European Federation of National Associations of Orthopaedics and Traumatology
European Instructional Lectures Volume 9 2009
European Federation of National Associations of Orthopaedics and Traumatology Committees and Task Forces EFORT Executive Committee
Standing Committees EAR Committee
Executive Board Prof. Dr. Karl-Göran Thorngren, President Prof. Dr. Miklós Szendrıi, Vice President Dr. Manuel Cassiano Neves, Secretary General Prof. Dr. Wolfhart Puhl, Immediate Past President Mr. Stephen R. Cannon, Treasurer Prof. Dr. Enric Caceres Palou, Member at Large Prof. Dr. Pierre Hoffmeyer, Member at Large Prof. Dr. Maurilio Marcacci, Member at Large Co-Opted Members Mr. John Albert Prof. Dr. Thierry Bégué Prof. Dr. George Bentley, Past President Prof. Dr. Nikolaus Böhler, Past President Dr. Karsten Dreinhöfer Dr. Roberto Giacometti Ceroni Prof. Dr. Klaus-Peter Günther Ass. Prof. Dr. Per Kjaersgaard-Andersen Prof. Dr. Karl Knahr
Scientific Coordination 10th EFORT Congress, Vienna 2009 Chairman Prof. Dr. Pierre Hoffmeyer Members Prof. Dr. George Bentley Prof. Dr. Nikolaus Böhler Prof. Dr. Enric Caceres Palou Mr. Stephen R. Cannon Dr. Manuel Cassiano Neves Prof. Dr. Alfred Engel Prof. Dr. Roberto Giacometti Ceroni Prof. Dr. Martti Hämäläinen Prof. Dr. Karl Knahr Prof. Dr. Philippe Neyret Prof. Dr. Miklós Szendrıi
Prof. Dr. Nikolaus Böhler, Dr. Gerold Labek Education Committee Prof. Dr. Enric Caceres Palou EIL Committee Prof. Dr. Wolfhart Puhl, Prof. Dr. Karl-Göran Thorngren Events Committee Dr. Manuel Cassiano Neves Finance Committee Mr. Stephen R. Cannon, Prof. Dr. Pierre-Paul Casteleyn Health Service Research Committee Dr. Karsten Dreinhöfer Portal Steering Committee Prof. Dr. Klaus-Peter Günther Publishing Committee Prof. Dr. George Bentley (Books), Prof. Dr. Klaus-Peter Günther (Portal), Prof. Dr. Wolfhart Puhl (Journal) Scientific Committee Prof. Dr. Pierre Hoffmeyer Venue Committee Prof. Dr. Miklós Szendrıi
Task Forces and Ad Hoc Committees Awards & Prizes Committee Prof. Dr. George Bentley Fora Prof. Dr. Thierry Bégué Liaison & Lobbying Committee Prof. Dr. Wolfhart Puhl Speciality Societies Committee Dr. Roberto Giacometti Ceroni Travelling & Visiting Fellowships Prof. Dr. Maurilio Marcacci
European Federation of National Associations of Orthopaedics and Traumatology
European Instructional Lectures Volume 9, 2009 10th EFORT Congress, Vienna, Austria
Edited by
George Bentley
Editor: Prof. Dr. George Bentley Royal National Orthopaedic Hospital Trust Stanmore, Middlesex HA 7 4LP, UK
[email protected] EFORT Central Office Technoparkstrasse 1 8005 Zürich, Switzerland www.efort.org
ISBN: 978-3-642-00965-5
e-ISBN: 978-3-642-00966-2
DOI: 10.1007/978-3-642-00966-2 Springer Dordrecht Heidelberg London New York Library of Congress Control Number: 2009926014 © EFORT 2009 This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilm or in any other way, and storage in data banks. Duplication of this publication or parts thereof is permitted only under the provisions of the German Copyright Law of September 9, 1965, in its current version, and permission for use must always be obtained from Springer. Violations are liable to prosecution under the German Copyright Law. The use of general descriptive names, registered names, trademarks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. Product liability: The publishers cannot guarantee the accuracy of any information about dosage and application contained in this book. In every individual case the user must check such information by consulting the relevant literature. Cover design: Frido Steinen-Broo, eStudio Calamar, Spain Printed on acid-free paper Springer is part of Springer Science+Business Media (www.springer.com)
Foreword
