticosteroid injection for trigger finger in adults. Cochrane
Database Syst Rev. 2009 January;(1):CD005617.
20. Avci S, Yilmaz C, Sayli U. Comparison of nonsurgical treatment
measures for de Quervain’s disease of pregnancy and lactation. J Hand
Surg Am. 2002 March; 27(2):322–4.
21. Marshall SC, Tardif G, Ashworth NL. Local corticosteroid injection
for carpal tunnel syndrome. Cochrane Database Syst Rev. 2007
April;(2):CD001554.
22. Chou R, Hashimoto R, Friedly J, Fu R, Bougatsos C, Dana T, Sullivan
SD, Jarvik, J. Epidural corticosteroid injections for radiculopathy and
spinal stenosis. Ann Intern Med. 2015 September; 163(5):373.
23. Chen S-K, Lu C-C, Chou P-H, Guo L-Y, Wu W-L. Patellar tendon
ruptures in weight lifters after local steroid injections. Arch Orthop
Trauma Surg. 2009 March; 129(3):369–72.
24. Nichols AW. Complications associated with the use of corticosteroids
in the treatment of athletic injuries. Clin J Sport Med. 2005 September;
15(5):370–5.
25. Webb ST, Ghosh S. Intra-articular bupivacaine: Potentially
chondrotoxic? Br J Anaesth. 2009 February; 102(4):439–41.
26. Bloom JE, Rischin A, Johnston RV, Buchbinder R. Image-guided versus
blind glucocorticoid injection for shoulder pain. Cochrane Database
Syst Rev. 2012 August;(8):CD009147.
20 Musculoskeletal injections in general
27. Combe B. Early rheumatoid arthritis: Strategies for prevention
and management. Best Pract Res Clin Rheumatol. 2007 February;
21(1):27–42.
28. Raynauld J-P et al. Safety and efficacy of long-term intraarticular steroid
injections in osteoarthritis of the knee: A randomized, double-blind,
placebo-controlled trial. Arthritis Rheum. 2003 February; 48(2):370–7.
29. Kennedy JC, Willis RB. The effects of local steroid injections on tendons:
A biomechanical and microscopic correlative study. Am J Sports Med.
1976 January; 4(1):11–21.
30. Gottlieb NL, Riskin WG. Complications of local corticosteroid
injections. JAMA. 1980 April; 243(15):1547–8.
31. Smith AG, Kosygan K, Williams H, Newman RJ. Common extensor
tendon rupture following corticosteroid injection for lateral tendinosis
of the elbow. Br J Sports Med. 1999 December; 33(6):423–5.
32. Fitzgerald AT, Hofmeister EP, Fan RA, Thompson MA. Delayed flexor
digitorum superficialis and profundus ruptures in a trigger finger
after a steroid Injection: A case report. J Hand Surg Am. 2005 May;
30(3):479–82.
33. Chechick A, Amit Y, Israeli A, Horoszowski H. Recurrent rupture of the
Achilles tendon induced by corticosteroid injection. Br J Sports Med.
1982 June; 16(2):89–90.
34. Ford LT, DeBender J. Tendon rupture after local steroid injection. South
Med J. 1979 July; 72(7):827–30.
35. Day S, Gelberman R, Patel AA, Vogt MT, Ditsios K, Boyer MI. Basal
joint osteoarthritis of the thumb: A prospective trial of steroid injection
and splinting. J Hand Surg Am. 2004 March; 29(2):247–51.
36. Courtney P, Doherty M. Joint aspiration and injection. Best Pract Res
Clin Rheumatol. 2005 June; 19(3):345–69.
37. Charalambous P, Tryfonidis M, Sadiq S, Hirst P, Paul A. Septic arthritis
following intra-articular steroid injection of the knee? A survey of current
practice regarding antiseptic technique used during intra-articular steroid
injection of the knee. Clin Rheumatol. 2003 December; 22(6):386–90.
38. Friedman SJ, Butler DF, Pittelkow MR. Perilesional linear atrophy and
hypopigmentation after intralesional corticosteroid therapy: Report
of two cases and review of the literature. Am Acad Dermatol. 1988
September; 19(3):537–41.
39. Papadopoulos PJ, Edison JD. Soft tissue atrophy after corticosteroid
injection. Cleve Clin J Med. 2009 June; 76(6):373–74.
References 21
40. Gray RG, Gottlieb NL. Intra-articular corticosteroids: An updated
assessment. Clin Orthop Relat Res. 1983 July–August;(177):235–63.
41. Hauser RA, Lackner JB, Steilen-Matias D, Harris DK. A systematic
review of dextrose prolotherapy for chronic musculoskeletal pain. Clin
Med Insights Arthritis Musculoskelet Disord. 2016 January; 9:CMAMD.
S39160.
2
Shoulder and elbow injections
HELEN TUNNICLIFFE AND HARVINDER PAL SINGH
INTRODUCTION
The shoulder is a ball-and-socket joint. Movement of the shoulder is not
isolated to one joint; it also involves the shoulder girdle (Figure 2.1) which
consists of the
1. Glenohumeral joint
2. Acromioclavicular joint
3. Scapulothoracic joint (pseudo-joint)
4. Subacromial space (pseudo-joint)
These work in harmony together, with movement being a finely timed
sequence of events. The shoulder has a large degree of movement and is
responsible for placing the hand for function. The socket is very shallow,
with a soft tissue labrum to aid stability, but a lot of stability comes from
the dynamic structures, namely the rotator cuff. The rotator cuff arises
Acromioclavicular
Subacromial space
joint
(pseudo-joint)
Subscapular area
Glenohumeral
(pseudo-joint)
joint
Figure 2.1 Bony anatomy of the shoulder showing the two joints and two
pseudo-joints.
23
24 Shoulder and elbow injections
Front view
Subscapularis
Back view
Supraspinatus
Infraspinatus
Supraspinatus
Teres minor
Figure 2.2 Muscles of the rotator cuff.
from the scapula and wraps around the humeral head, and help to centre the
ball in the socket (Figure 2.2).
When injury or pain occurs in the shoulder, quite often the firing of the
rotator cuff is affected/inhibited, leading to poor muscle patterning and a
chain of worsening pain and loss of movement.
HOW TO DIFFERENTIATE SHOULDER PAIN?
When treating a patient with shoulder pain, it is key to differentiate where the
pain is stemming from. It must not be forgotten that pain in the shoulder may
be referred from the other areas. Patients with shoulder conditions tend to
complain of pain primarily in the upper arm. The following areas of pain are
indicative of problems arising from the
1. Acromioclavicular joint: Pinpoint over the top of the shoulder.
2. Cervical spine: Neck and supraclavicular region.
3. Upper arm: Subacromial space or glenohumeral joint.
4. Scapula: Poor muscle patterning, especially if winging is present. In
addition, look for trigger points around the medial border of scapula,
which can be seen in fibromyalgia.
What is the role of physiotherapy in shoulder disorders? 25
WHAT IS THE ROLE OF PHYSIOTHERAPY IN
SHOULDER DISORDERS?
Physiotherapy should be considered as a first line of treatment for most shoulder
conditions. If delivered at the right time it can prevent the need for any further
intervention. Patients in pain often develop poor patterns of movement and
lose the ability to take the arm through full range. The range of movements
could be lost due to joint stiffness or pain (Video 2.1).
Patients who are passively stiff may require manual mobilisations
and self-stretching to overcome the stiffness. However, if the patient has
significant osteoarthritis in the glenohumeral joint, this is not normally
successful.
Improvement tests are a very useful way to determine if a patient can
modify the movement and break the poor patterning. These can involve many
techniques:
1. Facilitating the rotator cuff (resisting into gentle external rotation
strengthens the infraspinatus).
2. Moving the body around the arm (for example, placing the hand static
on a shelf or ball and squatting, or sliding the hand along a table and
leaning the body to achieve the movement).
3. Recruiting the kinetic chain (squatting or lunging whilst elevating the
arm).
4. Changing the start position (for example to supine, prone or leaning
forwards).
5. Hitching or depressing the shoulder girdle (useful if the patient has a
poor pattern and initiates movement by either fixing the scapula into
depression or hitching the shoulder girdle).
Improvement tests can consist of any alteration to position or muscle
activation, and the key is looking for an improvement in the pain or range of
movement. Fixing the hand decreases the weight of the arm, diminishing the
activation of the rotator cuff [1]. This leads to increased pain-free range of
motion and minimises compensation patterns (Video 2.2).
A combination of these techniques can be useful. Once an improvement
factor is found, this is the basis for the start of the personalised physiotherapy
regime. Exercise programmes should be individual and tailored to the
patients’ needs and goals. The shoulder exercises could be grouped into early
(restoring movement), mid (rotator cuff strengthening primarily), and late
26 Shoulder and elbow injections
(higher level end-stage rehabilitation). Once movement is restored, rotator
cuff recruitment, strengthening and endurance should be progressed using
functional patterns. Late-stage rehabilitation should be directed to the
patient’s specific functional demands or hobbies (Video 2.3). A useful resource
is the website http://ww.leicestershoulderunit.co.uk.
WHAT IS THE ROLE OF STEROID INJECTIONS
FOR SHOULDER DISORDERS?
Steroid injections are commonly used in the shoulder to treat conditions that
are not settling with rest, exercise, time, oral pain relief or physiotherapy.
Steroid and local anaesthetic are combined to provide an anti-inflammatory
effect to treat pain for the following common shoulder disorders:
●● Osteoarthritis
●● Impingement syndrome/bursitis/tendinopathy
●● Frozen shoulder/joint stiffness
●● Degenerative rotator cuff tears (when not considering surgical repair)
●● Calcific tendinitis
Inflammation is a common factor linking these disorders and is often
the driver of pain [2]. Steroid injections can also be used as a diagnostic
test to try and help clinically reason where the patient’s pain is coming
from. Studies have found that steroid injections in the shoulder are more
effective at providing short-term pain relief than the use of non-steroidal
anti-inflammatory drugs [3]. Steroid injection for shoulder pain leads to a
significant improvement in pain and function for up to 12 weeks [4]. This
provides a window for physiotherapy, therefore the two should be combined to
hopefully give longer-lasting results.
There are three typical sites for injection in the shoulder: (1) the
subacromial space, (2) the glenohumeral joint, and (3) the acromioclavicular
joint (ACJ). Please see later regarding conditions as to which area to inject
depending on the patient’s presentation. There is much debate as to whether
landmark-guided versus image-guided steroid injections are more effective,
but cost effectiveness and practicality of what services are available must be
considered. Sage [5] found that the difference between outcomes after the two
types of shoulder injections was very small.
Impingement/subacromial bursitis/tendinopathy 27
OSTEOARTHRITIS
Osteoarthritis can cause pain and limitation of movement in the shoulder.
It is more common in the older patient, primarily 60 years or older, or can
develop earlier due to shoulder trauma. The acromioclavicular joint and/or the
glenohumeral joint can be affected. Osteoarthritis in the acromioclavicular joint
is more common, and patient presents with pain at the end of range of elevation
pain during hand behind the back movements. Pain is often pinpointed over the
lateral tip of the clavicle, with patients pointing directly to the acromioclavicular
joint. Osteoarthritis of the glenohumeral joint is less common and presents with
a more global loss of range of movement, especially external rotation. Crepitus is
often felt throughout the range. A plain x-ray is useful to confirm osteoarthritic
changes and exclude other disorders that present with loss of external rotation
such as frozen shoulder or locked posterior dislocation. Steroid injections can
be useful in early arthritis, when the pain is often inflammatory in nature; but in
more advanced severe cases, the injections may not be beneficial in the long term.
However, it is often used as a treatment choice to try to delay joint replacement,
especially in younger patients. Studies have found an increase risk of infection by
up to 40% if the patient has received a steroid injection within 3 months of joint
replacement and injection, and therefore should be avoided for patients who are
awaiting a joint replacement [6,7].
For acromioclavicular osteoarthritis, injection of this joint should be
considered in symptomatic patients. The acromioclavicular is a very small
joint, therefore accuracy in localising this joint is low without image guidance.
In a cadaveric study, Peck et al. [8] observed that only 40% of palpation-
guided injections accurately went into the acromioclavicular joint compared
to 100% with ultrasound guidance. However, Hegedus et al. [9] found that
despite many injections around the shoulder not being accurate, patients still
improved in symptoms.
IMPINGEMENT/SUBACROMIAL
BURSITIS/TENDINOPATHY
Impingement is one of the most common disorders of the shoulder. The cause
of pain in these patients is not fully understood. Proponents of extrinsic
theory of impingement syndrome believe that the tendons of the rotator cuff
28 Shoulder and elbow injections
Impingement
Acromioclavicular joint
Bone spurs
Irritation
to bursa
Figure 2.3 Figure showing subacromial bursa of the shoulder and impingement
during elevation of the shoulder.
and the subacromial bursa, which lie under the surface of the acromion, are
pinched as the arm is elevated, causing pain on movement (Figure 2.3). On
the other hand, the cause of pain is believed to be due to inflammation as per
the intrinsic theory.
The most common presentation is a painful arc as the patient elevates the
arm, around 60°–120° (Figure 2.4).
Pain is often located in the upper arm rather than in the shoulder itself.
Movement is not normally restricted but can be painful in the mid arc of
abduction. Patients are commonly 40–60 years of age. Diagnosis needs to
be reconsidered in patients under the age of 40 years, as their impinging
symptoms could be secondary to instability.
Impingement is a blanket term, and covers pinching of the tendons,
bursitis, tendinopathy and swollen tendons, so the favoured term used now
is subacromial pain syndrome [10]. Generally, the space under the acromion
Impingement/subacromial bursitis/tendinopathy 29
180° Acromioclavicular
painful arc
170°
Painless 120°
Glenohumeral
painful arc
45°–60°
Painless
Figure 2.4 Figure showing painful arc of the shoulder.
is reduced and compromised and becomes inflamed. Posture contributes, as
a protracted shoulder girdle and chin poke posture reduces the subacromial
space. A winging scapula also worsens this problem. Pectoralis muscle
tightness and a tight posterior capsule also makes the shoulder sit forward
again decreasing the subacromial space.
Physiotherapy is the first line of treatment for impingement symptoms,
and many patients improve with this alone. However, if a patient is struggling
to perform the exercises prescribed by the physiotherapist, or if the pain is
persistent despite physiotherapy, then an injection may be indicated. The
injection should be performed into the subacromial space, and the patient
should recommence their physiotherapy regime within a week post injection.
30 Shoulder and elbow injections
Kang et al. [11] found that unguided subacromial injections were 70% accurate
and the patient improves whether the injection was accurate or not, therefore
palpation guided is normally adequate. For the technique, see the section ‘How
to Inject the Subacromial Space’.
FROZEN SHOULDER/JOINT STIFFNESS
Frozen shoulder, also known as adhesive capsulitis, is a painful condition in
which the patient presents with an insidious onset of pain affecting usually
the upper arm around the distal deltoid insertion. Frozen shoulder commonly
affects patients in the 40–60 years’ age group. The pain can be quite extreme in
the early stages, known as the freezing stage. Movement is then progressively lost
and the shoulder becomes stiff and ‘frozen’. There is a gradual loss of both active
and passive glenohumeral joint motion resulting from progressive fibrosis and
ultimate contracture of the glenohumeral joint capsule [12]. In frozen shoulder,
pain does improve over time, but the patient can be left with residual stiffness
and improvement can take more than a couple of years, so earlier treatment is
indicated. It is described as a self-limiting condition, with duration averaging
from 1 to 3 years [13]. It is common in diabetics especially if uncontrolled
[14]. The capsule, which is normally loose and elastic to allow full range of
motion, becomes inflamed and contracted. Movement is lost and the shoulder
becomes passively stiff, especially external and internal rotation. X-rays must be
performed to exclude other pathologies like osteoarthritis. Physiotherapy can
help to restore movement via exercises, stretching and mobilisations. However,
if the patient is in significant pain an injection into the glenohumeral joint can
be offered to help reduce the pain so that physiotherapy can be commenced.
Koh [15] found that steroid injection with physiotherapy was superior to
physiotherapy alone in the short term and should be used especially in the early
stages when pain is the predominant presentation. The technique for this is the
same as for osteoarthritis of the shoulder, described later. Physiotherapy should
commence approximately one-week post injection to optimise the window of
pain relief to enable effective stretching and mobilising.
DEGENERATIVE ROTATOR CUFF TEARS
The rotator cuff tendons lose blood supply with age and become more fragile.
Degenerative tears usually occur in those over 70 years of age. Tears can occur
Diagnostic injection 31
in a degenerative manner without trauma due to the fragile nature of the
avascular tendon. Often these tears are not suitable for repair, as it is likely
to fail due to the friable nature of the tissues, and often fatty atrophy of the
muscle has occurred so these patients cannot be rehabilitated despite surgical
repair. A chronic degenerative rotator cuff tear could present on x-ray with a
high-riding humeral head, as it has lost the dynamic pull of the cuff muscles.
This leads to a reduction in the subacromial space, so often the patient’s pain
is impinging in nature. The loss of muscle function can present with a patient
having difficulty actively elevating the arm, leading to functional difficulties.
The first line of treatment should again be physiotherapy to help rehabilitate
the anterior deltoid [16]. However, if the patient struggles to perform the
exercises, then an injection into the subacromial space could be utilised to
provide pain relief. Again, the patient should recommence the physiotherapy
regime within a week post injection to maximise the window of pain relief
the injection provides. Acute traumatic rotator cuff tears in patients under 70
should not be injected if a surgical repair is in consideration [17].
CALCIFIC TENDINITIS
Calcific tendinitis is a painful condition in which calcium hydroxyapatite crystals
are deposited in the rotator cuff tendon [18] (Figure 2.5). This causes an increase in
pressure and a chemical reaction which is extremely painful. It is not known what
causes this, but commonly it presents patients 30 to 60 years old, is more common
in diabetics and can disperse itself with time. However, due to the painful nature
of the condition, injection is often the treatment of choice to help relieve the
pain. Maugars et al. [19] found that majority of patients with calcifications had
significant improvements in pain and function following subacromial injection.
The patient is then able to move and exercise more freely, and the problem can
settle. The injection should be in the subacromial space for this condition.
DIAGNOSTIC INJECTION
A patient can sometimes present with multiple pathologies around the
shoulder, and it can be unclear which is the predominant site of their pain.
For example, a patient with glenohumeral joint osteoarthritis on x-ray might
have symptoms stemming from the subacromial space due to impingement,
or a patient with impinging symptoms may be stemming from the ACJ.
32 Shoulder and elbow injections
Figure 2.5 X-ray showing calcific deposit in the rotator cuff (arrow).
Local anaesthetic can be injected in isolation and the patient reassessed after
30 minutes to differentiate the location of the patient’s symptoms.
WHAT ARE THE CONTRAINDICATIONS FOR
INJECTION OF THE SHOULDER?
The following are absolute and relative contraindications.
Absolute:
●● Allergy
●● Local or systemic infection
●● Active rash/broken skin at site of injection
●● Uncontrolled coagulopathy/bleeding diathesis/anticoagulation
●● Fracture/unstable joint
Relative:
●● Injection in tendon regions at high risk of rupture
●● Needle phobia
Which drugs to use? 33
●● Pregnant or breastfeeding patient
●● Prosthetic joint (a subacromial injection can be performed if the rotator
cuff is intact)
WHAT ARE THE RISKS?
The patient should be informed of the risk of infection (<0.001%) and risk
of allergic reaction, and diabetics should be informed that it may cause an
increase in their blood sugars for up to a week and can cause facial flushing.
Tendon rupture can occur although uncommon (0.1%). In superficial
injections, there is a risk of fatty atrophy and skin depigmentation, but
these are only possible with ACJ injections and do not normally occur in
subacromial or glenohumeral joint injections. The patient should also be
informed of the risk of flare which can cause a worsening of symptoms for
24–48 hours’ post injection. Patients should be advised to rest and avoid
repetitive heavy use of the upper limb for 24–48 hours’ post injection to reduce
the risk of steroid flare. The patient should also be informed that the injection
may not work. Verbal informed consent should be taken and this documented
in the medical notes. Informed consent requires a discussion with the patient
regarding the risks and potential benefits of injection with the patient. Written
information should also be provided.
Repetitive injections over short timescales can increase the risk of
infection and tendon rupture. It is therefore not recommended to perform a
repeat injection within a 3-month period. It is not generally recommended to
perform more than two or three injections for the same condition unless a long
period of time (that is a matter of years) has passed. Repetitive injections tend
to become less effective, and can lead to osteonecrosis or steroid arthropathy.
If injections do not work they should not be repeated; alternative treatment
options should be considered.
WHICH DRUGS TO USE?
Which local anaesthetic is commonly used?
●● 1–4 mL of 1% or 2% lidocaine can be mixed with Depo-Medrone or
individually in separate syringes.
●● Bupivacaine is a long-acting, local anaesthetic and is preferred for
diagnostic injections.
34 Shoulder and elbow injections
BOX 2.1 Where, how and who can perform shoulder and
elbow injections?
Primary Image Trained
Site care?a guidance? AHP?a
Glenohumeral joint Yes No Yes
Acromioclavicular joint No Yes No
Subacromial space Yes No Yes
Tennis elbow Yes No Yes
Golfer’s elbow Yes No Yes
Abbreviation: AHP, allied health professional.
a These injections should only be performed by appropriately trained
personnel
who have knowledge of local anatomy and good clinical skills.
Which formulations are preferred for
joint injections?
Depo-Medrone is the steroid preparation which is listed for most injections,
but an equivalent dose of another corticosteroid, for example triamcinolone
(40 mg) with 0.5% bupivacine can be used. 9 mL is the recommended volume,
as it is useful to get the steroid around the space.
Hyaluronan also has anti-inflammatory benefits, as well as coating pain
receptors, stimulating endogenous synovial fluid production and lubrication
effects. It also seems to have a role in degenerative synovial joint disease where
surgery is not indicated (Box 2.1).
HOW TO INJECT THE GLENOHUMERAL JOINT?
The glenohumeral joint is most easily accessed from the posterior approach.
The patient sits with their arm resting at their side with the shoulder in neutral
rotation resting on their lap. The sulcus between the head of the humerus and
acromion is identified with the hand (Figure 2.6). From behind, palpate the
tip of the acromion and identify the coracoid process (Figure 2.7). The needle
is inserted 2.5 cm inferior and medial to the posterolateral corner of the
acromion and directed anteriorly towards the coracoid process (Figure 2.8).
How to inject the glenohumeral joint? 35
Figure 2.6 Markings for posterior approach to the glenohumeral joint with
the arrow pointing towards 2.5 cm inferior and medial to the posterior border
of acromion for entry of the needle.
Figure 2.7 Front view indicating the markings for the coracoid process (arrow)
for the direction of the needle for glenohumeral joint.
36 Shoulder and elbow injections
Figure 2.8 Posterior approach to the glenohumeral joint with index finger
placed over the acromion and the needle entry from the posterior point aiming
towards the tip of the index finger.
The plunger should push with great ease and no resistance if you are in the
glenohumeral joint.
●● Needle: 18G or 21G, inserted to a depth of approximately 4 cm
●● Steroid: Depo-Medrone 40 mg
ANTERIOR APPROACH TO THE
GLENOHUMERAL JOINT?
Injection can be done for the glenohumeral joint from the anterior approach
with needle entry 1 cm inferior to the acromioclavicular joint and medial
towards the head of humerus, lateral to the coracoid process by 1 cm and
directed posteriorly at a slight superior and lateral angle. The anterior approach
is less commonly used than the posterior due to the relative proximity of the
large vessels and brachial plexus. Again, an 18-gauge needle should slip into
the joint completely and the injection have no resistance (Figure 2.9).
How to inject the acromioclavicular joint? 37
Figure 2.9 Anterior approach to glenohumeral joint injection. Portal is 1 cm
lateral to coracoid process aiming for the glenoid.
HOW TO INJECT THE ACROMIOCLAVICULAR
JOINT?
Where there is diagnostic uncertainty, this injection should be undertaken
under ultrasound guidance to aid accurate placement of the injection.
The acromioclavicular joint is identified 1 cm medially from the tip of the
acromion. It can be felt to move when the shoulder is shrugged. The patient
sits with their arm hanging by their side and the needle is inserted at an
angle of 30° medially as the joint sits at an angle and at an angle of about
70° to the horizontal. This can be a difficult joint to inject, but ‘walking’
the needle slowly and gently across the acromion can help in identifying
the acromioclavicular joint. The joint is a small joint with a volume of
about 2–3 mL (Figure 2.10). Mark the acromion and the end of clavicle and
your site of entry. Use 1 mL of triamcinolone and 1 mL of 2% lidocaine.
In obese people, it can be very difficult to palpate the joint and injection is
38 Shoulder and elbow injections
Figure 2.10 Picture showing surface marking for the injection to the
acromioclavicular joint. Note the angle of the needle to the joint.
better performed under image intensifier guidance. Warn patients about
discoloration and thinning of the skin, which can occur after this injection.
●● Needle: 25G, inserted 1 cm
●● Steroid: Depo-Medrone 20 mg
HOW TO INJECT THE SUBACROMIAL SPACE?
The patient sits with the arm hanging by their side (Video 2.4). This opens the
subacromial space between the acromion and humeral head. The lateral edge
of the acromion should be palpated and the needle inserted below the midpoint
of the acromion. Mark the skin entry point 2.5 cm medial to the point of the
posterior point of the acromion and 2.5 cm inferior. Mark the entry point with
the sheathed needle. Palpate the anterior acromion to show the direction the
How to inject the subacromial space? 39
Figure 2.11 Picture showing posterior portal for injection into the subacromial
space with the needle entering 2.5 cm medial and inferior to acromion and the
index finger pointing to the anterior tip of acromion.
needle will go (Figure 2.11). A long needle should be placed at a depth of 2–3 cm
anterior to the posterolateral corner of the acromion and the syringe plunger
should push easily with no resistance during injection. If any resistance is
encountered, the needle should be withdrawn and readjusted aiming more
superiorly under the acromion, as the common error is to inject into the rotator
cuff tendon. This should be avoided due to the proteolytic nature of
corticosteroids.
●● Needle: 21G, inserted 3 cm
●● Steroid: Depo-Medrone 40 mg
This space can also be accessed through the lateral portal by asking the
patient to relax the arm by their side and aiming from the lateral side in
the middle of the acromion about 1–2 cm away from the lateral edge of the
acromion. This approach has a higher risk of an injection into the rotator cuff
tendon (Figure 2.12).
40 Shoulder and elbow injections
Figure 2.12 Figure showing a lateral approach to injection of the subacromial
space approximately 1–2 cm lateral to the lateral edge of the acromion.
HOW TO INJECT THE ELBOW JOINT?
Elbow osteoarthritis is uncommon and injection of the joint should only be
undertaken following appropriate imaging. The elbow capsule houses the
radio-humeral, radio-ulnar and humero-ulnar joints (Figure 2.13). The joint
is most easily accessed from a lateral approach. The patient sits with the elbow
at 90° of flexion. The needle is inserted into the space between the head of the
radius and the olecranon process of the humerus, with the needle parallel to
the top of the radius (Figure 2.14).
●● Needle: 25G, inserted 2 cm
●● Steroid: Depo-Medrone 40 mg
HOW TO INJECT FOR TENNIS ELBOW?
Tennis elbow is a chronic degeneration of a tendon on the lateral side of
the elbow. It is also known as ‘lateral epicondylitis’. Usual treatment of this
How to inject for tennis elbow? 41
Figure 2.13 Image showing markings for the lateral portal for injection into
the elbow joint.
Figure 2.14 Illustration of injection technique into the elbow joint. The needle
is inserted into the space between the head of the radius and the olecranon
process of the humerus, with the needle parallel to the top of the radius.
42 Shoulder and elbow injections
Figure 2.15 The injection for the lateral epicondylitis is usually given at the
most tender point just distal to the lateral epicondyle and is spread around the
point in a pepper-pot technique.
condition is physiotherapy and analgesia or strapping. If the condition does
not respond to the aforementioned treatments, injections are often used.
Steroid injections are the most commonly used injections, but they generally
wear off after a few months and may need repeating. The role of steroid
injections is highly controversial. More recently platelet-rich plasma (PRP)
injections have shown to be more effective than steroid injections but are
much more expensive.
The cause of this condition is repetitive use of the extensor tendons at the
elbow, originating from the extensor carpi radialis brevis (ECRB) tendon,
and usually the injection is given into the most tender point just distal to the
lateral epicondyle. The injection is usually spread over the area in a pepper-pot
technique. Be aware of the skin discoloration, and fat necrosis is common after
this technique and it can be very painful (Figure 2.15).
HOW TO INJECT FOR GOLFER’S ELBOW?
Golfer’s elbow is a chronic degeneration of a tendon of the medial side of the
elbow. It is also known as ‘medial epicondylitis’. The causes are like tennis
elbow. Although the exact cause of golfer’s elbow is not known, it does tend
How to inject for golfer’s elbow? 43
Figure 2.16 Figure showing injection for golfer’s elbow that is usually given
at the most tender point just distal to the medial epicondyle and is spread in
the area in a pepper-pot technique. Be aware of injecting into the ulnar nerve.
to occur after repetitive use of the forearm and wrist. It is does not only affect
golfers. Usual treatment of this condition is physiotherapy and analgesia
or strapping. If the condition does not respond to the above treatments,
injections are often used.
The disease is usually due to tendinopathy to the affected flexor muscles
just distal to the tip of the medial epicondyle. The injection is given into the
most tender point just distal to the medial epicondyle and injection is usually
spread over the area in a pepper pot technique. Be aware of skin discoloration,
and fat necrosis is common after this technique and it can be very painful.
Also refrain from injecting into the ulnar nerve that is just posterior to the
medial epicondyle (Figure 2.16).
TAKE-HOME MESSAGES
●● Always take informed consent, and discuss risks and benefits
(address expectations).
●● Injection is used for pain relief only.
44 Shoulder and elbow injections
●● Ask the patients to rest the joint for 24–48 hours post injection
(initially pain gets worse).
●● Always combine injection with physiotherapy, which should
ideally commence within 1–2 weeks of injection.
●● Warn patients that repeated injections pose greater risks and are
less likely to be effective and can damage joints.
VIDEOS
Video 2.1 Physiotherapy for frozen or stiff shoulder.
(https://youtu.be/_3ojJMPvxhY)
Video 2.2 Physiotherapy for painful shoulder.
(https://youtu.be/2NsgqaSt4lE)
Video 2.3 Shoulder exercises (strengthening and late rehabilitation).
(https://youtu.be/3OhD-xq6ivI)
Video 2.4 How to perform injection for subacromial impingement.
(https://youtu.be/rDc61zXwwEE)
REFERENCES
1. Fujisawa H, Suenaga N, Minami A. Electromyographic study during
isometric exercise of the shoulder in head-out water immersion.
J Shoulder Elbow Surg. 1998;7(5):491–4.
2. Saccomanni B. Inflammation and shoulder pain – A perspective on
rotator cuff disease, adhesive capsulitis, and osteoarthritis: Conservative
treatment. Clin Rheumatol. 2009;28(5):495–500.
3. Zheng XQ, Li K, Wei YD, Tie HT, Yi XY, Huang W. Nonsteroidal anti-
inflammatory drugs versus corticosteroid for treatment of shoulder
pain: A systematic review and meta-analysis. Arch Phys Med Rehabil.
2014;95(10):1824–31.
4. Zufferey P, Revaz S, Degailler X, Balague F, So A. A controlled trial of
the benefits of ultrasound-guided steroid injection for shoulder pain.
Joint Bone Spine. 2012;79(2):166–9.
References 45
5. Sage W, Pickup L, Smith TO, Denton ER, Toms AP. The clinical and
functional outcomes of ultrasound-guided vs landmark-guided
injections for adults with shoulder pathology – A systematic review and
meta-analysis. Rheumatology (Oxford). 2013;52(4):743–51.
6. Schairer WW, Nwachukwu BU, Mayman DJ, Lyman S, Jerabek
SA. Preoperative hip injections increase the rate of periprosthetic
infection after total hip arthroplasty. J Arthroplasty. 2016;31(9
Suppl):166–9.e1.
7. Bedard NA, Pugely AJ, Elkins JM, Duchman KR, Westermann RW,
Liu SS, Gao Y, Callaghan JJ. The John N. Insall Award: Do intraarticular
injections increase the risk of infection after TKA? Clin Orthop Relat
Res. 2017;475(1):45–52.
8. Lim CS, Miles J, Peckham TJ. Current practice of obtaining informed
consent for local steroid injection among the shoulder and elbow
surgeons in United Kingdom. Scott Med J. 2010;55(3):32–4.
9. Hegedus EJ, Zavala J, Kissenberth M, Cook C, Cassas K, Hawkins
R, Tobola A. Positive outcomes with intra-articular glenohumeral
injections are independent of accuracy. J Shoulder Elbow Surg.
2010;19(6):795–801.
10. Diercks R, Bron C, Dorrestijn O, Meskers C, Naber R, de Ruiter T,
Willems J, Winters J, van der Woude HJ. Guideline for diagnosis and
treatment of subacromial pain syndrome: A multidisciplinary review by
the Dutch Orthopaedic Association. Acta Orthop. 2014;85(3):314–22.
11. Kang MN, Rizio L, Prybicien M, Middlemas DA, Blacksin MF.
The accuracy of subacromial corticosteroid injections: A comparison
of multiple methods. J Shoulder Elbow Surg. 2008;17(1 Suppl):61S–66S.
12. Neviaser AS, Hannafin JA. Adhesive capsulitis: A review of current
treatment. Am J Sports Med. 2010;38(11):2346–56.
13. Maund E et al. Management of frozen shoulder: A systematic review and
cost-effectiveness analysis. Health Technol Assess. 2012;16(11):1–264.
14. Ewald A. Adhesive capsulitis: A review. Am Fam Physician.
2011;83(4):417–22.
15. Koh KH. Corticosteroid injection for adhesive capsulitis in primary
care: A systematic review of randomised clinical trials. Singapore Med
J. 2016;57(12):646–57.
16. Ainsworth R. Physiotherapy rehabilitation in patients with
massive, irreparable rotator cuff tears. Musculoskeletal Care. 2006;
4(3):140–51.
46 Shoulder and elbow injections
17. Lazarides AL, Alentorn-Geli E, Choi JH, Stuart JJ, Lo IK, Garrigues
GE, Taylor DC. Rotator cuff tears in young patients: A different disease
than rotator cuff tears in elderly patients. J Shoulder Elbow Surg.
2015;24(11):1834–43.
18. Siegal DS, Wu JS, Newman JS, Del Cura JL, Hochman MG. Calcific
tendinitis: A pictorial review. Can Assoc Radiol J. 2009;60(5):263–72.
19. Maugars Y et al. Treatment of shoulder calcifications of the cuff: A
controlled study. Joint Bone Spine. 2009;76(4):369–77.
3
Hand and wrist injections
SUNIL GARG
INTRODUCTION
Hand and wrist conditions such as arthritis of the first carpometacarpal joint,
De Quervain’s tenosynovitis, trigger finger and carpal tunnel syndrome are
commonly seen in primary care, physiotherapy assessments, rheumatology
and orthopaedic clinics. Most of these conditions can be diagnosed by
taking a focused history and performing specific clinical examinations.
Early diagnosis and simple interventions such as modification of life style,
physiotherapy, targeted joint and soft tissue injections can help in initial
management of these conditions.
Musculoskeletal injections are an established therapy, embedded in
standard clinical practice for many years. This chapter aims to provide
contemporary, evidence-based approach to soft tissue and joint injections,
and demonstrates simple yet effective techniques in management of common
wrist and hand conditions.
Soft tissue and joint injections discussed in this chapter can be given by
trained practitioners in the field of general/family practice, orthopaedics,
pain medicine, rheumatology, radiology and physiotherapy. It cannot be
overemphasised that knowledge of local and regional anatomy and good clinical
skills are essential for the practitioners who are performing these injections
(Box 3.1).
CARPAL TUNNEL SYNDROME
Carpal tunnel syndrome (CTS) is an entrapment neuropathy caused by
compression of the median nerve as it travels through the carpal tunnel within
the wrist (Figure 3.1). It is the most common nerve entrapment neuropathy.
47
48 Hand and wrist injections
BOX 3.1 A guidance to the setting of hand and wrist
injections
Site Primary care?a Image guidance? Trained AHP?a
Carpal tunnel Yes USG can be useful Yes
De Quervain’s Yes USG can be useful Yes
1st CMCJ Yes Fluoroscopy can be useful Yes
Trigger finger Yes No Yes
Abbreviations: AHP, allied health professional; CMCJ, carpometacarpal joint; USG,
ultrasound guidance.
a These injections should only be performed by appropriately trained personnel
who have knowledge of local anatomy and good clinical skills.
Figure 3.1 The surface marking of the carpal tunnel and course of the median
nerve.
Carpal tunnel syndrome 49
Early symptoms of CTS include numbness, tingling and pain (that increases
at night) in the thumb, digits 2 and 3, and the radial half of digit 4. Weakness,
clumsiness and temperature changes also are common complaints. In the
early presentation of the disease, symptoms most often present at night when
lying down and are relieved during the day. Patients with CTS may report
improvement in symptoms when they flick their hand and wrist. With further
progression of the disease, symptoms may also be present during the day,
especially with certain repetitive activities, such as drawing, typing or playing
video games. In more advanced disease, symptoms can be constant.
What causes CTS?
CTS is multifactorial. A specific cause is not known, but it is most likely any
condition that generates increased pressure in the carpal tunnel and results
in the obstruction of venous outflow. This leads to further oedema, causing
constriction and potential ischaemia to the median nerve with dysfunction
of axonal transport. Any of the nine flexor tendons travelling through
the carpal tunnel can become inflamed and compress the median nerve.
Typical occupations of patients with CTS include those who use computers
for extended periods of time, construction workers (especially those using
equipment that have vibration), and any other occupation that requires
frequent, repetitive movement.
Diagnosis of CTS is based on clinical presentation, examination and
nerve conduction studies. There is no single clinical sign diagnostic of CTS.
Direct compression of the median nerve, Phalen’s test and Tinel’s sign are the
commonest clinical signs used by clinicians worldwide. The sensitivity and
specificity of these tests is variable. The benefit and value of electrodiagnostic
testing in CTS is also debated. Current best evidence suggests that the
combination of clinical diagnosis and electrodiagnosis of CTS can better confirm
the diagnosis than either alone. On the other hand, the practice of carrying
out nerve conduction studies in all patients with suspected CTS can lead to a
delay in definitive treatment, entailing substantial additional costs. The author
therefore reserves nerve conduction studies for cases when clinical diagnosis
is in doubt.
How is CTS treated?
The only confirmed disease-modifying treatment for CTS is surgical
decompression and release of the median nerve. Non-surgical treatment,
50 Hand and wrist injections
however, is tried in most cases and can be effective in early presentation.
Conservative treatment includes the use of splints, lifestyle modification,
physiotherapy, use of anti-inflammatories and local steroid injection.
The most likely mechanism of action of corticosteroid injections is by
reduction in inflammation and swelling in the carpal tunnel. Cochrane
Review evidence suggests that there is short-term improvement of symptoms
following a steroid injection for CTS. The longer-term effects beyond 3 months
are uncertain [1–3].
What is the technique of steroid injection?
It is advisable to provide the patient with an information leaflet before the
steroid injection (Video 3.1). Rest the patient’s hand and wrist on a stable
surface such as the consultation table. Figure 3.1 illustrates the surface
marking of the carpal tunnel and the course of the median nerve. Palpate
anatomical landmarks on the volar aspect of the wrist are the palmaris
longus tendon and proximal wrist crease. The palmaris longus can be easily
located by asking the patient to join the tips of thumb and little finger which
makes this tendon prominent (Figure 3.2). The point of needle entry is just
ulnar to the palmaris longus and proximal to the wrist crease (Figure 3.3).
Figure 3.2 Showing how to locate the palmaris longus tendon.
Carpal tunnel syndrome 51
Figure 3.3 Showing the approximate entry point of needle for carpal tunnel
injection.
Some patients do not have a palmaris longus, and if this is the case, the
injection site can be just ulnar to the midline of the wrist or just ulnar to the
flexor carpi radialis tendon. Identify the area to be injected, the point of
entry and direction of needle travel. Clean the skin with an antiseptic and
let it dry. A 5 mL syringe is used. The injection constituents are mixed: 1 mL
(40 mg) of steroid (Kenalog) and 2 mL of local anaesthetic (lignocaine 1%).