The 10th Congress of the European Federation of National Associations of Orthopaedics and Traumatology (EFORT) is the most important combined congress of the national societies in Europe. At present a total of 36 societies are members of this organisation. The major goal of EFORT is to bring current knowledge of diseases and trauma of the musculoskeletal system to all European surgeons and additionally to welcome colleagues from all over the world to join us in sharing our daily work experience. In the scientific programme the instructional lectures form a very basic and important part of the Congress. In Vienna a total of 25 sessions are included in the programme. The authors come from all over Europe and they discuss topics from many different fields of trauma and orthopaedics. These lectures not only give the opportunity for us to be informed about various diseases, but they are also influenced by the authors’ experience based on the treatment philosophy in their own country – again an opportunity to widen the European horizon. They are aimed at both the general orthopaedic surgeons and the young residents and trainees who want to widen their knowledge in different topics of orthopaedic and trauma surgery. As the chairman of the Local Organising Committee I thank all the authors for providing their presentation for publication in this volume. I also address my special thanks to Professor George Bentley for organising this edition. I am confident that this book will have the same respected place in the library of the participating orthopaedic surgeons as do all the previous ones. Vienna, Austria
Karl Knahr
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Preface
This is the 9th volume of the European Instructional Lectures, which contains more new material, which will be presented during the 10th EFORT Congress in Vienna by distinguished authors from across Europe. As in former volumes the chapters cover a range of topics, concentrating on both the essentials of the subjects and the latest thinking and technology. Additionally, the authors are from different countries and centres, which reflect the variety of modern European orthopaedic and traumatology practice and their special experience and philosophy. Special thanks are due to these authors who have been called upon to do other tasks, such as paper reviewing and chairing Specialist Symposia and Free Paper sessions, and all of them have responded generously. Without this spirit of collaboration by our colleagues in the National and Specialty Societies, EFORT would not flourish. The preparation and printing of this volume was by the Internationally-recognised Springer team, enthusiastically led by Gabriele Schroeder, to whom we are very grateful. I wish also to thank Larissa Welti, Régine Brühweiler, Sabrina Wolf and the EFORT Central Office for their unfailing support. EFORT has now exceeded 220 essays in the 9 volumes of Instructional Lectures since the series first began at the opening Congress in Paris in 1993. With this in mind we wish to dedicate this volume to the memory of the life and work of our dear colleague Professor Frantz Langlais, tragically and prematurely taken from us in 2007. Stanmore, UK
George Bentley
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Contents
General Orthopaedics Current Status of Arthroplasty Registers in Europe . . . . . . . . . . . . . . . . . . N. Böhler and Gerold Labek
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National Registration of Hip Fractures in Sweden . . . . . . . . . . . . . . . . . . . . Karl-Göran Thorngren
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Current Status of Articular Cartilage Repair. . . . . . . . . . . . . . . . . . . . . . . . Emmanuel Thienpont
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Thromboprophylaxis After Major Orthopaedic Surgery: State of the Art . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Alexander G.G. Turpie
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Paediatrics DDH: Diagnosis and Treatment Strategies . . . . . . . . . . . . . . . . . . . . . . . . . . R. Graf
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Slipped Capital Femoral Epiphysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . C. Zilkens, M. Jäger, Y-J. Kim, M.B. Millis, and R. Krauspe
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Major Joint Contractures in Children. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Deborah M. Eastwood
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Trauma Damage-Control Orthopaedic Surgery in Polytrauma: Influence on the Clinical Course and Its Pathogenetic Background . . . . . . . . . . Hans-Christoph Pape
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Fractures and Non-Unions of the Clavicle. . . . . . . . . . . . . . . . . . . . . . . . . . . Patrick Simon
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Proximal Humeral Fractures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . C. Torrens
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Fixation of Intertrochanteric Femoral Fractures . . . . . . . . . . . . . . . . . . . . . Vilmos Vécsei and Stefan Hajdu
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Surgical Management of Distal Tibial Fractures in Adults . . . . . . . . . . . . . Mathieu Assal and Richard Stern
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Contents
Upper Limb and Hand The Distal Radio-Ulnar Joint: Functional Anatomy, Biomechanics, Instability and Management . . . . . . . . . . . . . . . . . . . . . Panayotis N. Soucacos and Nickolaos A. Darlis
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Distal Radius Fractures: Evolution in the Treatment Standard of Care 2009 . . . . . . . . . . . . . . . Antonio Abramo and Philippe Kopylov
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Dupuytren’s Contracture . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Hanno Millesi
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Spine Low Back Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . R. Eyb and G. Grabmeier
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Hip Total Hip Arthroplasty: A Comparison of Current Approaches . . . . . . . . Martin Krismer
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How to Do a Cemented Total Hip Arthroplasty . . . . . . . . . . . . . . . . . . . . . . Eduardo Garcia-Cimbrelo
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How to Do a Cementless Hip Arthroplasty . . . . . . . . . . . . . . . . . . . . . . . . . . Klaus-Peter Günther, Firas Al-Dabouby, and Peter Bernstein
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Knee How to Treat a Meniscal Lesion? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Olivier Charrois and The GREC Group
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Soft-Tissue Balance in Total Knee Arthroplasty. . . . . . . . . . . . . . . . . . . . . . David E. Beverland
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Revision Total Knee Arthroplasty with Bone Loss . . . . . . . . . . . . . . . . . . . . Josef Hochreiter and Karl Knahr
219
Foot and Ankle Ankle Arthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . X. Crevoisier
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Hallux Rigidus: Arthroplasty or Not? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . S. Giannini, F. Vannini, R. Bevoni, and D. Francesconi
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Contributors Preface
Antonio Abramo Hand and Upper Extremity Unit, Department of Orthopaedics, Lund University Hospital, Lund, Sweden Firas Al-Dabouby Department of Orthopaedic Surgery, University Hospital Carl Gustav Carus Dresden, Fetscherstr. 74, D-01307 Dresden, Germany Mathieu Assal Orthopaedic Surgery Service, University Hospital of Geneva, Switzerland,
[email protected] Peter Bernstein Department of Orthopaedic Surgery, University Hospital Carl Gustav Carus Dresden, Fetscherstr. 74, D-01307 Dresden, Germany David E. Beverland Outcomes Unit, Musgrave Park Hospital, Belfast, BT9 7JB, UK,
[email protected] Roberto Bevoni Via Pupilli 1, 40136 Bologna, Italy,
[email protected] Nikolaus Böhler AKH Linz, Orthopaedic Department, Krankenhausstrasse 9, A-4020 Linz, Austria,
[email protected] Olivier Charrois Clinique Arago, 95 Boulevard Arago, 75014 Paris, France,
[email protected] Xavier Crevoisier Centre Hospitalier Universitaire Vaudois (CHUV), Site Hôpital Orthopédique, Pierre-Decker 4, 1011 Lausanne, Switzerland,
[email protected] Nickolaos A. Darlis Department of Orthopaedic Surgery, University of Athens, School of Medicine, Athens, Greece Deborah M. Eastwood Department of Paediatric Orthopaedics, Great Ormond St Hospital for Children and the Royal National Orthopaedic Hospital, London, UK,
[email protected] Richard Eyb Donauspital, Orthopädische Abteilung, Sozialmedizinisches Zentrum Ost, Langobardenstrasse 122, 1220 Wien, Austria,
[email protected] D. Francesconi Via Pupilli 1, 40136 Bologna, Italy,
[email protected] Eduardo Garcia-Cimbrelo Hospital La Paz, Universidad Autónoma de Madrid, Paseo de la Castellana 261, Madrid 28046, Madrid, Spain,
[email protected]
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Sandro Giannini Via Pupilli 1, 40136 Bologna, Italy,