The total volume can vary but try not to inject more than 5 mL. Insert the
blue/orange needle ulnar to the palmaris longus tendon at the level of the
proximal wrist crease directing the needle towards the mouth of carpal
tunnel. Insert the needle approximately 5 mm–8 mm (depending upon the
subcutaneous fat) in the direction of carpal tunnel. Always aspirate before
injecting. Do not inject against resistance. If there is severe pain during
injection, reposition the needle. After injection, withdraw the needle and
gently massage the injection site to spread the solution and apply a sterile
dressing. Ensure the appropriate disposal of sharps. The patient should be
advised to wait in the surgery for 30 minutes following injection or
alternatively ensure that they are accompanied by a responsible adult for
that time. Most patients report improvement in symptoms within 2 weeks
of the injection.
52 Hand and wrist injections
What are the complications of
steroid injection?
Patients may experience some redness, swelling and pain following the
injection, but this usually disappears in 2 to 3 weeks. There are reports of
accidental damage to a vessel or tendon. A good knowledge of local anatomy
is therefore vital to avoid the risks. The way the needle is placed is of particular
importance as intraneural injection will cause an inflammatory reaction
within the sheath of the nerve. This can lead to persistent symptoms and
significant damage of the median nerve. Histological studies and studies of
micro neural circulation have indicated that steroids can cause neurotoxicity.
DE QUERVAIN’S TENOSYNOVITIS
De Quervain’s stenosing tenosynovitis is a painful condition of the base of
thumb and wrist characterised by thickening of the sheath of the abductor
pollicis longus (APL) and extensor pollicis brevis (EPB) tendons. These tendons
cross under the extensor retinaculum in the first dorsal compartment of the
wrist. The condition takes its name from the Swiss physician De Quervain
who first described a case series of five patients in 1895. Risk factors include
repetitive or forceful manual work and pregnancy. The patient typically
complains of pain over the radial styloid process upon the use of thumb and
wrist. On clinical examination, there is tenderness over the radial side of the
wrist and symptoms can be elicited clinically by means of Finkelstein’s test
(deviating the wrist to the ulnar side while grasping the thumb, resulting in
pain).
What is the treatment of de quervain’s
tenosynovitis?
Non-surgical treatment includes rest, splinting and physiotherapy.
Corticosteroid injection is the mainstay of treatment for those patients who
do not respond to the aforementioned. Other described treatments include
acupuncture, hyaluronic acid injections, ultrasound-guided percutaneous
needle tenotomy, platelet-rich plasma injection and prolotherapy. Surgery is
reserved for failure of conservative modalities and involves release of the first
dorsal compartment.
De Quervain’s tenosynovitis 53
A number of randomised controlled trials have shown that corticosteroid
injection results in a statistically significant increase in resolution of
symptoms, pain relief and increased function in the treatment of De Quervain’s
disease [4–6].
What is the technique of steroid injection?
The steroid injection can be done with or without ultrasound guidance
(Video 3.2). The use of ultrasound increases the accuracy of steroid placement.
The simple method of steroid injection without the use of ultrasound scan is
also very effective (up to 70% patients experience pain relief by one to two
injections).
The injection is best done in the clinic setting. The aim of injection is to
place the steroid into the tendon sheath of the APL and EPB within the first
dorsal compartment of the extensor retinaculum.
Rest the ulnar border of the wrist over the edge of a consultation table that
may allow ulnar deviation of the wrist with the hand hanging down exposing
the radial aspect of the wrist.
Palpate the anatomical landmarks of the anatomical snuffbox: the tip of
the radial styloid, and tendons of the EPB and APL (Figure 3.4). Identify the
area to be injected, the point of entry (distal to proximal) and direction of
needle travel (distal to proximal). Clean the skin over the radial styloid with
antiseptic and let it dry. Load the syringe with steroid and local anaesthetic
Figure 3.4 Surface marking of APL, EPB, radial styloid and extensor pollicis
longus (EPL) (anatomical snuffbox).
54 Hand and wrist injections
Figure 3.5 The technique of injection for De Quervain’s.
in a 5 mL syringe, total volume around 3 mL (volume can vary but try and
not inject more than 5 mL). Insert the needle approximately 1 cm proximal
to the radial styloid, aiming for the sheath of the EPB and APL tendons,
almost parallel to the tendons. Insert the blue needle for 1–2 cm, remaining
superficial to the tendon substance (Figure 3.5). Aspirate and inject, spreading
the 3 mL of solution in a 1 cm area. Withdraw the needle and gently massage
the injection site to spread the solution and then apply a sterile dressing.
Most patients report symptomatic relief within 10 days of the injection.
The chances of failure of injection are slightly high in obese patients and in
those patients with abnormal anatomy. As a general rule, if one injection done
in the primary care has not worked, the patient should be referred to see a
consultant. Alternative diagnosis of first carpometacarpal joint arthritis and
intersection syndrome should also be considered before attempting a second
injection. Multiple injections should be avoided. If two steroid injections fail
and the diagnosis of De Quervain’s is confirmed, then a surgical release is
recommended.
FIRST CARPOMETACARPAL JOINT
OSTEOARTHRITIS
Arthritis at the base of thumb is a common painful condition of old age, more
common in women in the fifth to seventh decades. The main symptoms of first
carpometacarpal joint osteoarthritis (1st CMCJ OA) are pain and stiffness at
First carpometacarpal joint osteoarthritis 55
the base of the thumb. The thumb performs a very important role in the hand,
enabling grip and pinch movements.
Examination findings include tenderness on compression of the CMCJ,
limited range of motion, crepitation, a bony prominence resulting from
osteophyte formation and radial subluxation of the base of the first metacarpal.
Radiographic changes of 1st CMCJ OA include varying degrees of joint-space
narrowing and periarticular bony sclerosis dividing the condition into four
grades of severity.
What causes 1st CMCJ OA?
The aetiology of 1st CMCJ OA is complex. It stems from weakness or laxity of
the basal thumb joint ligaments causing instability and subluxation. In time,
this leads to degeneration of articular cartilage.
What is the treatment of 1st CMCJ OA?
A range of non-operative and operative management options can be used
to treat 1st CMCJ OA. A range of surgical techniques have been employed
over the years, but the mainstay is trapeziectomy. This can be performed with
or without ligament interposition, although this may confer no additional
benefit. Other surgical options include joint replacement or fusion. First-line
treatment includes activity modification, analgesic and anti-inflammatory
tablets, physiotherapy, acupuncture and splints to support the thumb.
When these first-line treatments cease to control symptoms, intra-articular
injections can be considered [7–9]. Significant improvement in pain and
hand function can be achieved with a single corticosteroid injection. The
duration of symptomatic improvement can vary significantly, and the level of
improvement achieved is not related to the radiological stage. Some surgeons
prefer to use hyaluronic acid instead of steroids.
What is the injection technique for
1st CMCJ OA?
Rest the ulnar aspect of the wrist on a stable surface such as the consultation
table, exposing the base of thumb and anatomical snuffbox (Video 3.3). Palpate
the bony base of the first metacarpal and feel it from distal to proximal as it
suddenly dips into a soft spot, which is essentially the 1st CMCJ (Figure 3.6).
Clean the skin with antiseptic and let it dry. Load the 5 mL syringe with 40 mg
56 Hand and wrist injections
Figure 3.6 The surface marking of the first metacarpal base and radial styloid.
of Kenalog (1 mL) steroid and 2 mL of local anaesthetic (lignocaine 1%).
Distract the thumb to open up the 1st CMCJ. Insert the needle towards the base
of first metacarpal aiming for 1st CMCJ as shown in Figure 3.7. Advance the
needle for 5 mm to 1 cm. Aspirate and inject the solution, which would flow
without much resistance if the needle is in joint space.
Figure 3.7 Showing the entry point and direction of needle for 1st CMCJ OA
injection.
Trigger finger 57
TRIGGER FINGER
Trigger finger is a common finger ailment thought to be caused by
inflammation and subsequent narrowing of the A1 pulley, which causes pain,
clicking, catching and loss of motion of the affected finger.
What causes trigger finger?
Although it can occur in anyone, it is seen more frequently in the diabetic
population and in women, typically in the fifth to sixth decade of life. The initial
complaint associated with trigger finger is usually a painless clicking with digital
manipulation. Further development of the condition can cause the catching to
become more frequent and painful with both flexion and extension, and be
related as occurring at either the metacarpophalangeal (MCP) or proximal
interphalangeal joints. A painful nodule, a result of intratendinous swelling,
may be palpated in the palmar MCP area. The patient may report MCP stiffness
or swelling in the morning, or that they awaken with the digit locked and that it
loosens throughout the day. A history of recent trauma to the area may also be
reported. With continued deterioration the finger may present locked in flexion,
requiring passive manipulation to achieve full extension. This occurs because
the flexor mechanisms of the digit are generally strong enough to overcome the
restrictive and narrowed A1 pulley, while the extensors are not. The diagnosis is
usually fairly straightforward, but other pathological processes such as fracture,
tumour or other traumatic soft tissue injuries must be excluded.
What is the treatment of trigger finger?
Treatment modalities include splints, corticosteroid injections or surgical
release. A corticosteroid injection given at the base of the A1 pulley is usually the
first line of treatment in most patients with relief reported in majority [10–12].
Splints are only offered if the patient refuses corticosteroid injection.
Does the corticosteroid injection work?
The risks following the injection are low. The main complication is self-
limiting pain at the injection site. Other complications are rare, and include
dermal or subcutaneous atrophy, hypopigmentation of the skin, infection
of the flexor sheath and, rarely, rupture of the flexor tendon. Erratic glucose
58 Hand and wrist injections
levels for up to 1 week after the injection are seen commonly in diabetics.
Corticosteroid injection with lidocaine was more effective than lidocaine
alone at 4 weeks (relative risk = 3.15; 95% confidence interval, 1.34 to 7.40)
in a couple of randomised controlled studies that involved 63 participants.
Thirty-four patients were allocated to receive corticosteroid and lidocaine
(Xylocaine) injection, whereas 29 patients received lidocaine alone injection.
No adverse events or side effects were reported [11,12].
What is the technique of trigger
finger injection?
The corticosteroid injection is best given in the clinic setting (Video 3.4). The
aim is to get the steroid into the space between the A1 pulley and the flexor
tendon avoiding the tendon substance. After explaining the procedure, and
its risks and benefits in detail, rest the patient’s hand on a stable surface such
as the consultation table, exposing the palm and the base of fingers. Palpate
the anatomical landmarks of the flexor tendon along the A1 pulley. It might
be possible to palpate the triggering nodule within the flexor tendon. Identify
the area of the A1 pulley (surface marking as shown in Figure 3.8) and the
approximate proximal edge of the A1 pulley (roughly the distal palmar
crease). This is the point of entry of the needle. Clean the skin with antiseptic
and let it dry. Load the 2 mL syringe with 1 mL steroid (Kenalog) and 1 mL
of local anaesthetic (lignocaine 1%). Use an orange needle to enter sharply into
the skin along the flexor tendon at the mouth of the A1 pulley surface mark.
Advance the orange needle for approximately 5 mm remaining superficial to
the tendon substance (Figure 3.9). Remaining outside the tendon sheath can
be tricky. The author’s preferred technique is to ask the patient to move the
finger into flexion and extension, and check if the needle also moves with the
finger. Withdraw the needle until it stops to move with the finger, aspirate and
inject spreading the steroid into the A1 pulley area. Finally, place a sticky
dressing over the injection site.
Most patients report symptomatic relief within 10 days of the injection.
Triggering recurs in some patients who should be offered another injection
or surgical release of A1 pulley. A second injection is typically half as likely to
succeed as the initial treatment. Surgery on the other hand is almost always
successful with a low complication rate [10].
Surgery of trigger finger entails releasing the A1 pulley under local
anaesthetic by a trained healthcare professional.
Trigger finger 59
Figure 3.8 The location of A1 pulleys.
Figure 3.9 The direction of needle for trigger finger injection.
60 Hand and wrist injections
TAKE-HOME MESSAGES
●● Focused history taking and examination is the key to diagnosis.
●● Most steroid injections for the wrist and hand are safe and easy to
perform in an outpatient setting by an experienced clinician.
●● Steroids injections are both diagnostic and therapeutic.
●● Knowledge of local anatomy is the key to a safe and successful
injection.
●● If one injection is not successful, alternative diagnosis and
further investigations should be considered.
VIDEOS
Video 3.1 How to perform injection for CTS.
(https://youtu.be/lyxKisHEABM)
Video 3.2 How to perform injection for De Quervain’s tenosynovitis.
(https://youtu.be/4IJUXMcOQOE)
Video 3.3 How to perform injection for 1st CMCJ OA.
(https://youtu.be/AqZxP3wQ7k8)
Video 3.4 How to perform injection for trigger finger.
(https://youtu.be/nxUbSuceroM)
REFERENCES
1. Atroshi I, Flondell M, Hofer M, Ranstam J. Methylprednisolone
injections for the carpal tunnel syndrome: A randomized, placebo-
controlled trial. Ann Intern Med. 2013; 159(5):309–17.
2. Chen PC, Chuang CH, Tu YK, Bai CH, Chen CF, Liaw M. A Bayesian
network meta-analysis: Comparing the clinical effectiveness of local
corticosteroid injections using different treatment strategies for carpal
tunnel syndrome. BMC Musculoskelet Disord. 2015 November; 16:363.
3. Burton C, Chesterton LS, Davenport G. Diagnosing and managing carpal
tunnel syndrome in primary care. Br J Gen Pract. 2014 May; 64(622):262–3.
4. Ashraf MO, Devadoss VG. Systematic review and meta-analysis on
steroid injection therapy for de Quervain’s tenosynovitis in adults. Eur
J Orthop Surg Traumatol. 2014 February; 24(2):149–57.
References 61
5. Peters-Veluthamaningal C, van der Windt DA, Winters JC, Meyboom-de
Jong B. Corticosteroid injection for de Quervain’s tenosynovitis.
Cochrane Database Syst Rev. 2009 July; (3):CD005616.
6. Cavaleri R, Schabrun SM, Te M, Chipchase LS. Hand therapy versus
corticosteroid injections in the treatment of de Quervain’s disease: A
systematic review and meta-analysis. J Hand Ther. 2016 January–March;
29(1):3–11.
7. Aebischer B, Elsig S, Taeymans J. Effectiveness of physical and
occupational therapy on pain, function and quality of life in patients
with trapeziometacarpal osteoarthritis – A systematic review and meta-
analysis. Hand Ther. 2016 March; 21(1):5–15.
8. Fowler A, Swindells MG, Burke FD. Intra-articular corticosteroid
injections to manage trapeziometacarpal osteoarthritis – A systematic
review. Hand (NY). 2015 December; 10(4):583–92.
9. Hamasaki T, Lalonde L, Harris P, Bureau NJ, Gaudreault N, Ziegler
D, Choinière M. Efficacy of treatments and pain management for
trapeziometacarpal (thumb base) osteoarthritis: Protocol for a
systematic review. BMJ Open. 2015 October; 5(10).
10. Ryzewicz M, Wolf JM. Trigger digits: Principles, management, and
complications. J Hand Surg Am. 2006 January; 31(1):135–46.
11. Chambers RG Jr. Corticosteroid injections for trigger finger. Am Fam
Physician. 2009 September; 80(5):454.
12. Peters-Veluthamaningal C, van der Windt DA, Winters JC, Meyboom-de
Jong B. Corticosteroid injection for trigger finger in adults. Cochrane
Database Syst Rev. 2009 January; (1):CD005617.
4
Hip and knee injections
ASHWIN KULKARNI AND KIMBERLY LAMMIN
INTRODUCTION
This chapter discusses injections into the hip and knee joints, and soft tissues
around these, covering indications, contraindications, how to administer
them and alternative therapies.
The most commonly performed injections around the hip joint are those
given into the lateral soft tissues around the hip for greater trochanteric pain
syndrome (GTPS). Intra-articular injections to the hip are less common and
generally routinely performed in the hospital setting with image intensifier
guidance. The most commonly performed injections around the knee joint
are intra-articular injections (and aspirations).
Injections into the soft tissues lateral to the hip and intra-articular knee joint
injections are usually given in an outpatient or primary care setting without any
imaging support, although ultrasound-guided injections have been increasingly
used around the lateral aspect of the hip, particularly in recalcitrant cases.
Injections into the hip joint, iliopsoas tendon, sacroiliac joint, ischial
tuberosity and hamstring area require imaging support to ensure accuracy and
avoid important structures such as nerves and blood vessels. Injections around
the knee which tend to routinely be performed with image guidance are Hoffa’s
fat pad, proximal tibiofibular joint and distal iliotibial band injections (Box 4.1).
INJECTIONS AROUND THE HIP JOINT
Greater trochanteric pain syndrome
Greater trochanteric pain syndrome (GTPS) is a common condition, previously
known as trochanteric bursitis. The underlying pathological anomaly is not
63
64 Hip and knee injections
BOX 4.1 A guidance to the setting of hip and knee
injections
Site Primary care?a Image guidance? Trained AHP?a
GTPS Yes No Yes
Hip joint No Yes No
Knee joint Yes No Yes
Abbreviations: AHP, allied health professional; GTPS, greater trochanteric pain
syndrome.
a These injections should only be performed by appropriately trained personnel
who have knowledge of local anatomy and good clinical skills.
solely bursitis, but also includes tendinopathy (gluteus medius and minimus
tendons), enthesopathy, degeneration (similar to the pathology in rotator
cuff problems), and external coxa saltans (snapping hip due to the iliotibial
band sliding over the greater trochanter) [1]. There may be an inflammatory
element, however, this is not the case in all patients.
Patients typically complain of lateral hip pain that is there almost all the
time. It may be related to activity, but often progresses to being present at rest
and is particularly prominent when lying on the affected side, disturbing sleep.
There are no specific diagnostic criteria for GTPS [2]. If patients complain
about pain in the groin, the hip joint must be suspected as a potential cause
of the pain in addition to trochanteric pain, and investigations performed
accordingly (anteroposterior [AP] pelvis x-ray). Up to two-thirds of patients
with GTPS have coexisting low back pain or hip osteoarthritis [3].
Clinical examination of patients with GTPS reveals a full range of
movement of hip joint, but often all movements are painful with the pain felt
laterally over the trochanteric area and tenderness at this site.
There are no specific investigations required to confirm the diagnosis
of GTPS and often imaging is only undertaken if the condition is
resistant to treatment, particularly if there is no response to injection. If
investigations are undertaken they initially include a plain hip x-ray (AP
pelvis and lateral views) of the affected hip to rule out arthritis. If this is
normal and there is doubt as to the diagnosis, ultrasound or MRI of the
hip can be done to confirm the diagnosis. MRI has a higher sensitivity
and specificity [4].
Patients with hip dysplasia can present with lateral or anterolateral hip
pain. A dysplastic hip can present in young patients with a labral tear and
anterolateral hip overload, or in older patients with early arthritis.
What are the indications and contraindications for lateral soft tissue hip injection? 65
WHAT ARE THE INDICATIONS AND
CONTRAINDICATIONS FOR LATERAL
SOFT TISSUE HIP INJECTION?
Indications for injection
●● Diagnostic injection
●● Therapeutic
– Trochanteric bursitis
– Trochanteric tendinopathy
– Soft tissue pain
– Inflammatory disease with localised trochanteric pain
– Enthesopathy
Contraindications to injection
●● Allergy
●● Local or systemic infection
●● Local skin breakdown or rash
●● Uncontrolled diabetes
●● Coagulopathy
●● Tendons at risk of rupture
●● Technical difficulty
●● Total hip replacement (relative)
●● Failure of a previous injection (relative)
Relative contraindications to injection
Previous failure of an injection is a relative contraindication to further
injection, as the reason for failure may be a technical error with the previous
injection not being given at the correct location. The presence of a hip
replacement on the same side is also a relative contraindication. The joint
surgery may have created a channel from lateral aspect of the hip directly
into the hip joint and therefore injection in this area may potentially pass
directly into the prosthetic hip joint, carrying a significant risk of introducing
infection in the joint. Many surgeons will still consider performing the
injection in cases of greater trochanteric pain syndrome, but only in a sterile
environment (e.g. operating theatre).
66 Hip and knee injections
Conditions in which injection may not work
1. Concurrent hip arthritis
2. Dysplastic hip
3. Deep tissue pain
4. Broad area of pain
5. Inflammatory disorder with widespread enthesitis
6. Sacroiliac pain
HOW TO PREPARE AND WHAT IS THE
TECHNIQUE FOR GTPS INJECTION?
The injection should be performed in appropriate premises where resuscitation
equipment and staff are available (Video 4.1).
Equipment required
●● Gloves
●● Antiseptic solution
●● Drawing up needle (no filter if using steroid)
●● Needle for injecting
●● Syringe
●● Local anaesthetic
●● Steroid
●● Cotton wool/swab
●● Sterile dressing
Pre-procedure checks
●● Correct patient
●● Confirm the indication for injection
●● Contraindications excluded
●● Is the patient on anticoagulants?
●● Any relevant allergies?
●● Procedure appropriately explained to the patient
●● Consent (verbal or written)
How to prepare and what is the technique for GTPS injection? 67
Patient position
The injection is best given with the patient in a lateral decubitus position with
the affected side up. Slight flexion of the hip and knee improves stability while
lying in this position (Figure 4.1).
Figure 4.1 (Top to bottom): Patient positioning and landmarks for GTPS
injection.
68 Hip and knee injections
Procedure
Approach the patient from behind and reassure them that you will explain
each step and warn them before performing the injection.
Locate and mark the site of the injection, palpate and confirm the site
of maximal tenderness, and then ask the patient not to change position, as
a change in position can move the tender spot away from the marked area
(Figure 4.1). Marking can be performed with a permanent marker; however,
most of these are affected by the skin preparation solution, so the mark may
wash away.
Use standard sterile precautions for injection. Use skin preparation and
the no-touch technique. Isolate the area with a sterile drape/drapes.
Use a 20 mL syringe and long green needle or angiocath needle for
injection. The length of the needle is critical in ensuring it can be delivered to
the target tissue which is often deeper than anticipated. Use a different needle
for aspiration of drugs and giving the injection.
The needle for injection is generally inserted at 90° to the skin, as the
desired injection site is deep, adjacent to the greater trochanter. Always
aspirate before injecting. Once the injection has been given, apply the sterile
dressing.
The patient should be asked about pain after the injection to assess the
effect and can be asked to keep a pain diary for up to 6 weeks post procedure.
Generally patients are asked to stay for 20 minutes after the procedure in
outpatients to ensure no adverse reactions occur.
Post-procedure follow-up is common at 6 or 12 weeks to assess the effect
of the injection and whether it has continued to work.
WHAT ARE THE INJECTION CONTENTS?
The local anaesthetic used can be long acting or short acting, or a mixture of
both. If a long-acting local anaesthetic is used, then the effects may not be evident
before the patient leaves the clinical setting, and therefore immediate feedback
as to whether the injection has improved the symptoms may not be possible.
The steroid used with the local anaesthetic can be either 80 mg of Kenalog or
Depo-Medrone. There is only limited evidence regarding the selection of which
local anaesthetic and steroid, but there is evidence showing greater improvement
with higher doses of steroid (80 mg rather than 40 mg) [3]. A 20 mL syringe is
required, which allows sufficient volume for dispersion locally.
What are the treatment options for GTPS? 69
WHAT IS THE EFFICACY OF INJECTIONS
FOR GTPS?
Trochanteric area injections work best when there is a single source of pain that
can be located pinpoint rather than a large area of tenderness or pain where
the target area is simply too large. The volume of the injection can aid it in
diffusing around the exact injection site, but not covering too large an area.
Injections have been shown to yield temporary symptomatic relief, with
recurrence of symptoms after a few months [5]. Higher doses of steroids (80 mg)
have demonstrated a greater effect than smaller doses [6].
Although ultrasound image guidance can be used to target specific tissues,
it has not been shown to increase the efficacy of the injections [7,8].
The injection may be the only treatment offered or one of multiple simultaneous
treatments, especially giving the injection to facilitate active physiotherapy.
WHAT ARE THE TREATMENT OPTIONS
FOR GTPS?
Despite being originally thought to be a self-limiting condition, a number of
patients suffer with GTPS, which lasts for a prolonged period and is recalcitrant
despite trials of several treatment modalities. Physiotherapy is most frequently
the first treatment tried and steroid injections are frequently used to supplement
this intervention (Video 4.2).
There are many available treatment options, both conservative and
operative, which are shown in the following lists.
Extracorporeal shock wave therapy (ESWT) is a newer treatment option
which involves a course of shock wave therapy rather than a single treatment.
It is still being investigated in trials, but the current evidence suggests that it
yields a good but delayed effect [9].
Surgical intervention is generally reserved for severe recalcitrant cases, in
which multiple previous conservative treatment options have failed.
Conservative treatment options
●● Analgesia
●● Anti-inflammatory medications
●● Activity modification
●● Ice or heat therapy
70 Hip and knee injections
●● Weight reduction
●● Physiotherapy (therapeutic exercise)
●● Manual therapy
●● Deep-heating modalities (e.g. ultrasound)
●● Transcutaneous electrical nerve stimulation (TENS)
●● Acupuncture
●● Local corticosteroid injections (blind or fluoroscopically guided)
●● Platelet-rich plasma (PRP) injection
●● Dry needling
●● ESWT
●● Local anaesthetic patches (sustained release)
●● Foot orthotics
Operative treatment options
●● Bursectomy
●● Iliotibial band lengthening (ITB)
●● Gluteal tendon repair
●● Trochanteric reduction osteotomy
INTRA-ARTICULAR HIP INJECTIONS:
INTRODUCTION
Intra-articular hip injections are performed in both adults and paediatric
patients. In the latter group this is most commonly in the form of injection of
contrast media in the assessment of developmental dysplasia or aspiration of
the hip to exclude infection. This is done in a hospital setting.
In adults there are a number of indications for hip injections, with the
commonest being diagnostic. Diagnostic injection is performed to elicit whether
the pain is originating from the hip itself (or to quantify the amount of pain from
the hip in cases of multiple sources) or whether the pain originates from extra-
articular structures around the hip (the spine or the sacroiliac joints). Diagnostic
hip injections have been shown to be sensitive and specific in differentiating
between intra-articular and extra-articular hip and spinal causes of hip pain [10].
There are a number of approaches via which the injection can be given and
the approaches differ based on whether the patient is an adult or a paediatric
patient. In adults the injections are usually given via anterior or lateral
approaches; in children the medial approach is often used.
What are the indications and contraindications for intra-articular hip injections in adults? 71
Intra-articular hip injections can be performed without image guidance;
however, they are most frequently performed with image guidance, as this
has been shown to increase the accuracy [11]. The commonest form of image
guidance is fluoroscopy, with or without the use of contrast, but ultrasound
guidance has also been utilised. Fluoroscopy often requires the patient to
attend on a second occasion to undergo the injection and involves exposure to
radiation, but ultrasound guidance requires a learning curve and the expense
of the equipment required.
WHAT ARE THE INDICATIONS AND
CONTRAINDICATIONS FOR INTRA-ARTICULAR
HIP INJECTIONS IN ADULTS?
Indications for injection
●● Diagnostic (elicit pain source or percentage of pain from hip)
●● Therapeutic
– Osteoarthritis
– Inflammatory arthropathies
– Femoroacetabular impingement
– Labral tear
Contraindications to injection
●● Allergy
●● Local or systemic infection
●● Local skin breakdown or rash
●● Uncontrolled diabetes
●● Coagulopathy
Substances that can be injected into
the hip joint
●● Local anaesthetic
●● Corticosteroids
●● Hyaluronic acid
●● PRP
72 Hip and knee injections
PREPARATION AND TECHNIQUE FOR INTRA-
ARTICULAR HIP INJECTION (IN ADULTS)
The injection should be performed in appropriate premises where resuscitation
equipment and staff are available.
Equipment required
●● Gloves
●● Skin prep solution
●● Drawing up needle (no filter if using steroid)
●● Needle for injecting
●● Syringe
●● Local anaesthetic
●● Steroid
●● Cotton wool/swab
●● Sterile dressing
Pre-procedure checks
●● Correct patient
●● Confirm the indication for injection
●● Contraindications excluded
●● Is the patient on anticoagulants?
●● Any relevant allergies?
●● Procedure appropriately explained to the patient
●● Consent (verbal or written)
Patient position
The patient should be positioned lying supine on a radiolucent table to allow
for x-ray guidance.
Anterior approach
After the patient is prepped and draped, the spinal needle can be lain on the
skin over the femoral neck in line with the centre of the neck, and x-rays
Preparation and technique for intra-articular hip injection (in adults) 73
taken to confirm this position. The entry point for injection will be on
this line, over the proximal portion of the neck; it can be marked with a
sterile skin marker. The entry point will lie in the groin skin crease. Before
inserting the needle, palpation should be performed for the femoral pulse
to ensure the entry point marked is not overlying the femoral neurovascular
structures. The needle is inserted at a 45° angle aiming proximally and
towards the midline.
L ateral approach
After the patient is prepped and draped, the spinal needle can be lain on the
skin to confirm on x-ray that the needle entry point laterally will allow the
needle to pass over the greater trochanter and into the hip joint.
Procedure
Reassure the patient that you will explain each step and warn the patient
before performing the injection.
For both approaches a spinal needle will be required. Local anaesthetic can
be given to the skin and fascia prior to insertion of the spinal needle, but many
surgeons use only local anaesthetic into the hip itself. If local anaesthetic is
given into the skin and fascia with the anterior approach, the patient may
experience temporary numbness in the distribution of the femoral nerve if
the injection disperses around the nerve.
Always aspirate before injecting
Injection of radiopaque dye may be given to confirm that the needle is in the
hip joint, although not all surgeons use this, and adverse reaction to the dye
can occur.
Once the injection has been given, apply a sterile dressing.
The patient should be asked about pain after the injection to assess the
effect and can be asked to keep a pain diary for up to 6 weeks post procedure.
Generally patients are asked to stay for 20 minutes after the procedure in
outpatients to ensure no adverse reactions occur.
Post-procedure follow-up is commonly at 6 or 12 weeks to assess the effect
of the injection and whether it has continued to work.
74 Hip and knee injections
Injection contents
If using local anaesthetic to the skin and fascia, this will generally be short-
acting to allow a rapid onset in order to give the injection. Either short-
or long-acting local anaesthetic can then be given into the hip joint with
80 mg of steroid. A 20 mL syringe will be required for the steroid and local
anaesthetic for the hip. In addition two 5 mL or 10 mL syringes will be
required for the more superficial local anaesthetic and radiopaque dye, if
being used.
WHAT IS THE EFFICACY OF HIP INJECTIONS?
There is limited evidence for routinely using therapeutic injections in
femoroacetabular impingement and labral tears, but diagnostic injections can
be helpful [12].
Corticosteroids have been shown to be more effective in alleviating pain in
hip osteoarthritis than hyaluronic acid and PRP [13].
There is evidence that a higher dose of steroid (80 mg rather than 40 mg)
prolongs the effect of the injection [14]. However, the total volume of the
solution injected did not improve the efficacy [15].
INJECTIONS AROUND THE KNEE JOINT:
INTRODUCTION
The commonest site for injections around the knee is into the joint itself.
Other sites where image-guided injections using ultrasound or x-ray are given
around the knee are
1. Fat pad injection for localised pain in Hoffa’s fat pad (deep to the patella
tendon) with ultrasound guidance
2. The proximal tibiofibular joint, using ultrasound or x-ray guidance
3. The distal iliotibial band (ITB) for ITB friction syndrome, with
ultrasound guidance
Injection containing steroid into tendons around the knee are best avoided
for fear of rupture of the tendons.
What are the indications and contraindications for intra-articular knee joint injection? 75
WHAT ARE THE INDICATIONS AND
CONTRAINDICATIONS FOR INTRA-ARTICULAR
KNEE JOINT INJECTION?
Indications
●● Diagnostic
●● Therapeutic
– Early osteoarthritis of the knee
– Inflammatory arthritis of the knee
– Degenerate meniscal tear with early arthritis without mechanical
symptoms
– Crystal deposition disease gout/pseudogout
Knee injections can be diagnostic or therapeutic. Diagnostic injections
can be performed injecting either local anaesthetic alone or with steroid to
confirm the source of pain, or an aspiration to send fluid for microbiological
and/or biochemical examination.
Contraindications
1. Allergy
2. Local or systemic infection
3. Local skin breakdown or rash
4. Uncontrolled anticoagulation or bleeding in the joint
5. Uncontrolled diabetes
6. Fracture, osteochondral injury or ligament injury
Relative contraindications
The presence of a prosthetic joint is a relative contraindication. Injection
containing steroid can be given in a prosthetic joint (total or partial joint
replacement), if indicated, by an appropriately experienced orthopaedic
surgeon in an operating theatre with sterile antiseptic precautions. It should
not be given in an outpatient or ward setting because of the risk of introducing
infection.
76 Hip and knee injections
PREPARATIONS AND TECHNIQUE FOR
KNEE INJECTION
The injection should be performed in appropriate premises where resuscitation
equipment and staff are available (Video 4.3).
Equipment required
●● Gloves
●● Skin prep solution
●● Drawing up needle, (no filter if using steroid)
●● Needle for injecting
●● Syringe
●● Local anaesthetic
●● Steroid
●● Cotton wool/swab
●● Sterile dressing
Pre-procedure checks
●● Correct patient
●● Confirm the indication for injection
●● Contraindications excluded
●● Is the patient on anticoagulants?
●● Any relevant allergies?
●● Procedure appropriately explained to the patient
●● Consent (verbal or written)
Patient position
The patient position for knee joint injection is determined by the approach.
Approaches to intra-articular knee joint injection:
●● Lateral suprapatellar
●● Medial suprapatellar
●● Medial to patellar tendon
●● Lateral to patellar tendon
Suprapatellar approach 77
SUPRAPATELLAR APPROACH
Patient position
The patient position is usually supine with the knee relaxed and extended or
in slight flexion (up to 20°), reclining on the examination couch (Figure 4.2). If
the patient is wheelchair bound or otherwise unable to transfer to/comfortably
remain supine on the couch, then with the patient sitting the foot can be
placed on a footstool to achieve the necessary extended position of the knee.
The lateral suprapatellar approach is easiest, as for the medial approach, the
contralateral leg lies in the way. The suprapatellar approach is very difficult in
patients who have had a previous patellectomy, as the necessary bony landmarks
are not present, and also in patients with a fixed flexion of the knee, preventing
the desired leg position of extension from being achieved. In these patients
approaches lateral or medial to the patellar tendon may be easier.
Figure 4.2 Lateral suprapatellar approach for knee injection.
78 Hip and knee injections
Injection site and landmarks
Palpate the patella and locate the proximal pole. The injection site is in the
soft spot lying between the proximal pole of the patella and the femur, either
laterally or medially. The soft spot is easier to palpate if the patient is relaxed,
and if there is an effusion present it may be more obvious to palpate. The
needle is inserted deep into the patella, in line with the upper pole of the
patella. Resistance is usually felt when entering the joint, confirming the intra-
articular placement.
APPROACHES ADJACENT TO THE
PATELLAR TENDON
Patient position
The knee should be flexed at 90°. This can be achieved by letting the patient
remain in a chair or hanging the leg off the end/side of the examination couch.
Injection site and landmarks
Palpate the knee to locate and mark the patella, patellar tendon, and medial
and lateral joint lines (Figure 4.3). The injection, via either the medial or
lateral approach, is given into the joint line anteriorly, adjacent to the patellar
tendon. The location is felt as a soft spot between the patella, tibial plateau
and patellar tendon, approximately 1 cm proximal to the tibial plateau. The
injection enters the joint piercing the skin at 90° to the skin, parallel to the
tibial plateau and aiming towards the centre of the knee (notch).
Caution should be taken regarding how deeply to insert the needle, as the
needle tip may hit the articular cartilage or pass into the anterior cruciate
ligament, given the direction of insertion. When entering the joint resistance
will be felt, confirming intra-articular placement of the needle tip, and at this
point the needle should not be passed any farther.
For all approaches
Reassure the patient that you will explain each step and warn the patient before
performing the injection. Use standard sterile precautions for injection. Use skin
preparation and the no-touch technique. Isolate the area with a sterile drape(s).
Approaches adjacent to the patellar tendon 79
Figure 4.3 Medial and lateral portals (X) for knee joint.
Insert the needle as per the selected approach. Always aspirate before injecting.
Use a 20 mL syringe and long green needle or angiocath needle for
injection. In patients with a very high body mass index (BMI), a spinal needle
may be required. At the end of the injection cover the area with a sterile
dressing.
Aspiration of the joint fluid to empty the joint before injection is not
necessary but can improve discomfort in patients with tense effusion. If you
are planning to aspirate and then inject the joint, ensure you have a sufficient
number of syringes available and you do not lose the position of needle in the
joint or contaminate the needle by touching an unsterile area.
After the injection ask the patient to sit at the edge of the couch and move
the knee joint several times to allow dispersion of the injection in the joint.
Generally patients are asked to stay for 20 minutes after injection in outpatient
to ensure safety. It is best to ask the patient to keep a diary of pain on a daily
basis for 6 weeks, and the patient is reviewed after 6 to 12 weeks.
80 Hip and knee injections
WHAT ARE THE KNEE INJECTION CONTENTS?
Either short-acting or long-acting local anaesthetic, or a mixture of both can
be used with 80 mg of either Kenalog or Depo-Medrone in a 20 mL syringe.
This allows sufficient volume for dispersion. If a short-acting local anaesthetic
is used, it allows instant pain relief indicating the injection has reached the
target.
WHAT IS THE EFFICACY OF KNEE
INJECTIONS?
Steroid injection has been shown to be more effective when there is a knee
joint effusion present [16]. Larger doses of steroids (80 mg) have been shown to
prolong the effect of the injection [17].
WHAT ARE VARIOUS TREATMENT OPTIONS
FOR OSTEOARTHRITIS OF THE KNEE?
Conservative
●● Analgesia
●● Anti-inflammatory medications
●● Activity modification
●● Ice or heat therapy
●● Weight reduction
●● Physiotherapy (quadriceps exercises particularly effective in
patellofemoral osteoarthritis)
●● Manual therapy
●● Deep-heating modalities (e.g. ultrasound)
●● TENS
●● Acupuncture
●● Local corticosteroid injections
●● PRP injection
●● Hyaluronic acid injections
●● Local anaesthetic patches (sustained release)
●● Foot orthotics
●● Braces
What are the potential complications and risks of all injections 81
Operative
●● Partial/total knee replacement
●● Osteotomy (high tibial or distal femoral)
The evidence supports the use of corticosteroid injections for moderate to
severe pain in osteoarthritis, but there is insufficient evidence for hyaluronic
acid [18] or PRP [19].
WHAT ARE THE POTENTIAL COMPLICATIONS
AND RISKS OF ALL INJECTIONS AROUND
AND INTO THE HIP AND KNEE?
Potential complications from steroid injection
1. Infection
2. Tendon rupture
3. Post-injection flare up of symptoms
4. Osteonecrosis/steroid arthropathy
5. Facial flushing
6. Menstrual irregularity
7. Elevated blood sugar in diabetic patients
8. Fainting
9. Local or systemic hypersensitivity
10. Tissue atrophy, nodule formation, skin discoloration
Risks of injections
1. Pain
2. Worsening of symptoms
3. Post-injection flare up of symptoms
4. Infection
5. Fat atrophy
6. Skin discoloration
7. Bleeding
8. Tendon rupture
9. Poor diabetes control
10. Persistent pain
82 Hip and knee injections
11. Recurrence of pain
12. Further surgery
SUMMARY
There are a number of injections that are routinely performed for
musculoskeletal conditions affecting the hip and knee joints, and
soft tissues surrounding these. The most commonly performed in
the outpatient/primary care setting are lateral soft tissue injection
for greater trochanteric pain syndrome and intra-articular knee
joint injection. Other injections that can be performed, including
intra-articular hip joint injections, are more commonly done with
imaging support.
TAKE-HOME MESSAGES
●● Corticosteroid injections for greater trochanteric pain syndrome
are one of the most commonly used treatments for this condition.
●● Injection into the lateral soft tissues over the greater trochanter,
without image guidance, is a safe and effective treatment
modality for greater trochanteric pain syndrome which can be
performed in the outpatient/primary care setting.
●● Intra-articular hip injections are most commonly performed in
hospital with image guidance.
●● Intra-articular knee injections can be given for pain management
in osteoarthritis.
●● Intra-articular knee injections can safely be given in the
outpatient/primary care setting.
VIDEOS
Video 4.1 How to perform injection for trochanteric pain syndrome.
(https://youtu.be/9uRrjjg2PAo)
Video 4.2 Physiotherapy for trochanteric pain syndrome.
(https://youtu.be/F20xnQNFDJ8)
References 83
Video 4.3 How to perform injection for knee joint.
(https://youtu.be/K7C2tFnkDBY)
REFERENCES
1. Williams BS, Cohen SP. Greater trochanteric pain syndrome: A review
of anatomy, diagnosis and treatment. Anaesth Analg. 2009;108:1662–70.
2. Geraci A, Sanfilippo A, D’Arienzo M. Greater trochanteric pain
syndrome: What is this meaning? Orthop Muscular Syst. 2011;1:101.