[email protected] Georg Grabmeier Donauspital Orthopädische Abteilung Sozialmedizinisches Zentrum Ost Langobardenstrasse 122 1220 Wien, Austria Reinhard Graf Allgemeines u. Orthopädisches Landeskrankenhaus, 8852 Stolzalpe, Austria,
[email protected] Klaus-Peter Günther Department of Orthopaedic Surgery, University Hospital Carl Gustav Carus Dresden, Fetscherstr. 74, D-01307 Dresden, Germany,
[email protected] Stefan Hajdu Department of Trauma Surgery, Vienna Medical University, Währinger Gürtel 18-20, 1090-Wien, Austria,
[email protected] Josef Hochreiter Department of Orthopaedic Surgery, St. Vincent’s Hospital, Linz, Austria,
[email protected] Marcus Jäger Department of Orthopaedic Surgery, University Hospital of Düsseldorf, Moorenstrasse 5, 40225 Düsseldorf, Germany Young-Jo Kim Children’s Hospital Boston, Harvard Medical School, Department of Orthopaedic Surgery, 300 Longwood Avenue, Boston, MA 02115, USA Karl Knahr Department II of Orthopaedic Surgery, Orthopaedic Hospital Speising, Vienna, Austria,
[email protected] Philippe Kopylov Hand and Upper Extremity Unit, Department of Orthopaedics, Lund University Hospital, Lund Sweden,
[email protected] Rüdiger Krauspe Department of Orthopaedic Surgery, University Hospital of Düsseldorf, Moorenstrasse 5, 40225 Düsseldorf, Germany,
[email protected] Martin Krismer Department of Orthopaedics, Innsbruck Medical University, Anichstrasse 35, A-6020 Innsbruck, Austria,
[email protected] Gerold Labek Medical University Innsbruck, Orthopaedic Department, Anichstrasse 35, A-6020 Innsbruck, Austria Hanno Millesi Wiener Privatklinik, Pelikangasse 15 1090 Wien, Austria,
[email protected] M.B. Millis Children’s Hospital Boston, Harvard Medical School, Department of Orthopaedic Surgery, 300 Longwood Avenue, Boston, MA 02115, USA Hans-Christophe Pape University of Aachen, Chairman, Department of Orthopaedics, Pauwelstreet 30, 52074 Aachen, Germany
[email protected] Patrick Simon Centre Hospitalier Saint Joseph - Saint Luc 20, quai Claude Bernard 69365 Lyon, France,
[email protected] Panayotis N. Soucacos Department of Orthopaedic Surgery, University of Athens, School of Medicine, Athens, Greece,
[email protected] Richard Stern Orthopaedic Surgery Service, University Hospital of Geneva, Switzerland
Contributors
Contributors
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Emmanuel Thienpont University Hospital Saint Luc, U.C.L., Avenue Hippocrate 10, 1200 Brussels, Belgium,
[email protected] Karl-Göran Thorngren Department of Orthopaedics, Lund University Hospital, SE-221 85 Lund, Sweden,
[email protected] Carlos Torrens Orthopaedic Department, Hospital del Mar, Passeig Marítim 25-29, 08003 Barcelona, Spain,
[email protected] Alexander G.G. Turpie McMaster University, 237 Barton Street East, Hamilton, Canada, ON L8L 2X2,
[email protected] F. Vannini Via Pupilli 1, 40136 Bologna, Italy,
[email protected] Vilmos Vécsei Department of Trauma Surgery, Vienna Medical University, Währinger Gürtel 18-20, 1090-Wien, Austria Christoph Zilkens Department of Orthopaedic Surgery, University Hospital of Düsseldorf, Moorenstrasse 5, 40225 Düsseldorf, Germany
Current Status of Arthroplasty Registers in Europe1 N. Böhler and Gerold Labek
Introduction National Arthroplasty Registers in Scandinavia have proved to be an important and valid instrument to assess the longterm performance of joint arthroplasty procedures and to lead to an improvement in the long-term outcome of arthroplasty [1–8]. Improved quality of joint arthroplasty effects a reduction of costs in public health care by avoiding revision surgery [9]. Starting with the Swedish National Knee Register (Lund, 1975) [10] and the Swedish National Hip Register (Gothenburg, 1979) they have had a high impact on Orthopaedic procedures in Scandinavia and worldwide. In Sweden, for instance, the revision burden as an essential indicator could be substantially reduced. Due to data in the register, products with inferior performance such as Boneloc bone cement were rapidly detected [11]. The product was taken from the market wordwide in 1995. Moreover, the effects of procedures such as the mini-invasive approach, of operating experience [12] or the administration of antibiotics could be evaluated and, as a consequence, standardised improvements could be suggested. Even though the results obtained from arthroplasty registers were accepted by the scientific community worldwide and were often quoted, efforts to establish similar projects in other countries were not really successful. For example,
N. Böhler () AKH Linz, Orthopaedic Department, Krankenhausstrasse 9, A-4020 Linz, Austria e-mail:
[email protected]
an ambitious project in Germany, the German Arthroplasty Register e.V. in Göttingen [13], as well as the European Implant Register Committee by EFORT were discontinued after a few years. A multitude of different projects were and still are designated as registers. As there was no commonly-accepted definition of a register, the definition of an Arthroplasty Register was worked out by close dependence on the Scandinavian experience and was finally determined by the European Arthroplasty Register with all European National Arthroplasty Registers participating. These are the aims of a Register: ● Registration of ALL primary and revision operations in a defined area in a central database. ● Follow the implant until it has to be revised, the patient dies or emigrates. ● Definition of Revision (= Failure): at least one part of the implant has to be revised. Other large-scale documentation should be considered as multi-centre studies or surveys. The completeness of data is decisive for the quality of the results drawn from a register. Registers in Scandinavia were the first to prove that area-wide data collection is possible [14–18]. The high quality of statements on activities and results within whole National territories is unique in science. One of the essential criteria is that the bias which is inevitable when working with samples can largely be avoided on a National scale.
Historical Review and Methods 1
International Websites of National Arthroplasty Registers including National Arthroplasty Register Reports and Publications are presented on the EFORT-Website: http://www.efort.org/ getdoc/1b923b01-41d2-4587-bac2-7ca7a11e613e/ArthoplastyRegisters.aspx
Within the scope of an EFORT project in Romania it was decided in 1999 to found a National arthroplasty register. Afterwards, in rapid succession, the Slovak Orthopaedic Society also decided to establish a National arthroplasty
G. Bentley (ed.), European Instructional Lectures. European Instructional Course Lectures 9, DOI: 10.1007/978-3-642-00966-2_1, © 2009 EFORT
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register and the Hungarian Register, founded in 1998, expressed its willingness to co-operate, the opportunity for supra-National co-operation became self-evident. EFORT was given responsibility for these activities, and consequently the EFORT Executive Committee launched the “European Arthroplasty Register” (EAR) project in June 2001. All existing National registers, at that time the Scandinavian Registers, were prepared to join the project and make their experience available to the network. In order to be able to support the increasing number of network activities in the best possible way a non-profit association, EFORT-EAR, was founded in 2005. This association closely co-operates with EFORT. There are multiple organisational links between EFORT and EFORT-EAR. Further information is available from the Internet on www.ear.efort.org. Membership requires either operating a National register according to the EFORT-EAR definition or an exisiting project for the foundation of a National register that is supported by the relevant National orthopaedic society. The EAR network supports initiatives for the foundation of National arthroplasty registers by National orthopaedic societies. These activities are primarily based on the exchange of experience, passing on information for discussions, for instance with health authorities, and the interchange of solutions for common problems in organisation, documentation and evaluation. Particular central standards are being laid down, such as Minimal Datasets, for example, that comprise all parts of information to be collected in a National register. These standardisation efforts aim at improving the supranational comparison of reports. Where necessary central services shall help registers to fulfil their tasks as economically as possible. A central product data base would be one example. Implant tracking is a pre-condition for any kind of evaluation. Setting up a database comprising