3. Reid D. The management of greater trochanteric pain syndrome: A
systematic review of the literature. J Orthop. 2016;13(1):15–28.
4. Kong A, VanderVliet A, Zadow S. MRI and US of gluteal tendinopathy in
greater trochanteric pain syndrome. Eur Radiol. 2007 July;17(7):1772–83.
5. Stephens MB, Beutler AI, O’Connor FG. Musculoskeletal injections: A
review of the evidence. Am Fam Physician. 2008 October;78(8):971–6.
6. Shbeeb MI, O’Duffy JD, Michet CJ Jr, O’Fallon WM, Matteson EL.
Evaluation of glucocorticosteroid injection for the treatment of
trochanteric bursitis. J Rheumatol. 1996;23:2104–6.
7. Estrela GQ, Furtado R, Natour J, Narimatsu S, Rosenfeld A. THU0352
Blinded vs ultrasound-guided corticosteroid injections for the treatment
of greater trochanteric pain syndrome: A randomized controlled trial.
Ann Rheum Dis. 2014;73(suppl.):304.
8. Cohen SP, Strassels SA, Foster L, Marvel J, Williams K, Crooks
M, Gross A, Kuriharra C, Nguyen C, Williams N. Comparison of
fluoroscopically guided and blind corticosteroid injections for greater
trochanteric pain syndrome: Multicenter randomized controlled trial.
BMJ. 2009;338:b1088.
9. Rompe JD, Sagal NA, Cacchio A, Funa JP, Morral A, Maffuli N. Home
training, local corticosteroid injection, or radial shockwave therapy
for greater trochanteric pain syndrome. Am J Sports Med. 2009
October;37(10):1981–90.
10. Deshmukh AJ et al. Accuracy of diagnostic injection in differentiating
source of atypical hip pain. J Arthroplasty. 2010;25(6 suppl.):129–33.
11. Kurup H, Ward P. Do we need radiological guidance for hip joint
injections? Acta Orthop Belg. 2010;76:205–7.
12. Chandrasekaran S, Lodhia P, Suarez-Ahedo C, Vemula SP, Martin TJ,
Domb BG. Symposium: Evidence for the use of intra-articular
cortisone or hyaluronic acid injection of the hip. J Hip Preserv Surg.
2016 April;3(1):5–15.
84 Hip and knee injections
13. Krych AJ, Griffith TB, Hudgens JL, Kuzma SA, Sierra J, Levy BJ. Limited
therapeutic benefits of intra-articular cortisone injection for patients
with femoro-acetabular impingement and labral tears. Knee Surg Sports
Traumatol Arthrosc. 2014;22:750–5.
14. Robinson P, Keenan Am, Conaghan PG. Clinical effectiveness and dose
response of image-guided intra-articular corticosteroid injection for
hip arthritis. Rheumatology. 2007;46:285–91.
15. Young R, Harding J, Kingsly A, Bradley M. Therapeutic hip injections:
Is the injection volume important? Clin Radiol. 2012;67:55–60.
16. Ayral X. Injections in the treatment of osteoarthritis. Best Pract Res Clin
Rheumatol. 2001;15:609–26.
17. Arroll B, Goodyear-Smith F. Corticosteroid injections for arthritis of
the knee: Meta-analysis. BMJ. 2004;328:869.
18. NICE guideline. Osteoarthritis: Care and management (CG177). 2014.
19. NICE guideline. Platelet-rich plasma injections for osteoarthritis of the
knee (IPG491). 2014.
5
Foot and ankle injections
BOBBY MOBBASSAR SIDDIQUI, ANNETTE JONES,
AND MANEESH BHATIA
INTRODUCTION
Symptoms related to the foot and ankle are a common presentation in
primary and secondary care. Pain is the leading symptom that is disclosed
at presentation; 63% of patients cite this as the reason for referral [1]. Steroid
injections for foot and ankle problems can be helpful in relieving patients’
symptoms and improving the quality of life. In addition, they can be good
adjuncts to other non-operative measures such as physiotherapy. Sometimes
they can help in ‘buying time’ towards more definitive surgical treatment or
useful in patients who are high risk for surgery.
Since the 1960s corticosteroid injections have been used in treating a
variety of musculoskeletal conditions [2]. Peterson et al. [1] reported 64% of
patients showed a significant improvement in pain scores following intra-
articular injections. The commonest intra-articular injections used in foot
and ankle include ankle joint, first metatarsophalangeal joint, tarsometatarsal
joints and sinus tarsi. Soft tissue foot and ankle injections are most commonly
used for Morton’s neuroma, intermetatarsal bursitis, plantar fasciitis, ankle
impingement and retrocalcaneal bursitis [3].
Image guidance increases the accuracy (and therefore efficacy) of
pharmacological injections. It serves as both a diagnostic and therapeutic
measure and can easily be performed in the outpatient setting. Fluoroscopy
and ultrasonography are the commonly used image guidance. X-ray guidance
is useful for joints, whereas ultrasound is used for soft tissue injections.
Image guidance must be used for injections for tendinopathies and most
foot and ankle joints. The injections which can be performed without image
guidance by an experienced clinician who has a good knowledge of foot and
85
86 Foot and ankle injections
ankle anatomy are the ankle joint, first metatarsophalangeal joint, Morton’s
neuroma, plantar fasciitis, ankle impingement and sinus tarsi syndrome.
WHAT ARE THE IMPORTANT ANATOMICAL
CONSIDERATIONS?
Osseous structures
There are 26 bones within the foot and ankle: 7 tarsal bones, 5 metatarsals
and 14 phalanges. The tarsal bones are composed of the talus, calcaneum,
navicular, cuboid and three cuneiform bones.
The foot can be subdivided into three regions: the hindfoot (talus and
calcaneum), the midfoot (navicular, cuboid and three cuneiforms) and the
forefoot (metatarsals and phalanges). See Figure 5.1.
(a)
Hindfoot
Tarsal bones
Midfoot
Metatarsals (1–5)
Forefoot
Phalanges
Figure 5.1 (a) Basic subdivision of the foot and ankle bones (dorsal view).
(Continued)
What are the important anatomical considerations? 87
(b)
Talus
Calcaneum
Navicular
Cuboid
Medial, middle,
lateral cuneiforms
(c)
Talus
Subtalar joint
(posterior facet)
Calcaneum
Figure 5.1 (Continued) (b) Osteology of the hindfoot and midfoot (dorsal
view). (c) Osteology of the hindfoot (posterior view).
A number of important neurovascular and tendinous structures cross the
foot and ankle, and the clinician should remain vigilant of their course to
reduce the risk of iatrogenic injury.
Vascular structures
The two main arteries of the foot are the posterior tibial artery and the dorsalis
pedis artery.
88 Foot and ankle injections
Tibialis anterior
Extensor digitorum
Longus
Superficial Neurovascular
peroneal nerve bundle
Extensor hallucis
longus
Neurovascular
bundle
Figure 5.2 Anatomy of the anterior ankle and foot dorsum showing tendons
and neurovascular structures.
The dorsalis pedis artery is the termination of the anterior tibial artery
which lies on the anteromedial surface of the ankle, most commonly between
the tendons of the extensor hallucis longus (EHL) and extensor digitorum
longus (EDL) (Figure 5.2). The artery is accompanied by the deep peroneal
nerve as a neurovascular bundle and can be endangered during medial
injections of the ankle; ensuring that injections remain medial to the tibialis
anterior tendon minimises this risk.
The posterior tibial artery can be found at the posteromedial aspect of the
ankle joint. It can be identified by a point approximately halfway between
the apex of the medial malleolus and the Achilles tendon. Posteromedial
What are the important anatomical considerations? 89
injections are rarely indicated without image guidance due to the high risk of
neurovascular damage and should not be attempted.
Tendinous structures
The tibialis anterior tendon lies on the anteromedial aspect of the ankle joint
and is easily seen by asking the patient to dorsiflex and invert the foot which
makes it more prominent (see Figure 5.2). The tendon serves as an important
landmark for anteromedial injections into the medial ankle. The clinician
should remain medial to this tendon when injecting this area.
The EHL tendon runs on the dorsomedial aspect of the foot and is an
important landmark when considering injections to the great toe.
The EDL tendon runs on the anterolateral aspect of the ankle and lateral
aspect of the foot. It is an important landmark when injecting the ankle joint,
as the clinician should remain lateral to this structure. Asking the patient to
extend their toes can help identify this structure.
Nervous structures
The superficial peroneal nerve supplies sensation to the dorsum of the foot,
except the first dorsal web space. It can be identified by placing the foot into a
plantar-flexed and supinated/inverted position (Figure 5.3). At the ankle joint
it runs immediately lateral to the tendons of EDL and can be at risk during
lateral ankle injections (see Figure 5.2).
(a) (b)
Figure 5.3 Course of superficial peroneal nerve in the foot, with (a) plantar
flexion and (b) highlighted.
90 Foot and ankle injections
The sural and saphenous nerves supply sensation to the lateral and medial
borders of the foot respectively. The sural nerve runs between the Achilles
and peroneal tendons.
The saphenous nerve (a sensory terminal branch of the femoral nerve) runs
on the anteromedial aspect of the ankle. It is approximately 1 cm anterior
from the palpable apex of the medial malleolus and is potentially at risk with
medial ankle injections. It is accompanied by the long saphenous vein, which
can lead to extensive venous bleeding if damaged.
WHAT ARE THE TECHNIQUES OF INJECTION?
In general, there are two techniques for foot and ankle injections: direct and
indirect. In the direct technique the local anaesthetic and steroid are mixed
together and injected at the same time. This is useful for soft tissue injections,
for example Morton’s neuroma and plantar fasciitis.
On the other hand, the indirect technique is useful for intra-articular
injections (e.g. ankle or first metatarsophalangeal joint). About 5–10 mL of
quick-acting local anaesthetic (lignocaine 1%) is injected first using a 10 cc
syringe. Following this, it is easier to explore the joint space. Once the needle
has entered the joint space without resistance, in most cases, a drop or two of
joint fluid backs out of the needle. This is a useful sign that the needle is in the
right place. If image guidance is available, then an arthrogram is performed
following injection of a radiopaque dye using a 5 cc syringe. This confirms the
intra-articular placement of the needle. The steroid is then injected (using a
1–2 cc syringe), which should flow freely.
For most foot and ankle injections, a blue needle (23 gauge) is sufficient. The
use of different sizes of syringes is advocated specially when using radiopaque
dye to avoid confusion between local anaesthetic and radiopaque dye.
WHAT DRUGS ARE USED COMMONLY FOR
FOOT AND ANKLE INJECTIONS?
Local anaesthetic
The choice of local anaesthetic is based on personal preference. The authors
use lignocaine 1%, as it is quick acting. For soft tissue injections (direct
technique) 1 mL of local anaesthetic is adequate. For intra-articular injection
Interdigital (Morton’s) neuroma 91
(indirect technique) up to 10 mL of local anaesthetic can be infiltrated in soft
tissues adjacent to the joint.
Steroids
For intra-articular injections, steroids with low solubility (e.g. Kenalog) are
advised, as they have a longer duration of action. Corticosteroid preparations
with higher solubility (e.g. Depo-Medrone) are chosen for soft tissue injections,
as they have fewer cutaneous and soft tissue side effects. About 1 mL (40 mg)
of steroid is adequate for most foot and ankle injections.
WHAT IS THE ROLE OF IMAGING FOR FOOT
AND ANKLE INJECTIONS?
The two main imaging modalities used are fluoroscopy or ultrasound
guidance. In general, soft tissue structures are best visualised and injected
using ultrasonography. Injections for noninsertional or insertional Achilles
tendinopathy, retrocalcaneal bursitis and tibialis posterior tendinopathy must
be performed under ultrasound guidance.
Fluoroscopy (x-ray guidance) can delineate joints accurately. The use of
radiopaque dye is a useful adjunct to confirm intra-articular injections. Joints
that are markedly degenerate with significant joint narrowing and osteophytes
usually require image guidance to ensure correct needle placement. Joints
within the midfoot and hindfoot are best injected primarily under image
guidance, given their high degree of congruence (thus, difficult entry) and
close proximity to neurovascular structures (Box 5.1).
INTERDIGITAL (MORTON’S) NEUROMA
Morton’s neuroma is a very common cause of forefoot pain. It is a benign
condition caused by thickening of the interdigital nerve and reactive
hypertrophy of the perineural tissues as opposed to a true neuroma.
Although the true aetiology is not fully understood, it is thought that
chronic compression of the interdigital nerve remains the main cause.
Typically, the second and third interdigital nerves are most commonly
affected. The most common differential diagnosis is synovitis of the second
metatarsophalangeal joint (MTPJ). The other conditions that can mimic
92 Foot and ankle injections
BOX 5.1 A guidance to the setting of foot and ankle
injections
Primary Image Trained
Site care?a guidance? AHP?a
Morton’s neuroma Yes USG can be Yes
useful
Plantar fascia Yes USG can be Yes
useful
First MTPJ Yes Fluoroscopy can No
be useful
Other foot joints No Yes No
Ankle joint Yes Fluoroscopy can No
be useful
Achilles No USG No
Retrocalcaneal bursa No USG No
Tibialis posterior No USG No
Abbreviations: AHP, allied health professional; USG, ultrasound guidance; MTPJ,
metatarsophalangeal joint.
a These injections should only be performed by appropriately trained personnel
who have knowledge of local anatomy and good clinical skills.
Morton’s neuroma include arthritis of the second MTPJ, Freiberg’s disease,
plantar plate tear or bone marrow oedema (stress response) of metatarsals.
The diagnosis of Morton’s neuroma is typically made clinically, although in
equivocal cases, ultrasound scan, MRI scan or injection of local anaesthetic
can be used. It has been shown that clinical examination has 98% accuracy as
compared to ultrasound scan to detect Morton’s neuroma. Approximately 74%
of patients describe burning pain, whereas 60% report numbness or altered
sensation. The most useful clinical test is the thumb index finger squeeze test
with sensitivity of 96% [4].
The published literature does not support the role of insoles for treatment
of Morton’s neuroma. The authors of two separate randomised controlled
trials concluded that custom-made orthotics and shoewear modification
did not make any significant improvement in symptoms [5,6]. On the other
hand, there are a number of studies reporting good outcome following
steroid injection for this condition. In general, 50% of patients report
improved symptoms following steroid injection lasting up to one year. There
Interdigital (Morton’s) neuroma 93
has been no study which has reported a long-term outcome of steroid
injection for Morton’s neuroma. It has been shown that steroid injections
are superior to insoles or local anaesthetic injection [6,7]. One study reports
that the effect of steroid injection is better if the injection is performed earlier
[8]. Most studies show that there is no correlation between size of Morton’s
neuroma and effect of steroid injection. One randomised controlled
trial has reported that there is no significant difference in pain scores,
patient reported outcomes and injection failure rates (patients requiring
further injections or excisions) between injections that were performed by
ultrasound-guided or sham (not ultrasound guided) technique. The take-
home message from this paper was that in the presence of a clear diagnosis
of Morton’s neuroma, a trained clinician who understands the forefoot
anatomy may perform an injection without ultrasound guidance with good
and safe results [9].
Injection technique
Morton’s neuroma injections can be performed using dorsal or plantar
approaches (Video 5.1). The main advantage of a plantar approach is that it
avoids the skin changes which can follow a dorsal injection. Also one does
not need to go very deep with the needle, as Morton’s neuroma is a plantar
structure. However, the plantar skin is quite sensitive, so plantar injections
can be very uncomfortable for the patient. The other disadvantage is that
there are no visible anatomical landmarks for guidance for a plantar
injection.
On the dorsal side, the extensor tendons serve as a good landmark, and the
injection site is in between the soft tissue space of the adjacent toe tendons. This
advantage makes the dorsal approach favourable and is used by most clinicians.
The patient needs to be counselled regarding possible hypopigmentation
following a dorsal injection (Figure 5.4a).
The needle entry site is approximately 2 cm proximal to the web space.
The clinician’s other hand is used to support and steady the foot (Figure
5.4b). The clinician should not encounter any resistance to injection at first,
however there is a slight ‘give’ as the intermetatarsal ligament is penetrated.
This signifies that the clinician is in the vicinity of the Morton’s neuroma,
which lies deep to this structure. The other practical tip is to observe splaying
of the adjacent toes once the injection is performed, which is due to pressure of
the injected fluid into the intermetatarsal space.
94 Foot and ankle injections
(a) (b)
Figure 5.4 (a) Skin hypopigmentation following injection. (b) Dorsal approach
for Morton’s neuroma injection, highlighting extensor tendons.
PLANTAR FASCIITIS
The plantar fascia is a thick band of connective tissue known as an
aponeurosis – formed of white collagen fibre bundles – comprising of a deep
central band, and lesser medial and lateral fibrous bands. From its proximal
fibrocartilaginous attachment to the medial tuberosity of the calcaneum, the
plantar aponeurosis runs distally before dividing into five bands which attach
through several slips to the plantar plates of the metatarsophalangeal joints,
bases of the proximal phalanges and the flexor tendon sheaths, collateral
ligaments, and deep transverse metatarsal ligaments [10]. It contributes to
the biomechanical function of the foot, supporting the medial longitudinal
arch and the first MTPJ via the ‘windlass mechanism’. During the propulsive
gait phase when the toes are dorsiflexed, the plantar fascia tenses resulting
in elevation of the longitudinal arch and shortening of the toes. It further
assists with shock absorption during the loading stance phase of gait, when
pronation of the forefoot, resulting in a flattening of the medial longitudinal
arch and subsequent stretch of the plantar fascia.
Plantar fasciitis is rather a misnomer, as the underlying pathology is
regarded as a degenerative rather than an active inflammatory condition.
Plantar fasciitis 95
Repetitive traction and overuse injury is thought to result in micro-tears
which provoke an inflammatory response. Histology findings include
fibroblastic proliferation and chronic granulomatous tissue. A common
finding on ultrasound or MRI scan is an increased thickness of the plantar
fascia, the normal dorsoplantar thickness being 3 mm. Doubt remains as to
whether the x-ray finding of medial tuberosity calcaneal heel spur is a result
of the pathological process of plantar fasciitis [11]. An estimated 15%–25% of
normal population has a heel spur, and this incidence increases with obesity
and age. On the other hand, 50% of plantar fasciitis patients have a heel spur.
Most foot and ankle surgeons believe that a heel spur does not require surgical
intervention.
Risk factors for plantar fasciitis
●● Prolonged standing, increase in running distance or intensity
●● High body mass index (BMI)
●● Tight Achilles tendon
●● Inappropriate footwear (poor cushioning)
Typical presenting symptoms
●● Pain and tenderness at the fascia’s insertion at the calcaneus’s medial
plantar tuberosity.
●● Pain described as a burning sensation, worse on first rising after a
period of rest (first-step pain).
In the first instance a conservative approach to management would
consist of
●● Activity modification/advice/reassurance
●● NSAIDs (non-steroidal anti-inflammatory drugs)
●● Stretches for plantar flexor muscles and plantar fascia
●● Consideration of orthotic insoles
●● Rolling foot on ice bottle to relieve symptoms
●● Occasionally consideration of night splints
Through appropriate selection of the aforementioned modalities, patients
generally report improvement in their symptoms within a few weeks, though
full resolution may take up to 6 months [12]. Extracorporeal shock wave
therapy (ESWT) provides a successful adjunct for patients with persistent
symptoms. Gerdesmeyer et al. [13] demonstrated significant improvements
in pain scales, functional measurements and quality of life scores in their
subjects compared to baseline at 12 weeks and 12 months follow-up.
96 Foot and ankle injections
A recent randomised controlled trial (RCT) compared steroid injections
with joint mobilisations/stretching [14]. At 3, 6 and 12 weeks follow-up, both
groups showed significant improvements in patients’ pain relief and functional
outcomes compared with their baseline, with greater improvements in the
injection group. However, the noted improvements continued only in the joint
mobilisations/stretching group at one-year follow-up.
Caution is advised in the use of steroid injections given the high rates of
plantar fascia rupture: One study concluded that of the 35 patients that had
been diagnosed with a complete plantar fascia rupture, 33 had had a prior
steroid injection [15].
As a first line of treatment, the authors recommend physiotherapy in the first
instance, with effective utilisation of the aforementioned modalities (Video 5.2).
If this fails to provide adequate symptom relief, steroid injection may be
considered as the next line of treatment. Injections aim to provide enough pain
relief in order for the patient to be compliant with a regime of stretching exercises
(Figure 5.5).
(a) (b) (c)
(d)
Figure 5.5 (From top left, clockwise) Common physiotherapy stretching
exercises for treatment of plantar fasciitis.
First metatarsophalangeal joint 97
Alternative treatments such as autologous blood injection, including
platelet-rich plasma (PRP) have been advocated within the United Kingdom,
by NICE (National Institute for Health and Care Excellence). This is on the
understanding that although it is safe to administer, there is limited evidence to
show that it is an effective treatment (NICE guidance IPG437). PRP injections
are outside the direct regulation of the U.S. Food and Drug Administration
and remain an ‘off-label’ treatment for plantar fasciitis [16]. They are discussed
in greater detail in Chapter 7.
Injection technique
The patient positioning is variable based on clinician’s preference (Video 5.3).
If a supine position is selected, external rotation of the affected leg is helpful
to direct injection to the medial heel. Some clinicians, on the other hand,
prefer a semilateral position with the affected foot lowermost. The prone
position has the advantage of easy access for injection. The tender area on the
medial heel is palpated and marked. The soft tissue immediately distal to that
serves as the entry point of the needle (Figure 5.6). The patient should be
reassured as this is often the maximal point of tenderness. Body habitus
dictates the needle choice (blue 23G versus green 21G). Once the needle has
touched the plantar border of medial calcaneum, it is withdrawn slightly and
the injection is performed. Care should be taken not to inject into the fat pad
at the base of the foot [17].
Patients should avoid any strenuous activity or stretching for the next 48
hours and some may experience a flare up of their symptoms during this time.
Stretching exercises/ physiotherapy should be commenced 1–2 weeks after a
successful steroid injection.
FIRST METATARSOPHALANGEAL JOINT
Hallux rigidus, or arthritis of the first MTPJ, is the commonest degenerative
disease of the foot, affecting 2.5% of patients over the age of 50 years [18]. The
aetiology is not fully understood and the majority of cases are idiopathic. Other
risk factors are positive family history (in two-thirds of cases), inflammatory
arthropathy and metabolic disorders. Trauma is also cited as a cause, as with
most other degenerative joint diseases [19].
Patients present along a spectrum depending upon the severity of disease.
Initially a painful dorsal prominence is noted that interferes with shoewear
98 Foot and ankle injections
Figure 5.6 Injection site for plantar fasciitis.
and restricts terminal (and often painful) dorsiflexion. Aggravating activities
such as ascending stairs, running (especially during push-off) and push-ups
are typical. In advancing disease, pain throughout any range of movement
and a positive ‘grind-test’ is elicited. Radiographs show typical joint space
narrowing and prominent dorsal osteophytosis.
First metatarsophalangeal joint 99
Treatments are directed towards the severity of disease and can be divided
into early or advanced hallux rigidus. Early interventions involve the use of
NSAIDs, avoiding aggravating activities, stiff insoles with a Morton’s extension
or rocker-bottom soles (to limit first MTPJ movement) and injections within
the joint. Injection of the joint may also help defer surgical treatment in cases
of intrusive symptoms. Injections have been effective in providing temporary
relief (up to 3 months’ duration) as shown in a RCT comparing the use of
hyaluronic acid and steroid injections [20]. Overall, non-surgical measures can
offer significant relief from the symptoms in the hallux rigidus. A retrospective
review of non-surgical treatments found success rates in 55% of patients with
hallux rigidus [21].
Surgical intervention is commonly divided into joint sparing or joint
sacrificing. Joint sparing procedures involve cheilectomy, osteotomies and
synthetic cartilage interposition (SCI).
A cheilectomy involves removal of the prominent dorsal osteophyte and
resection of up to one-third of the dorsal metatarsal head. Multiple studies
have shown good results with mild to moderate hallux rigidus, with one
long-term study showing >90% subjective and objective improvement
[22]. Osteotomies act to increase dorsiflexion range of movement, whilst
sacrificing plantar flexion. Definite conclusions regarding the effectiveness
of osteotomies cannot be drawn from the current evidence [23]. Joint
sacrificing procedures involve joint arthrodesis (which currently remains
the ‘gold standard’ treatment for advanced hallux rigidus). A multicentre,
international RCT comparing SCI and arthrodesis found equivalent pain
scores and similar rates of further surgery in both groups [24]. A systematic
review by Korim et al. [25] found overall union rates in arthrodesis at 93.5%,
irrespective of the fixation method used. A further systematic review found
superior results in foot and ankle scores, favouring arthrodesis over total
joint replacement [26]. Other choices include joint arthroplasty, although
they have fallen out of favour due to poor results and survivorship. Finally,
joint excision can be performed, although this is typically reserved for elderly
and low-demand patients.
Injection technique
The patient position is supine (Video 5.4). The first MTPJ line is palpated and
marked (this can be done by dorsiflexion and plantar flexion). The EHL tendon
should be identified and protected. The needle entry point is either medial or
lateral to EHL tendon (Figure 5.7).
100 Foot and ankle injections
(a) (b)
Figure 5.7 (a) Surface anatomy of the first MTPJ and (b) injection site.
An ‘indirect approach’ is useful for this injection. The skin and soft tissue
are infiltrated with 5–10 mL of 1% lignocaine with orange 25G or blue 23G
needle. Blue needle 23G is used for intra-articular placement of steroid. The
needle should be directed at 60°–70° to the plane of the foot and directed distally;
this matches the slope of the joint and reduces the risk of chondral injury [27].
Distraction of toe can help to open up the joint space.
There should be minimal resistance during injection; the needle should be
re-sited if resistance is encountered.
ANKLE (TIBIOTALAR) JOINT
The ankle remains the most commonly injected joint (97% of members of the
American Academy of Orthopaedic Surgeons performed this procedure),
with patients typically presenting with pain and/or loss of function and
movement. Injections help to delineate between intra- and extra-articular
pathology and guide subsequent treatment [2]. Aspiration can be performed
to help distinguish between infective and crystal arthropathy in the acute
setting.
Ankle osteoarthritis (OA) is a growing problem, with approximately 1%
of the world’s population being affected. Primary OA of the ankle joint is
Ankle (tibiotalar) joint 101
relatively uncommon. The vast majority of cases are secondary to significant
ligament or bone injury. In a large case series by Salzman et al. [28], 70% of
ankle arthritis was secondary to trauma; 12% due to rheumatoid disease and
only 7% of cases had no underlying cause (primary ankle OA). Damage to the
articular surface at the time of injury, or chronic cartilage overloading due to
incongruity and residual instability, has been implicated in the development
of ankle OA, with often a 20-year lag from time of injury to disabling joint
degeneration [29].
Progressive pain and limited range of ankle movements are typical
complaints from patients with ankle OA. The pain is often described as
burning and deep seated; it may be localised to a specific part of the ankle or
to the hindfoot in general. As the disease progresses, analgesics and cessation
of weight-bearing activities become ineffective; rest pain, and intrusive night
pain become more frequent [30].
Clinical examination will often lead to the diagnosis: a reduction in ankle
movements, presence of stiffness, crepitus, effusion and joint line tenderness are
commonly observed. Plain radiographs can confirm ankle OA and also the state
of surrounding joints (CT can also help in this regard), whereas MRI scanning can
delineate chondral and peri-articular soft tissue pathology in subtler cases [30].
Early degenerative changes can be managed non-operatively with
NSAIDs, activity modification, ankle braces and shoewear modifications.
Targeted exercises aim to improve muscle recruitment that act on the ankle
joint (Figures 5.8 and 5.9).
Intra-articular injections can also help provide respite from symptoms,
reduce the inflammation in surrounding tissues, and also buy time until
a definitive procedure is performed. End-stage ankle arthritis is treated
surgically: the two main options are ankle arthrodesis (performed through
either open or endoscopic means) or total ankle replacement. Both options
have risks and benefits, and the literature does not currently favour one
intervention over the other. A large multicentre UK RCT (TARVA) is currently
in progress to answer this very question, with results due in the near future.
In a recent review of the literature, Lawton et al. [31] demonstrated a higher
overall complication rate after arthrodesis, but a higher reoperation rate for
revision after total ankle replacement. They also found a more symmetric gait
and less impairment on uneven surfaces after total ankle replacement. The
authors concluded that the choice of surgery ultimately depends on the choice
of the surgeon and tailored to suit each patient [31].
Injections also play a role in treating peri-articular pathologies, such as
ankle impingement.
102 Foot and ankle injections
(a) (b)
(c) (d)
(e) (f )
Figure 5.8 (a) Inversion against resistance band, (b) eversion against resistance
band, (c) ankle plantar flexion, (d) ankle dorsiflexion, (e) single leg stance, (f)
wobble board.
Ankle (tibiotalar) joint 103
(a) (b)
(c) (d)
Figure 5.9 (a) Double-heel raise, (b) single-heel raise, (c) and (d) single-leg
heel raises with pre-stretch.
Ankle impingement syndromes have been defined as the loss of physiological
tibiotalar range of movement as a result of bony or soft tissue overgrowth or
by the presence of accessory ossification centres [32]. There are a variety of
impingement syndromes, which are classified anatomically in relation to the
tibiotalar joint. Although they may have similar aetiologies, they can present
with distinct clinical signs.
104 Foot and ankle injections
Chief among them is anterior ankle impingement. Typically, anterior
impingement syndrome is a common source of chronic anterior ankle pain,
often seen in athletes or football players, where repetitive micro-trauma to
the cartilaginous rim (when the anterior tibia and talus come into contact)
through dorsiflexion or ball striking leads to the development of intra-capsular
bony spurs (Figure 5.10). Patients typically complain of anterior ankle pain
on dorsiflexion (e.g. in squatting, sprinting or stair-climbing), and tenderness
with a reduced range of terminal dorsiflexion on clinical examination [33].
Diagnosis is mainly clinical, although lateral radiographs can clinch the
diagnosis with the appearance of bony osteophytes.
Non-surgical treatment, in the form of analgesics, NSAIDs, activity
modification/avoidance and intra-articular injection (to settle any synovial
irritation and inflammation and provide pain relief) help in early stages of
the disease where there is an absence of degenerative changes in the ankle.
Surgery in the form of either open or endoscopic removal of bony spurs,
Figure 5.10 Anterior ankle impingement. The arrows indicate bone spurs whereas
the solid triangle represents thickened anterior capsule of the ankle joint.
Ankle (tibiotalar) joint 105
hypertrophied synovium and scar tissue has been shown to be effective, as
long as there is no evidence of joint space narrowing, which is related to much
poorer outcomes overall. Tol et al. [34] reported excellent outcomes in 77% of
patients treated endoscopically at 5 years, whereas Coull et al. [35] reported
a 92% satisfactory outcome, following open surgery (provided there were no
degenerative changes on pre-operative radiographs) at a mean follow-up of
7.3 years.
Posterior ankle impingement is a common cause of posterior ankle
pain, which is worsened on plantar flexion. The talus and surrounding soft
tissues become compressed between the posterior tibia and the calcaneum,
resulting in typical inflammation and pain. Soft tissue structures at risk
of impingement include the flexor hallucis longus (FHL) tendon, and
posterior talofibular and posterior tibiofibular ligaments. The majority of
cases show the presence of an ‘os trigonum’ or an elongated lateral talar
process called the ‘Steida process’. These anomalies increase the likelihood
of impingement. Posterior ankle impingement is seen in athletes, especially
downhill runners, footballers and ballet dancers, where repetitive plantar
flexion is expected [33].
Radiographs can often detect bony abnormalities as mentioned early.
Ultrasonography (often detecting a thickened posterior capsule) and MRI
(showing thickening of the posterior capsule and ligaments, bony oedema
and fluid within the FHL sheath) can help where radiographic changes are
not so obvious [36].
Treatment is mainly conservative. In the presence of an os trigonum,
injection of local anaesthetic into the synchondrosis under fluoroscopic
control can be both diagnostic and therapeutic [37] (Figure 5.11). In the
(a) (b)
Figure 5.11 (a) Injection site for posterolateral impingement. (b) Fluoroscopy
view highlighting os trigonum (blue arrow) and needle tip at os trigonum.
106 Foot and ankle injections
absence of an os trigonum and presence of clinical posterior impingement,
Robinson and Bollen [38] found that ultrasound-guided dry-needling with
local anaesthetic and steroid gave relief in all of their patients with no residual
or recurrent symptoms at 31 months mean follow-up.
Grice et al. [3] found injections helped patients with soft tissue ankle
impingement. Ninety percent of patients received significant improvement in
symptoms following injection, with 46% of patients remaining asymptomatic
2 years later [3].
In persisting symptoms, surgery to excise an os trigonum, Steida process
or any associated pathological soft tissue, with or without release of the FHL
tendon, can be performed, achieving good results [33].
Injection technique
Injections to the ankle joint can be performed through anterolateral or
anteromedial approach (Figures 5.12). In a cadaveric study by Heidari et al.
[39], anterolateral injections were shown to be more reliable in achieving
intra-articular position than the anteromedial approach. In our experience
both approaches are equally effective.
(a) (b)
Figure 5.12 (a) Anterolateral ankle injection site. Dotted line represents course
of superficial peroneal nerve. (b) Anteromedial ankle injection site.
Sinus tarsi syndrome 107
ANTEROMEDIAL ANKLE INJECTION TECHNIQUE
The patient position is supine with the foot plantar-flexed on the couch surface
to open up the joint space (Video 5.5). The bony landmarks (see earlier) of the
ankle joint should be identified. From the medial malleolus, the clinician’s
finger can be ‘walked’ laterally in line with the ankle joint-line (which can be
confirmed by asking the patient to dorsiflex and plantar flex). A ‘soft spot’ will
eventually be felt, indicating the approximate needle entry point. The tibialis
anterior tendon (which can be made prominent against resisted dorsiflexion
and inversion) also serves as another landmark, and the injection site should
remain medial to this.
Following sterile preparation of the ankle, the needle is directed slightly
cephalad and posterolaterally until there is a sudden loss of resistance,
confirming joint entry. There should be very minimal resistance during
injection.
ANTEROLATERAL ANKLE INJECTION TECHNIQUE
A similar manner can be adopted for anterolateral injections: the lateral
malleolus and EDL tendon serve as bony and soft tissue landmarks respectively
(Video 5.6). The clinician’s finger can be ‘walked’ medially from the lateral
malleolus, along the joint line. The EDL tendon (made prominent by asking
the patient to extend their toes) should be identified and the injection should
remain lateral to it.
SINUS TARSI SYNDROME
Sinus tarsi syndrome (STS) remains a poorly understood process. It is thought
to chiefly arise from a severe inversion injury to the ankle, generating enough
force to damage the strong ligaments (the interosseous talocalcaneal ligament
and the cervical ligament) that lie within the sinus tarsi [40,41].
Initially, bleeding and inflammation can lead to an increase in intra-
sinus pressure and irritation to nearby neurovascular structures (including
branches of the deep peroneal nerve). Later, the resultant subtalar joint
instability can lead to persistent synovitis and eventual degenerative joint
disease. Acute injuries as a result of jumping sports or stepping off a high
curb can lead to STS. Chronic conditions such as hindfoot deformities or
inflammatory arthropathy (e.g. rheumatoid arthritis or gout) can also be a
cause of STS [41].
108 Foot and ankle injections
Clinically the patient reports pain over the lateral hindfoot, corresponding
to the sinus tarsi, which is exacerbated on weight bearing and/or varus stressing
of the hindfoot. The patient may also complain of subjective instability when
walking on uneven ground.
Diagnosis of this condition can be difficult. Radiographs are often normal
[42] and MRI findings often do not correlate well with pathology found at
arthroscopy [43].
Injections into the sinus tarsi are thus critical in the diagnosis of STS.
Several studies have cited symptom relief following local anaesthetic injection
as a key diagnostic criterion [41,42,44].
As a therapeutic measure, injections within the sinus tarsi, alongside
NSAIDs, have been shown to significantly improve patient symptoms. Kuwada
[45] showed symptom resolution in 63% of their cohort, with a further 22%
reporting symptom improvement.
Conservative management may also include physiotherapy, NSAIDs,
orthotic insoles, use of ice for acute flare-ups and advice regarding appropriate
footwear.
Injection technique
The patient is placed in a decubitus position with the symptomatic foot
uppermost. Injection to the sinus tarsi is made laterally. The needle is inserted
perpendicular to the skin, just immediately inferior to the lateral malleolus
to gain access to the sinus tarsi [46] (Figure 5.13a). There should be no bony
resistance and in cases of acute inflammation, usually some fluid backs out.
X-ray can be used to confirm needle placement in sinus tarsi (Figure 5.13b).
TARSOMETATARSAL JOINTS
Osteoarthritis of the tarsometatarsal joints (TMTJs) is the second most common
site of arthritis within the foot. Fracture–dislocations of the tarsometatarsal
joint (often referred to as a ‘Lisfranc’ injury) can lead to secondary TMTJ
OA. Approximately 20% of tarsometatarsal joint injuries are missed on initial
examination.
With established OA of the TMTJs, diagnosis of the most symptomatic
joint can be challenging. In a review by Myerson [47], the author commented
on the poor correlation between radiographic joint degeneration and patient-
reported pain. Although, the more mobile third and fourth TMTJs would
Tarsometatarsal joints 109
(a) (b)
Figure 5.13 (a) Injection site for the sinus tarsi. (b) X-ray showing tip of the
needle in sinus tarsi.
exhibit severe changes, the relatively immobile second TMTJ is often the main
source of pain [47]. Thus, the role of selective TMTJ local anaesthetic injection
can be vital in localising the most offending joint, directing treatment.
Initial treatment of TMTJ OA is non-operative, through the use NSAIDs,
moulded insoles, rocker-bottom shoes or immobilisation using ankle–
foot orthoses. Image-guided steroid injections for TMTJ arthritis can be
successful, specially in early arthritis.
If the injections fail to provide lasting relief in symptoms, surgical
treatment is in the form of arthrodesis of the first, second and/or third TMTJ.
Following fusion, most patients remain satisfied with the level of pain relief
and functional capacity [47].
Injection technique
Image-guided injection and ‘indirect technique’ (described earlier) is
commonly employed. These joints can be identified by dorsiflexing and
plantar flexing the respective metatarsal (MT) head. This can be done by
holding the MT head between the clinician’s thumb and index finger, and
gently balloting in a dorsal and plantar direction. Movement at the desired
TMTJ can be palpated using the clinician’s other hand.
110 Foot and ankle injections
First TMTJ
The first TMTJ is often the easiest TMTJ to be identified. The tibialis anterior
tendon should be identified and the injection site should be immediately
medial to this, so as to reduce the risk of penetration of the tibialis anterior
tendon, and subsequent iatrogenic rupture. Intra-articular placement and
confirmation is conducted as described earlier.
Second and third TMTJs
Initial palpation of the fourth and fifth TMTJs serves as an anatomical
landmark. A thumb is placed at the fourth TMTJ and immediately medial
to this is the third TMTJ. It is important to remember that the second TMTJ
is more proximal than the first and third TMTJs, as it is recessed into the
cuneiforms to form the Lisfranc joint (see Figure 5.1a). Both the second and
third TMTJs can be accessed via a single injection (Figure 5.14).
Fourth and fifth TMTJs
The base of the fifth MT is the anatomical landmark, running a thumb
proximally and distally to this, approximates the fourth/fifth TMTJ. Pronating
(a) (b)
Figure 5.14 (a) Surface markings of second TMTJ. (b) Fluoroscopy view
indicating injection into second TMTJ.
Videos 111
and supinating the midfoot helps delineate the base of the fifth MT, increasing
accuracy further. The needle should be placed and advanced in a dorsal to
plantar direction, along the joint line. As with the second and third TMTJ,
only a single injection is required due to the communication between the
fourth and fifth TMTJs.
TAKE-HOME MESSAGES
●● The foot and ankle have complex anatomy due to a number
of joints, tendons and ligaments. Clinical diagnosis and good
knowledge of regional anatomy is the key to success following
injection.
●● Image guidance increases accuracy of injection to soft tissue
structures and joints. Ultrasound is best used for soft tissue
structures, whereas fluoroscopy is better for joints. Tendons (e.g.
Achilles and tibialis posterior) should not be injected blindly.
●● Injection is not the first line of treatment for plantar fasciitis.
Stretching exercises of plantar fascia and calf muscles should be
encouraged once the pain has improved (usually 1–2 weeks after
injection) to prevent recurrence.
●● Foot and ankle injections have a diagnostic as well as therapeutic
role. The injections are particularly effective for early arthritis.
●● Local side effects of steroid injections include skin
depigmentation, fat atrophy, iatrogenic ligament and tendon
atrophy or rupture.