all products available on the relevant markets is one of the most complex and time-consuming tasks of every register that has to be carried out in co-operation with the producers. A co-operation will thus enable all partners to improve data quality at a lower expenditure. EFORT also supports register activities through its wide range of publication facilities. Within the scope of the EFORT homepage (www.efort.org) all websites of National Arthroplasty Registers have been combined in a user-friendly way. Futhermore publication activities are supported through essential results achieved in the course of EFORT and National conferences. Of course the EAR project also comprises scientific activities. These activities as with all communication within the network of National Registers are run via the
N. Böhler and G. Labek Fig. 1 Number of National Arthroplasty Register projects started
20 18 16
Start of Arthroplasty Registers
14 12 10 8 6 4 2 0 1970s
1980s
1990s
2000-
EAR Office at the Orthopaedic University Hospital of Innsbruck, Austria. The variety of projects in nearly all European countries and the rapidly growing number of register foundations within the last 10 years clearly demonstrate the value and necessity of activities of that kind (Fig. 1). At present 27 registers in 24 countries are members of the EAR. In most of these countries register activities are carried out by one organisation. However, the splitting of activities into several centres, each dealing with a particular joint, is a promising alternative as examples in Sweden and Denmark have shown (Table 1).
Basic Requirements for the Development and Activities of a National Arthroplasty Register Arthroplasty Registers are very complex projects requiring co-operation with a variety of experts and stakeholders. Over the past few years the development of various National registers has shown that several aspects are crucial for successful implementation. 1. The register has to be an integral part of the National health-care system. Registers exclusively based on scientific motivation and the support of academic institutions were not able to cope with the diverse problems and requirements alone, notwithstanding the strong personal
Current Status of Arthroplasty Registers in Europe
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Table 1 Arthroplasty registers according to EAR definitions worldwidea Country
Founded
Status
Data collection
Data validation published
Sweden – Knee Sweden – Hip Finland Norway Denmark – Hip Denmark – Knee New Zealand Hungary Australia Canada Czech Rep. Romania Moldova Turkey Slovakia Austria England and Wales (NJR) Lithuania France Portugal Netherlands Italy
1975 1979 1980 1987 1995 1997 1998 1998 1999 2000 2001 2001 2002 2002 2002 2002 2003 2005 2006 2006 2006 2006 2006 2006 Submitted for agreement 2008 2008 2008 2006
Nationwide Nationwide Nationwide Nationwide Nationwide Nationwide Nationwide Incomprehensive Nationwide Nationwide Incomprehensive Nationwide Incomprehensive In reorgansiation Nationwide Pilot phase Nationwide Pilot phase Pilot phase Pilot phase Pilot phase Inhomogenous according to the development in the regions Project Project Project
Yes Yes Yes Yes Yes No No No No No No No No No No No No No No No No No
Croatia Bulgaria Germany
Active Active Active Active Active Active Active Active Active Active Active Active Active In reorgansiation Active Active Active Pilot phase Pilot phase Pilot phase Pilot phase Regional registers to be combined Project Project Project Pilot phase Pilot phase Project Pilot project
Pilot phase (30% coverage) Pilot phase Project Pilot project
No No No No
Switzerland Israel Luxembourg Spain
No No No
a
Deadline, 1 Jan 2009
commitment of those involved. Under the prevailing circumstances, particularly the solution of data privacy issues and achieving completeness in data collection can only be handled in co-operation with Institutions pertaining to the public health sector. Furthermore, longterm funding of a high-quality national register through a professional association or academic institution alone has proved difficult. 2. A professional, central structure should be available for data collection and evaluation in order to be able to meet the manifold requirements in an appropriate way. 3. The specific implementation is strongly dependent on the legal framework, particularly with regard to data protection. In some countries there are very stringent restraints