VIDEOS
Video 5.1 How to perform injection for Morton’s neuroma.
(https://youtu.be/vKSr3dnOSCc)
Video 5.2 How to do exercises for plantar fasciitis.
(https://youtu.be/iNYNhnBJ7-0)
Video 5.3 How to perform injection for plantar fasciitis.
(https://youtu.be/7ZLX2i0tE5I)
Video 5.4 How to perform injection for arthritis of big toe (hallux rigidus).
(https://youtu.be/K2DLvAPpWwg)
112 Foot and ankle injections
Video 5.5 H
ow to perform injection for ankle joint using anteromedial
approach.
(https://youtu.be/Hxy6nZ4CGDU)
Video 5.6 H
ow to perform injection for ankle joint using anterolateral
approach.
(https://youtu.be/_ZGxeNoTMGQ)
REFERENCES
1. Peterson CK, Buck F, Pfirrman CWA, Zanetti M, Hodler J.
Fluoroscopically guided diagnostic and therapeutic injections
into foot articulations: Report of short-term patient responses
and comparison between various injection sites. Am J Radiol.
2011;197:949–53.
2. Johnson JE, Klein SE, Putnam RM. Corticosteroid injections in the
treatment of foot & ankle disorders: An AOFAS survey. Foot Ankle Int.
2011;32(4):394–9.
3. Grice J, Marsland D, Smith G. Efficacy of foot and ankle corticosteroid
injections. Foot Ankle Int. 2017;38(1):8–13.
4. Mahadevan D, Venkatesan M, Bhatt R, Bhatia M. Diagnostic accuracy
of clinical tests for Morton’s neuroma compared with ultrasonography.
J Foot Ank Surg. 2015;54:549–53.
5. Kilmartin TE, Wallace WA. Effect of pronation and supination orthosis
on Morton’s neuroma and lower extremity function. Foot Ankle Int.
1994;15(5):252–62.
6. Saygi B, Yildrim Y, Saygi EK, Kara H, Esemenli T. Morton neuroma:
Comparative results of two conservative methods. Foot Ankle Int. 2005;
26(7):556–9.
7. Thomson CE, Beggs I, Martin DJ, McMillan D, Edwards RT, Russell
D, Yeo ST, Russell IT, Gibson JN. Methylprednisolone injections for
the treatment of Morton neuroma: A patient-blinded randomized trial.
J Bone Joint Surg [Am]. 2013;95-A:790–8.
8. Markovic M, Crichton K, Read JW, Lamb P, Slater HK. Effectiveness of
ultrasound-guided corticosteroid injection in the treatment of Morton’s
neuroma. Foot Ankle Int. 2008;29(5):483–7.
9. Mahedevan D, Attwal M, Bhatt R, Bhatia M. Corticosteroid injection for
Morton’s neuroma with or without ultrasound guidance. Bone Joint J.
2016;98-B:498–503.
References 113
10. Hossain M, Makawana N. “Not Plantar Fasciitis”: The differential
diagnosis and management of heel pain syndrome. Orthopaedics
Trauma. 2011;25(3):198–206.
11. Singh D, Angel J, Bentley G, Trevino SG. Fortnightly review: Plantar
fasciitis. Br Med J. 1997;315:172–5.
12. Cornwall MW, McPoil TG. Plantar fasciitis: Etiology and treatment.
J Orthop Sports Phys Ther. 1999;29:756–60.
13. Gerdesmeyer L et al. Radial extracorporeal shock wave therapy is safe
and effective in the treatment of chronic recalcitrant plantar fasciitis:
Results of a confirmatory randomized placebo-controlled multicenter
study. AM J Sports Med. 2008;36:2100–9.
14. Celik D, Kus G, Sirma SO. Joint mobilization and stretching exercise
vs steroid injection in the treatment of plantar fasciitis: A randomized
control study. Foot Ankle Int. 2016;37(2):150–6.
15. Lee HS, Choi YR, Kim SW, Lee JY, Seo JH, Jeong JJ. Risk factors
affecting chronic rupture of the plantar fascia. Foot Ankle Int.
2014;35(3):258–63.
16. Beitzel K, Allen D, Apostolakos J, Russell RP, McCarthy MB, Gallo
GJ, Cote MP, Mazzocca DA. US definitions, current use and FDA
stance on use of platelet-rich plasma in sports medicine. J Knee Surg.
2015;28(1):29–34.
17. Tallia AF, Cardone DA. Diagnostic and therapeutic injection of the
ankle and foot. Am Fam Physician. 2003;68(7):1356–63.
18. Lam A, Chan JJ, Surace MF, Vulcano E. Hallux rigidus: How do I
approach it? World J Orthop. 2017 May;8(5):364–71.
19. Ho B, Baumhauser J. Hallux rigidus. EFORT Open Rev. 2017
January;2(1):13–20.
20. Pons M, Alvarez F, Solana J, Viladot R, Varela L. Sodium hyaluronate in
the treatment of hallux rigidus. A single-blind, randomized study. Foot
Ankle Int. 2007 January;28(1):38–42.
21. Grady JF, Axe TM, Zager EJ, Sheldon LA. A retrospective analysis
of 772 patients with hallux limitus. J Am Podiatr Med Assoc. 2002
February;92(2):102–8.
22. Coughlin MJ, Shurnas PS. Hallux rigidus. J Bone Joint Surg AM. 2004
September;86-A Suppl 1(Pt 2):119–30.
23. Polzer H, Polzer S, Brumann M, Mutschler W, Regauer M. Hallux
rigidus: Joint preserving alternatives to arthrodesis – A review of the
literature. World J Orthop. 2014 January;5(1):6–13.
114 Foot and ankle injections
24. Baumhauser JF et al. Prospective, randomized, multi-centered clinical
trial assessing safety and efficacy of a synthetic cartilage implant versus
first metatarsophalangeal arthrodesis in advanced hallux rigidus. Foot
Ankle Int. 2016;37(5):457–69.
25. Korim MT, Mahedevan D, Ghosh A, Mangwani J. Effect of joint
pathology, surface preparation and fixation method on union frequency
after first metatarsophalangeal joint arthrodesis: A systematic review of
the English literature. Foot Ankle Surg. 2017 September;23(3):189–94.
26. Stevens J, de Bot RTAL, Hermus JPS, van Rhijn LW, Witlox AM.
Clinical outcome following total joint replacement and arthrodesis for
hallux rigidus: A systematic review. JBJS Rev. 2017 November;5(11):e2.
27. de Cesar Netto C, da Fonseca LF, Nascimento FS, O’Daley AE, Tan
EW, Dein EJ, Godoy-Santos AL, Schon LC. Diagnostic and therapeutic
injections of the foot and ankle – An overview. Foot Ankle Surg. 2017.
28. Salzman CL, Salamon ML, Blanchard GM, Huff T, Hayes A, Buckwalter
JA, Amendola A. Epidemiology of ankle arthritis: Report of a
consecutive series of 639 patients from a tertiary orthopaedic center.
Iowa Orthop J. 2005;25:44–6.
29. Horisberger M, Valderrabano V, Hintermann B. Posttraumatic
ankle osteoarthritis after ankle-related fractures. J Orthop Trauma.
2009;23(1):60–7.
30. Barg A, Pagenstert GI, Hügle T, Gloyer M, Wiewiorski M, Henninger
HB, Valderrabano V. Ankle osteoarthritis. Etiology, diagnostics and
classification. Foot Ankle Clin N Am. 2013;18:411–26.
31. Lawton CD, Butler BA, Dekker RG II, Prescott A, Kadakia A, Kadakia
AR. Total ankle arthroplasty versus ankle arthrodesis – A comparison
of outcomes over the last decade. J Orthop Surg Res. 2017;12(1):76.
32. Witteveen AGH, Siervelt IN, Blankevoort L, Kerkhoffs GM, van Dijk
CN. Intra-articular sodium hyaluronate injections in the osteoarthritic
ankle joint: Effects, safety and dose dependency. Foot Ankle Surg.
2010;16:159–63.
33. Hopper MA, Robinson P. Ankle impingement syndromes. Radiol Clin
N Am. 2008;46:957–71.
34. Tol JL, Verheyen CP, van Dijk CN. Arthroscopic treatment of anterior
impingement in the ankle. J Bone J Surg Br. 2001;83:9–13.
35. Coull R, Raffiq T, James LE, Stephens MM. Open treatment of anterior
impingement of the ankle. J Bone J Surg Br. 2003;85-B(4):550–3.
References 115
36. Cerezal L, Abascal F, Canga A, Pereda T, Garcia-Valtuille R, Perez-
Carro L, Cruz A. MR imaging of ankle impingement syndromes. Am J
Roentgenol. 2003;181:551–9.
37. Mitchell MJ, Bielecki D, Bergman AG, Kursunoglu-Brahme S, Sartoris
DJ, Resnick D. Localization of specific joint causing hindfoot pain:
Value of injecting local anaesthetics into individual joint during
arthrography. Am J Roentgenol. 1995;164:1473–6.
38. Robinson P, Bollen SR. Posterior ankle impingement in professional
soccer players: Effectiveness of sonographically guided therapy. Am J
Roentgenol. 2006;187:W53–8.
39. Heidari N, Pichler W, Grechenig S, Grechenig W, Weinberg AM.
Does the anteromedial or anterolateral approach alter the rate of joint
puncture in injection of the ankle? A cadaver study. J Bone Joint Surg
(Br). 2010;92-B:176–8.
40. Lee KB, Bai LB, Song EK, Jung ST, Kong IK. Subtalar arthroscopy for
sinus tarsi syndrome: Arthroscopic findings and clinical outcomes of
33 consecutive cases. Arthroscopy. 2008;24(10):1130–4.
41. Klausner VB, McKeigue ME. The sinus tarsi syndrome. A cause of
chronic ankle pain. Phys Sports Med. 28(5):75–80.
42. Taillard W, Meyer JM, Garcia J, Blanc Y. The sinus tarsi syndrome. Int
Orthopaed (SICOT). 1981;5:117–30.
43. Lee KB, Bai LB, Park JG, Song EK, Lee JJ. Efficacy of MRI versus
arthroscopy for evaluation of sinus tarsi syndrome. Foot Ankle Int.
2008;29(11):1111–6.
44. O’Connor D. Sinus tarsi syndrome: A clinical entity. J Bone Joint Surg.
1958;40:720–6.
45. Kuwada GT. Long-term retrospective analysis of the treatment of sinus
tarsi syndrome. J Foot Ankle Surg. 1994;15:349–53.
46. Pekarek B, Osher L, Buck S, Bowen M. Intra-articularcorticosteroid
injections: A critical literature review with up-to-date findings. Foot.
2011;21:66–70.
47. Myerson MS. The diagnosis and treatment of injury to the tarsometatarsal
joint complex. J Bone Joint Surg (Br). 1999;81-B:756–63.
6
Image-guided injections in
orthopaedics
SANGOH LEE AND RAJ BHATT
INTRODUCTION
Image-guided intervention is thought to increase accuracy, improve symptom
relief and clinical outcome compared to the non-image-guided cohort. It is
important to be aware of the indications for image-guided intervention, the
characteristics of medications that are used and their associated potential
side effects. Thorough preparation and correct positioning of the patient is
integral to, if not the most aspect of, a successful image-guided intervention.
This chapter will discuss various image-guided techniques including bursa,
tendon/paratenon, joint and neuroma injections that are used in orthopaedics.
It will focus on how to overcome common pitfalls when it comes to therapeutic
injections of musculoskeletal systems.
Physical activity across the population is increasing with the young
acquiring more sports-related injuries and the elderly living longer resulting
in greater prevalence of degenerative joint disease. As a consequence, there is
increased in demand for image-guided diagnosis and appropriate intervention.
Due to the superficial nature of most musculoskeletal structures, there is large
practice of non-image-guided anaesthetic and steroid injections for symptom
relief. It is widely believed that this practice cannot accurately target the area
of interest, however the majority of patients will report some degree of benefit.
This is likely secondary to local diffusion effect and systemic spread of locally
injected medication. On the contrary, image-guided intervention gives real-
time information of the needle position and provides an accurate assessment
of the anatomy in which the medication is injected [1,2]. Henkus et al. found
that accurate injection via image guidance decreased pain and improved
functional score, whereas inadvertent injection in adjacent structures caused
117
118 Image-guided injections in orthopaedics
significant increase in pain [3]. Image guidance can be achieved by various
modalities including fluoroscopy, ultrasound (US), computed tomography
(CT) or magnetic resonance imaging (MRI). Image-guided injections become
more relevant in smaller joints, as it is difficult to identify these joints with
clinical assessment alone. Blind injection into adjacent structures can give
false-negative results leading to significant escalation of treatment including
surgery, which can be avoided with accurate image-guided intervention. This
chapter will therefore discuss the various image-guided techniques, focusing
on USS-guided intervention, and how to overcome common pitfalls when it
comes to therapeutic injections of musculoskeletal systems.
WHAT AND WHEN TO PERFORM
IMAGE-GUIDED INJECTIONS?
Indications
Steroid injections reduce inflammation, relieve pain and allow improvement
in function of the affected musculoskeletal systems. Their effect is usually
short-lived, therefore rehabilitation with physiotherapy, analgesia and relief
of causative biomechanical stress is paramount. Damaged cells from acute
trauma, repetitive stress injuries or inflammatory arthritis act as antigen, which
instigate an inflammatory cascade to the affected area. Although this facilitates
increased blood flow and healing process, prolonged inflammatory state can be
counterproductive causing scarring, oedema and loss of normal function leading
to significant morbidity. This process of angiogenesis is associated with pain in
tendinopathies. Corticosteroids act to inhibit cell-mediated immune response
and vascular permeability, reducing recruitment of cytokines, leukocytes and
macrophages. It also reduces pain and prostaglandin formation, which is an
important mediator of inflammatory cascade. Its action in cellular inflammatory
response seen in conditions such as rheumatoid arthritis is multifactorial
and downregulation of inflammatory mediators such as collagenase, human
leucocyte antigen (HLA)–DR, tissue inhibitor of metalloproteinase and
complements (C2 and C3) is thought to play an important part in reducing
inflammation [4]. In chronic repetitive stress injuries, there is usually an absence
of cellular inflammatory response, and the action of corticosteroids in this
category is less well documented. Thus, the term tendinopathy is more appropriate
than tendinitis. Local anaesthesia (LA) is also used in combination with
corticosteroids to primarily provide quick symptomatic relief and to confirm
What and when to perform image-guided injections? 119
Table 6.1 Indications for articular and periarticular
corticosteroid injections
Inflammatory arthritis
• Adult and juvenile rheumatoid arthritis
• Crystal-induced arthritis (gout, pseudogout)
• Spondyloarthritis (reactive and psoriasis)
Osteoarthritis
Periarticular/soft tissue conditions
• Bursitis
• Epicondylitis
• Adhesive capsulitis
• Tenosynovitis
• Carpal tunnel syndrome
• Baker’s cyst
• Ganglia
• Plantar fasciitis
that the area injected is the cause of the patient’s symptoms. The conditions in
which image-guided corticosteroids/anaesthetic injections are indicated can be
broadly divided into inflammatory arthritis, osteoarthritis caused by chronic
mechanical degeneration and periarticular/non-joint-related conditions caused
by chronic repetitive injuries or other immune-mediated pathologies (Table 6.1)
[5]. Image-guided injections are indicated once conservative treatment such
as physiotherapy and medical therapy have failed, before moving onto a more
radical treatment involving surgery.
Medications used in musculoskeletal injections include a combination
of LA and steroid injections. LA provides immediate symptom relief and
confirmation that the correct area has been injected, whereas steroid is used
to provide short- to medium-term symptom relief (Figure 6.1).
Corticosteroids
The most commonly used steroids in the United Kingdom include
methylprednisolone (Depo-Medrone, Pfizer Limited, Kent, UK) and
triamcinolone acetonide (Kenalog, E.R Squibb & Sons Limited, Middlesex,
UK). Different preparations of corticosteroids will have varying duration
of action and potency, which depends on the concentration, solubility and
chemical composition (e.g. particle size and tendency to aggregate). However,
120 Image-guided injections in orthopaedics
Figure 6.1 Commonly used local anaesthesia and steroid preparation in our
musculoskeletal radiology department. From left: 1% lidocaine, 2.5 mg/mL
levobupivacaine, 40 mg/mL Depo-Medrone.
these characteristics can also increase the risk of complications such as
tissue atrophy, tendon and fascial rupture, although these risks remain
low [6]. Intra-articular sepsis, bacteraemia and intra-articular fracture are
absolute contraindications to intra-articular corticosteroid injections, as it is
thought that this can exacerbate sepsis and retard bone healing [7]. Relative
contraindications include severe juxta-articular osteopenia, coagulopathy
and injection of joint three times that year or within 6 weeks. Corrections
or withholding of anticoagulation is controversial, however correcting the
international normalised ratio (INR) of greater than 2 is thought to be a safe
practice [7] (Table 6.2).
COMPLICATIONS
There are several potential or hypothetical complications to intra-articular
steroid injections. Although the risk is low, it is important to be mindful of
What and when to perform image-guided injections? 121
Table 6.2 Chemical composition of commonly used corticosteroid injectable
Triamcinolone
Steroid preparations Methylprednisolone acetonide
Equivalent potency (mg) 4 4
Solubility (% wt/vol) 0.001 (Medium) 0.0002 (Low)
Maximum particle size (µm) >500 >500
Particle aggregation Few Extensive
Volume of intra-articular Small 4–10 mg Small 2.5–10 mg
injectiona Medium 10–40 mg Medium 5–10 mg
Large 20–80 mg Large 40 mg
Duration of action [8,9] 8–56 days 14–66 days
Source: MacMahon PJ et al., Radiology, 2009, 252(3):647–61.
a Small joints = Metacarpophalangeal, facet and acromioclavicular, Medium joints =
Elbow and wrist, Large joints = Knee, shoulder and ankle.
potential risks and explain them to the patient as part of acquiring consent
for the intervention.
COMPLICATIONS RELATED TO THE JOINT
Septic arthritis is the most severe and feared complication of intra-articular
injections. However, due to the aseptic or the “no-touch” technique performed
by most practitioners, this is a rare complication, occurring in approximately
1/14,000–15,000 injections [10]. It usually occurs a couple of days after the
injection, which is an important differentiating factor from steroid flare,
which is a more common complication. This inflammatory type of reaction
to steroid injection closely mimics septic arthritis; however it occurs much
sooner than septic joint, settling after 2 to 3 days. There is also the hypothetical
complication of steroid-induced arthropathy, which is primarily based on
animal studies and case reports [10].
COMPLICATIONS RELATED TO SOFT TISSUE
Complications related to soft tissue include peri-articular calcification,
tendon rupture and skin pigmentation and atrophy. Soft tissue calcification is
known to occur following steroid injection, especially with triamcinolone
hexacetonide. It is thought that insoluble particles cause an immune-mediated
granulomatous response causing calcification. Triamcinolone acetonide
is up to 10 times more water soluble, and therefore is the preferred choice of
122 Image-guided injections in orthopaedics
medication [11]. Triamcinolone is also known to cause subcutaneous fat, skin
atrophy and depigmentation, and therefore is not recommended for superficial
injections. Depigmentation is seen more commonly in dark-skinned patients and
can take up to 2 months to manifest, which mostly resolves after 12 months.
Intratendinous steroid injection is associated with tendon rupture, and it is
thought to be secondary to non-inflammatory degeneration of collagen at the
myotendinous junction [12]. This highlights the importance of image-guided
injection of steroid: deep enough to prevent superficial lipoatrophy but not too
deep as to cause intratendon injection, increasing the risk of tendon rupture and
significant morbidity.
SYSTEMIC COMPLICATIONS
Flushing post steroid injection is a phenomenon not uncommonly seen and
is thought to be a systemic histamine-mediated response. It usually occurs
several hours after the injection and can last up to a day, and antihistamine
has been used to ease the symptoms. Corticosteroids-induced hyperglycaemia
can occur in previously well-controlled diabetics, with effects lasting for
several days. Therefore, diabetic patients should be informed and blood sugar
monitored closely subsequent to steroid injections [13].
Local anaesthesia
Lidocaine is a fast action local anaesthetic agent with short duration of action
(2–4 hours). Levobupivacaine is slightly slower acting with longer duration
of action (6–8 hours). The role of LA is to provide immediate symptom relief
during the duration of the intervention. This allows a better experience for the
patient with less chance of anxiety-induced complications such as vasovagal
episodes. It also provides immediate feedback to the clinicians that the
location of injection is indeed the cause of the patient’s symptoms, which aids
in confirming the diagnosis.
SIDE EFFECTS
Studies have shown the chondrotoxic effect of LA to bovine articular
chondrocytes [14,15]. Levobupivacaine due to its longer duration of action has
been shown to be more chondrotoxic than lidocaine. Adrenaline-containing
LA has been shown to cause significant chondrotoxicity, likely due to its
vasoconstrictive effect and lowered pH, and should not be used for intra-
articular injections [16]. However, over several decades the injections have
How to perform image-guided injections? 123
shown no significant chondrotoxic effect of LA in clinical practice. This is likely
as the concentration of LA used in clinical practice is far less than that used in
clinical studies. Synovial fluid and active absorption of LA in patients are also
likely to aid in dissipation of the chondrotoxic effect of LA. Levobupivacaine
is also thought to have less cardiovascular and central nervous system toxicity
when compared to similar medications such as bupivacaine and ropivacaine
despite having similar potency. The most common adverse effect encountered
with levobupivacaine is hypotension [17].
HOW TO PERFORM IMAGE-GUIDED
INJECTIONS?
Preparation
Simple and clear instruction and information should be provided to the
patient to reduce their anxiety and improve overall experience when
acquiring an informed consent. This can be verbal or written depending
on the local policies. It is then important to position the patient in such a
way that will give plenty of space to carry out the procedure with a clear,
unobstructed route for needle placement. This should take into consideration
whether you are right or left handed, where the USS machine is located,
height of the couch, how comfortable the patient is in that position, and the
ability to carry out the procedure without straining yourself, as this will
increase the risk of contaminating the sterile field during the procedure.
It is thus advised to perform the procedure from the side closest to the area
being injected. Forward planning is therefore imperative for a successful,
uncomplicated procedure. Aseptic technique should be used with routine
sterilisation measures to reduce the risk of infection, especially when
joint prosthesis is being injected. This involves cleaning the skin with
chlorhexidine, utilisation of sterile drape, gloves and USS cover. Needles
and syringes should be opened from their packets and passed to the clinician
via the “no-touch” technique (Figure 6.2).
Techniques
There are two commonly used techniques employed when performing USS-
guided injections depending on the size, depth and location of the target.
124 Image-guided injections in orthopaedics
Figure 6.2 Commonly used equipment in USS-guided injections. These items
are kept in strictly sterile field and include the ChloraPrep stick, USS probe
cover, sterile gloves, different sizes of needles for different joints, syringes
filled with medication and gauze.
IN-VIEW APPROACH
The in-view approach is when the needle is placed in line with the USS probe
along its long axis so that the needle is visible along its route. There are obvious
benefits to seeing the needle at all times so that there is certainty where the
needle is placed. This technique is useful mostly for biopsies, and injection of
large and deep structures. The skin is punctured in line with the centre of the
USS probe at its short axis, slightly away from the USS probe depending on
the depth of the target. Deep structures will require skin puncture to be made
close to the USS probe, whereas superficial structures mean skin puncture
should be made relatively distant from the USS probe in order to visualise the
trajectory of the needle. It is important to visualise the tip of the needle at all
times, especially before the medication is injected, to prevent injection into
adjacent soft tissue structures. When the needle tip is lost, small adjustments
with the USS probe in a steady sweeping motion are made until the needle tip
is found and note is made of the path that the needle has taken. The USS probe
is then placed back into the correct position and the needle slightly retracted
and position readjusted before it is advanced in a correct path. The bevel of
How to perform image-guided injections? 125
(a) (b)
Figure 6.3 In-view approach of the talonavicular joint. (a) There is joint
effusion and synovial thickening in keeping with synovitis. The needle can be
seen throughout its length with the clearly visible needle tip with its bevel
positioned within the joint. (b) The USS probe is positioned longitudinally
along the dorsum of the foot with the needle placed in line with the probe.
the needle should be kept superiorly as to prevent inadvertent injury to deeper
structures and rotated 180° before the injection is performed. Anechoic fluid
distension should be seen whether the joint, bursa or soft tissue is injected to
confirm the correct position. Small blebs of hyperechoic foci can sometimes
be seen, which represent blebs of air from the needle or syringe (Figure 6.3).
OUT-OF-VIEW APPROACH
The out-of-view approach is used for superficial and small joint injections
where direct visualisation of the needle tract may not be necessary. It is also
a useful technique when an adjacent body part gets in the way of allowing
the needle to be inserted at the end of the USS probe. A position is marked
in the middle of the USS probe along its long axis and the needle inserted
perpendicular to the probe straight down into the target without the need for
any significant angulation. The needle tip should become visible on the USS
image at the area of interest (Figure 6.4).
Tendon/paratenon intervention
Tendons are mostly surrounded by tendon sheath that allow smooth gliding
without causing friction. Alteration to this mechanism, either by misuse or
repetitive stress injury, can cause degeneration of the tendon itself causing
tendinopathy or inflammation of the tendon sheath causing tenosynovitis.
Angiogenesis is thought to play a part in this pathology, which is thought
126 Image-guided injections in orthopaedics
(a)
(b)
Figure 6.4 Out-of-view approach of tarsometatarsal joint. (a) Linear high
echogenicity can be seen at the centre of the joint, which is the needle tip
coming into view of the USS. (b) The needle is positioned parallel to the short
axis of the USS probe and inserted perpendicular to the joint. The needle
cannot be traced along its entire length as is seen in the in-view approach. This
approach is used for superficial and small joint injections.
to cause pain and predisposing the tendon to degeneration and tear.
Hydroxyapatite crystals can also form within the tendon substance as a
response to repetitive injury causing calcific tendinopathy, which can cause
tendon degeneration, pain and reduced range of motion. There are certain
tendons that do not have tendon sheath, such as the Achilles tendon. These
tendons are surrounded by paratenon instead, which can also become irritated
causing paratenonitis.
Inflammatory tenosynovitis causes fluid distension of the tendon sheath,
which allows corticosteroid and LA injection to be relatively straightforward.
How to perform image-guided injections? 127
(a) (b)
Figure 6.5 (a) Injections of tendon sheaths in tenosynovitis. Injection of long
head of the biceps tendon sheath. The long head of the biceps can be seen
as a round structure traversing through the bicipital groove of the humerus.
(b) The USS probe is positioned along the short axis of the long head of the
biceps tendon within the bicipital groove. The needle is inserted in plane with
the USS probe.
However, careful assessment of the underlying tendon should be made as
steroid injection can predispose to tendon rupture if there is pre-existing
injury. The needle can be inserted either along the long or short axis of the
tendon sheath depending on the accessibility. As previously described, it is
important to keep the needle tip in view at all times as inadvertent penetration
and injection of the tendon itself can cause tendon injury and rupture. Correct
needle position should see fluid distension of the tendon sheath throughout
its length. If there is no evidence of uniform fluid distension along the tendon
sheath, it implies the needle is either outside the tendon sheath or within
the tendon itself, therefore the injection should be stopped immediately and
needle repositioned. Paratenon injection is similar in technique to tendon
sheath injection; however, there is no paratenon anterior to the Achilles
tendon, therefore post-injection fluid distension will only be seen on three
sides of the Achilles tendon (Figures 6.5 and 6.6).
Dry needling therapy
USS-guided dry needling therapy is reserved for those who have tendinopathy
and failed conservative management. USS allows identification of tendinopathic
tissue which is targeted for treatment, whilst the normal tendon substance is
left undisrupted. The needle is guided towards the tendinopathic tissue under
USS guidance, taking care not to cause injury to the articular cartilage or the
surrounding structure. Once in a satisfactory position, the needle is fenestrated
approximately 15 times for the duration of 40 seconds. The patient subsequently
128 Image-guided injections in orthopaedics
(a1) (b)
(a2) (c)
Figure 6.6 Injections of tendon sheaths in tenosynovitis. (a1) Injection of the
first extensor compartment due to De Quervain’s tenosynovitis. The image
is a cross-sectional view of compartment 1 with a needle seen entering the
tendon sheath from the left side. The medication is injected deep into the
tendon to reduce the risk of subcutaneous fat atrophy and skin pigmentation.
(a2) The longitudinal view of the first compartment extensor tendons with
neovascularity in keeping with tendinopathy. (b) The needle can be seen with
its tip at the iliopsoas tendon sheath. The iliopsoas tendon can be seen in its
cross section as an echogenic focus (highlighted by a dotted circle). (c) Cross-
sectional USS image of the tibialis posterior tendon. The needle can be seen
within the distended tendon sheath.
undergoes a strict physiotherapy regimen that includes unresisted movement
for 2 days followed by band-resistance exercises and regular exercises at
50% usual intensity weight by day 6 [18]. It is thought that fenestration of
the degenerate tendon causes disruption of the scar tissue, whilst localised
bleeding stimulates growth factor-β and basic fibroblasts that stimulate
organised tendon healing and remodelling [19]. Increased cellular and matrix
proliferation is the cause for increased echogenicity of the fenestrated tendon
on USS with resolution of patients’ symptoms [18] (Figure 6.7).
High-volume injection therapy
Association between neo-angiogenesis and pain in chronic tendinopathy
is documented, especially in Achilles and patella tendons. It is thought that
How to perform image-guided injections? 129
(a) (b)
Figure 6.7 USS-guided dry needling. (a) The needle can be seen within the
tendon substance of the tendinopathic Achilles tendon. Dry needling causes
disruption of the scar tissue and localised haemorrhage, which stimulates
growth factors that allow tendon healing. (b) The USS probe is positioned along
the plane of the Achilles tendon and the needle placed in line with the probe.
chronic degenerative changes lead to a hypoxic environment that drives
secretion of vascular growth factors leading to abnormal, disorganised new
vessel formation [20]. The mechanism of pain due to neo-angiogenesis is
not fully understood; however, it is thought to be due to direct ingrowth of
vessels in tendon substance or associated nerves that grow with the vessels.
In the Achilles tendon, neo-angiogenesis is predominantly found anteriorly
between the Kager’s fat and Achilles tendon substance. High-volume injection
(HVI) is a USS-guided therapy where a needle is inserted to this ventral
surface and large volume of saline injected in addition to corticosteroid and
LA mixture. The theory is that it will strip away any scar tissue, pathological
blood vessels and nerves formed that cause pain which prevent rehabilitation.
Resteghini and Yeoh found that neo-vascularity had significantly reduced 3
months post-HVI and there was a decrease in the tendon thickness at the
site of recalcitrant mid-Achilles tendinopathy [21]. Significant improvement
was also noted in terms of pain relief, which allowed better compliance
with physiotherapy involving an eccentric exercise programme (Figures 6.8
and 6.9).
Calcium barbotage
Calcific tendinosis occurs secondary to deposition of calcium hydroxyapatite
crystals and predominantly occurs around the rotator cuff and gluteal
tendons. It is usually a self-limiting condition, which sees calcium resorption
130 Image-guided injections in orthopaedics
(a) (b)
Figure 6.8 (a) Longitudinal and (b) transverse view of insertional Achilles
tendinopathy. There is marked thickening and neovascularity. The vessels are
seen arising from Kager’s fat pad and paratenon superficially. Pathological
new blood vessels and nerves are thought to cause pain and prevent
rehabilitation.
(a)
(b) (c)
Figure 6.9 HVI of Achilles tendon (different patient to Figure 6.8). (a) The needle
can be seen superficial to the tendinopathic Achilles tendon. (b) The needle is
also positioned deep to the Achilles tendon to get circumferential distension
of the paratenon away from the tendinopathic recalcitrant Achilles tendon.
Distension via saline causes disruption of scar tissue and neovascularisation
that contribute to pain. (c) The USS probe is positioned perpendicular to the
Achilles tendon and the needle inserted in line with the probe entering the
skin from the lateral approach.
How to perform image-guided injections? 131
spontaneously. However, in some patients, chronic tendinopathy ensues
with worsening pain and functional impairment. Calcium in supraspinatus
tendon can cause pain upon abduction of the shoulder due to mechanical
impingement. Success of the procedure entirely depends on the number of
calcium present and consistency of the calcium. Hard calcium usually appears
on USS as well-defined and bright echogenic foci with posterior acoustic
shadowing, whereas softer calcium appears ill-defined and less echogenic.
Percutaneous needle aspiration and lavage of these intra- and peritendinous
calcium have correlated with clinical improvement [22]. The patient’s arm is
positioned by their side with palm facing down in order to provide a degree
of internal rotation. It is important to remove all air from the syringe as any
air injected into the bursa can cause artefact that may impair visualisation
of the target area. Under USS guidance, a 22-gauge needle is inserted into
the calcium via the in-view approach maintaining constant visualisation
of the needle position. Once the needle tip is at the centre of the calcium
conglomerate, a small amount of local anaesthesia is injected into the calcium
and plunger of the syringe depressed and relaxed repeatedly whilst rotational
movement is made with the needle. Extracted calcium is seen as chalky debris
floating within the syringe. The subacromial bursa is injected once more, this
time with LA and corticosteroid mixture, preferably with a different needle
as the barbotage needle has tendency to become blocked after aspiration
(Figure 6.10).
Bursal injection
Bursa is a synovial-lined structure found between bone and adjacent soft
tissue that secrete lubricating synovial fluid to allow smooth, frictionless
gliding motion of the joint. Bursa can become inflamed through repetitive
stress injury, infection, medication and autoimmune conditions such as
rheumatoid arthritis. They usually contain a minimal amount of fluid that is
difficult to detect on USS. However, active bursitis leads to fluid distension of
the bursa with echogenic rind-like debris causing internal echoes. The active
inflammation can itself cause symptoms such as pain and restrictive
movement; however, its enlargement can cause mechanical impingement,
commonly seen in subdeltoid/subacromial bursa. Abduction of the arm will
cause bunching up of the bursa, which pinches between the supraspinatus
tendon and acromion leading to pain. It is important not to put too much
pressure with the USS probe, as this can dissipate the fluid to different parts
of the bursa masking its true extent of pathology. Colour flow is also seen
132 Image-guided injections in orthopaedics
Figure 6.10 Supraspinatus calcium barbotage. The needle can be seen
entering the calcium hydroxyapatite crystal within the supraspinatus tendon
under the in-view approach.
when there is presence of active bursitis. The technique of bursal injection is
similar to other musculoskeletal (MSK) injections described earlier. Informed
consent, patient positioning, sterile field and needle visualisation is key to
successful injection (Video 6.1, Table 6.3, Figures 6.11 and 6.12).
Table 6.3 Examples of commonly
occurring bursitis that can be
treated with USS-guided injections
Types of bursitis by location
Prepatellar
Trochanteric
Olecranon
Subacromial/subdeltoid
Achilles
Retrocalcaneal
Intermetatarsal
Iliopsoas
How to perform image-guided injections? 133
(a)
(b) (c)
Figure 6.11 Bursal injection. (a) The needle can be seen entering the
subacromial/subdeltoid bursa, which is distended in keeping with bursitis.
The underlying curvilinear structure is the supraspinatus tendon, which can
cause pain as the distended bursa impinge on the acromion. (b) Subacromial/
subdeltoid bursal distension can be seen as medication is injected. (c) The arm
is kept in an internal rotation with the palmar side facing down. This brings out
the supraspinatus tendon from beneath the acromion. The USS probe is placed
along the long axis of the supraspinatus tendon and the needle inserted in line
with the USS probe.
(a) (b)
Figure 6.12 Bursal injection. (a) The needle can be seen at the tip of the
greater trochanter. Fluid can be seen superficially in keeping with trochanteric
bursitis. (b) The needle is positioned within the retrocalcaneal bursa that is
distended by mixed echogenic fluid in keeping with severe retrocalcaneal
bursitis. The superficial oval structure (outlined by dotted circle) is thickened,
tendinopathic Achilles tendon.
134 Image-guided injections in orthopaedics
Joint injection
Joint injections are performed when conservative and medical therapy
have failed to ease the symptoms in osteoarthritis and sero-positive/
negative arthropathy. Large joints are relatively simple to visualise on USS
and the needle can be inserted according to ease of accessibility, area of
most joint effusion or synovial thickening (Video 6.2). The suggested
method is to use the in-view approach to track the needle placement in
order to avoid capsular injury or adjacent structures as the needle traverses
into the joint. The in-view approach is however more difficult to utilise on
smaller joints, as they are more superficial. Therefore it is often difficult
to place the needle into the joint at an angle, which is often required in the
in-view approach. This technique is made harder by the presence of
osteophytes and adjacent anatomical barriers and difficulty getting
adequate patient positioning. These joints include mid-/hindfoot, toe and
hand injections. Therefore, the out-of-view approach is recommended by
placing a needle in the middle of the USS probe and going straight down
into the joint perpendicular to the skin surface. Careful skin marking over
the joint is required in order to achieve intra-articular injection. The
needle tip can often appear in the middle of the USS screen and guided
into the joint (Figures 6.13 and 6.14).
Figure 6.13 Injection of the metatarsophalangeal joint (MTPJ). The needle can
be seen positioned within the MTPJ distended by joint effusion. Underlying
bone should be carefully examined for erosions, as synovitis of these peripheral
joints are associated with inflammatory arthritis.
How to perform image-guided injections? 135
(a) (b)
Figure 6.14 Joint injections. (a) The needle can be seen entering the posterior
glenohumeral joint. (b) The needle can be seen entering the hip joint anteriorly
at the femoral head and neck junction.
Neuroma injection
Neuroma is a lesion associated with nervous tissue and can be broadly divided
into neoplastic and non-neoplastic. Neoplastic neuromas are usually benign,
however they can undergo malignant transformation and these types of
neuromas are outside the scope of this chapter. Traumatic neuromas occur at
the site of recent trauma, such as surgery or amputation. This occurs at the end
of the injured nerve fibres and is secondary to disorganised and unregulated
regeneration of nervous tissue. They are closely related to superficial scars and
can often be painful, especially if present in weight-bearing areas found in an
amputated limb that is in contact with prosthesis (Figure 6.15).
(a) (b)
Figure 6.15 Post-traumatic neuroma at the site of below-knee amputation.
(a) Hypoechogenic lesion can be seen adjacent to the cortex of proximal tibia,
closely related to the neurovascular bundle. (b) A needle can be seen in close
proximity to the neuroma which is located on the right side of the image.
136 Image-guided injections in orthopaedics
(a)
(b) (c)
Figure 6.16 Morton’s neuroma. (a) Hypoechogenic focus can be seen within
the third web space of the forefoot in keeping with Morton’s neuroma, which
is closely related to the neurovascular bundle. A useful landmark is to examine
the pulsatile artery that traverses with the interdigital nerve. (b) The needle
can be seen as a white dot in the middle of the neuroma. (c) The USS probe is
placed longitudinally along the plantar aspect of the forefoot at the third web
space. The needle is placed in line with the USS probe on the dorsal surface
and inserted into position.
The commonest type of neuroma that is encountered in MSK injection
however is plantar interdigital neuroma of the foot, also known as Morton’s
neuroma. This occurs due to compression of the common interdigital nerve
that runs under the transverse metatarsal ligament. Thus, it is not a true
neoplasm and histology demonstrates perineural fibrosis, oedema and local
vascular proliferation [23]. It commonly occurs within the third metatarsal
web space, and patients present with pain or paraesthesia radiating from
midfoot to toes, which is reproducible by lateral compression of the forefoot.
USS is an effective method of diagnosing Morton’s neuroma. The USS probe
is placed longitudinally along the plane of the foot on the plantar surface
starting with the first metatarsal web space. Morton’s neuroma is seen as a
focal area of hypoechogenicity that displaces dorsally upon lateral
How to perform image-guided injections? 137
compression of the forefoot. Once identified, LA and corticosteroid can be
injected for short- to medium-term symptom relief. The USS probe is placed
again on the plantar surface and a 23G needle is inserted into the dorsal
surface and guided into the centre of the neuroma. Then 3 mL of local
anaesthesia and corticosteroid mixture is injected, which should see
distension of the neuroma and adjacent bursa (Video 6.3). Patients are
recommended to rest for a day, avoiding strenuous exercise for 5 days.
Greenfield et al. have reported total symptom relief after a series of
corticosteroid injections in 30% of cases with 80% of patients showing
complete or improved pain relief at 2-year follow-up [24]. Other single-
injection studies have however shown disappointing long-term outcome,
which may suggest repeated injections can improve long-term outcome in
non-surgical treatment of Morton’s neuroma [25,26]. However, these are
invariably associated with increased complications related to corticosteroids
such as plantar fat pad atrophy, hyperpigmentation and dermal thinning
(Figure 6.16).
TAKE-HOME MESSAGES
●● Image-guided intervention significantly increases needle position
accuracy, greater improvement in symptom relief and clinical
outcome when compared to the non-image-guided cohort.
●● Image-guided injections are indicated once conservative
treatment such as physiotherapy and medical therapy have failed.
●● Local anaesthesia provides immediate symptom relief, whereas
corticosteroid is used to provide short- to medium-term
symptom relief. There are different preparations available
depending on which structure is being injected and the required
duration of desired effect.
●● The in-view approach is used for soft tissue biopsies, and injection
of large and deep structures, whereas the out-of-view approach
is useful for superficial and small joint injections where direct
visualisation of the needle track may not be necessary.
●● Meticulous preparation with careful patient positioning, strict
aseptic technique and needle visualisation is key to a successful
injection.
138 Image-guided injections in orthopaedics
VIDEOS
Video 6.1 How to perform ultrasound-guided subacromial injection.
(https://youtu.be/8Soe89QPJc8)
Video 6.2 How to perform ultrasound-guided hip injection.
(https://youtu.be/gw4okfmael8)
Video 6.3 How to perform ultrasound-guided injection for Morton’s neuroma.
(https://youtu.be/YZSpHfWqO0w)
REFERENCES
1. Soh E, Li W, Ong KO, Chen W, Bautista D. Image-guided versus blind
corticosteroid injections in adults with shoulder pain: A systematic
review. BMC Musculoskelet Disord. 2011;12(1):137.
2. Eustace JA, Brophy DP, Gibney RP, Bresnihan B, FitzGerald O.
Comparison of the accuracy of steroid placement with clinical
outcome in patients with shoulder symptoms. Ann Rheum Dis.
1997;56(1):59–63.
3. Henkus HE, Cobben LPJ, Coerkamp EG, Nelissen RGHH, Van Arkel
ERA. The accuracy of subacromial injections: A prospective randomized
magnetic resonance imaging study. Arthroscopy. 2006;22(3):277–82.
4. Firestein G, Paine M, Littman B. Gene expression (collagenase,
tissue inhibitor of metalloproteinases, complement, and HLA-DR) in
rheumatoid arthritis and osteoarthritis synovium. Arthritis Rheum.
1991;34(9):1094–105.
5. Caldwell JR. Intra-articular corticosteroids. Drugs. 1996;52(4):507–14.
6. Nichols AW. Complications associated with the use of corticosteroids
in the treatment of athletic injuries. Clin J Sport Med. 2005;15(5):370–5.
7. MacMahon PJ, Eustace SJ, Kavanagh EC. Injectable corticosteroid and
local anesthetic preparations: A review for radiologists. Radiology.
2009;252(3):647–61.
8. Bird HA, Ring EF, Bacon PA. A thermographic and clinical comparison
of three intra-articular steroid preparations in rheumatoid arthritis.
Ann Rheum Dis. 1979;38(1):36–9.
9. Blyth T, Hunter JA, Stirling A. Pain relief in the rheumatoid knee
after steroid injection: A single-blind comparison of hydrocortisone
succinate, and triamcinolone acetonide or hexacetonide. Rheumatology.
1994;33(5):461–3.
References 139
10. Gray RG, Gottlieb NL. Intra-articular corticosteroids. An updated
assessment. Clin Orthop Relat Res. 1983;177:235–63.
11. Conti RJ, Shinder M. Soft tissue calcifications induced by local
corticosteroid injection. J Foot Surg. 1991;30(1):34–7.
12. Smith AG, Kosygan K, Williams H, Newman RJ. Common extensor
tendon rupture following corticosteroid injection for lateral tendinosis
of the elbow. Br J Sport Med. 1999;33:423–5.
13. Habib G, Safia A. The effect of intra-articular injection of betamethasone
acetate/betamethasone sodium phosphate on blood glucose levels in
controlled diabetic patients with symptomatic osteoarthritis of the
knee. Clin Rheumatol. 2009;28(1):85–7.
14. Karpie JC, Chu CR. Lidocaine exhibits dose- and time-dependent
cytotoxic effects on bovine articular chondrocytes in vitro. Am J Sports
Med. 2007;35(10):1621–7.
15. Chu CR, Izzo NJ, Papas NE, Fu FH. In vitro exposure to 0.5%
bupivacaine is cytotoxic to bovine articular chondrocytes. Arthroscopy.
2006;22(7):693–9.
16. Dragoo JL, Korotkova T, Kanwar R, Wood B. The effect of local
anesthetics administered via pain pump on chondrocyte viability. Am
J Sports Med. 2008;36(8):1484–8.
17. Foster RH, Markham A. Levobupivacaine: A review of its pharmacology
and use as a local anaesthetic. Drugs. 2000;59(3):551–79.
18. Settergren R. Treatment of supraspinatus tendinopathy with ultrasound
guided dry needling. J Chiropr Med. 2013;12(1):26–9.
19. Rudzki JR, Adler RS, Warren RF, Kadrmas WR, Verma N, Pearle AD,
Lyman S, Fealy S. Contrast-enhanced ultrasound characterization of
the vascularity of the rotator cuff tendon: Age- and activity-related
changes in the intact asymptomatic rotator cuff. J Shoulder Elb Surg.
2008;17(1 Suppl):96S–100S.
20. Ohberg L, Alfredson H. Ultrasound guided sclerosis of neovessels in
painful chronic Achilles tendinosis: Pilot study of a new treatment. Br
J Sports Med. 2002;36(3):173–7.
21. Resteghini P, Yeoh J. High-volume injection in the management of
recalcitrant mid-body Achilles tendinopathy: A prospective case series
assessing the influence of neovascularity and outcome. Int Musculoskelet
Med. 2012;34(3):92–100.
22. Del Castillo-González F, Ramos-Álvarez JJ, Rodríguez-Fabián G,
González-Pérez J, Calderón-Montero J. Treatment of the calcific
tendinopathy of the rotator cuff by ultrasound-guided percutaneous
140 Image-guided injections in orthopaedics
needle lavage. Two years prospective study. Muscles Ligaments Tendons
J. 2014;4(2):220–5.
23. Bourke G, Owen J, Machet D. Histological comparison of the third
interdigital nerve in patients with Morton’s metatarsalgia and control
patients. Aust N Z J Surg. 1994;64(6):421–4.
24. Greenfield J, Rea J, Ilfeld FW. Morton’s interdigital neuroma. Indications
for treatment by local injections versus surgery. Clin Orthop Relat Res.
1984;(185):142–4.
25. Bennett GL, Graham CE, Mauldin DM. Morton’s interdigital neuroma:
A comprehensive treatment protocol. Foot Ankle Int. 1995;16(12):760–3.
26. Rasmussen MR, Kitaoka HB, Patzer GL. Nonoperative treatment of
plantar interdigital neuroma with a single corticosteroid injection. Clin
Orthop Relat Res. 1996;(326):188–93.
7
Platelet-rich plasma injections
KEVIN ILO AND FAZAL ALI
INTRODUCTION
Platelet-rich plasma (PRP) is thought to have great potential in the process
of tissue healing and has become an emerging treatment option, specifically
for tendinopathies. In vitro studies have been promising, but clinical results
have often been variable. It is essential to understand the variability in PRP
and its production that may help to explain this. PRP has many theoretical
advantages and is being utilised as an alternative to surgery for common
musculoskeletal conditions. This chapter will discuss the theory surrounding
PRP, the evidence behind its indications and a protocol for injection.
Acute and chronic musculoskeletal injuries are common and are a
leading presenting complaint to healthcare professionals. These injuries can
potentially be difficult to manage, leading to chronic pain and disability. Due
to the significance of this issue there has been a drive to develop innovative
treatments. Ferrari et al. first developed PRP for use in cardiac surgery in
1987 [1]. PRP has also been known as platelet-rich fibrin, platelet-rich fibrin
matrix, platelet concentrate, fibrin sealant and platelet rich in growth factors.
Optimism surrounds PRP as a result of its theoretical ability to encourage
tissue regeneration. In 2008, the International Olympic Committee published
a consensus on the importance of molecular mechanisms in connective tissue
and skeletal muscle injury and healing. It envisaged the popularity and use
of autologous growth factors in musculoskeletal injuries would inevitably
increase, which it has done. However, although there is optimism regarding
the therapeutic abilities of PRP, it does not replace the first-line management
of musculoskeletal injuries.
Animal and in vitro studies have reported advantages of PRP for tissue
regeneration [2]. These reports show that platelets contain growth factors
and cytokines that can encourage tissue healing. Additionally, PRP can be
141
142 Platelet-rich plasma injections
produced quickly from the patients’ own blood, making it an ever-available
resource which does not initiate an immune response. There are numerous
human clinical studies evaluating the efficacy of PRP and whilst many show
good results, not all have such positive outcomes. The principles of treatment
may be comparable but there is no standard for PRP production and use. This
has led to disparities in the collection, preparation and application of PRP,
resulting in inconsistent methods making it difficult to compare between studies.
Furthermore, it is essential to understand that PRP is autologous and
consequently is affected by the condition of the patient. In human clinical
studies which test PRP, the PRP is not all from the same subject, and
differences between individuals will produce differences in the efficacy of
the PRP produced. Nevertheless, there are still many reports illustrating the
efficacy of PRP and its effectiveness in the treatment of certain musculoskeletal
complaints.
WHAT IS PLATELET-RICH PLASMA?
Plasma is the non-cellular component of blood and its largest single
component. PRP by definition is plasma with a platelet concentration above
baseline. There are many different commercially available preparations of
PRP, resulting in variable characteristics of the product. However, the objective
of PRP is to concentrate platelets three to five times the baseline platelet counts
of a concentration of at least 1,000,000 platelets/µL [3].
Platelets are well known for their role in haemostasis. They are also heavily
involved in inflammation and tissue repair. During the process of tissue
healing, the first cells to arrive at the site of injury are platelets. Platelets consist
of organelles, tubules and granules (alpha and dense). There are more than
1100 types of proteins identified inside platelets or on their surface. Platelets
become activated once they aggregate, with plasma fibrinogen playing a vital
role in the aggregation process. Once platelets are activated they release the
contents of their alpha and dense granules [4].
Alpha granules release growth factors which regulate cell differentiation
and proliferation, and are imperative for tissue healing. The main growth
factors are summarised in Table 7.1. The combined effect of these growth
factors is to stimulate cellular proliferation and production of extracellular
matrix and collagen at the site of injury [4]. Utilising autologous concentrated
growth factors to promote healing is the foundation of PRP treatment.
Other proteins such as blood fibrin, vitronectin and fibronectin proteins
Classification of PRP 143
Table 7.1 Function of growth factors in PRP
Growth factor Function
Platelet-derived growth Fibroblast chemotaxis, mesenchymal cells
factor (PDGFa-b) and osteoblast proliferation, collagen
synthesis, angiogenesis
Epidermal growth factor Endothelial chemotaxis/angiogenesis,
(EGF) mesenchymal cells proliferation, collagen
synthesis
Vascular endothelial growth Angiogenesis, proliferation of endothelial
factor (VEGF) cells
Transforming growth Mesenchymal cell proliferation, collagen
factor-beta (TGF-β) synthesis, endothelial chemotaxis and
angiogenesis
Basic fibroblast growth Growth and proliferation of mesenchymal
factor (bFGF) cells, chondrocytes and osteoblasts
Connective tissue growth Fibrosis, angiogenesis and platelet adhesion
factor (CTGF)
Platelet-derived epidermal Proliferation of keratinocytes and fibroblasts,
growth factor epidermal regeneration
Platelet factor 4 Chemotaxis for fibroblasts and neutrophils,
promotes coagulation
are also concentrated in PRP. They are involved in the migration of epithelial
cells, osteoinduction, and in the repair of conjunctive, epithelial and bone
tissues [3].
CLASSIFICATION OF PRP
PRP can be prepared and administered in different ways. These variables can
influence the effectiveness of PRP, which in turn can contribute to reported
variable results. A recent systematic review highlighted that the reporting of PRP
preparation protocols in clinical studies was very inconsistent and the current
reporting of PRP preparation and composition did not facilitate comparison
of the PRP products [5]. This highlighted and suggested standardisation of
PRP preparation protocols and composition. Consequently, it is essential to
recognise the differences between PRP products to allow comparison between
studies and provide reproducibility.
144 Platelet-rich plasma injections
There are several commercially available PRP products, and their major
differences include:
●● Platelet concentration: This is extremely variable between different PRP
products. The optimum platelet concentration is still unknown and
PRP products such as autologous conditioned plasma (Arthrex ACP)
are based on producing a lower platelet concentration when compared
to other PRP products. This is a result of the theory that platelet
concentrations greater than four times over baseline have shown to
cause an inhibitory effect on cell proliferation.
●● Leukocyte presence: The presence of leukocytes is dependent on
the centrifuge process. Whether leukocyte presence is beneficial is
debated. Leukocytes are known to have an essential role in tissue
healing, however, there is evidence that neutrophils release matrix
metalloproteinase, which can have a detrimental effect.
●● Anticoagulant utilisation: In order to prevent early activation of platelets,
an anticoagulant can be used. The consequence is the pH can be changed,
which can have an effect on the platelets and released growth factors.
●● Activator utilisation: It is contentious whether activation of PRP is
necessary, as it is argued that the in vivo environment stimulates activation.
In order to better categorise PRP preparations, Dohan Ehrenfest et al.
classified PRP products into four groups depending on their leucocyte and
fibrin content [6] (Table 7.2):
●● P-PRP, pure platelet-rich plasma
●● L-PRP, leukocyte and platelet-rich plasma
●● P-PRF, pure platelet-rich fibrin
●● L-PRF, leukocyte and platelet-rich fibrin
WHICH PRP PREPARATION IS BEST?
Due to variables involved in the production and administration of PRP
products, it is difficult to identify which preparation is the most effective.
Regarding tendinopathies, a recent meta-analysis of randomised controlled
trials by Fitzpatrick et al. evaluated the effectiveness of PRP. They established
that leucocyte-rich PRP had a greater positive outcome when treating
tendinopathies [7].
They also noted the importance of injection technique. An optimum
technique would involve the use of 1 to 2 mL of local anaesthetic injected first
What can PRP be utilised for? 145
Table 7.2 Classification of PRP products
PRP type Product name (manufacturer)
Pure platelet-rich plasma Cell separator PRP (experimental)
(P-PRP) PRGF/Endonet (BTI)
Vivostat PRF (Vivolution)
Nahita PRP (Nahita)
Autologous conditioned plasma (Arthrex)
Leukocyte and platelet-rich Curasan (Kleinostheim)
plasma (L-PRP) PCCS PRP (3I)
Magellan PRP (Magellan APS)
GPS PRP (Biomet)
Angel PRP (Sorin Group)
Smart Prep (Harvest Technologies)
Biomet GPS III (Biomet)
Plateltex (Plateltex)
Regen PRP (RegenLab)
Friadent PRP (Friadent-Schutze)
Ace PRP (Surgical Supply and Surgical
Science Systems)
Pure platelet-rich fibrin Fibrinet, PRFM (Cascade Medical)
(P-PRF)
Leukocyte and platelet-rich Choukrons PRF
fibrin (L-PRF) Cascade (MSF)
Intra-Spin L-PRF (Intra-Lock Inc)
just superficial to the tendon. This is followed by leucocyte-rich PRP injected
intratendinously using a peppering technique under ultrasound guidance.
WHAT CAN PRP BE UTILISED FOR?
In the field of orthopaedics, PRP has been utilised for many purposes. It
has been used during surgery to stimulate healing of damaged tissues.
PRP has also been applied in the treatment of different musculoskeletal
pathologies such as osteoarthritis, ligament injuries, cartilage injuries and
bone healing.
Tendinopathy is a common musculoskeletal condition. It is also commonly
termed as tendonitis, which implies that it occurs as a result of inflammation.
146 Platelet-rich plasma injections
Yet histology has displayed degeneration with absent or little inflammation
[8]. This may explain why non-steroidal anti-inflammatory medication and
steroid injections, which have been frequently used for chronic tendinopathy,
have not always been successful. Nevertheless it is plausible that inflammation
and degradation work together in the pathogenesis of tendinopathy [9]. As a
result there are many different treatment options, but resolution of symptoms
can be difficult, which can lead to chronic pain and dysfunction. Once
conservative treatments have failed there is the option of surgery, but this is
not without risk. PRP is emerging as a safe non-surgical treatment which has
gained popularity as a treatment option.
L ateral epicondylitis
Also known as tennis elbow, lateral epicondylitis is the most common condition
of the elbow with a prevalence of 1%–3% [10] (Video 7.1). Lateral epicondylitis
is thought to be an overuse injury instigated by eccentric overload of the
common extensor origin. It is common amongst manual workers and those
who perform repetitive gripping and lifting tasks. Symptoms are commonly
lateral elbow pain with resisted wrist extension and weakened grip. Patients
will typically have point tenderness at the extensor carpi radialis brevis
insertion into lateral epicondyle (which is just distal to the tip of the lateral
epicondyle).
As a common tendinopathy, the effectiveness of PRP as a treatment for lateral
epicondylitis has been extensively studied. A recent meta-analysis of randomised
controlled trials comparing PRP to steroid injections for lateral epicondylitis
showed encouraging results [11]. It established that PRP was more effective in
relieving pain and improving function in the intermediate and long term (up to
one year). Another recent systematic review has also shown favourable results
for PRP and both recommended the use of PRP as a treatment option for lateral
epicondylitis [12].
Patella tendinopathy
Also known as ‘jumpers knee’, patella tendinopathy is usually activity-related
anterior knee pain with localised tenderness at the inferior border of the
patella. It commonly affects young adults, especially athletes who perform
repetitive jumping. This leads to micro-tears and degeneration within the
patella tendon. Diagnosis is clinical, but ultrasound or MRI can be performed,
which will illustrate tendon thickening.
What can PRP be utilised for? 147
Enginsu et al. specifically investigated the use of PRP in the treatment of
chronic persistent patella tendinopathy [13]. Their study showed that PRP gave
encouraging clinical results and has the potential to achieve a satisfactory
outcome in the treatment of difficult chronic persistent patella tendinopathy.
A randomised controlled trial by Vetrano et al. investigated PRP versus
shock wave therapy for treatment of patella tendinopathy in athletes [14]. This
study showed PRP injections led to better midterm clinical results compared
with focused shock wave therapy in the treatment of patella tendinopathy in
athletes.
Non-insertional achilles tendinopathy
Non-insertional Achilles tendinopathy is characterised by pain, swelling and
thickening of the mid-substance of Achilles tendon (Video 7.2). It is
commonly associated with competitive and recreational sporting athletes.
PRP has been shown to resolve chronic Achilles tendinopathy which failed
conservative managements for a minimum of 6 months [15]. Medium term (4
years) outcome for PRP in chronic Achilles tendinopathy has also shown overall
good results [16].
Plantar fasciitis
Plantar fasciitis is characterised by sharp heel pain caused by inflammation of
the plantar fascia at its origin of the calcaneus. Typically, the pain of plantar
fasciitis is worse when the patient gets out of bed or at the end of the day after
prolonged standing. Diagnosis is clinical, with tenderness on palpation of the
calcaneum; however, radiographs can identify a plantar heel spur.
A recent meta-analysis compared the effectiveness of autologous blood
products, shock wave therapy and corticosteroids in the treatment of plantar
fasciitis. The conclusion was PRP was the most effective treatment [17].
Another recent systematic review concluded that PRP injection therapy may
be beneficial over purely conservative treatment and other injection therapy
modalities in the treatment of plantar fasciitis. However, they reiterated that
the current evidence is promising but limited, and further high-quality research
is required [18].
Quadriceps tendinopathy
Currently there are no studies on the efficacy of PRP in quadriceps tendinopathy.
148 Platelet-rich plasma injections
Rotator cuff tendinopathy
Rotator cuff tendinopathy is a common cause of shoulder weakness and
reduced range of movement. As rotator cuff tendinopathy is caused by
progressive and degenerative changes, its prevalence increases with age and
can cause chronic pain and disability. Diagnosis can be made clinically and
confirmed with imaging such as ultrasound and MRI.
A randomised controlled trial by Rha et al. concluded that PRP injections
lead to a progressive reduction in pain and disability when compared to dry
needling [19]. This benefit was still present at 6 months after treatment.
Another study by Scarpone et al. concluded that a single ultrasound-
guided, intra-lesional injection of PRP resulted in safe, significant sustained
improvement of pain, function and MRI outcomes in participants with
refractory rotator cuff tendinopathy [20]. These findings suggest that
treatment with platelet-rich plasma injections is safe and useful for rotator
cuff disease.
DOES PRP HAVE ANY CONTRAINDICATIONS?
Absolute: Sepsis, infection at target site, haemodynamic instability, platelet
dysfunction, critical thrombocytopenia
Relative: Recent fever, cancer, symptomatic anaemia, low platelet count,
recent and frequent non-steroidal anti-inflammatory or antiplatelet use
Complications and adverse effects
As with all invasive procedures there is the risk of infection, bleeding, damage
to surrounding structures and pain. There are theoretic complications such as
damage to tendon and tendon rupture. However, the complications for a PRP
injection are essentially similar as those for steroid injections. Additionally,
PRP is deemed safe due its autologous nature and there is no reported evidence
of a systemic reaction to a PRP injection.
The therapeutic effectiveness of PRP depends greatly on the condition of
the patient. Factors such as anti-inflammatory and anti-platelet medications
are well recognised to effect platelet function. Furthermore, variables such
as gender, age and systemic diseases can potentially influence the efficacy of
platelets.
PRP injection protocol 149
PRP INJECTION PROTOCOL
PRP product utilised: Biomet GPS III (Biomet Inc)
1. Patient and equipment preparation: The entirety of the procedure must
be performed using an aseptic technique with utilisation of sterile
equipment. The procedure can be performed without an assistant;
however, it is essential to prepare all equipment first. The patient needs
to be in a comfortable position (ideally on an examination couch) to
allow access for venepuncture and PRP injection to the site of interest.
2. PRP preparation: Although preparation and delivery are essentially
similar between most PRP products, each production system contains
different equipment. Therefore, it is important to understand the steps
and equipment required to produce PRP (Figures 7.1 to 7.6).
3. Local anaesthetic infiltration: Demarcate the exact area of tenderness
with a permanent marker in order to localise the area to inject the
PRP for best effect. Prepare the skin with a antiseptic agent such as
chlorhexidine gluconate. Local anaesthetic used for analgesia will make
the procedure easier and less uncomfortable for the patient. Take a
10 mL syringe with a 21G needle and withdraw 5 mL of 2% lignocaine.
Then inject, using a 23G needle, 2–3 mL of local anaesthetic (2%
lignocaine) just superficial to the tendon. (Note: It is best to inject the
local anaesthetic at least 5 minutes before the PRP injection. Therefore,
Figure 7.1 In the 60 mL syringe withdraw 5 mL of anticoagulant (ACD-A). Then
withdraw 55 mL of blood into the syringe.
150 Platelet-rich plasma injections
Figure 7.2 Next, 55 mL of patient’s bloods with 5 mL of anticoagulant is
inserted into the separator tube.
Figure 7.3 Place the separator tube into the centrifuge, place the appropriate
counterbalance opposite and set centrifuge at 3200 rpm.
PRP injection protocol 151
Figure 7.4 Post centrifugation, the top layer is platelet-poor plasma, the
middle layer is platelet-rich plasma and the bottom layer is red cells.
Figure 7.5 Extract the platelet-poor plasma using the 30 mL syringe.
152 Platelet-rich plasma injections
Figure 7.6 Withdraw 2 mL PRP using the 10 mL syringe, then gently shake the
tube for 30 s and withdraw the remaining PRP.
an appropriate time to do this is during centrifugation of the whole
blood) (Figure 7.7).
4. PRP injection technique: Using sterile gloves, attach a 23G needle to
the syringe of PRP. Place the needle perpendicular to the skin in the
centre of the previously demarcated area of tenderness. Advance the
needle through the skin, subcutaneous fat and into the tendon. Then
inject a small volume of PRP (<1 mL), withdraw the needle just out
of the tendon and then back into the tendon in a different position
within the demarcated area, injecting a small volume of PRP in each
area. Continue this ‘peppering’ manoeuvre 15 times throughout the
demarcated area. If the PRP finishes before this it is important to
continue as dry needling, which has been shown to be effective in
tendinopathies (Figures 7.8 to 7.11).
5. Place a dressing over the site of injection: The injected limb should
remain in the same position for approximately 15 minutes to keep the
PRP localised to the injection site.
PRP injection protocol 153
Figure 7.7 Local anaesthetic injection administered superficially to Achilles
tendon.
Figure 7.8 PRP injection administered.
154 Platelet-rich plasma injections
Figure 7.9 PRP injection to patella tendon.
Figure 7.10 PRP administered to quadriceps tendon.
PRP injection protocol 155
Figure 7.11 PRP administered for lateral epicondylitis.
Post-procedure protocol
Post PRP injection, patients can expect an increase in pain, swelling and
sometimes stiffness, which can last for one week. Over-the-counter non-steroidal
medication should be prohibited as they may inhibit the healing effect of PRP.
The stages of tendon healing are an inflammatory phase, repair phase
and remodelling phase. The initial inflammatory phase involves increased
vascular permeability, as there is recruitment of inflammatory cells to the
site of injury together with activation of platelets and formation of a fibrin
clot. The repair phase commences towards the end of the inflammatory
phase and can last up to 6 weeks. In this phase, there is collagen formed in a
disorganised fashion as there is an increase in cellularity and angiogenesis.
The last phase is the remodelling phase, where there is a decrease in cellularity
and neovascularisation, with an increase in type I collagen [21].
Currently the optimum rehabilitation of tendons treated with PRP is
in contention. During the initial inflammatory phase, the aim is to protect
156 Platelet-rich plasma injections
Table 7.3 Post-PRP treatment tendon protection
Affected tendon Immobilisation
Lateral epicondylitis Wrist splint
Patella/quadriceps tendinopathy Partial weight bearing with
crutches and Richards splint
Achilles tendinopathy, plantar fasciitis Partial weight bearing with
crutches and walking boot
Rotator cuff tendinopathy Shoulder sling
the tendon. To decrease risk of tendon injury, stretching and strengthening
are avoided. During the repair phase, scar formation can result in
contracture, which should be avoided with mobilisation. Stretching and
strengthening should commence during the repair phase. During the
remodelling phase, eccentric strengthening exercises can be initiated.
There should be a gradual increase in exercise for preparation to safe return
to activities/sports.
In the initial stage, there should be protection and immobilisation of the
affected tendon (Table 7.3). It is debatable how long the affected tendon should
be immobilised for, if at all. However, there are available and published post-
PRP injection rehabilitation protocols.
Exercise is crucial for healing following PRP and we recommend initiating
a rehabilitation program within one week of PRP injection. At this point,
physiotherapy emphasises gentle range of movement, stretching and isometric
strengthening with light resistance.
By weeks 2–3, eccentric strengthening exercises optimal with increasing
loads as tolerated are commenced.
This rehabilitation program by Lana et al. [22] has been suggested after
a review of the literature and can be utilised for all tendons. This is the
rehabilitation program advocated by the authors, however, this should be used
in conjunction with a physiotherapist and adjusted to the age, condition and
expectations of the patient.
DAY 0–3
Precautions:
●● Consider non-weight-bearing/protected weight bearing for lower limb
procedures
PRP injection protocol 157
●● Avoid non-steroidal anti-inflammatory drugs (NSAIDs)
●● Limited ice
Rehabilitation:
●● Active range of movement
DAYS 4–14
Precautions:
●● Progress to weight bearing as tolerated
●● Wean off protective orthosis/crutches
●● Avoid NSAIDs
●● Avoid ice
Rehabilitation:
●● Active range of movement
WEEKS 2–6
Precautions:
●● Avoid NSAIDs
●● Avoid ice
Rehabilitation:
●● Static stretching with progression to dynamic stretching (avoid ballistic
stretching)
●● High-repetition isotonic strengthening without accentuated eccentric
phase of contraction
●● Kinetic chain rehabilitation
●● Low-intensity energy system training
●● Consider manual therapy such as cross-fibre friction massage
WEEKS 6–12
Precautions:
●● None
Rehabilitation:
●● Eccentric strengthening
●● Power training as applicable
158 Platelet-rich plasma injections
●● Intensified energy system training as applicable
●● Sports-specific drills as applicable, typically later in phase
WEEKS 12 AND SO ON
●● Sport conditioning and injury prevention programme
●● Return to sport and desired activities
The authors would advocate that the patient can be permitted to
recommence sporting activities once they have finished the rehabilitation
programme. Resolution of symptoms should also be a target prior to starting
sport activities. As the process of tendon healing can take weeks to months,
patients should be informed of this and to persist with their rehabilitation. If
there is not full resolution of symptoms after completion of the rehabilitation
programme, another PRP injection can be performed. There should be at least
12 weeks between PRP injections.
TAKE-HOME MESSAGES
●● Tendinopathies are difficult to treat and it is advised that PRP
be used in chronic cases, with more that 3 months of symptoms
which is refractory to conservative management. In cases where
conservative measures have failed, PRP can be utilised as an
alternative to surgery.
●● It is important to understand the differences between different
preparations and administration of PRP products. Current
evidence suggests leucocyte-rich PRP is best utilised for
treatment of tendinopathies.
●● PRP injections are best done using a small volume of local
anaesthetic initially for pain relief, followed by administration of
PRP using a peppering technique.
●● Although there has been encouraging and positive outcomes
for the use of PRP in treating some tendinopathies, there is a
need for high-quality randomised controlled trials to accurately
understand its effectiveness with all tendinopathies.
References 159
VIDEOS
Video 7.1 How to perform PRP injection for tennis elbow.
(https://youtu.be/Epw6bNOVNYM)
Video 7.2 How to perform PRP injection for Achilles tendinopathy.
(https://youtu.be/nT_VkS2EdnQ)
REFERENCES
1. Ferrari M, Zia S, Valbonesi M, Henriquet F, Venere G, Spagnolo S,
Grasso MA, Panzani I. A new technique for hemodilution, preparation
of autologous platelet-rich plasma and intraoperative blood salvage in
cardiac surgery. Int J Artif Organs. 1987;10(1):47–50.
2. Roffi A, Di Matteo B, Krishnakumar GS, Kon E, Filardo G. Platelet-
rich plasma for the treatment of bone defects: From pre-clinical rational
to evidence in the clinical practice. A systematic review. Int Orthop.
2017;41(2):221–37.
3. Marx RE. Platelet-rich plasma: Evidence to support its use. J Oral
Maxillofac Surg. 2004;62(4):489–96.
4. Cole BJ, Seroyer ST, Filardo G, Bajaj S, Fortier LA. Platelet-rich
plasma: Where are we now and where are we going? Sports Health.
2010;2(3):203–10.
5. Chahla J, Cinque ME, Piuzzi NS, Mannava S, Geeslin AG, Murray IR,
Dornan GJ, Muschler GF, LaPrade RF. A call for standardization in
platelet-rich plasma preparation protocols and composition reporting:
A systematic review of the clinical orthopaedic literature. J Bone Joint
Surg Am. 2017;99(20):1769–79.
6. Dohan Ehrenfest DM, Rasmusson L, Albrektsson T. Classification of
platelet concentrates: From pure platelet-rich plasma (P-PRP) to leucocyte-
and platelet-rich fibrin (L-PRF). Trends Biotechnol. 2009;27(3):158–67.
7. Fitzpatrick J, Bulsara M, Zheng MH. The effectiveness of platelet-rich
plasma in the treatment of tendinopathy: A meta-analysis of randomized
controlled clinical trials. Am J Sports Med. 2017;45(1):226–33.
8. Alfredson H, Ljung BO, Thorsen K, Lorentzon R. In vivo investigation of
ECRB tendons with microdialysis technique – No signs of inflammation
but high amounts of glutamate in tennis elbow. Acta Orthop Scand.
2000;71(5):475–9.
160 Platelet-rich plasma injections
9. Abate M, Silbernagel KG, Siljeholm C, Di Iorio A, De Amicis D, Salini
V, Werner S, Paganelli R. Pathogenesis of tendinopathies: Inflammation
or degeneration? Arthritis Res Ther. 2009;11(3):235.
10. Verhaar JA. Tennis elbow. Anatomical, epidemiological and therapeutic
aspects. Int Orthop. 1994;18(5):263–7.
11. Mi B, Liu G, Zhou W, Lv H, Liu Y, Wu Q, Liu J. Platelet rich plasma
versus steroid on lateral epicondylitis: Meta-analysis of randomized
clinical trials. Phys Sportsmed. 2017;45(2):97–104.
12. Arirachakaran A, Sukthuayat A, Sisayanarane T, Laoratanavoraphong
S, Kanchanatawan W, Kongtharvonskul J. Platelet-rich plasma versus
autologous blood versus steroid injection in lateral epicondylitis:
Systematic review and network meta-analysis. J Orthop Trauma.
2016;17(2):101–12.
13. Enginsu M, Lokmaoğlu R, Selimoğlu Ş, Korkmaz E. Use of platelet-
rich plasma (PRP) for the treatment of chronic persistent jumper’s knee.
Orthop J Sports Med. 2014;2(3 Suppl):2325967114S00267.
14. Vetrano M, Castorina A, Vulpiani MC, Baldini R, Pavan A, Ferretti
A. Platelet-rich plasma versus focused shock waves in the treatment of
jumper’s knee in athletes. Am J Sports Med. 2013;41(4):795–803.
15. Monto RR. Platelet rich plasma treatment for chronic Achilles
tendinosis. Foot Ankle Int. 2012;33(5):379–85.
16. Filardo G, Kon E, Di Matteo B, Di Martino A, Tesei G, Pelotti P, Cenacchi
A, Marcacci M. Platelet-rich plasma injections for the treatment of
refractory Achilles tendinopathy: Results at 4 years. Blood Transfus.
2014;12(4):533–40.
17. Hsiao MY, Hung CY, Chang KV, Chien KL, Tu YK, Wang TG.
Comparative effectiveness of autologous blood-derived products,
shock-wave therapy and corticosteroids for treatment of plantar
fasciitis: A network meta-analysis. Rheumatology (Oxf). 2015;54(9):
1735–43.
18. Franceschi F, Papalia R, Franceschetti E, Paciotti M, Maffulli N, Denaro
V. Platelet-rich plasma injections for chronic plantar fasciopathy: A
systematic review. Br Med Bull. 2014;112(1):83–95.
19. Rha DW, Park GY, Kim YK, Kim MT, Lee SC. Comparison of the
therapeutic effects of ultrasound-guided platelet-rich plasma injection
and dry needling in rotator cuff disease: A randomized controlled trial.
Clin Rehabil. 2013;27(2):113–22.
References 161
20. Scarpone M, Rabago D, Snell E, Demeo P, Ruppert K, Pritchard P,
Arbogast G, Wilson JJ, Balzano JF. Effectiveness of platelet-rich plasma
injection for rotator cuff tendinopathy: A prospective open-label study.
Glob Adv Health Med. 2013;2(2):26–31.
21. Sharma P, Maffulli N. Tendon injury and tendinopathy: Healing and
repair. J Bone Joint Surg Am. 2005;87(1):187–202.
22. Lana JFSD, Santana MHA, Belangero WD, Luzo ACM. Platelet-Rich
Plasma; Regenerative Medicine: Sports Medicine, Orthopedic, and
Recovery of Musculoskeletal Injuries. Springer Science and Business
Media; 2013.
8
Visco-supplementation injections
ZAID ABUAL-RUB AND SANJEEV ANAND
INTRODUCTION
Intra-articular administration of hyaluronic acid (HA) is now a widely used
therapy for the treatment of symptomatic osteoarthritis (OA). Hyaluronic
acid, also called hyaluronan, is a naturally occurring polymer with a
simple chemical structure that has been identified and described as a major
component of all three structures of the joint functional unit: synovium,
synovial fluid and extracellular cartilage matrix (ECM). In OA, there is a
decrease in the elastic and viscous properties of synovial fluid that results
from reduction in the molecular weight and concentration of HA in the
synovial fluid.
Analgesics remain the first-line therapy in symptomatic OA in
international guidelines. However, Visco-supplementation has shown a better
pain effect than that of paracetamol and comparable to that of non-steroidal
anti-inflammatory drugs (NSAIDs) with better risk–benefit ratio, therefore
offering a potential alternative to conventional first-line therapy especially in
the elderly with multiple co-morbodities and medications [1].
Paracetamol is a well-tolerated analgesic but has low efficacy. While opioids
show greater analgesic effect, they are associated with poor tolerance. On the
other hand, NSAIDs fall in between paracetamol and opioids with regard to
efficacy. They are not recommended as a long-term treatment due to their
potential gastrointestinal, cardiovascular and renal side effects.
Visco-supplementation is a medical procedure in which a preparation of
highly purified hyaluronic acid is injected directly into the intra-articular space
of an arthritic joint aiming to increase joint lubrication. In addition, it helps
in restoration of the normal metabolic homeostasis of the intra-articular
microenvironment in the joints of osteoarthritis patients. It was first used
in the 1970s in eye surgery and was described for use in osteoarthritis in the
163
164 Visco-supplementation injections
1980s by Balasz. Intra-articular use of HA was approved in Japan and Italy in
1987, in Canada since 1992, in most of Europe since 1995, and in the United
States since 1997 [1,2].
WHAT IS THE STRUCTURE OF HA?
HA is a high molecular weight linear polysaccharide containing alternating
N-acetyl-D-glucosamine and D-glucuronic acid residues linked by β (1–4)
and β (1–3) bonds [3]. HA is found ubiquitously in the ECM of all vertebrate
tissues, although its concentration and binding partners vary. Although
classically considered an extracellular molecule, the presence of HA in the
cytoplasm and the nucleus was suggested as early as the 1970s and was
convincingly confirmed in the 1990s [4]. Although intracellular HA has been
suggested to play important roles in inflammation, its intracellular functions
remain largely unknown [5].
HA is uniquely synthesised at the plasma membrane rather than in
the Golgi apparatus, as is typical of other glycosaminoglycans (GAGs) [3].
Synthesis of mammalian HA is accomplished by a family of membrane-bound
glycosyltransferases composed of three isozymes: hyaluronan synthases
(HAS) 1, 2 and 3.
Although the three HAS isoforms are similar and synthesise an identical
product, they exhibit differences in half-life and stability, the rate of HA synthesis,
and affinity for HA substrates, all of which potentially affect the regulation of HA
synthesis and biological function [6]. Of particular interest is the finding that the
three HAS enzymes synthesised HA of varying molecular masses.
HA can be broadly classified according to their molecular weight (MW)
and formulation type:
●● Solutions of low MW (500–1200 kDa)
●● Solutions of high MW (6000 kDa)
●● Cross-linked HA
●● Solutions of non-animal stabilised HA (NASHA)
HOW DOES HA WORK?
The non-clinical basic science literature provides evidence for numerous
mechanisms in which HA acts on joint structures and function. The binding
What are the indications for usage? 165
of HA to cluster of differentiation (CD) 44 receptor has been to reported to be
the biological cause of the following mechanisms:
●● Chondroprotection – Intra-articular HA has been shown to reduce
chondrocytes apoptosis, while increasing chondrocyte proliferation [7].
●● Proteoglycan and glycosaminoglycan (GAG) synthesis – As OA
progresses, intrinsic proteoglycans and GAG concentrations decline
within cartilage. There is evidence demonstrating that intra-articular
HA stimulated proteoglycan synthesis delaying OA progression [8].
Intra-articular HA treatment is also shown to increase endogenous
production of GAG and intrinsic HA.
●● Anti-inflammatory – Interleukin-1β (IL-1β) is known to demonstrate
pro-inflammatory effects, and HA was found to inhibit IL-1β expression
through binding to CD44, which explains its anti-inflammatory effect [9].
●● Mechanical – The viscous nature of HA treatment is shown to lubricate
the joint capsule, preventing degeneration through decreased friction.
It also provides cushioning to absorb pressure and vibration within the
joint that otherwise may lead to chondrocyte degradation [10].
●● Analgesic – HA analgesic effects have been shown to occur at
mechanosensitive stretch-activated ion channels, where channel activity
is significantly decreased upon HA binding, as well as, it reduces the
action of joint nociceptors, which provides pain reduction within the
joint [11].
WHAT ARE THE INDICATIONS FOR USAGE?
The indications for use of intra-articular HA can be classified according to:
●● Severity of OA – Moderate OA is the indication of choice for visco-
supplementation, efficacy being better in moderate joint space
narrowing (Kellgren and Lawrence grades 2 and 3), whichever the joint.
Some studies, however, have reported efficacy in highly advanced knee
OA (grade 4), in which HA injection can provide interim relief awaiting
arthroplasty [12].
●● Compartmental involvement – In the knee, it is indicated in tibio-
femoral OA. The response rate was found to be less effective, around
50% in patellofemoral OA [13].