concerning the collection and evaluation of personal data. Usually these countries possess public health institutions holding the necessary authorisations. 4. Task assignment within the central register organsiation should take into account the main areas of expertise of the individual partners. Public health institutions, such as the BQS in Germany or STAKES in Finland, possess high technical and organisational skills regarding data collection and evaluation, and in initiating feedback mechanisms, which have proved essential for the success of the Scandinavian Registers. Science-oriented institutions, such as the Universities of Gothenburg, Lund or Bergen, are also capable of providing highly professional work; however, adequate and long-term funding should
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be guaranteed. Experience has shown that this is generally difficult in the critical start-up phase of register projects, and that projects of this kind often depend on the strong, voluntary and time-consuming commitment of the persons involved. 5. Data interpretation should involve professional specialists. These experts should be authorised by way of nomination by the scientific professional associations concerned. The delegated expert group should consist of experienced and esteemed executive members of the professional associations and of younger colleagues. During the start-up phase of a register it is often underestimated that the need for basic work such as literature research or detailed evaluations increasingly rises in the course of time. Established staff members, who usually have a variety of other responsibilities, will hardly be able to personally do this kind of work. The selection and training of staff as regards the very specific handling of register datasets takes time, and younger members of such committees should be given the opportunity gain the association’s confidence for handling sensitive data. The prospect of high-level publications on the basis of register data usually represents an adequate factor of motivation for qualified colleagues. 6. The close involvement of professional associations is a central point in putting the knowledge gained into practice and thus increasing the potentials for improvement. Intensive feedback mechanisms and scientific discussions within the framework of regular congresses and special meetings are essential in order to approach physicians with the findings and to foster implementation in their everyday decisions in the treatment of patients. The sole publication of reports or one-sided communication through public health Institutions is insufficient.
Registers in Orthopaedics There are perhaps several favourable circumstances that make registers more successful in arthroplasty than in any other field of medicine. (a) Serious problems of an arthroplasty to a high percentage lead to revision, and nearly every revision has to do with a problem of or at the implant. (b) Every operation, no matter if primary or revision, usually involves good documentation comprising all important contents of a register so that the documentation can easily be integrated into the daily working routine.
N. Böhler and G. Labek
(c) The contents to be documented in successful registers barely leave any scope for subjective interpretation. The time or method of documentation is thus less sensitive than it would be with clinical scores, for instance, that involve a high subjective portion of questions. The long-term result is the most important parameter for the success of an operation so that the longitudinal registration of patients – as held in a register – is superior as compared to cross-sectional evaluation. Therefore evaluations from arthroplasty registers are focussed on survival rates. Other contents that are also important in assessing the success of an operation, subjective patient satisfaction, for instance, can also be investigated in close connection with register documentation. However, their registration is organised differently from the registration of key contents. The simultaneous use of different documentation systems may produce essential progress if employed supplementarily [19–23].