●● Associated conditions with OA
166 Visco-supplementation injections
– Inflammatory flare – In acute inflammation, with severe effusion,
visco-supplementation is not indicated. Synovitis has been shown
to be associated with accelerated joint cartilage degradation.
Moreover, it impairs the efficacy of HA, less by dilution in the
effusion fluid than due to enzymes and oxidants (hyaluronidases,
free radicals) degrading the HA chains [14].
– Subchondral bone lesion – Acute intense mechanical pain with
extensive bone oedema, bone fissure or stress necrosis on MRI
does not respond to HA and should be managed by non-weight-
bearing [12].
– Radiological chondrocalcinosis – There is no contraindication
under the condition that there is no gout-like acute inflammation
[14]. According to some reports, it is a factor of good response to
HA [15].
●● Post-operative use
– Knee arthroscopy – There is evidence of improved pain and
function in the short-term post-operative period (3–6 weeks) over
bupivacaine when intra-articular HA was infiltrated following
arthroscopic knee surgery [16].
WHAT IS THE RECOMMENDED DOSE FOR
HIGH MOLECULAR WEIGHT HA?
●● Hyman G-F 20
– Synvisc® (MW 6 million Da) – Chemically cross-linked hyaluronan
containing hylan A and B polymers produced from chicken combs.
A dose of 16 mg/2 mL is injected once a week for 3 weeks, or as
48 mg/6 mL given in a single injection (Synvisc-One®).
●● Sodium hyaluronate
– Hyalgan® (MW 500–730 kDa) – Administered once a week (1 week
apart) for a total of 3 to 5 weeks, at a dose of 20 mg/2 mL per
injection.
– Ostenil-plus® (MW 1–2 million Da) – Highly purified, natural,
non-chemically modified product combined with mannitol, single
injection at a dose of 40 mg/2 mL per injection.
– Supartz® (MW 620–1170 kDa) – Administered once a week (1 week
apart) for a total of 3 to 5 weeks, at 25 mg/2.5 mL per injection.
Is HA clinically effective? 167
IS HA CLINICALLY EFFECTIVE?
Although HA is most commonly used for knee osteoarthritis, it has also
been used in the shoulder, hip and ankle OA with studies in the literature
describing effectiveness in those joints (Box 8.1).
Knee
Data indicates that intra-articular HA preparations provide OA pain relief that
is comparable to or greater than that observed with conventional treatment,
NSAIDs, intra-articular corticosteroids, arthroscopic lavage, physical therapy
and exercise [17].
In a literature review published in 2004, in which a total of 13 randomised
controlled trials and 5 case series were included, there were conflicting results
with regard to trials of the low-molecular weight HA with more studies
demonstrating improvement in symptoms, whereas the trials of the high-
molecular weight HA had more consistent results indicating pain relief and
better functioning [18].
●● Lateral suprapatellar –
A line drawn vertically 1 cm superior to
proximal margin of patella, intersecting with a line drawn along the
posterior margin of the patella, to mark the entry point of the needle.
The needle is inserted parallel to the floor and is directed medially
(Figure 8.1).
●● Anteromedial and anterolateral approaches – Place the knee in flexion
and palpate the patella tendon. At the midpoint of the tendon, move
about 1 cm medially or laterally and palpate a soft spot which marks the
BOX 8.1 Where, how and who can perform HA injections
Site Primary care?a Image guidance? Trained AHP?a
Shoulder Yes No No
Hip No Yes No
Knee Yes No Yes
Ankle No Yes No
Abbreviation: AHP, allied health professional.
a These injections should only be performed by appropriately trained personnel
who have knowledge of local anatomy and good clinical skills.
168 Visco-supplementation injections
(a) (b) (c)
Figure 8.1 (a–c) Lateral suprapatellar portal for knee.
Figure 8.2 Anteromedial and anterolateral portals for knee.
needle entry point. Insert the needle with the tip aimed in a 45-degree
angle into the centre of the joint (Figure 8.2).
Hip
HA efficacy in OA of the hip remains controversial. In 2003, visco-
supplementation was included initially in international guidelines
for treatment of hip OA as a result of promising results, as shown in a
Is HA clinically effective? 169
meta-analysis in 2006 [19]. However, more recent evidence found no superiority
of HA hip injections over placebo [20]. In subgroup analysis, it was noticed
that poor effect may be secondary to advanced hip OA, presence of synovitis
and effusion, as well as poor access with a single injection administration.
In a subgroup of early hip OA without effusion, HA injection administered
under ultrasound (US) guidance was superior to placebo and corticosteroids.
Despite the relatively low level of evidence of the included studies, HA
injection under fluoroscopic or ultrasound guidance can potentially be effective
alternative in early hip OA. However, HA cannot be recommended as standard
therapy in hip OA for wider populations, and therefore the indications remain
a highly individualised matter.
●● Hip injection surface marking – The patient lies supine with the limb
in neutral rotation (patella facing forward). The tip of the greater
trochanter is identified and marked, the anterior superior iliac spine
(ASIS) is marked, and a line is drawn between them at the junction
between the upper third and lower two-thirds, lying at the soft spot (one
can feel the anterior border of the gluteus medius); this is marked as the
needle entry point (Figure 8.3a).
●● Hip arthrogram – Hip injection is recommended and usually performed
under fluoroscopy guidance to confirm the intra-articular position of
the needle as demonstrated earlier (Figure 8.3b).
Ankle
The use of fluoroscopy, computed tomography (CT), or US guidance can
increase accuracy of infiltration. The current available evidence suggests that
(a) (b)
Figure 8.3 (a) Hip surface markings. (b) Hip injection under fluoroscopy.
170 Visco-supplementation injections
visco-supplementation of the ankle joint is effective and improves functional
outcome scores but without evidence of superiority over other conservative
treatment measures. There is no data indicating which groups of patients
benefit from this therapy, which is the best treatment regimen, the best
technique to perform the procedure and the role of imaging techniques
(fluoroscopy, US, CT) [21].
●● Anterolateral approach – This approach avoids potential injury to
the anterior tibial artery and the deep peroneal nerve. However, the
superficial peroneal nerve is at risk and one should try to identify and
stay lateral to it. The needle is inserted at the joint line midway between
the base of the lateral malleolus and the lateral border of the extensor
digitorum longus, advancing the needle perpendicular to the fibular
shaft (Figure 8.4).
Anterior tibial artery
Lateral malleolus Medical malleolus
Anterolateral entry
point Anteromedial entry
point
Extensor digitorum longus
Extensor hallucis longus Tibialis anterior
Dorsalis paedis artery
Figure 8.4 Anterolateral and anteromedial approaches to ankle joint (marked
by crosses).
Is HA clinically effective? 171
●● Anteromedial approach – Identify the ankle joint line, the medial
malleolus, and the tendons of extensor hallucis longus and tibialis
anterior. Identify the space between the base of the medial malleolus
and the medial border of the tibialis anterior. Insert and advance the
needle perpendicular to the tibial shaft (Figure 8.4).
Shoulder
The limited evidence in literature is in favour of a beneficial effect of intra-
articular HA in the shoulder joint for OA with an intact rotator cuff. Significant
improvement in pain, function and satisfaction following two or three injections
at 6 months follow-up has been reported [22]. In comparison to those findings,
a recent systematic review found that despite good efficacy at follow-up with
intra-articular HA, when compared to placebo, the efficacy never reaches the
minimal clinically important difference at any of the follow-up points [23].
●● Anterior approach – Palpate the coracoid process and the humeral
head. With the arm in internal rotation (internal rotation is achieved
by placing the hand in lap of the patient), the joint space can be felt as a
groove lateral to the coracoid process. Direct the needle slightly laterally
and superiorly into the glenohumeral joint space (Figure 8.5).
●● Posterior approach – The needle is inserted 1–2 cm inferior and medial
to the posterior tip of the acromion, then directed anteriorly and
medially toward the coracoid (Figure 8.6).
Is HA safe?
There have been no major systemic safety issues reported. The most common
adverse reaction associated with visco-supplementation is the occurrence of a
Figure 8.5 Anterior approach for shoulder injection.
172 Visco-supplementation injections
Figure 8.6 Posterior approach for shoulder injection.
local reaction at the injection site [24]. This reaction is thought to be associated
with higher-molecular weight HA products, and is typically mild and self-
limited, resolving within 1 to 3 days.
A severe inflammatory acute response called pseudo-sepsis has been
described and mainly associated with repeated HA injections. The
pathogenesis of the condition is not known and thought to be immune-
mediated. It is defined by five classic clinical criteria:
●● Marked inflammation of the joint, typically with significant effusion
and pain, normally occurring within 24 to 72 hours after injection.
●● Occurring more often after exposure to more than one injection.
●● Sepsis or pseudogout is ruled out by the absence of infectious agents and
calcium pyrophosphate crystals in the synovial fluid.
●● Synovial fluid may include high numbers of mononuclear cells (largely
macrophages, with occasional neutrophils, and an increased percentage
of eosinophils) infiltrating from the surrounding membrane.
●● Not self-limiting and requires clinical intervention, usually in the form
of NSAIDs, or arthrocentesis and intra-articular steroid injection.
IS HA COST-EFFECTIVE?
The cost effectiveness of intra-articular HA can be realised with reduction
of NSAID use and the possibility of delaying total knee replacement, which
can reduce the need for costly revision procedures. Because different intra-
articular hyaluronan formulations require different numbers of injections and
office visits, are associated with variable treatment costs, and provide varying
degrees of efficacy, not all intra-articular hyaluronan formulations may be
equally cost-effective over time [17].
What are the recommendations of national/international guidelines? 173
Studies published in the recent years found that intra-articular HA cost
utility per quality-adjusted life year (QALY) was cost-effective when compared
to conventional care or when used in addition to conventional care versus
conventional care only [25].
WHAT ARE THE RECOMMENDATIONS OF
NATIONAL/INTERNATIONAL GUIDELINES?
United Kingdom:
●● National Institute for Health and Care Excellence (NICE) 2014 – NICE
does not recommend the use of intra-articular hyaluronan injections for
the management of osteoarthritis.
United States:
●● American Medical Society for Sports Medicine (AMSSM) 2015 – In a
network meta-analysis of the relevant literature to compare the effect of
visco-supplementation injection (HA) on patients with knee OA versus
intra-articular corticosteroids (IAS) and placebo, it was found that
participants receiving HA were 15% and 11% more likely to respond to
treatment than those receiving IAS and placebo, respectively. Subsequently,
the AMSSM ‘recommended’ the use of visco-supplementation injections
for Kellgren and Lawrence (KL) grade 2–3 knee OA in those patients above
60 years of age based on high-quality evidence demonstrating benefit.
For patients under the age of 60 years, AMSSM ‘suggested’ use of visco-
supplementation based on moderate-quality evidence.
●● American Association of Orthopaedics Surgeons (AAOS) 2013 –
The two primary changes recommended in the 2013 guidelines that
differ from the 2009 clinical practice guideline (CPG) included the
recommended dosage of acetaminophen which was reduced from
4000 mg to 3000 mg a day, and intra-articular HA is no longer
recommended as a method of treatment for patients with symptomatic
osteoarthritis of the knee. The 2009 guidelines review was inconclusive
regarding this treatment method.
●● Fourteen studies (three high-strength studies and 11 moderate-strength
studies) assessed intra-articular HA injections. Meta-analyses of
WOMAC (Western Ontario and McMaster Universities Osteoarthritis
Index) pain, function and stiffness subscales scores all found
174 Visco-supplementation injections
statistically significant treatment effects, none of the improvements met
the minimum clinically important improvement thresholds.
●● American College of Rheumatology (ACR) 2012 – The guideline
recommends the use of intra-articular HA injection for the treatment
of OA of the knee in adults, in accordance with the ACR 2012 OA
guidelines. It is indicated for management of osteoarthritis in patients
who are not good candidates or who do not respond to other treatment
options.
International:
●● Osteoarthritis Research Society International (OARSI) 2014 – The
OARSI published a guideline for the non-surgical management of knee
osteoarthritis based on the evidence published between 2009 and 2013.
A voting panel of 13 members (including seven rheumatologists,
two orthopaedic surgeons, two physical therapists, one primary care
practitioner and clinical guideline methodologist, and one physical
therapy and rehabilitation specialist) was formed that voted on the
appropriateness, therapeutic benefit and overall risk of each treatment
modality. It recommended that intra-articular HA was inappropriate
in multiple-joint OA and uncertain in knee-only OA. The inconsistent
conclusions among the meta-analyses and conflicting results regarding
intra-articular HA safety influenced the panel votes.
TAKE-HOME MESSAGES
●● Intra-articular high molecular weight HA has shown durable
effect in improving pain and function with effect onset at 4
weeks, peaking at 8 weeks and continuing up to 24 weeks.
Favourable outcomes are reported in mild/moderate
osteoarthritis without effusion.
●● Pseudo-sepsis is a recognised adverse effect that should be
anticipated, recognised and treated.
●● Clinicians are advised to familiarise themselves with their
national guidelines to guide their management.
●● Patients with no response or at high risk to conventional
pharmacological treatments may benefit from intra-articular HA.
Treatment should be tailored to patients individually.
References 175
●● At present, the inconsistent recommendations provided for intra-
articular HA treatment make it difficult for clinical professionals
to determine its appropriateness when treating patients with knee
osteoarthritis.
REFERENCES
1. Wen DY. Intra-articular hyaluronic acid injections for knee
osteoarthritis. Am Fam Physician. 2000;62(3):565–70.
2. George E. Intra-articular hyaluronan treatment for osteoarthritis. Ann
Rheum Dis. 1999;57(11):637–40.
3. Laurent TC, Fraser JR. Hyaluronan. FASEB J. 1992 April;6(7):2397–404.
4. Eggli PS, Graber W. Association of hyaluronan with rat vascular
endothelial and smooth muscle cells. J Histochem Cytochem.
1995;43:689–97.
5. Hascall VC, Majors AK, de la Motte CA, Evanko SP, Wang A, Drazba
JA, Strong SA, Wight TN. Intracellular hyaluronan: A new frontier for
inflammation? Biochim Biophys Acta. 2004;1673:3–12.
6. Itano N et al. Three isoforms of mammalian hyaluronan synthases have
distinct enzymatic properties. J Biol Chem. 1999;274(35):25085–92.
7. Brun P, Panfilo S, Daga Gordini D, Cortivo R, Abatangelo G. The
effect of hyaluronan on CD44-mediated survival of normal and
hydroxyl radical-damaged chondrocytes. Osteoarthritis Cartilage. 2003
March;11(3):208–16.
8. Williams JM, Zhang J, Kang H, Ummadi V, Homandberg GA. The
effects of hyaluronic acid on fibronectin fragment mediated cartilage
chondrolysis in skeletally mature rabbits. Osteoarthritis Cartilage. 2003
January;11(1):44–9.
9. Sasaki A, Sasaki K, Konttinen YT, Santavirta S, Takahara M, Takei H,
Ogino T, Takagi M. Hyaluronate inhibits the interleukin-1beta-induced
expression of matrix metalloproteinase (MMP)-1 and MMP-3 in human
synovial cells. Tohoku J Exp Med. 2004 October;204(2):99–107.
10. Lu HT, Sheu MT, Lin YF, Lan J, Chin YP, Hsieh MS, Cheng CW,
Chen CH. Injectable hyaluronic-acid-doxycycline hydrogel therapy in
experimental rabbit osteoarthritis. BMC Vet Res. 2013 April;9:68.
176 Visco-supplementation injections
11. Peña EL, Sala S, Rovira JC, Schmidt RF, Belmonte C. Elastoviscous
substances with analgesic effects on joint pain reduce stretch-activated
ion channel activity in vitro. Pain. 2002 October;99(3):501–8.
12. Lussier A, Civino AA, McFarlane CA, Olzinski WP, Potasner WJ,
De Medicic R. Viscosupplementation with hylan for the treatment of
osteoarthritis: Findings from clinical practice in Canada. J Rheumatol.
1996;23:1579–85.
13. Clarke S, Lock V, Duddy J, Sharif M, Newman JH, Kirwan JR. Intra-
articular hylan GF-20 (Synvisc) in the management of patellofemoral
osteoarthritis of the knee (POAK). Knee. 2005;12:57–62.
14. Legré-Boyera V. Viscosupplementation: Techniques, indications,
results. Orthop Traumatol Surg Res. 2015;101:S101–S108.
15. Conrozier T et al. Factors predicting long-term efficacy of hylan
GF-20 viscosupplementation in knee osteoarthritis. Joint Bone Spine.
2003;70:128–33.
16. Anand S, Singisetti K, Srikanth KN, Bamforth C, Asumu T, Buch
K. Effect of sodium hyaluronate on recovery after arthroscopic knee
surgery. J Knee Surg. 2016 August;29(6):502–9.
17. Waddell DD. Viscosupplementation with hyaluronans for osteoarthritis
of the knee: Clinical efficacy and economic implications. Drugs Aging.
2007;24(8):629–42.
18. Aggarwal A, Sempowski IP. Hyaluronic acid injections for knee
osteoarthritis. Systematic review of the literature. Can Fam Physician.
2004;50:249–56.
19. Fernandez-Lopez JC, Ruano-Ravina A. Efficacy and safety of
intraarticular hyaluronic acid in the treatment of hip osteoarthritis: A
systematic review. Osteoarthritis Cartilage. 2006;14:1306–11.
20. Qvistgaard E et al. Intra-articular treatment of hip osteoarthritis: A
randomized trial of hyaluronic acid, corticosteroid, and isotonic saline.
Osteoarthritis Cartilage. 2006;14:163–70.
21. Faleiro TB, Schulz RS, Jambeiro JES, Tavares Neto A, Delmonte FM,
Daltro GC. Viscosupplementation in ankle osteoarthritis: A systematic
review. Acta Ortop Bras. 2016;24(1):52–4.
22. Silverstein E, Leger R, Shea KP. The use of intra-articular hylan G-F
20 in the treatment of symptomatic osteoarthritis of the shoulder: A
preliminary study. Am J Sports Med. 2007 June;35(6):979–85.
References 177
23. Colen S, Geervliet P, Haverkamp D, Van Den Bekerom MP. Intra-
articular infiltration therapy for patients with glenohumeral
osteoarthritis: A systematic review of the literature. Int J Shoulder Surg.
2014 October;8(4):114–21.
24. Bellamy N, Campbell J, Robinson V, Gee T, Bourne R, Wells G.
Viscosupplementation for the treatment of osteoarthritis of the knee.
Cochrane Database Syst Rev. 2006;2:CD005321.
25. Rosen J, Sancheti P, Fierlinger A, Niazi F, Johal H, Bedi A. Cost-
effectiveness of different forms of intra-articular injections
for the treatment of osteoarthritis of the knee. Adv Ther. 2016
June;33(6):998–1011.
9
Practical prolotherapy
ROGER OLDHAM
WHAT IS PROLOTHERAPY?
The term ‘prolotherapy’ was introduced by Hackett in 1958 and derives
from the Latin proles meaning ‘generation’ or ‘growth’ [1]. The technique
has also been called ‘sclerotherapy’ from the Greek sklera meaning ‘hard’.
Prolotherapy describes the injection of non-pharmacological irritants and
hyperosmolar solutions into dysfunctional joints, capsules, tendons, ligaments
and entheses. These agents produce a controlled injury and inflammation with
the expectation of improving blood flow, and initiating and promoting the
healing cascade which results in deposition and hypertrophy of collagen [2].
The tissues treated are mainly lax or torn ligaments, areas of tendinopathy
and enthesopathy, and lax joint capsules. Once any instability or laxity is
corrected, pain relief usually follows (Figures 9.1 and 9.2).
HISTORY
400 bc Hippocrates II of Kos, the Greek physician, employed the insertion of
hot needles for recurrent shoulder dislocation [3].
1832 Sclerosing agents injected into hernias, hydroceles, varicose veins
and haemorrhoids [3,4].
1930 Hackett, Gedney, and Shuman began injecting ligaments with
sclerosants [1].
1930 Schultz treated temporomandibular joint (TMJ) dysfunction with irritant
injections and published his results after 20 years’ experience [5].
1936 Rice et al. showed fibrosis occurring 15 hours after sclerosing
injections which was dense and firm by 7 days and in compact
bundles by 18 days [6].
1955 Rice’s findings were corroborated by Hackett and he stated that this
therapy resulted in stabilisation of unstable joints [7].
179
180 Practical prolotherapy
Figure 9.1 Femoral attachment and joint line of medial collateral ligament of
the knee showing hypervascularity 1 week after the first of three injections of
P2G proliferant in lidocaine.
WHAT ARE THE INDICATIONS AND
CONTRAINDICATIONS?
The following conditions respond best to prolotherapy:
●● Joint instability – Including impingement syndromes, especially of the ankle,
and recurrent shoulder dislocation and acromioclavicular joint subluxation.
●● Pelvic pain – Especially sacroiliac dysfunction, symphysis pubis
instability and iliolumbar ligament pain.
●● Patients who have experienced only temporary, but definite, benefit
following manipulation.
●● Non-specific mechanical spinal pain – Particularly associated with
increased pain, tightness and tenderness of the surrounding muscles
which may be compensating for underlying ligament laxity.
●● Referred upper or lower limb pain in the absence of clinically significant
radicular compression.
What are the indications and contraindications? 181
Figure 9.2 For comparison here is the same scan as in Figure 9.1 at the pes
anserinus end which had not been injected with proliferant.
●● Persistent steroid resistant, non-specific, post-traumatic or surgical synovitis.
●● Enthesopathies, tendinopathy, plantar fasciitis.
●● Capsular laxity of the ankle where there is recurrent ligament
insufficiency.
●● Cervical headache, TMJ dysfunction and Barré-Liéou syndrome.
●● Osteoarthritis (OA) where joint laxity is a factor aggravating pain, e.g.
medial compartment OA of the knee secondary to lateral collateral
ligament laxity.
●● Patellofemoral pain associated with maltracking or recurrent patellar
dislocation.
●● Symptomatic spondylolisthesis and frequent recurrent acute
(discogenic) lumbago.
●● Miscellaneous – Core necrosis of the Achilles tendon, Osgood-Schlatter
disease (Figures 9.3 to 9.5).
The contraindications are the same as for any injection, e.g. local or general
sepsis, and where surgical treatment is indicated.
182 Practical prolotherapy
(a)
(b)
Figure 9.3 (a) Initial MRI scan of 77-year-old male keen tennis player with core
necrosis of the Achilles tendon. (b) Axial view.
What are the indications and contraindications? 183
Figure 9.4 The same patient 3 months after a single intratendinous injection
of P2G.
Figure 9.5 After three proliferant injections and 6 months after the first injection.
184 Practical prolotherapy
WHAT ARE THE ADVANTAGES,
DISADVANTAGES AND SIDE EFFECTS?
Prolotherapy is drug-free and allows the body to heal efficiently with minimal
scarring.
It is cheap. However, in the author’s opinion, this is one of the reasons for
its lack of uptake, as there is no pharmaceutical company willing to fund a
randomised controlled trial.
There is little or no intrinsic pain relief, which enables rehabilitation to
proceed safely and rapidly once the ligament is healed and the joint stable,
as there is no masking of pain such as occurs with steroids. The speed of
healing and stability without splinting helps to minimise deconditioning.
It is unnecessary to wait for soft tissue swelling to settle before injecting
proliferant.
The osmotic effect of injecting the hyperosmolar solution causes rapid
swelling of the injured structure and almost immediate correction of the
instability. It is therefore possible to re-examine the structure to check accurate
placement and/or possible related injury which can be subsequently injected.
Because of the aforementioned effect, the practitioner will soon discover
common multiple injury patterns for him- or herself.
Ligament laxity is an important risk factor in the development of
osteoarthritis and this can be relatively easily corrected with prolotherapy.
Based on the author’s personal experience, it is rare to make a patient
worse. Either prolotherapy will be effective or there will be no change, because
the wrong structure was treated or because prolotherapy is inappropriate.
Apart from the usual problems with the needle-shy patients, the only real
disadvantage is the fact that to achieve a good result one needs a significant
inflammatory reaction which will cause increased discomfort, swelling and
stiffness for 1 to 3 days. This can be minimised by good injection technique
ensuring even dispersal of multiple small aliquots (0.3 mL or less) of the
irritant solution and immediate mobilisation.
Severe afterpain is usually due to poor technique in injecting too much
proliferant in one spot. Usually this is manageable with patient reassurance.
Accidental injection of a nerve, e.g. the cutaneous branch of the saphenous
nerve when injecting a pes anserinus injury, may very rarely cause mild
neuritic symptoms for a month or so but will always resolve. Recovery from
these side effects can be speeded by the administration of decreasing doses of
oral steroids but is rarely necessary.
Getting started 185
Cutaneous nerve involvement will rarely cause mild numbness for 2 or
3 months.
Tenderness especially of a superficial structure, e.g. supraspinous ligament,
is usual but is not a problem and always resolves within a month.
Serious allergic reactions or anaphylaxis is extremely rare but, as with
injection therapy of any kind, should not be carried out unless facilities for
treatment are immediately available.
Particular care is needed to avoid injection into the subdural and pleural
spaces and major blood vessels and nerves especially when using phenol,
and teaming up with a radiological colleague is advised for imaging in
such areas.
WHAT IS THE CURRENT EVIDENCE?
Despite poor evidence, prolotherapy has become increasingly used by sports
and primary care physicians, podiatrists and orthopaedic surgeons, particularly
when treating elite athletes [8,9].
Objective results such as histological evidence and increasing use of
ultrasonography show clear regenerative change [10] (Figures 9.6 and 9.7).
A detailed review of the literature on the effect of dextrose injections was
carried out by Hauser et al. in 2016. They concluded that dextrose prolotherapy
was supported for the treatment of tendinopathies, knee and finger joint OA,
and spinal/pelvic pain [11].
Little emphasis has been placed on joint stability, which is the main
symptom in the author’s experience in treating sports injuries and non-athletes.
Instability can be most effectively treated with prolotherapy.
GETTING STARTED
Solutions
The simplest proliferant is hypertonic dextrose (d-glucose) diluted in 1%
lidocaine. This is readily available from any pharmacy as 50% glucose (25G in
50 mL). A reasonably strong solution is made by diluting 3 mL 50% dextrose
with 7 mL 1% lidocaine producing a 15% dextrose solution. For intra-articular
injections increase this to 5 mL 50% dextrose to which is added 5 mL 1%
lidocaine to obtain a 25% dextrose solution.
186 Practical prolotherapy
Figure 9.6 Chronic patellar tendinopathy of 18 months’ duration (22 May
2008).
Figure 9.7 The same patient after three prolotherapy injections (26 June
2008).
Preparation and needle technique 187
After trying many different substances over a 25-year period, the author
prefers P2G or P25G which contains:
Phenol 2.5%
Glucose monohydrate 25% in water for injection.
Glycerin 25%
This is obtainable in the United Kingdom as ‘Sclerosing Solution for
Injection’ and is manufactured by Torbay PMU, Paignton, Devon. It is supplied
in 10 mL multidose bottles. This is more effective than pure dextrose probably
because the glycerol is broken down more slowly than the dextrose prolonging
healing, and also the phenol is more highly irritant. This is diluted by mixing
4 mL of sclerosant with 6 mL of 1% lidocaine producing a 40% concentration
of sclerosant. Phenol may be left out when injecting intra-articularly and
dextrose only injected, but it has been shown to be safe and less than excreted
daily by the kidney [12].
The advantage of these solutions over blood products is that they are
simple to use and the reaction is predictable and controllable. If, for example,
a footballer is playing with a chronically lax ankle, he can be effectively treated
with a 30% solution on a Monday in the knowledge that he will be fit to train
on Thursday and play on Saturday. If he is sidelined with, for example, a grade
II medial collateral knee ligament (MCL) injury, it is advisable to initiate
treatment with a 40% mixture.
In some cases, autologous blood, platelet-rich plasma, bone marrow and
adipose tissue have been used [13].
PREPARATION AND NEEDLE TECHNIQUE
Prolotherapy can only be performed competently with the knowledge of
clinical orthopaedic tests of ligamentous and joint instability, referred
pain of ligamentous origin, surface anatomy, and an ability to visualise
deep structures in three dimensions. It can be usefully practised alongside
physiotherapy, manipulation, trigger point therapy, attention to posture, pain
management, and general health measures. Routine procedures of consent
and strict attention to sterility apply as with any injection.
Non-steroidal anti-inflammatory drugs (NSAIDs) should ideally be
discontinued 4 days before injection, but occasionally one has to treat a patient
on long-term steroids and the author does not find this to be a contraindication.
188 Practical prolotherapy
A few millilitres of 1% lidocaine administered through an orange 25G
25 mm needle to the skin will help nervous patients initially. This needle is
long enough, for example, to inject anterior talofibular, calcaneofibular and
deltoid ligaments at the ankle and can be left in situ whilst the syringe is
changed to one containing the proliferant/lidocaine mixture.
It is important to inject into the ligament substance down to the periosteum
at the enthesis. For efficacy and safety, do not inject proliferant initially unless
in contact with the bone. A few drops are injected here and continued as the
needle is withdrawn along the line of the ligament. No more than 0.3 mL
should be injected in any one place. With experience one is soon able to feel
the variable resistance to injection corresponding with the deficient fibres.
The second and third treatment sessions should produce increased resistance
to injection as the fibres form and thicken. It is difficult to inject a normal
ligament.
Most ligaments can be injected, without any form of imaging, with
anatomical knowledge and bony landmarks. Ultrasound guidance can be
helpful for localised lesions but in general the whole structure, not just the
injured section, will produce a better result.
Sacroiliac joints can easily be injected using the technique described by
Cyriax, as it is the posterior and interosseous ligaments which are at fault, not
the synovial joint [14]. With the patient prone and a pillow under the abdomen,
a 2-inch 21G green needle is inserted just beyond the midline midway between
the anterior and posterior superior iliac spine (ASIS and PSIS) at 60° from the
vertical and directed down to the joint injecting lidocaine at intervals between
the two bony points. After several minutes a 22G 90 mm spinal needle is then
inserted through the posterior and interosseous ligaments and 6–10 mL of
diluted proliferant injected at multiple points when in contact with the bone
and slowly withdrawn until ligament resistance is felt to subside.
●● Always commence injection with bone contact at the enthesis.
●● The key to tolerability and efficacy is effective dispersal of the proliferant.
●● Practise 3D visualisation and feel resistance to injection.
Frequency
Intervals between treatments have been recommended as 3 to 4 weeks based
on the timescale of the phases of wound healing. In practice, however, the
author has found good responses varying between twice weekly to once every
2 weeks depending on the lesion, patient’s reaction, duration and urgency.
Preparation and needle technique 189
Weekly injections would be a good starting point. Most lesions can repair with
three treatments with good technique, but occasionally up to six sessions may
be required. If treatment is to be effective an approximate reduction in laxity
of 50% should occur with each treatment.
Aftercare
Advise the patient of an increased bruised feeling, swelling and stiffness
lasting an average of 2 days. The patient and physiotherapist need to be
reminded that the inflammation is improving blood flow and this should
be encouraged not suppressed. Therefore, NSAIDs, ice and immobilisation
are replaced by simple analgesics, heat and immediate mobilisation. ‘Reduced
gravity’ treadmills are ideal for early rehabilitation after lower limb therapy.
Walking, low friction cycling and jogging in a pool should immediately be
encouraged. It is aggravated by attempting to ‘mix and match’ prolotherapy
with standard orthopaedic splinting, as this will result in severe pain
and stiffness. It cannot be emphasised enough that non-athletic patients,
after spinal, pelvic or lower limb treatment, should repeatedly walk short
distances even on the day of injections, rather than resting, to avoid
unpleasant afterpain and stiffness.
In summary it is MEAT (movement, exercise, analgesics, treatment) and not
RICE (rest, ice, compression, elevation) following prolotherapy.
Patients should be warned that tenderness (not pain) may persist for a
month or so, but this is just a sign of continued healing.
Time to achieve full benefit depends on the severity, complexity and
duration of the injury; secondary degenerative or compensatory changes
which may have occurred; age of the patient; and structural length of any
injured ligaments. A grade II injury of an anterior talofibular ligament (ATFL)
will resolve in 10 to 14 days, whereas an MCL will take 3 to 4 weeks.
Most patients notice subjective increased stability or balance after the first
treatment, but occasionally there may be no obvious benefit and therefore
patience is required. If the second treatment fails to improve, then one needs
to reassess. Not all symptoms improve at once, for example a patient with
sacroiliac joint (SIJ) dysfunction will usually first notice an improvement in
morning stiffness before pain starts to subside. Failure to respond altogether
is a sign that pathology lies elsewhere or surgery is required.
●● Educate the patient to expect bruised discomfort and stiffness. ‘It will be
worse before better’.
190 Practical prolotherapy
●● Immediate movement but not rest or stressing the joint is essential.
●● Improvement may not occur or be transient after the first injection; it is
a course.
TIPS FROM 25 YEARS’ EXPERIENCE
Those who are not experienced with prolotherapy (and are familiar with the
technique of injecting steroids) tend to aim for the pain area. This is often
not the case when using prolotherapy. Injecting an anterolateral impingement
point with a proliferant will increase the degree of impingement and pain when
it is the lax deltoid ligament which requires treatment.
Cervical pain, whiplash, cervical headache
and cervical-related dizziness
Injection of the facets and fascial laminar attachments is tricky and requires
imaging and experience, but most patients can be improved by simply injecting
the supraspinous and nuchal ligaments from the occiput to D1. This is possible
by injecting small aliquots from 10 mL of proliferant at intervals through a
2-inch 21G green needle using three, almost horizontal, needle punctures.
Injecting from the cranial end with bone contact reduces the risk of dural
puncture.
Bending the needle to about 15° at the hub prior to injection eases the
procedure here as in many areas. The patient will feel as though there is a
brace at the back of the neck but will be gratified by an immediate increased
range of movement, improvement in forward head posture and ease of
full shoulder abduction. This is due to reduced muscle tension resulting
from increased strength from turgidity of the ligaments produced by the
hyperosmolar fluid.
Acromioclavicular joint subluxation
Instability of the acromioclavicular joint is easy to demonstrate clinically
or on stressing during ultrasonography. It usually responds well to three
intra-articular injections of the proliferant. It is not necessary to inject the
costoclavicular ligament even in professional rugby players.
Tips from 25 years’ experience 191
Recurrent dislocation of the shoulder
and impingement syndrome
After years of tediously injecting the rotator cuff, glenoid labrum and capsule,
the author has found that three intra-articular injections of 10 mL of 25%
dextrose at weekly intervals is sufficient to stabilise glenohumeral joints
in most cases, even in rugby forwards and in the presence of significant
pathology. Increased resistance with smaller volumes will be felt with
subsequent injections.
Check the apprehension test before and immediately after injection.
Intra-articular injection will also often cure impingement by preventing
upward subluxation of the humeral head in abduction caused by capsular laxity
provided there is no significant osteophytosis. As always test impingement
signs before and immediately after the injection as a prognostic indicator. If
the painful arc disappears, subsequent sclerosant injections are likely to be
successful.
Tennis and golfer’s elbows
Prolotherapy will help in resistant cases and should be injected into all tender
areas sometimes, therefore including the radiohumeral joint and annular
ligament as well as the enthesis. Subsequent injections should produce
progressive localisation of tenderness. The aim should be to get the patient
80% pain-free, as otherwise an unnecessary number of injections is needed.
Once this is achieved time will do the rest.
Lumbar pain, recurrent acute lumbago
and spondylolisthesis
As in the cervical spine, injection of the lower three facets and deep fascial
attachments have been practised for years and require imaging, but injection
of the supraspinous and interspinous ligaments from L3 to S1 using a 2-inch
21G needle will help most patients. A 15°-bent 2-inch 21G needle is inserted
2 inches above the sacrum in the midline. Multiple small volume injections of
proliferant mixture are then injected with bony contact down to the sacrum
and then rotated through 180° as far superiorly as possible after an initial
injection of lidocaine. The L5/S1 interspace requires extra care to avoid dural
192 Practical prolotherapy
puncture, as the ligament here is deficient and subdural space relatively
superficial.
Pelvic/sacroiliac/lumbar pain associated with
pelvic tilt and apparent leg length inequality
The common pattern by far is a patient who stands with a raised right iliac
crest and apparent right leg shortening. If a different pattern is found (and
many are described) just ask the patient to stand with relaxed core muscles and
abdomen for a few seconds and the above pattern will mostly become apparent.
The dysfunctional SIJ (posteriorly upwardly rotated right or anteriorly and
downwardly rotated left SIJ/innominate) is the one which is relatively fixed.
This is most easily determined by the standing hip flexion test. The patient
stands with arms supported for balance and slowly flexes the hip and knee
to 90°. The examiner pushes their thumb up under the PSIS and places their
other thumb on the sacrum as a reference point. In the functional SIJ the
thumb rotates downwards with the PSIS during the test. On the dysfunctional
side the thumb remains stationary or moves laterally. Confirmation is sought
by testing straight leg raise. The dysfunctional side will produce a straight leg
raise (SLR) 10°–15° less than the normal side and/or there is a sensation of
hamstring and gluteal tightness.
The dysfunctional SIJ is the one that requires injection. This seems
paradoxical and may cause confusion, but it is the hypermobile side which,
because of excessive movement, becomes ‘locked’. Following the procedure,
the pelvic tilt and apparent leg length inequality should disappear as the
osmotic effect of the hyperosmolar injection produces increased turgidity,
with temporary strengthening of the ligaments and SIJ realignment. The
previously reduced SLR should recover because the SIJ becomes ‘unlocked’
and rotates slightly on full hamstring stretch. It should be emphasised
to the patient that the ligament will be strengthened not stiffened and the
resulting reduction in compensatory muscle tension will loosen not stiffen
movement. No manipulation is required, as the increased ligament turgidity
is enough to ‘realign’ the joint. When beginning, inject both SIJs if in doubt.
Occasionally the ileal attachment of the iliolumbar ligament and rarely the
sacral attachments of the sacrotuberous and/or sacrospinous ligaments will
appear to be the cause of the pain and may also need injecting.
If after two or three injections at weekly/fortnightly intervals the deformity
recurs, consider injecting the symphysis pubis to further stabilise the
Tips from 25 years’ experience 193
innominate. If malalignment continues, the interspinous and intervertebral
ligaments from L3 to S1 may require treatment to improve core strength and
muscle balance. This occurs in only about 5% of patients.
Most of these patients will have asymptomatic laxity of the ankle (usually
right deltoid), which will presumably cause proprioceptive input imbalance
contributing to pelvi-lumbar muscle tonal inequality and the pelvic torsion.
Those who are starting prolotherapy should try the effect of injecting the
deltoid ligament if SIJ injections appear too daunting to start with. Again
check the pelvic tilt, leg length inequality, and SLR before and after treatment.
It is rare to see a footballer with recurrent hamstring, adductor or rectus
sprain, or osteitis pubis who has not got sacroiliac dysfunction on the affected
side. Treating this as well as the injury will speed recovery and help to prevent
recurrence.
Symphysis pubis instability and osteitis pubis
In addition to injecting the symphysis it is important to treat the dysfunctional
SIJ to reduce the torsion on this joint. If sacroiliac dysfunction switches
sides, symphysis pubis instability is likely. Instability of the symphysis is not
necessarily painful. The whole innominate requires stabilisation and injection
of the dysfunctional SIJ ligaments and any ankle laxity requires proliferant
injections.
This will cure many cases of osteitis pubis by reducing the stress
across the joint and can be recommended before considering intravenous
bisphosphonate, which may then be avoided. In addition to injecting the SIJ
and ankle, any adductor fissure should be injected if symptomatic.
Medial collateral ligament injury
Early (immediate) mobilisation and removal of the splint is essential
otherwise severe stiffening may result. The knee should be rested in
extension with only the heel supported when sitting. These injuries are
commonly associated with lateral collateral ligament (LCL) laxity. This is
especially the case in intractable proximal lesions. The asymptomatic LCL
laxity causes the knee to go into slight varus then when side-footing a ball
there is a sudden strain on the proximal MCL attachment causing further
pain and breakdown. Functional LCL laxity does not usually show any
abnormality on MRI.
194 Practical prolotherapy
Medial osteoarthritis of the knee
Always look for LCL laxity, which is often present despite a normal MRI
appearance. Treating this will help offload the medial compartment and often
reduce pain for prolonged periods.
Patellar subluxation, lateral patellofemoral
osteoarthritis and patellar tendinopathy
Patellar subluxation, lateral patellofemoral osteoarthritis and patellar
tendinopathy will all improve by injecting the medial patellofemoral ligament,
which will improve maltracking and shearing stress on the proximal patellar
tendon. The homolateral SIJ is very often also dysfunctional and causes
switching off of the quadriceps. The vastus medialis obliquus weakness
further aggravates the condition and the dysfunctional SIJ should be treated
if present.
Using this technique in cases of patellar tendinopathy, injection of
the tendon itself is often unnecessary unless there is a large defect on
ultrasonography.
Always test the knee by checking for lateral maltracking on squatting and
for correction of deviation and reduced pain after injection of the MPFL.
L ateral ankle ligament and
syndesmosis injury
The author has never seen injury to anterior tibiofibular ligament (ATFL) or
calcaneofibular ligament (CFL) without there being accompanying deltoid
ligament laxity. A syndesmosis injury (mostly anterior inferior tibiofibular
ligament [AITFL]) will almost always only occur in an ankle with underlying
mortise instability. Check the deltoid ligament by forcing the shin back and
forth with the knee flexed at 90°, heel fixed on the couch and ankle flexed
at 90°. Always inject the deltoid! Ultrasonography of the deltoid ligament in
these cases usually shows lack of deep fibres, but again the ligament on MRI
imaging is usually normal. Often a positive dial test will be rendered negative
after injection of the deltoid ligament alone.
High-grade II ATFL injuries are often reported on MRI as grade III. If
prolotherapy injection produces an immediate increase in stability from the
osmotic effect of the hyperosmolar solution, treat as grade II.
Tips from 25 years’ experience 195
Deltoid ligament laxity and anterolateral
or posterior ankle impingement
Deltoid ligament laxity is common and almost never shows up on MRI.
The ligament stretches without tearing and then renders the ankle unstable
and liable to ATFL injury, or anterolateral or posterior impingement
syndrome. Never inject the painful anterolateral impingement area as
this will make it worse. Occasionally a medial submalleolar steroid
injection is necessary once the deltoid ligament is stable and lateral gutter
opened up.
Ankle joint capsule laxity
If stabilising the ankle ligaments fails, or the injury is chronic or recurrent,
or there has been previous surgery with scarring causing a poor response
to prolotherapy, consider capsular laxity. Capsular laxity at the ankle (and
knee) is not uncommon. This is easily treated with 2 or 3 fortnightly intra-
articular injections of 25% dextrose. Often the resistance to the initial
injection is poor even when injecting 10 mL of fluid, further confirming
the diagnosis. With subsequent injections the resistance will increase with
smaller volumes.
Once confidence in these simple techniques is achieved, teaming up with
a musculoskeletal radiologist and further reading will allow more conditions
to be identified and treated [15,16].
TAKE-HOME MESSAGES
●● The scientific evidence regarding prolotherapy is poor.
●● Some pain, swelling and stiffness following sclerosant injection
are common.
●● MEAT (movement, exercise, analgesics, treatment) is advised
following prolotherapy injections.
●● Examine the patient before and immediately after the injection to
check benefit.
●● Consider capsular laxity if prolotherapy of ligaments results in
only temporary benefit especially in chronic recurrent cases.
196 Practical prolotherapy
ACKNOWLEDGEMENT
I wish to record the help of Dr Raj Bhatt, MBBS MD FRCR, Consultant
Musculoskeletal Radiologist at the University Hospitals of Leicester and
Spire Leicester Hospital for his help and expertise over many years and for
providing imaging.
REFERENCES
1. Hackett GS. Ligament and Tendon Relaxation Treated by Prolotherapy.
3rd ed. Springfield, IL: Charles C Thomas; 1958. 5th ed. Oak Brook, IL:
Institute in Basic Life Principles; 1991.
2. Banks AR. A rationale for prolotherapy. J Orthop Med. 1991;13(3):54–9.
3. Adams F. Hippocrates. Baltimore: Williams and Wilkins; 1946.
4. Manoil L. Histological effects of injections of various sclerosing
solutions. Arch Surg. 1938;36.
5. Schultz L. Twenty year’s experience of treating hypermobility of the
temporomandibular joints. Am J Surg. 1956 December;92:925–8.
6. Rice CO, Mattson H. Histologic changes in the tissues of man and
animals following the injection of irritating solutions intended for the
cure of hernia. Ill Med J. 1936;271–8.
7. Hackett GS. Joint stabilisation: An experimental histologic study on
ligament proliferation. Am J Surg. 1955;89.
8. Rabago D, Slattengren A, Zgierska A. Prolotherapy in primary care
practice. Prim Care. 2010;37:65–80.
9. Schnirring L. Are your patients asking about prolotherapy? Physician
Sportsmed. 2000;28(8):15–7.
10. Dorman TA, Ravin TH. Diagnosis and Injection Techniques in
Orthopaedic Medicine. Baltimore: Williams and Wilkins; 1991.
11. Hauser RA, Lackner JB, Steilen-Matias D, Harris DK. A systematic
review of dextrose prolotherapy for chronic musculoskeletal pain. Clin
Med Insights Arthritis Musculoskelet Disord. 2016;9:139–59.
12. Banks AR. Safety of phenol in prolotherapy. J Orthop Med. 1996;18(1):23.
13. Alderman D, Alexander RW, Harris GR, Astourian PC. Stem cell
prolotherapy in regenerative medicine: Background, theory and
protocols. J Prolotherapy. 2011;3(3):689–708.
References 197
14. Cyriax J. Textbook of Orthopaedic Medicine. Vol. 2. 10th ed. London:
Baillière Tindall; 1980:318–20.
15. Ravin TH, Cantieri MS, Pasquarello GJ. Principles of Prolotherapy.
Denver, CO: American Academy of Musculoskeletal Medicine; 2008.
16. Hutson M, Ward A. Oxford Textbook of Musculoskeletal Medicine. 2nd
ed. Oxford, England: Oxford University Press; 2016.
10
Extracorporeal shock
wave therapy
RANDEEP S. AUJLA AND PHILIPPA TURNER
INTRODUCTION
Extracorporeal shock wave therapy (ESWT) provides a non-invasive option to
treat chronic soft-tissue conditions that have notoriously been difficult to treat.
A course of weekly treatments, lasting three to four weeks, provides a safe and
easy to administer intervention with the benefit of minimal transient side
effects. This chapter will focus on providing information regarding the use
of extracorporeal shock wave therapy and its efficacy for key musculoskeletal
areas.
ESWT has been used to treat musculoskeletal conditions for over 20 years.
Following the successful use of extracorporeal shock wave lithotripsy to
treat renal/ureteric stone disease in urology, ESWT has emerged as an
acceptable and non-invasive method to manage disease of tendons and other
musculoskeletal pathologies. About 80%–85% of randomised controlled trials
from the Physiotherapy Evidence Database (PEDro) have shown a positive
outcome [1].
WHAT IS IT?
ESWT is a non-invasive procedure whereby shock waves are passed through
the skin to the targeted area using a handheld probe attached to either a
portable or freestanding device (Figure 10.1). Shock waves are audible, pulsed,
low-energy sound waves that are applied for approximately 3 to 5 minutes
at a time. The oscillations cause a local pressure increase to between 5 and
120 MPa within 5 ns. The shock waves then provide mechanical stimulus to the
tissue to ignite biological changes.
199
200 Extracorporeal shock wave therapy
(a) (b)
Figure 10.1 Hand-held and standing Extracorporeal Shockwave Therapy
Devices.
ESWT has been used in multiple forms across studies. The basic options
include radial or focused pulses, but there are also possibilities of low- or high-
energy modes. There is no scientific evidence that either radial or focused is
superior to the other, but there is evidence that insufficient energy applied to
the treatment area does affect the benefit [1]. The optimum treatment protocol
consists of three to four treatment sessions at weekly intervals that deliver
2000 impulses per session.
HOW DOES IT WORK?
The exact mechanism of action on tissues of ESWT is unknown. Overall it
is said to reduce inflammation, break up scar tissue and stimulate healing.
This is done through neovascularisation, direct suppressive effects on
nociceptors, direct stimulation of healing pathways and hyperstimulation
mechanisms.
The main physiological changes observed in the area of treatment are local
angiogenesis and neurogenesis [2]. It has also been proposed that mechanical
micro-trauma promotes the local inflammatory cascade, and a catabolic
process is utilised to remove damaged tissues constituents.
What are the contraindications? 201
In tendinopathy, there has been evidence to encourage the theory that
hyperstimulation analgesia has a key role. Initial increase followed by long-term
decrease in substance P in treated areas has supported this [3]. Also ESWT has
been found to increase production of TGFb1 and IGF-1 that results in tenocyte
activation, which has been hypothesised to aid in tendon healing [4].
WHAT ARE THE EVIDENCE-BASED
INDICATIONS?
Strong evidence:
●● Chronic calcific rotator cuff tendinopathy
●● Chronic plantar fasciitis
●● Achilles tendinopathy
Moderate evidence:
●● Chronic lateral epicondylitis
●● Greater trochanteric pain syndrome
●● Proximal hamstring tendinopathy
●● Patella tendinopathy
●● Non-union of fractures
Limited evidence:
●● Medial epicondylitis
●● Primary long bicipital tenosynovitis
●● Osteonecrosis of femoral head
●● Myofascial pain syndrome
WHAT ARE THE CONTRAINDICATIONS?
●● Malignant tumour in the shock wave field
●● Local infection
●● Pregnancy
●● <18 years of age
●● Blood clotting disorder
●● Neurological or vascular insufficiencies
●● Cardiac pacemaker/defibrillator
202 Extracorporeal shock wave therapy
●● Previous surgery (relative contraindication)
●● Anti-coagulant or anti-platelet use (relative contraindication)
●● Peripheral nerve compression neuropathy (relative contraindication)
WHAT ARE THE SIDE EFFECTS/RISKS?
There is usually some pain during the procedure. The skin following treatment
can be red, bruised, tender, swollen and even have reduced cutaneous sensation.
These effects are all temporary and should resolve within one week. There
are reports of Achilles tendon rupture 2 weeks after ESWT treatment session,
associated with falls in a couple of patients. The patients should be advised that
if the underlying tendon substance is weak or degenerate, there is a small risk
of rupture of the tendon following ESWT.
CLINICAL APPLICATIONS AND EVIDENCE
Notarnicola et al. [5] assessed prognostic factors in the successful usage of
ESWT in a wide variety of conditions in 355 patients. They found an overall
success rate of 46%; male gender and a high body mass index were predictors of
successful treatment. Interestingly there was no difference in relation to age,
work/sporting activity, co-morbidities, type of tendinopathy and density of
energy delivered [5]. This study however did encompass multiple pathologies in
a heterogeneous group of patients.
SHOULDER
Calcific rotator cuff tendinopathy
The overall prevalence of shoulder pain in the United Kingdom population
is estimated to be around 7%, rising to 26% in the elderly. Rotator cuff
calcification is a relatively common disease of unknown cause, characterised
by the presence of calcium hydroxyapatite crystal deposition in tendons.
Diagnosis is reached through clinical history, examination and radiology,
with ultrasound being the most effective, sensitive and inexpensive.
The initial treatment of choice is conservative, typically including rest,
analgesics, non-steroidal anti-inflammatory drugs (NSAIDs), rehabilitation
Elbow 203
and corticosteroid injections. Favourable results have been seen in 90%–99%
of cases [6,7]. Several options are available for patients who fail non-surgical
treatment, including ESWT, ultrasound-guided needle lavage and surgical
debridement. These modalities alleviate pain by eliminating the calcific deposit.
Treatment by ESWT can be used prior to invasive procedures such as
surgical debridement. Its use in non-calcific rotator cuff tendinopathy was
first mentioned in medical literature around 20 years ago. Its efficacy and low
morbidity is well demonstrated. However, the evidence for this is now limited
with focus remaining on the calcific form of rotator cuff tendinopathy.
The National Institute of Health and Care Excellence (NICE) in the United
Kingdom has published guidance on the treatment of calcific rotator cuff
tendinopathy of the shoulder. The guidance supports the use of focused ESWT
in those cases recalcitrant to conservative measures such as NSAIDs, analgesics,
corticosteroids, aspiration or lavage. There is no consensus on the most efficacious
ESWT generator, number of sessions, number of impulses, frequency, energy
level, use of anaesthesia or method of localisation, which shows heterogeneous
therapeutic outcomes and hinders comparison across research studies. Research
published in the last decade has shown a degree of efficacy, but the devices,
treatment protocols and endpoints differ from one publication to another.
Resolution of calcification was significantly greater in high-energy ESWT
than in placebo, whereas results for low-energy ESWT were inconclusive. In
eight randomised controlled trials (RCTs) comparing low- versus high-energy
ESWT, high energy seemed to be more efficient in resolving calcium deposits. It
was also more effective in terms of reducing pain, improving function and inducing
resorption of calcification. ESWT did not effectively treat non-calcific tendinosis.
In summary, regarding pain, function, resorption of calcification (which
appears to be dose-dependent), safety, non-invasiveness, reduced recovery time
after application and cost-effectiveness, ESWT is an efficacious and efficient
alternative to surgery for rotator cuff calcific tendinopathy. In non-calcific
rotator cuff tendinosis, there is no evidence in favour of low-dose- or high-
dose-focused ESWT versus placebo, each other or other treatments.
ELBOW
L ateral epicondylitis
Lateral elbow tendinopathy or epicondylitis is a common musculoskeletal
condition that affects 1%–3% of the adult population. Males and
204 Extracorporeal shock wave therapy
females are affected equally, and it commonly presents between the ages of
35 and 50 years. However, it can occur at any age in the sporting/physically
active population.
The tendinous origin of the extensor carpi radialis brevis is the area of
most pathologic change. Although the actual cause of the clinical condition
of lateral elbow tendinopathy is unknown, correlations with specific repetitive
movements for more than 2 hours a day, handling tools >1 kg, handling loads
>20 kg at least 10 times/day, low job control and low social support at work
have been identified as risk factors.
The initial research investigating the treatment of lateral
elbow tendinopathy with ESWT showed conf licting results. A Cochrane
Review in 2005 found there to be platinum level evidence that ESWT
provides little or no benefit in terms of improving pain and function in
lateral elbow tendinopathy. The authors, however, did not differentiate
between acute and chronic cases, they failed to consider the use of different
shock wave devices or treatment protocols, and did not comment on the
use of local anaesthesia. This has led to questions over the validity of this
initial review.
Early studies between 2002 and 2008 showed a variety of poor results
as a result of poor methodology. More recently there have been higher
quality RCTs that have taken place, and there are now numerous clinical
trials showing very good results for ESWT in treatment of lateral elbow
tendinopathy [8].
Trials comparing ESWT with surgery [9], corticosteroid injections [10] and
physical therapy [11] have all failed to show inferiority of ESWT.
The current evidence base appears to be adequate to support the use of
ESWT for lateral elbow tendinopathy with symptoms lasting beyond 3 months.
Although, further research is needed to investigate the best treatment regimens
to be utilised. There have been no studies demonstrating the effectiveness of
ESWT for medial epicondylitis.
HIP
Greater trochanteric pain syndrome
Greater trochanteric pain syndrome (GTPS) is a disorder that affects the lateral
side of the hip. It is commoner in women and most frequently affects people
aged 40–60. Over recent decades, there has been a range of names for this
Hip 205
condition, due to uncertainty over the exact pathological cause. Originally,
the trochanteric bursa was thought to be the primary problem; however, it is
now thought the tendons of the abductors and external rotators, particularly
gluteus medius, are involved.
Clinical diagnosis is commonly made based on the site of pain, i.e. greater
trochanter, buttock and upper lateral thigh. Examination reveals tenderness
on palpation of the posterolateral aspect of the greater trochanter; however,
other criteria have been observed, such as pain on lying on the affected side.
There is variation in diagnostic criteria, which increases the risk of diagnostic
error and may result in erroneous conclusions being drawn regarding
treatment effectiveness.
Rompe et al. [12] enrolled 229 patients with refractory unilateral GTPS
that were sequentially assigned to a home training program (n = 76), a
single local corticosteroid injection (25 mg prednisolone) (n = 75) or a
repetitive low-energy radial ESWT treatment (n = 78). Corticosteroid
injections were shown to be the most effective treatment modality within the
first month. ESWT and home-exercise-based therapy were both revealed more
effective at 15 months’ follow-up. Up to two-thirds of patients had significant
improvement in symptoms, however, 60% had recurrence at a mean of
4 months follow-up [13].
While ESWT provides promising medium-term outcomes, long-term
results over many years have not been studied. Patients with gluteal
tendinopathy have abductor muscle weakness and biomechanical variations
that potentially could result in relative overload of the abductor mechanism.
Reducing pain in the short-to-medium term with corticosteroid injection
or ESWT is unlikely to address these issues and may explain the long-term
failure of isolated ESWT.
In 2010, NICE produced guidelines for the treatment of refractory GTPS
with ESWT. However, evidence is limited in quality and quantity. Therefore,
this procedure should only be used with special arrangements for clinical
governance, consent and audit or research.
Chronic proximal hamstring tendinopathy
Chronic proximal hamstring tendinopathy is an overuse syndrome that is
usually managed by non-operative methods. One randomised control study
has looked at whether ESWT may be more effective than other non-operative
treatments for chronic proximal hamstring tendinopathy [14]. It concluded
ESWT is a safe and effective treatment for patients with chronic proximal
206 Extracorporeal shock wave therapy
hamstring tendinopathy, but as yet, there have been no other published studies
looking at this area of clinical use.
KNEE
Patella tendinopathy
Patella tendinopathy, also known as jumper’s knee or patellar tendinitis, is
a frequent problem for the athletic population, particularly those sports
involving jumping, rapid changes in direction and running. Prevalence
varies between 2% and 45% across a variety of sports and can depend
upon numerous factors such as training methods, sporting demands and
body habitus. Diagnosis is made via history and examination findings, and
confirmed using colour duplex sonography and/or MRI. The search continues
for an effective method to treat a chronically painful condition.
A scientific study on rabbit patellar tendons demonstrated that ESWT
increases collagen synthesis and collagen crosslinking during early healing of
tendons [15]. This theoretical laboratory-based finding has been translated into
clinical practice with good satisfaction rates in treating patellar tendinopathy
using ESWT.
Furia et al. [16] performed a retrospective review and found an
improvement in Visual Analogue Scale (VAS) scores at 1, 3 and 12 months
post-ESWT treatment. They had a satisfaction rate of 76% after a single
treatment session [16]. An RCT comparing radial and focussed ESWT found
no difference between the two. Nevertheless, both groups improved in their
Victoria Institute of Sport Assessment-Patella (VISA-P) score [17].
Studies have compared ESWT to surgery for chronic patella tendinopathy
and found little difference in outcomes between the two modalities [18]. In
a randomised controlled study, platelet-rich plasma (PRP) injections in the
athletic population led to better midterm clinical results compared to focused
ESWT in the treatment of jumper’s knee [19].
As per a recent systematic review the evidence for ESWT in patellar
tendinopathy is ‘ limited’ [20]. However, only two studies report poor
outcomes: one included only professional athletes during competition and
the other utilised an atypical protocol of one session of ESWT every 48–72
hours [19,21]. Overall satisfactory results with ESWT have been noted to be
62%–90%.
Foot and ankle 207
FOOT AND ANKLE
Achilles tendinopathy
The Achilles tendon is amongst the most prone tendon to overuse injury.
Achilles tendinopathy has been found in up to 18% of runners and accounts
for 4% of patients attending sports medicine clinics. It can affect both the
sporting and non-sporting population. Diagnosis is made via clinical history
and examination findings, and confirmed radiologically (using either colour
duplex sonography or MRI). Traditional treatments have involved activity
modification and physiotherapy that involved eccentric loading. These
methods are time consuming and are not always successful, and compliance
can be variable. For these reasons ESWT has been sought as an alternative
(Figure 10.2).
RCTs have been conducted comparing ESWT to either a placebo, no
intervention or eccentric exercises. In 2005, Costa et al. failed to show a
difference after 3 months of ESWT versus placebo in 49 patients [22]. In
contrast Rasmussen et al. [23] demonstrated an improvement in patient
reported outcome measures (PROMS) in a similar study. Rompe et al. [24]
demonstrated a statistical difference at 16 weeks of ESWT versus no
(a) (b)
Figure 10.2 Use of ESWT for insertional Achilles tendinopathy.
208 Extracorporeal shock wave therapy
intervention (24% versus 52%) but no difference when compared to eccentric
exercises (60% versus 52%). The same authors later showed that ESWT used
with an eccentric loading programme versus an eccentric loading programme
alone was statistically superior [25]. It has been shown that improved
symptoms can be noted in 78%–87% at 6- to 12-month follow-up [26,27].
Current literature suggests that the use of ESWT in conjunction with
eccentric loading programme may offer the best clinical results. The evidence
supports its use for mid-substance Achilles tendinopathy.
Plantar fasciitis
Plantar fasciitis is the commonest cause of heel pain and is usually self-
limiting. Diagnosis is based on clinical features from history and examination.
Radiological investigation is not usually required.
Plantar fasciitis continues to be managed non-surgically for most cases,
with 10%–20% developing chronic pain. In chronic recalcitrant cases ESWT
(Figure 10.3) has become a viable option with multiple RCTs showing
benefit over placebo [28,29]. However, there are some RCTs, including a
large multicentre RCT, that have failed to show any benefit of ESWT in this
difficult-to-treat cohort [30–32].
Aqil et al. performed a meta-analysis of RCTs in 2013, in which they
included seven studies (294 patients in ESWT group, 369 in placebo group) [33].
(a) (b)
Figure 10.3 Use of ESWT for plantar fasciitis.
References 209
The ESWT group showed improvements in VAS scores, heel pain when taking
initial steps, pressure meter readings and satisfaction. These improvements
were evident at 12 weeks after treatment. Across multiple studies patient
satisfaction rates varied from 55%–65%. Reductions in VAS scores were of a
similar level. Aqil et al. concluded that ESWT is a safe and effective treatment
in refractory cases of plantar fasciitis lasting more than 3 months.
TAKE-HOME MESSAGES
●● ESWT is safe and effective.
●● Scientific evidence shows significant benefit in plantar fasciitis,
calcific rotator cuff tendinopathy, Achilles tendinopathy and
lateral epicondylitis.
●● Any side effects experienced are temporary and should resolve
within a few weeks.
●● Main contraindications include malignant tumour in the
shock wave field, local infection, pregnancy, <18 years of
age, blood clotting disorder, anti-coagulant or anti-platelet
use, neurological or vascular insufficiencies, peripheral nerve
compression neuropathy, cardiac pacemaker or defibrillator, and
previous surgery.
REFERENCES
1. Schmitz C et al. Efficacy and safety of extracorporeal shock wave therapy
for orthopedic conditions: A systematic review on studies listed in the
PEDro database. Br Med Bull. 2015; 116(1):115.
2. Wang C-J, Ko J-Y, Kuo Y-R, Yang Y-J. Molecular changes in diabetic foot
ulcers. Diabetes Res Clin Pract. 2011; 94(1):105–10.
3. Maier M, Averbeck B, Milz S, Refior HJ, Schmitz C. Substance P and
prostaglandin E2 release after shock wave application to the rabbit
femur. Clin Orthop. 2003; 406(1):237–45.
4. Chen Y-J et al. Extracorporeal shock waves promote healing of
collagenase-induced Achilles tendinitis and increase TGF-β1 and IGF-I
expression. J Orthop Res. 2004; 22(4):854–61.
5. Notarnicola A, Maccagnano G, Tafuri S, Fiore A, Margiotta A,
Pesce V, Prognostic factors of extracorporeal shock wave therapy for
tendinopathies. Musculoskelet Surg. 2016; 100(1):53–61.
210 Extracorporeal shock wave therapy
6. Suzuki K, Potts A, Anakwenze O, Singh A. Calcific tendinitis of the
rotator cuff: Management options. J Am Acad Orthop Surg. 2014;
22(11):707–17.
7. Gardesmeyer L et al., Extracorporeal shock wave therapy for the
treatment of chronic calcifying tendonitis of the rotator cuff. JAMA.
2003; 290:2573–80.
8. Thiele S, Thiele R, Gerdesmeyer L. Lateral epicondylitis: This is still a
main indication for extracorporeal shockwave therapy. Int J Surg. 2015;
24:165–70.
9. Radwan YA, ElSobhi G, Badawy WS, Reda A, Khalid S. Resistant tennis
elbow: shock-wave therapy versus percutaneous tenotomy. Int Orthop.
2008;32(5):671–7.
10. Ozturan KE, Yucel I, Cakici H, Guven M, Sungur I. Autologous blood
and corticosteroid injection and extracoporeal shock wave therapy in
the treatment of lateral epicondylitis. Orthopedics. 2010;33(2):84–91.
11. Gündüz R, Malas FÜ, Borman P, Kocaoğlu S, Özçakar L. Physical
therapy, corticosteroid injection, and extracorporeal shock wave
treatment in lateral epicondylitis. Clin Rheumatol. 2012;31(5):807–12.
12. Rompe JD, Segal NA, Cacchio A, Furia JP, Morral A, Maffulli N. Home
training, local corticosteroid injection, or radial shock wave therapy
for greater trochanter pain syndrome. Am J Sports Med. 2009 October;
37(10):1981–90.
13. Sultan J, Lovell ME. Extracorporeal shockwave therapy for refractory
greater trochanteric pain syndrome. MOJ Orthop Rheumatol. 2015;
2(3):00050.
14. Cacchio A, Rompe JD, Furia JP, Susi P, Santilli V, De Paulis F. Shockwave
therapy for the treatment of chronic proximal hamstring tendinopathy
in professional athletes. Am J Sports Med. 2011 January; 39(1):146–53.
15. Hsu RW-W, Hsu W-H, Tai C-L, Lee K-F. Effect of shock-wave therapy on
patellar tendinopathy in a rabbit model. J Orthop Res. 2004; 22(1):221–7.
16. Furia JP, Rompe JD, Cacchio A, Del Buono A, Maffulli N. A single
application of low-energy radial extracorporeal shock wave therapy is
effective for the management of chronic patellar tendinopathy. Knee
Surg Sports Traumatol Arthrosc. 2013; 21(2):346–50.
17. van der Worp H, Zwerver J, Hamstra M, van den Akker-Scheek I, Diercks
RL. No difference in effectiveness between focused and radial shockwave
therapy for treating patellar tendinopathy: A randomized controlled
trial. Knee Surg Sports Traumatol Arthrosc. 2014; 22(9):2026–32.
References 211
18. Peers KH, Lysens RJ, Brys P, Bellemans J. Cross-sectional outcome
analysis of athletes with chronic patellar tendinopathy treated surgically
and by extracorporeal shock wave therapy. Clin J Sport Med. 2003;
13(2):79–83.
19. Vetrano M, Castorina A, Vulpiani MC, Baldini R, Pavan A, Ferretti
A. Platelet-rich plasma versus focused shock waves in the treatment of
jumper’s knee in athletes. Am J Sports Med. 2013; 41(4):795–803.
20. Larsson ME, Käll I, Nilsson-Helander K. Treatment of patellar
tendinopathy – A systematic review of randomized controlled trials.
Knee Surg Sports Traumatol Arthrosc. 2012; 20(8):1632–46.
21. Zwerver J, Hartgens F, Verhagen E, van der Worp H, van den Akker-
Scheek I, Diercks RL. No effect of extracorporeal shockwave therapy
on patellar tendinopathy in jumping athletes during the competitive
season: A randomized clinical trial. Am J Sports Med. 2011; 39(6):1191–9.
22. Costa ML, Shepstone L, Donell ST, Thomas TL. Shock wave therapy for
chronic Achilles tendon pain: A randomized placebo-controlled trial.
Clin Orthop. 2005; 440:199–204.
23. Rasmussen S, Christensen M, Mathiesen I, Simonson O. Shockwave
therapy for chronic Achilles tendinopathy: A double-blind, randomized
clinical trial of efficacy. Acta Orthop. 2008; 79(2):249–56.
24. Rompe JD, Nafe B, Furia JP, Maffulli N. Eccentric loading, shock-wave
treatment, or a wait-and-see policy for tendinopathy of the main body
of tendo Achillis. Am J Sports Med. 2007; 35(3):374–83.
25. Rompe JD, Furia J, Maffulli N. Eccentric loading versus eccentric loading
plus shock-wave treatment for midportion Achilles tendinopathy. Am J
Sports Med. 2009; 37(3):463–70.
26. Saxena A, Ramdath S, O’Halloran P, Gerdesmeyer L, Gollwitzer H.
Extra-corporeal pulsed-activated therapy (‘EPAT’ sound wave) for
Achilles tendinopathy: A prospective study. J Foot Ankle Surg. 2011;
50(3):315–9.
27. Fridman R, Cain JD, Weil L Jr, Weil L Sr. Extracorporeal shockwave
therapy for the treatment of Achilles tendinopathies: A prospective
study. J Am Podiatr Med Assoc. 2008; 98(6):466–8.
28. Malay DS et al. Extracorporeal shockwave therapy versus placebo for the
treatment of chronic proximal plantar fasciitis: Results of a randomized,
placebo-controlled, double-blinded, multicenter intervention trial.
J Foot Ankle Surg. 2006; 45(4):196–210.
212 Extracorporeal shock wave therapy
29. Gerdesmeyer L et al. Radial extracorporeal shock wave therapy is safe
and effective in the treatment of chronic recalcitrant plantar fasciitis:
Results of a confirmatory randomized placebo-controlled multicenter
study. Am J Sports Med. 2008; 36(11):2100–9.
30. Haake M, Buch M, Schoellner C, Goebel F, Vogel M, Mueller I, Hausdorf
J, Zamzow K, Schade-Brittinger C, Mueller HH et al. Extracorporeal
shock wave therapy for plantar fasciitis: Randomised controlled
multicentre trial. BMJ. 2003; 327(7406):75.
31. Buchbinder R, Ptasznik R, Gordon J, Buchanan J, Prabaharan V,
Forbes A. Ultrasound-guided extracorporeal shock wave therapy
for plantar fasciitis: A randomized controlled trial. JAMA. 2002;
288(11):1364–72.
32. Speed CA, Nichols D, Wies J, Humphreys H, Richards C, Burnet S,
Hazleman BL et al. Extracorporeal shock wave therapy for plantar
fasciitis. A double blind randomised controlled trial. J Orthop Res. 2003;
21(5):937–40.
33. Aqil A, Siddiqui MR, Solan M, Redfern DJ, Gulati V, Cobb JP.
Extracorporeal shock wave therapy is effective in treating chronic plantar
fasciitis: A meta-analysis of RCTs. Clin Orthop. 2013; 471(11):3645–52.
11
Novel treatments for the
management of chronic shoulder,
knee and hip joint pain
SADIQ BHAYANI
INTRODUCTION
What is radiofrequency?
Radiofrequency (RF) lesioning is a minimally invasive method of pain relief.
It involves generation of very high frequency alternating current (300–
500 kHz) from an RF generator which is delivered through an electrode via
an exposed tip of an insulated needle. This results in thermal energy that is
applied to the target nerve. Based on the temperature generated at the needle
tip, delivery of energy in pulses and the size of the lesion, it is further divided
into conventional radiofrequency (CRF), pulsed radiofrequency (PRF) and
cooled radiofrequency ablation (C-RFA).
RF lesioning of the target nerves involved in transmission of pain, thereby
improving pain, has been successfully used for over 4 decades. This chapter
details application of RF treatment of sensory nerves supplying to the
shoulder, knee and hip joint.
SHOULDER JOINT
Which nerves supply the shoulder joint?
Shoulder joint nerve supply comes from the brachial plexus. The suprascapular,
axillary and lateral pectoral nerves mainly innervate the shoulder joint.
In addition, there is small variable innervation from subscapular and
213
214 Novel treatments for the management of chronic shoulder, knee and hip joint pain
musculocutaneous nerves. The suprascapular nerve (SSN) contributes to
70% of sensory innervation of the shoulder joint. It supplies the posterior
shoulder joint capsule, acromioclavicular joint, coracoclavicular ligament,
coracoacromial ligament and subacromial subdeltoid bursa.
The SSN arises from the upper trunk of the brachial plexus and courses
laterally beneath the trapezius and omohyoid muscles and enters in the
supraspinous fossa via the suprascapular notch beneath the suprascapular
ligament. The suprascapular artery and vein pass above the suprascapular
ligament in the suprascapular notch, whereas the SSN passes below the
suprascapular ligament (Figure 11.1).
When to perform suprascapular nerve
block
Suprascapular nerve block can be used as a pain-relieving procedure following
shoulder trauma, surgery and for chronic shoulder pain syndrome secondary
to adhesive capsulitis, rotator cuff tears and glenohumeral osteoarthritis
(OA) [1–3].
How to perform suprascapular nerve block
and pulsed radiofrequency treatment
The SSN can be targeted either at the suprascapular notch or at the
suprascapular fossa [4,5]. Targeting the SSN at the notch using the blind or
landmark approach increases risk of pneumothorax, intravascular injections
and nerve injury [6,7]. This risk can be minimised by placing the needle in
the suprascapular fossa and placing the adequate volume of local anaesthetic
to block the SSN. The precision of needle tip placement in the notch or in the
fossa can be increased by using ultrasound, computed tomography (CT) scan
and fluoroscopy.
Ultrasound has several advantages including easy access; visualisation of
soft tissues, blood vessels, bony silhouette; live dynamic scanning; and real-
time needle visualisation. Therefore, use of ultrasound is preferred over the
other modalities of imaging and is described in this chapter.
The ultrasound scanning is performed with the patient in sitting position.
A high-frequency (6–13 MHz) linear probe is recommended given that the
nerve is quite superficial (less than 5 cm). The probe is positioned parallel to
Shoulder joint 215
Suprascapular A
Br. SA
Suprascapular N
Br. SS
Br. IA
Br. IS
Figure 11.1 Suprascapular nerve and its branches. The superior articular
branch (Br. SA) supplies to the coracohumeral ligament, subacromial bursa
and posterior aspect of the acromioclavicular joint capsule. The inferior
articular branch (Br. IA) supplies to the posterior joint capsule. Br. SS, branch to
supraspinatus; Br. IS, branch to infraspinatus. (Reproduced with the permission
of USRA, www.usra.ca.)
the scapular spine and then moved forward to visualise the suprascapular
fossa. This will show the trapezius and supraspinatus muscles (Figure 11.2a).
The suprascapular artery can be visualised using colour Doppler (Figure
11.2b). Then 5 mL of local anaesthetic and steroid is injected under real-time
guidance using either the ‘in plane’ or ‘out of plane’ approach [8].
216 Novel treatments for the management of chronic shoulder, knee and hip joint pain
(a)
(b)
Figure 11.2 (a) Ultrasound image of the suprascapular notch and the
content. (b) Colour Doppler shows suprascapular artery. (Reproduced with
the permission of USRA, www.usra.ca.)
PRF of the SSN is performed with the needle either inserted with in plane
or out of plane technique. The needle is positioned close to the nerve in the
suprascapular notch, and sensory and motor stimulation is performed before
lesioning. Two pulsed lesions with a needle tip temperature of 42°C for 2–3
minutes are recommended.
Knee joint 217
Outcome and summary
A randomised controlled trial in patients with adhesive capsulitis showed that
PRF lesioning of the SSN with ultrasound guidance combined with physical
therapy provided better and faster relief from pain and reduced disability
when compared with physical therapy alone. The effect can last up to 12 weeks
[9]. PRF of the suprascapular nerve is an effective treatment for chronic shoulder
pain, and the effect is sustained over a relatively long period in patients with
chronic intractable shoulder pain [10].
KNEE JOINT
Which nerves supply the knee joint?
The knee capsule innervation can be simplified into an anterior and a
posterior group of nerves called genicular nerves (superomedial, superolateral,
inferomedial and inferolateral) as shown in Figure 11.3. These nerves
mostly accompany the corresponding arteries. The femoral nerve (through
its muscular branches to the vastus medialis, intermedius and lateralis
muscles), saphenous nerve and common peroneal nerve (recurrent and lateral
retinacular branches) form the anterior group of genicular nerves. The sciatic
nerve (through its tibial branch) and obturator nerve (through its posterior
division) form the posterior group of genicular nerves [11] (Figure 11.3).
When to perform RF treatment of knee
genicular nerves
RF of sensory branches of the knee joint (genicular nerves) can be an
alternative treatment modality for the patients who are not surgical candidates
to undergo knee replacement (due to high medical comorbidities or patients
unwilling to undergo surgery) and patients with persistent chronic pain
following knee replacement.
How to perform RF treatment of knee
genicular nerves
The patient is placed in supine position with the knee slightly elevated. Three
genicular branches – superolateral, superomedial and inferomedial – are
218 Novel treatments for the management of chronic shoulder, knee and hip joint pain
DGA
SLGA
SMGA
SLGA
SMGA
MGA
ILGA
ILGA IMGA
IMGA
Genicular
arteries
SLGA: Superior lateral genicular artery/DGA: Descendent genicular artery/
SMGA: Superior medial genicular artery/ILGA: Inferior lateral genicular artery/
IMGA: Inferior medial genicular artery
Figure 11.3 Genicular arteries accompanied with genicular nerves.
(Reproduced with the permission of Dr Vincent Roques.)
targeted for RF treatment. These branches are ablated at the junction of the
lateral femoral shaft and the epicondyle, the junction of the medial femoral
shaft and the epicondyle, and the junction of the medial tibial shaft and the
epicondyle, respectively.
In addition to the aforementioned three nerves, lesion to medial
(retinacular) genicular branch from vastus intermedius can be performed at
the midline of the femoral shaft just above the patella. Anteroposterior (AP)
and lateral fluoroscopy guidance is used to advance the RF needles to meet the
bony end points. The stylet is removed and the RF probe is inserted through
the needle. Each nerve is treated with RF lesion of 60° for 150 seconds with
25 seconds of ramp time [12] (Figures 11.4 and 11.5).
Outcomes and summary
Application of RF neurotomy of genicular branches was first described in
2011. Choi et al. evaluated the effect of traditional RFA in a randomised,
Knee joint 219
Figure 11.4 RF treatment of genicular nerves of the knee under fluoroscopy
guidance. (Reproduced with the permission of Dr Vincent Roques.)
double-blinded and sham-controlled trial [13]. Ikeuchi et al. and Vas et al.
applied PRF neurotomy for genicular nerves [14,15].
The patients in the RF group had an improved pain score, osteoarthritis
score and global assessment at 4, 8, and 12 weeks, and 6 months
after the procedure and increase participation in physical therapy. RF
Superior medial genicular nerve
Superior lateral genicular nerve
Inferior medial genicular nerve
Figure 11.5 Superomedial, superolateral and inferomedial genicular nerves
radiofrequency needle positioning using fluoroscopy guidance.
220 Novel treatments for the management of chronic shoulder, knee and hip joint pain
treatment of genicular nerves supplying the knee joint has the potential to
reduce pain from osteoarthritis or chronic post-surgical pain following knee
replacement.
HIP JOINT
Which nerves supply the hip joint?
The innervation to the hip joint capsule is divided into anterior, anteromedial,
posteromedial and posterolateral areas, which are innervated by the articular
branches of the femoral, obturator, sciatic and superior gluteal nerves,
respectively [16].
The symptoms of hip osteoarthritis include groin, thigh and trochanteric
pain. Groin and thigh pain arise from the sensory branches of the obturator
nerve, whereas trochanteric pain arises from the sensory branches of the
femoral nerve.
When to perform RF treatment of hip
genicular nerves
RF of sensory branches of the hip joint (genicular nerves) can be an alternative
treatment modality for patients who are not surgical candidates to undergo
hip replacement secondary to comorbidities and patients unwilling to
undergo surgery and patients with persistent chronic pain following hip
replacement [17–21].
How to perform radiofrequency treatment
of hip genicular nerves
To target the sensory branch of the obturator nerve, the tip of the needle
is placed under fluoroscopy at the site below the inferior junction between
the ischium and the pubis. A sensory stimulation is performed to cause
paraesthesia and elicit groin and thigh pain. Then motor stimulation is
performed to exclude muscle contractions, indicating the presence of a motor
branch near the electrode.
To target sensory division of the femoral nerve the needle is inserted by
an anterolateral approach aiming for the tip of the needle to be placed below
Hip joint 221
Figure 11.6 Targets for needle positioning for radiofrequency lesioning of
articular branches (genicular nerves) of femoral and obturator nerves.
the anterior inferior iliac spine near the anterolateral margin of the hip joint
(Figure 11.6). Sensory and motor testing is performed to exclude femoral
muscle contraction.
After injection of local anaesthetic, RF lesion is performed at 80°C for
60 seconds.
The novel approach of using ultrasound to advance the needle to the
sensory division of obturator nerve has been described. Ultrasound can
allow the operator to safely avoid the critical structures like blood vessels and
increase the safety of the procedure [22] (Figure 11.6).
Outcome
Follow-up data at 6 months for the patients who had RF treatment of hip
genicular nerves revealed a statistically significant decrease in Visual
Analogue Scale (VAS) scores and Western Ontario and McMaster Universities
Osteoarthritis Index (WOMAC) scores, and a statistically significant increase
of Harris Hip Score [23].
222 Novel treatments for the management of chronic shoulder, knee and hip joint pain
CRYOTHERAPY
What is cryotherapy and how does it
work?
Cryotherapy is also known as cryoablation or cryoanalgesia. Its use over
50 years has proved to be safe with low incidence of adverse effects and
complications. The recent technical advances in the cryoprobes have
reawakened the interest in this technique of pain relief since its introduction
in 1961. In addition to the surgical placement of the cryoprobes, now it is
possible to deliver this treatment percutaneously. The availability of handheld
cryotherapy devices with skin warmers and advances in ultrasound technology
(for precise cryoprobe positioning) have made it possible to use this treatment
for chronic pain related to small, peripheral nerves.
Mechanism of action
The proposed mechanism of actions of cryotherapy leading to pain relief
involves the application of therapeutic cold temperature to peripheral nerves.
This leads to damage caused by freezing and formation of ice crystals leading
to reversible ablation due to Wallerian degeneration and nerve regeneration.
What are the clinical applications of
cryotherapy?
Cryotherapy had been used for chronic pain secondary to knee OA, facet
joint pain and sacroiliac joint pain leading to mechanical low back pain.
The retrospective data in a case series showed reduction in the Visual
Analogue Scale and Patient’s Global Impression of Change at 1 month after
cryoablation, with the best scores after 3 months. The majority of patients
experienced a clinically relevant degree of pain relief and improved function
after percutaneous cryotherapy [24].
The evidence to support the use of cryotherapy is only limited to case reports
at present. There are case reports describing its use for shoulder rotator cuff
repair and knee replacement surgery. Cryotherapy can provide multiple weeks
of pain relief. In the future it could be a practical alternative for the treatment
of prolonged post-surgical pain in a select group of surgical patients [25].
Lidocaine plasters 223
CAPSAICIN CREAM AND PATCH
What is capsaicin and how does it work?
Topical capsaicin cream and patches have been used to treat peripheral
neuropathic pain. The neuropeptide substance P has been implicated in the
pathogenesis of inflammation and pain in arthritis. Repeated application of
capsaicin cream can initially lead to enhanced sensitivity, followed by a period
with reduced sensitivity and persistent desensitisation secondary to depletion
of substance P and reduction in density of C-fibres.
What are the treatment applications and
evidence?
Results from a double-blind randomised study in patients with OA and
rheumatoid arthritis (RA) of the knee concluded that capsaicin cream is a safe
and effective treatment for OA and RA [26].
The reduction in visual analogue scales for pain, categorical pain scale
and physicians’ global evaluations were significantly high. Eighty percent of
the capsaicin-treated patients experienced a reduction in pain after 2 weeks of
treatment.
Another study demonstrated the efficacy of capsaicin cream for up to 1 year
of continuous use with its lack of systemic absorption and no potential for
serious systemic toxicity, in contrast to several other OA treatments [27].
LIDOCAINE PLASTERS
When to use the lidocaine plasters
Lidocaine 5% patches are licensed by the National Institute for Health and
Care Excellence (NICE) for the treatment option of post-herpetic neuralgia. But
these patches can also be used for the treatment of different types of superficial
neuropathic pain for, for example, diabetic polyneuropathy, chronic post
surgical pain (scar pain), localised neuropathic pain and OA knee.
In patients with moderate-to-severe OA of the knee, 2 weeks of treatment
with the lidocaine patch 5% significantly reduces the intensity of pain. The
224 Novel treatments for the management of chronic shoulder, knee and hip joint pain
results of this study coincide with previously reported improvements in pain
and physical function in the same patient population, as measured by the
WOMAC [28].
Lidocaine plasters offer advantages over systemic administration of
drugs by delivering the drug locally, reducing the risk of systemic adverse
effects, drug interactions and overdose. There are several advantages of
treatment with 5% lidocaine-medicated plasters: excellent tolerability
and safety, increased patients’ adherence to the treatment and continued
efficacy over the long-term. In patients who are frail and/or elderly and
those receiving multiple medications, lidocaine plasters are far better than
systemic analgesics. The good response to lidocaine plasters has allowed the
reduction, or even the withdrawal, of concurrent drugs and improved the
patients’ quality of life.
TAKE-HOME MESSAGES
●● Radiofrequency treatment of sensory nerves supplying to the
shoulder, hip and knee joints have potential to reduce pain and
is an option for the high-risk surgical patient and patients with
chronic post-surgical pain.
●● Cryotherapy or cryoanalgesia is a treatment modality that
involves application of cold temperature to the peripheral nerves
leading to Wallerian degeneration and reduction of pain.
●● Randomised controlled studies support the efficacy and safety of
capsaicin cream in knee pain.
●● Lidocaine plasters can be useful for the management of localised
neuropathic and osteoarthritic pain.
REFERENCES
1. Neal J, McDonald S, Larkin K, Polossar NL. Suprascapular nerve block
prolongs analgesia after nonarthroscopic shoulder surgery but does not
improve outcome. Anaesth Analg. 2003;96:982–6.
2. Emery P, Bowman S, Wedderburn L. Suprascapular nerve block
for chronic shoulder pain in rheumatoid arthritis. BMJ. 1989;299:
1079–80.
References 225
3. Jones DS, Chattopadhyay C. Suprascapular nerve block for the treatment
of frozen shoulder in primary care: A randomized trial. Br J Gen Prac.
1999;49:39–41.
4. Werthiem HM, Rovenstine EA. Suprascapular nerve block.
Anaesthesiology. 1941;2:541–5.
5. Gleeson AP, Graham CA, Jones I, Beggs I, Nutton RW. Comparison
of intra-articular lignocaine and suprascapular nerve block for acute
anterior shoulfer dislocation. Injury. 1997;28:141–2.
6. Dagiosse MJ, Wilson DJ, Glynn CJ. MRI and clinical study of an easy
and safe technique of suprascapular nerve blockade. Acta Anaesthe Belg.
1994;45:49–54.
7. Feigl GC, Anderhuber F, Dorn C, Pipam W. Modified lateral block of
suprascapular nerve—a safe approach and how much to inject? Reg
Anaesth Pain Med. 2007;32:488–94.
8. Peng P, Narouze S. Ultrasound-guided interventional procedures in
pain medicine: A review of anatomy, sonoanatomy, and procedures:
Part 1: Non axial structures. Reg Anaesth Pain Med. September–October
2009;34(5):458–74.
9. Wu Y, Ho C, Chen C, Li TY, Lee K. Ultrasound-guided pulsed
radiofrequency stimulation of the suprascapular nerve for adhesive
capsulitis: A prospective, randomized, controlled trial. Anesth Analg.
2014 September;119(3):686–92.
10. Jang JS, Choi HJ, Kang SH, Yang JS, Lee JJ, Hwang SM. Effect of pulsed
radiofrequency neuromodulation on clinical improvements in the
patients of chronic intractable shoulder pain. J Korean Neurosurg Soc.
2013 December;54(6):507–10.
11. Franco C, Buvanendran A, Petersohn J. Innervation of the anterior
capsule of the human knee implications for radiofrequency ablation
regional. Reg Anaesth Pain Med. 2015 July–August;40(4):363–8.
12. Vafi S, Gassan C, Hazem E, Tolba R, Lesley L. Application of cooled
radiofrequency ablation in management of chronic joint pain.
Techniques Region Anesth Pain Management. 18(4):137–44.
13. Choi WJ et al. Radiofrequency treatment relieves chronic knee
osteoarthritis pain: A double-blind randomized controlled trial. Pain.
2011;152(3):481–7.
14. Ikeuchi M, Ushida T, Izumi M, Tani T. Percutaneous radiofrequency
treatment for refractory anteromedial pain of osteoarthritic knees. Pain
Med. 2011;12(4):546–51.
226 Novel treatments for the management of chronic shoulder, knee and hip joint pain
15. Vas L, Pai R, Khandagale N, Pattnaik M. Pulsed radiofrequency of
the composite nerve supply to the knee joint as a new technique for
relieving osteoarthritic pain: A preliminary report. Pain Physician.
2014;17(6):493–506.
16. Birnbaum K, Prescher A, Hepler S, Heller K-D. The sensory innervation
of the hip joint—An anatomical study. Surg Radiol Anat. 1998;19:371–5.
17. Kawaguchi M, Hashizume K, Iwata T, Furuya H. Percutaneous
radiofrequency lesioning of the sensory branches of obturator and
femoral nerve for the treatment of hip joint pain. Reg Anesth Pain Med.
2001;26:576–81.
18. Fabrizio R, Carlo M, Giovanni A. Percutaneous radio-frequency
denervation in patients with contraindications for total hip arthroplasty.
Orthopedics. 2012;35:e302–5.
19. Locher S et al. Radiological anatomy of the obturator nerve and its
articular branches: Basis to develop a method of radiofrequency
denervation for hip joint pain. Pain Med. 2008;9:291–8.
20. Fukui S, Nosaka S. Successful relief of hip joint pain by percutaneous
radiofrequency nerve thermocoagulation in patients with
contraindications for hip arthroplasty. J Anesth. 2001;15:173–5.
21. Malik A, Simopolous T, Elkersh M, Aner M, Bajwa ZH. Percutaneous
radiofrequency lesioning of the sensory branches of obturator and
femoral nerve for the treatment of non-operable hip pain. Pain
Physician. 2003;6:499–502.
22. Gassan C, Tyler P, Joseph A. Use of ultrasound and fluoroscopy guidance
in percutaneous radiofrequency lesioning of the sensory branches of the
femoral and obturator nerves. Pain Practice. 2014;14(4):343–5.
23. Rivera F, Mariconda C. Percutaneous radiofrequency denervation in
patients with contraindications for total hip arthroplasty. Orthopaedics.
2012 March;35(3):e302–5.
24. Bellini M, Barbieri M. Percutaneous cryoanalgesia in pain management:
A case-series. Anaesthesiol Intensive Ther. 2015;47(4):333–5.
25. Ilfeld BM, Gabriel RA, Trescot AM. Ultrasound-guided percutaneous
cryoneurolysis providing postoperative analgesia lasting many weeks
following a single administration: A replacement for continuous
peripheral nerve blocks? A case report. Korean J Anesthesiol. 2017
October;70(5):567–70.
26. Deal CL, Schnitzer TJ, Lipstein E, Seibold JR, Stevens RM. Treatment
of arthritis with topical capsaicin: A double-blind trial. Clin Ther. 1991
May–June;13(3):383–95.
References 227
27. Schnitzer TJ, Pelletier JP, Haselwood DM, Ellison WT, Ervin JE, Gordon
RD, Lisse JR. Civamide cream 0.075% in patients with osteoarthritis
of the knee: A 12-week randomized controlled clinical trial with a
longterm extension. J Rheumatol. 2012 March;39(3):610–20.
28. Gammaitoni AR, Galer BS, Onawola R, Jensen MP, Argoff CE. Lidocaine
patch 5% and its positive impact on pain qualities in osteoarthritis:
Results of a pilot 2-week, open-label study using the Neuropathic Pain
Scale. Curr Med Res Opin. 2004;20(Suppl. 2):S13–9.
Index
A Analgesics, 163
Angiogenesis, 118, 125–126
AAOS, see American Association of
Ankle impingement
Orthopaedics Surgeons
anterior, 104–105
Abductor pollicis longus tendons
anterolateral ankle injection site,
(APL tendons), 52
106, 107
Achilles tendinopathy, 207–208
anteromedial ankle injection
Achilles tendon, 126
site, 106, 107
ACJ, see Acromioclavicular joint
posterior, 105–106, 195
ACR, see American College of
Ankle joint, 100; see also Foot and
Rheumatology
ankle injections
Acromioclavicular joint (ACJ), 26,
ankle dorsiflexion, 102
37–38; see also Shoulder
ankle plantar flexion, 102
and elbow injections
capsule laxity, 195
osteoarthritis, 27
double-heel raise, 103
subluxation, 190
eversion against resistance
Adhesive capsulitis, see Frozen
band, 102
shoulder
fluoroscopy view highlighting os
AITFL, see Anterior inferior
trigonum, 105
tibiofibular ligament
injection site, 105
American Association of
injection technique, 106
Orthopaedics Surgeons
intra-articular injections, 101
(AAOS), 173
inversion against resistance
American College of Rheumatology
band, 102
(ACR), 174
OA diagnosis, 101
American Medical Society
posterolateral, 105
for Sports Medicine
primary OA of, 100–101
(AMSSM), 173
single leg stance, 102
AMSSM, see American Medical
single-heel raise, 103
Society for Sports
syndromes, 103–104
Medicine
wobble board, 102
229
230 Index
Anterior inferior tibiofibular C
ligament (AITFL), 194
Calcaneofibular ligament (CFL), 194
Anterior superior iliac spine (ASIS),
Calcificrotator cuff tendinopathy,
169, 188
202–203
Anterior talofibular ligament
Calcific tendinitis, 31, 32; see also
(ATFL), 189
Shoulder and elbow
Anterior tibiofibular ligament
injections
(ATFL), 194
Calcific tendinopathy, 126
Anterolateral ankle injection site,
Calcium barbotage, 129, 131, 132;
106, 107; see also Ankle
see also Image-guided
joint
injections
Anteromedial ankle injection site,
Capsaicin cream and patch, 223;
106, 107; see also Ankle
see also Pain management
joint
treatments
Anteroposterior (AP), 64
Carpal tunnel syndrome (CTS), 47;
AP, see Anteroposterior
see also Hand and wrist
APL tendons, see Abductor pollicis
injections
longus tendons
aetiology of, 49
Arthritis, 54; see also First
complications of steroid
carpometacarpal joint
injection, 52
osteoarthritis
entry point of needle for carpal
Arthritis of first MTPJ, see Hallux
tunnel injection, 51
rigidus
locating palmaris longus
ASIS, see Anterior superior iliac
tendon, 50
spine
surface marking of carpal tunnel
ATFL, see Anterior talofibular
and course of median
ligament
nerve, 48
symptoms of, 49
B technique of steroid injection,
50–51
Basic fibroblast growth factor
treatment, 49–50
(bFGF), 143
CD, see Cluster of differentiation
bFGF, see Basic fibroblast growth
Cervical pain, 190
factor
Cervical-related dizziness, 190
BMI, see Body mass index
CFL, see Calcaneofibular ligament
Body mass index (BMI), 79, 95
Cheilectomy, 99
Bursa, 131
Chronic proximal hamstring
Bursal injection, 131–133; see also
tendinopathy, 205–206
Image-guided injections
Index 231
Clinical practice guideline no-touch technique to draw
(CPG), 173 injectate, 11
Cluster of differentiation patient response to, 13–14
(CD), 165 preparation, 8
Complementary therapies, 1 for radiculopathy, 6
Computed tomography (CT), 118, for shoulder and elbow
169, 214 pain, 5–6
Connective tissue growth factor for shoulder disorders, 26
(CTGF), 143 soft tissue injections, 13
Conventional radiofrequency structures amenable to unguided
(CRF), 213 injection and requiring
Cooled radiofrequency ablation image guidance, 12
(C-RFA), 213 for trigger finger and
Corticosteroid injections, 2; De Quervain’s disease, 6
see also Musculoskeletal— working mechanism, 2
injections Corticosteroids, 1–2, 118, 119
adjuncts available for, 15–16 -induced hyperglycaemia, 122
adverse effect of, 14 synthetic, 2
alternatives to, 16–17 CPG, see Clinical practice
in carpal tunnel syndrome, 6 guideline
common steroids, 7 CRF, see Conventional
complications of, 12, 14 radiofrequency
contraindications for, 3 C-RFA, see Cooled radiofrequency
corticosteroids around ablation
tendons, 13 Cryoablation, see Cryotherapy
equipment needed for, 9–11 Cryoanalgesia, see Cryotherapy
esterification reaction, 2 Cryotherapy, 222; see also Pain
for foot and ankle conditions, 5 management treatments
frequency, 12–13 CT, see Computed tomography
hip arthritis, 4 CTGF, see Connective tissue growth
without image guidance, 11–12 factor
indications and CTS, see Carpal tunnel syndrome
contraindications of, 2–3
injectable corticosteroid
D
agents, 7–8
for knee pain, 4 Degenerative rotator cuff tears,
and LA agents, 9 30–31; see also Shoulder
with local anaesthetics, 8–9 and elbow injections
for musculoskeletal pain, 4–6 Deltoid ligament laxity, 195
232 Index
Depo-Medrone, 34 Extensor pollicis brevis tendons
De Quervain’s tenosynovitis, 52; (EPB tendons), 52
see also Hand and wrist Extracellular cartilage matrix
injections (ECM), 163
steroid injection technique, Extracorporeal shock wave therapy
53–54 (ESWT), 69, 70, 95, 199
surface marking of APL, EPB, Achilles tendinopathy, 207–208
radial styloid and EPL, 53 calcificrotator cuff tendinopathy,
treatment, 52–53 202–203
Disease-modifying anti-rheumatic chronic proximal hamstring
drugs (DMARDs), 15 tendinopathy, 205–206
DMARDs, see Disease-modifying clinical applications and
anti-rheumatic drugs evidence, 202
Dry needling therapy, 127–128, 129; contraindications, 201–202
see also Image-guided elbow, 203–204
injections evidence-based indications, 201
foot and ankle, 207–209
greater trochanteric pain
E
syndrome, 204
ECM, see Extracellular cartilage hand-held and standing, 200
matrix hip, 204–206
ECRB, see Extensor carpi radialis knee, 206
brevis lateral elbow tendinopathy,
EDL, see Extensor digitorum longus 203–204
EGF, see Epidermal growth factor patella tendinopathy, 206
EHL, see Extensor hallucis longus plantar fasciitis, 208–209
Elbow joint, 40; see also Shoulder shoulder, 202–203
and elbow injections side effects/risks, 202
EPB tendons, see Extensor pollicis working mechanism, 200–201
brevis tendons
Epidermal growth factor (EGF), 143
F
Esterification, 2
ESWT, see Extracorporeal shock Femoral nerve, 217
wave therapy FHL, see Flexor hallucis longus
Exercise therapies, 16 First carpometacarpal joint
Extensor carpi radialis brevis osteoarthritis (1st CMCJ
(ECRB), 42 OA), 54; see also Hand and
Extensor digitorum longus (EDL), 88 wrist injections
Extensor hallucis longus (EHL), 88 aetiology of, 55
Index 233
entry point and direction of techniques of injection, 90
needle for, 56 tendinous structures, 89
injection technique for, 55–56 vascular structures, 87–89
surface marking of first Frozen shoulder, 30; see also Shoulder
metacarpal base and and elbow injections
radial styloid, 56
treatment, 55
G
1st CMCJ OA, see First
carpometacarpal joint GAGs, see Glycosaminoglycans
osteoarthritis Genicular nerves, 217
Flexor hallucis longus (FHL), 105 Glenohumeral joint, 34; see also
Flushing post steroid injection, 122; Shoulder and elbow
see also Image-guided injections
injections anterior approach to, 36–37
Foot and ankle injections, 85 markings for coracoid process, 35
anatomical considerations, 86 markings for posterior approach
ankle joint, 100–107 to, 35, 36
anterior ankle and foot dorsum, 88 Glycosaminoglycans (GAGs), 164
drugs commonly used for, 90 Golfer’s elbow, 42–43; see also
first metatarsophalangeal joint, Shoulder and elbow
97–100 injections
guidance to setting of, 92 prolotherapy, 191
interdigital neuroma, 91–94 Greater trochanteric pain syndrome
intra-articular injections, 85 (GTPS), 63–64, 204;
local anaesthetic, 90–91 see also Hip injections;
nervous structures, 89–90 Injection for GTPS
osseous structures, 86–87 conservative treatment options,
osteology of hindfoot and 69–70
midfoot, 87 efficacy of injections for, 69
plantar fasciitis, 94–97 operative treatment options, 70
role of imaging for, 91 GTPS, see Greater trochanteric pain
sinus tarsi syndrome, 107–108 syndrome
steroids, 91
subdivision of foot and ankle
H
bones, 86
superficial peroneal nerve in Hallux rigidus, 97; see also Foot
foot, 89 and ankle injections;
symptoms, 85 Metatarsophalangeal joint
tarsometatarsal joints, 108–111 aggravating activities, 98
234 Index
Hallux rigidus (Continued) Hip joint
cheilectomy, 99 nerve supply, 220
injection site, 100 outcome, 221
injection technique, 99–100 RF treatment, 220–221
joint sparing procedures, 99 treatments for management
osteotomies, 99 of, 220
risk factors, 97 HLA, see Human leucocyte antigen
SCI, 99 Human leucocyte antigen (HLA), 118
surface anatomy of first MTPJ, 100 HVI therapy, see High-volume
treatments, 99 injection therapy
Hand and wrist injections, 47 Hyaluronan, 34
carpal tunnel syndrome, 47–52 Hyaluronan synthases (HAS), 164
de quervain’s tenosynovitis, Hyaluronic acid (HA), 16,
52–54 163; see also Visco-
first carpometacarpal joint supplementation
osteoarthritis, 54–56 injections
guidance to setting of, 48 classification, 164
trigger finger, 57–59 clinical efficacy of, 167–172
HAS, see Hyaluronan synthases recommended dose for high
High-volume injection therapy molecular weight, 166
(HVI therapy), 128–129, structure, 164
130; see also Image-guided systemic safety issues, 171
injections usage indications, 165–166
Hip injections, 63; see also Greater working mechanism, 164–165
trochanteric pain
syndrome; Intra-articular
I
hip injections; Knee
injections IAS, see Intra-articular
complications and risks, 81–82 corticosteroids
efficacy of, 74 Iliotibial band lengthening (ITB), 70
greater trochanteric pain Image-guided injections, 117
syndrome, 63–64 advantages, 117
GTPS injection, 66–68 bursal injection, 131–133
guidance to setting of, 64 calcium barbotage, 129, 131, 132
indications and chemical composition
contraindications for of corticosteroid
lateral soft tissue, 65–66 injectable, 121
substances injected into hip complications, 120–122
joint, 71 corticosteroids, 119–120
Index 235
dry needling therapy, 127–128, 129 pre-procedure checks, 66
equipment used in USS-guided procedure, 68
injections, 124 INR, see International normalised
flushing post steroid injection, 122 ratio
high-volume injection therapy, Interdigital neuroma, 91; see also
128–129, 130 Foot and ankle injections
indications for articular and diagnosis of, 92
periarticular corticosteroid dorsal approach for, 94
injections, 119 injection technique, 93
indications to perform, 118–119 skin hypopigmentation
in-view approach, 124–125 following injection, 94
joint injections, 134–135 studies on, 92–93
local anaesthesia, 122–123 International normalised ratio
local anaesthesia and steroid (INR), 120
preparation, 120 Intra-articular corticosteroids
modalities, 118 (IAS), 173
neuroma injection, 135–137 Intra-articular hip injections,
out-of-view approach, 125, 126 70–71; see also Greater
preparation, 123 trochanteric pain
septic arthritis, 121 syndrome; Hip injections
soft tissue calcification, 121 anterior approach, 72–73
techniques, 123 aspirating before injecting, 73
tendon/paratenon intervention, contraindications to
125–127, 128 injection, 71
Impingement, 27–30; see also Ankle equipment required, 72
impingement; Shoulder indications for injection, 71
and elbow injections injection contents, 74
prolotherapy, 191 lateral approach, 73
Improvement tests, 25; see also patient position, 72
Shoulder and elbow preparation and technique
injections for, 72
Inflammatory tenosynovitis, 126 pre-procedure checks, 72
Injection for GTPS, 66; see also procedure, 73
Greater trochanteric pain Intra-articular knee joint
syndrome; Hip injections injection, 75; see also
equipment required, 66 Knee injections
injection contents, 68 In-view approach, 124–125; see also
patient positioning and Image-guided injections
landmarks for, 67 ITB, see Iliotibial band lengthening
236 Index
J novel treatments for
management of, 217
Joint; see also Image-guided
outcomes, 218, 220
injections
RF treatment, 217–218
injections, 134–135
sparing procedures, 99
Jumper’s knee, see Patella L
tendinopathy
LA, see Local anaesthesia
LA agent, see Local anaesthetic
agent
K
Lateral ankle ligament, 194
Kellgren and Lawrence (KL), 173 Lateral collateral ligament
KL, see Kellgren and Lawrence (LCL), 193
Knee injections, 74; see also Hip Lateral elbow tendinopathy, 203
injections Lateral epicondylitis, see Lateral
adjacent to patellar tendon, elbow tendinopathy;
78–79 Tennis elbow
complications and risks, Lateral patellofemoral
81–82 osteoarthritis, 194
contents, 80 LCL, see Lateral collateral
efficacy of, 80 ligament
guidance to setting of, 64 Lidocaine, 122–123; see also Pain
intra-articular knee joint management treatments
injection, 75 plasters, 223–224
medial and lateral portals for Lisfranc’ injury, 108; see also
knee joint, 79 Tarsometatarsal joints
preparations and technique Local anaesthesia (LA), 118,
for, 76 122–123
suprapatellar approach, 77–78 Local anaesthetic agent
treatment options for OA of (LA agent), 8
knee, 80–81 commonly used, 10
Knee joint properties of, 9
genicular arteries Lumbar pain, 191–192
accompanied with
genicular nerves, 218
M
genicular nerve treatment, 219
knee capsule innervation, 217 Magnetic resonance imaging
nerve supply, 217 (MRI), 118
Index 237
MCL, see Medial collateral knee National Institute of Health and
ligament Care Excellence (NICE), 4,
MCP, see Metacarpophalangeal 97, 173, 203, 223
MEAT (movement, exercise, Neuroma injection, 135; see also
analgesics, treatment), Image-guided injections
189 Morton’s neuroma, 136–137
Medial collateral knee ligament post-traumatic neuroma, 135
(MCL), 187 NHS, see National Health Service
Medial epicondylitis, see Golfer’s NICE, see National Institute
elbow of Health and Care
Medial OA of knee, 194 Excellence
Metacarpophalangeal (MCP), 57 Non-animal stabilised HA
Metatarsal (MT), 109 (NASHA), 164
Metatarsophalangeal joint Non-insertional achilles
(MTPJ), 91; see also tendinopathy, 147; see also
Hallux rigidus Platelet-rich plasma
Molecular weight (MW), 164 Non-medicinal treatments, 1
Morton’s neuroma, 136–137; see also Non-steroidal anti-inflammatory
Interdigital neuroma drugs (NSAIDs), 5, 95,
MRI, see Magnetic resonance 163, 187, 202
imaging NSAIDs, see Non-steroidal anti-
MSK, see Musculoskeletal inflammatory drugs
MT, see Metatarsal
MTPJ, see Metatarsophalangeal
O
joint
Musculoskeletal (MSK), 1; OARSI, see Osteoarthritis Research
see also Corticosteroid Society International
injections Off-the-shelf inserts, 15
injections, 1, 47, 132 Orthoses, 15
injuries, 141 Orthotics, 15
pain, 1 Osteitis pubis, 193
MW, see Molecular weight Osteoarthritis (OA), 27, 100,
163, 214; see also Knee
injections; Shoulder and
N
elbow injections
NASHA, see Non-animal of knee, 80–81
stabilised HA Osteoarthritis Research Society
National Health Service (NHS), 8 International (OARSI), 174
238 Index
Osteotomies, 99 alternative treatments, 97
Out-of-view approach, 125, 126; injection site for, 98
see also Image-guided injection technique, 97
injections management, 95
physiotherapy stretching
exercises for treatment
P
of, 96
Pain management treatments, 213 presenting symptoms, 95
capsaicin cream and patch, 223 randomised controlled
cryotherapy, 222 trial, 96
hip joint, 220–221 risk factors for, 95
knee joint, 217–220 Platelet-derived growth factor
lidocaine plasters, 223–224 (PDGFa-b), 143
PRF treatment, 214 Platelet factor 4, 143
RF lesioning, 213 Platelet-rich plasma (PRP), 42, 70,
shoulder joint, 213–217 71, 97, 141, 142, 206
SSN, 214 administering PRP for lateral
Paracetamol, 163 epicondylitis, 155
Paratenonitis, 126 administering PRP
Patellar subluxation, 194 injection, 153
Patellar tendinitis, see Patella administering PRP to quadriceps
tendinopathy tendon, 154
Patella tendinopathy, 146–147, 194, advantages of, 141–142
206; see also Platelet-rich adverse effects, 148
plasma alpha granules, 142
PDGFa-b, see Platelet-derived classification, 143–144, 145
growth factor contraindications, 148
PEDro, see Physiotherapy Evidence function of growth factors
Database in, 143
Pelvic/sacroiliac/lumbar pain, functions, 142
192–193 injection protocol, 149
Peroneal nerve, 217 injections, 4, 16
Pharmacological interventions, 1 lateral epicondylitis, 146
Physiotherapy Evidence Database local anaesthetic
(PEDro), 199 injection, 153
Plantar fasciitis, 94, 147, 208–209; non-insertional achilles
see also Foot and ankle tendinopathy, 147
injections; Platelet-rich patella tendinopathy, 146–147
plasma plantar fasciitis, 147
Index 239
post-procedure protocol, lateral ankle ligament, 194
155–158 lateral patellofemoral OA, 194
post-PRP treatment tendon lumbar pain, 191–192
protection, 156 medial OA of knee, 194
preparations, 144 osteitis pubis, 193
PRP injection to patella patellar subluxation, 194
tendon, 154 patellar tendinopathy, 194
quadriceps tendinopathy, pelvic/sacroiliac/lumbar pain,
147–148 192–193
rotator cuff tendinopathy, 148 preparation and needle
steps and equipment required technique, 187–190
to produce PRP, recurrent acute lumbago,
149–152 191–192
uses, 145–148 recurrent dislocation of shoulder
Posterior superior iliac spine and impingement
(PSIS), 188 syndrome, 191
PRF, see Pulsed radiofrequency solutions, 185, 187
Prolotherapy, 17, 179 spondylolisthesis, 191–192
acromioclavicular joint symphysis pubis instability, 193
subluxation, 190 syndesmosis injury, 194
advantages, disadvantages and tennis and Golfer’s elbows, 191
side effects, 184–185 tips from experience, 190
aftercare, 189–190 PSIS, see Posterior superior iliac
ankle joint capsule laxity, 195 spine
anterolateral or posterior ankle Pulsed radiofrequency
impingement, 195 (PRF), 213; see also
cervical pain and cervical- Pain management
related dizziness, 190 treatments
current evidence, 185, 186 treatment, 214
deltoid ligament laxity, 195
femoral attachment and joint
Q
line of medial collateral
ligament, 180 QALY, see Quality-adjusted
history, 179 life year
indications and Quadriceps tendinopathy, 147–148;
contraindications, see also Platelet-rich
180–183 plasma
intervals between treatments, Quality-adjusted life year
188–189 (QALY), 173
240 Index
R muscles of rotator cuff, 24
painful arc of, 29
RA, see Rheumatoid arthritis
Shoulder and elbow injections, 23
Radiofrequency lesioning (RF
anterior approach to
lesioning), 213; see also
glenohumeral joint, 36–37
Pain management
calcific tendinitis, 31, 32
treatments
contraindications for shoulder
Randomised controlled trial (RCT),
injection, 32–33
96, 203
degenerative rotator cuff tears,
RCT, see Randomised controlled
30–31
trial
diagnostic injection, 31–32
Recurrent acute lumbago, 191–192
differentiating shoulder pain, 24
Recurrent dislocation of
drug choice, 33–34
shoulder, 191
formulations for joint
RF lesioning, see Radiofrequency
injections, 34
lesioning
frozen shoulder/joint
Rheumatoid arthritis (RA), 223
stiffness, 30
RICE (rest, ice, compression,
impingement, 27–30
elevation), 189
improvement tests, 25
Rotator cuff; see also Platelet-rich
injecting acromioclavicular
plasma
joint, 37–38
calcification, 202
injecting elbow joint, 40
muscles, 24
injecting glenohumeral joint,
tendinopathy, 149
34–36
injecting golfer’s elbow, 42–43
injecting subacromial space,
S
38–40
Sacroiliac joint (SIJ), 188, 189 injecting tennis elbow, 40–42
Saphenous nerve, 90 local anaesthetic, 33
SCI, see Synthetic cartilage osteoarthritis, 27
interposition painful arc of shoulder, 29
Septic arthritis, 121 physiotherapy in shoulder
Shock waves, 199; see also disorders, 25–26
Extracorporeal shock risks, 33
wave therapy sites for injection in
Shoulder, 23 shoulder, 26
bony anatomy of, 23 steroid injections for shoulder
exercises, 25 disorders, 26
girdle, 23 subacromial bursa, 28
Index 241
Shoulder joint Syndesmosis injury, 194
nerve supply, 213 Synthetic cartilage interposition
PRF treatment, 214 (SCI), 99
suprascapular nerve block, 214 Synthetic corticosteroids, 2; see also
treatments for management of, Corticosteroids
213–217
ultrasound scanning, 214
T
Sinus tarsi syndrome (STS), 107;
see also Foot and ankle Tarsometatarsal joints (TMTJ), 108;
injections see also Foot and ankle
injection site for sinus tarsi, 109 injections
injection technique, 108 diagnosis, 108
x-ray showing needle in sinus first TMTJ, 110
tarsi, 109 fluoroscopy view indicating
SLR, see Straight leg raise injection into second, 110
Soft tissue fourth and fifth TMTJs, 110–111
calcification, 121 injection technique, 109
pathology, 16 second and third TMTJs, 110
Spondylolisthesis, 191–192 surface markings of second
SSN, see Suprascapular nerve TMTJ, 110
Steida process, 105 Temporomandibular joint
Steroid injections, see Corticosteroid (TMJ), 179
injections Tendinopathy, 125, 145–146; see also
Straight leg raise (SLR), 192 Impingement
STS, see Sinus tarsi syndrome Tendonitis, see Tendinopathy
Subacromial bursa, 28 Tendon/paratenon intervention,
Subacromial bursitis, see 125–127, 128; see also
Impingement Image-guided injections
Subacromial pain syndrome, see Tendons, 125
Impingement Tennis elbow, 40–42, 146; see also
Subacromial space, 38–40; see Platelet-rich plasma;
also Shoulder and elbow Shoulder and elbow
injections injections
Suprascapular nerve (SSN), 214; see prolotherapy, 191
also Pain management Tenosynovitis, 125
treatments TENS, see Transcutaneous electrical
block, 214 nerve stimulation
and branches, 215 TGF-β, see Transforming growth
Symphysis pubis instability, 193 factor-beta
242 Index
Tibiotalar joint, see Ankle joint Victoria Institute of Sport
TMJ, see Temporomandibular joint Assessment-Patella
TMTJ, see Tarsometatarsal joints (VISA-P), 206
Transcutaneous electrical nerve VISA-P, see Victoria Institute of
stimulation (TENS), Sport Assessment-Patella
70, 80 Visco-supplementation, 163
Transforming growth factor-beta Visco-supplementation injections,
(TGF-β), 143 163; see also Hyaluronic
Triamcinolone acetonide, 121–122 acid
Trigger finger, 57; see also Hand and for ankle, 169–171
wrist injections anteromedial and anterolateral
aetiology of, 57 portals for knee, 168
direction of needle for injection, cost-effectiveness, 172–173
59 effectiveness in joints, 167
effectiveness of corticosteroid, guidelines, 173–174
57–58 for hip, 168–169
injection technique, 58–59 for knee, 167–168
location of A1 pulleys, 59 lateral suprapatellar portal for
treatment, 57 knee, 168
recommended dose, 166
for shoulder, 171
U
usage indications, 165–166
Ultrasound (US), 118, 169 Visual Analogue Scale (VAS),
206, 221
V
W
VAS, see Visual Analogue Scale
Vascular endothelial growth factor WOMAC (Western Ontario and
(VEGF), 143 McMaster Universities
VEGF, see Vascular endothelial Osteoarthritis Index),
growth factor 173, 221
Musculoskeletal
Injections and
Alternative Options
A practical guide to
‘what, when, and how?’
Patient’s guide to steroid injection
Steroid injections are commonly performed for joint- or soft tissue- related
pain. This leaflet attempts to answer questions commonly asked by patients
about steroid injections.
How do steroid injections work?
The mechanism of action of these injections is complex. Steroids reduce the
body’s inflammatory and immune response at several levels. The net effect is
reduction in pain and inflammation at the injection site.
What are the indications of corticosteroid injections?
Corticosteroid injections play an important role in the management of various
musculoskeletal conditions. Common indications include arthritis of a
joint, inflammation around a nerve (e.g. carpal tunnel syndrome, Morton’s
neuroma) or inflammation around a tendon (tendinopathy, tenosynovitis or
tendonitis). The injections can give long- or short-term pain relief. In some
conditions, such as plantar fasciitis (inflammation of a band of tissue on the
sole of the foot), they provide a pain-free window for rehabilitation.
What are the contraindications of corticosteroid injections?
Steroid injections should not be administered in the following conditions:
●● Allergy or intolerance to drug
●● Overlying skin infection or broken skin
●● Fracture (a break in the bone)
●● Septic arthritis (infection of a joint)
●● Prosthetic joint (e.g. knee or hip replacement)
●● Unstable coagulopathy (bleeding disorder)
Steroid injections should be avoided in patients who are waiting for a Joint
replacement as this might increase the risk of infection post surgery.
What equipment is needed for corticosteroid injection?
Although many corticosteroid injections can be performed without specialist
equipment, image guidance (X-rays or ultrasound) may be necessary for
Patient’s guide to steroid injection 3
smaller joints in the hands and feet, deep structure (e.g. hip joint) and some
soft tissue injections (particularly if in close proximity to tendons, nerves or
blood vessels).
Is the injection painful?
In most cases, the injection will cause some discomfort or pain. Usually, local
anaesthetic is used to reduce the pain associated with steroid injection. The
local anaesthetic is either mixed with the steroid injection or given just before
the injection. Some numbness may be experienced following injection, and
this can last for a few hours depending on the local anaesthetic used.
What are the risks and side effects of a steroid injection?
Most steroid injections cause no complications, but, like all medications
and procedures, there are potential risks. In about 10% cases the steroid can
cause an increase in pain for the first day or two after injection, a so-called
steroid flare. This usually settles with time, and simple painkillers such as
paracetamol can help. There is a small risk of infection with a steroid injection.
If the joint or skin becomes hot, red or swollen, or you feel feverish and
unwell you should seek help from your doctor or local hospital. The injection
can result in bleeding. This risk is increased if you are on blood thinning
medication. Steroid injections can cause thinning and colour changes of
the skin around the site that has been injected. More general side effects,
such as mood changes, sleep disturbance and facial flushing, can also occur
temporarily. Diabetic patients can expect to experience a rise in blood sugar
levels after steroid injections.
What I can and can’t do after a steroid injection?
Usually, your doctor will advise you on this specifically depending on why
the injection has been given. As local anaesthetic is often used, it is safest to
avoid driving until this has worn off completely. Steroid injection can weaken
a tendon or ligament leading to rupture. You should avoid strenuous exercise,
heavy lifting or running for 2 weeks after an injection.
How often can a steroid injection be performed?
There is no hard and fast rule about this. General belief is that too many
injections may potentially weaken the soft tissue structures including tendons
and ligaments or increase the risk of infection. It has been shown that repeated
injections can become ineffective over a period of time. In general, steroid
injections should not be repeated for 3 months.
4 Patient’s guide to steroid injection
Do all patients respond to corticosteroid injections?
The degree and duration of pain relief following corticosteroid injection is
unpredictable. There is some evidence that patients with early arthritis benefit
more and for a longer duration compared to those with more severe arthritis.
In general, if patients are going to respond to a steroid injection, they tend to
respond after the first injection. Patients who have gained no symptom relief
or functional benefit from two injections should probably not continue with
repeat injections because the likelihood of improvement is small.
What is the role of pain killers and anti-inflammatory medicines after
steroid injection?
Depending on the indication, there are many additional treatments which
can complement the effect of steroid injection. For chronic conditions such
as arthritis, many patients may take regular analgesia such as paracetamol
and non-steroidal anti-inflammatory drugs (NSAIDs). These should be
continued following steroid injection. Immediately after the procedure, they
help to control pain after the local anaesthetic effects wear off. They also
help in managing symptoms in case of steroid flare. Similarly, for patients
receiving treatment for inflammatory conditions such as rheumatoid arthritis,
administration of disease modifying anti-rheumatic drugs (DMARDs) should
not be stopped.
What is the role of physiotherapy and when can it be started following
steroid injection?
For many soft tissue presentations, corticosteroid injections are themselves
adjuncts to other treatment modalities. Physiotherapy is the mainstay of ini-
tial management for many conditions (e.g. plantar fasciitis, tendinopathies,
adhesive capsulitis of shoulder). Steroid injections are administered to reduce
pain and inflammation sufficiently to do stretching and strengthening exer-
cises under the supervision of physiotherapists. In most cases, physiotherapy
can be started 1-2 weeks following steroid injection.
Note: If you have any further questions about steroid injections that you feel has
not been answered, be sure to ask your doctor to answer them before proceeding.