Basic Principles in Interpreting Register Data of Other Countries EAR is engaged in methodological research in the medical device sector with the objective of improving the benefit for the users. In evaluating register data the following aspects should be taken into account: 1. In its basic data, a National register reflects the National standards and circumstances characterising the public health system of a country. This allows for consideration of the particular factors of influence even in compact questionnaires as long as one sticks to the respective area. The datasets of a register also reflect a complex sequence of treatments in which the implant only represents one part. For example, in the Norwegian Register the cemented SP stem showed a significantly inferior performance than the average. All revisions could be traced back to one single hospital [24]. Statements of this kind may be lost in evaluations for annual routine reports. As the primary purpose of a National arthroplasty register is quality improvement in the National surgical performance and a broad International discussion of such cases does not promote co-operation on the national level, it is not sensible to consider such findings in the annual report of a National register. The mechanisms that make register data very valid on a National scale may lead to wrong conclusions in the individual case if the National circumstances are ignored.
Current Status of Arthroplasty Registers in Europe
Evaluations from aggregated, multi-National datasets lack direct connection to the general situation and are thus not suited for conclusions on a national level. Therefore, as long as data are available from a National register, these data will always have to be regarded superior for conclusions on a National scale. However, National registers are limited. The use of implants differs significantly in different countries. The validity of statements principally depends on the size of the sample. The Inter-OP cup, which was taken from the market because of a production error resulting in lubricant residues at the surface and lacking osteointegration, served as an example for calculating an estimate: It was carried out by means of the Fischer’s Exact Test with the usual α error margin of 0.05 and a β error margin of 0.2 to find out how many implants a year would be necessary to be able to rapidly record serious problems in an efficient register. When the first US press articles suggested increasing loosening of the implant an extraordinary evaluation of the datasets of the Swedish Hip Register was carried out. With 30 primary implants, already five revisions were documented after 1.5 years. The revision rate of 16.7% was significantly above average. Assuming a revision rate of 17% with a comparative value of 1% on the general average 54 primarily-treated patients would be necessary to achieve statistical significance. Even with an assumed comparative value of 5% – as an assumption for a compromised dataset in an ad hoc evaluation – only 117 patients would be required to make a register an effective early warning system. The estimate that 100 patients per year would be a sufficient sample for the registration of serious problems therefore seems to be plausible. In the Swedish Hip Register [25], however, only 11 cup and 7 stem implants reach this limit. Even if these implants represent the major market share with 88% and 87% a multitude of implants, revision implants, or newly introduced systems that are registered less frequently cannot be sufficiently controlled in the National register of a mediumsized country. In these cases aggregated datasets may offer valuable additional data. Moreover, the effects of National health systems, which differ greatly in Europe, on long-term results can only be compared through supra-National evaluations. At present it is a common practice that implant producers internationally do not clearly assign a product name to a particular implant. Very similar designations are used for different products in different countries. This practice does not only impede the unambiguous assignment of products for register
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publications but is also problematic for the web-based search of literature and for meta-analyses. A fundamental change of these marketing mechanisms cannot be expected. However, the problem can be solved by referring to the product number. This requires a complete and continuously updated list of all products – including product number, product designation, and country – that can be extended by specific product information and categorisation. Thus product registration for registers could be carried out by means of the usual bar code scanners. 2. In order to increase the value of National register reports outside the original country standardisation in certain parameters and definitions would be desirable. As an alternative they could be summarised in supra-National reports according to internationally concerted guidelines. At present, such standardisation does not even exist in Scandinavia [26].
Benefits the Individual Surgeon Can Derive from Registers 1. Arthroplasty registers compile valid information of high accuracy enabling the surgeon to re-consider individual decisions with regard to the outcome and adjust them accordingly. 2. Implants and surgical techniques can be evaluated faster and more accurately, thus allowing for quicker and more target-oriented implementation of improvements in everyday clinical practice. 3. Within the scope of the EUPHORIC (www.euphoricproject.eu) EU project the validity of different scientific data sources was checked against each other. The results were surprising, to some extent alarming. (a) With regard to the revision rate, meta-analyses in clinical sample-based literature show a statistically significant deviation from register data. (b) Authors of implants are clearly over-represented in the scientific literature, most of them show a statistically significant bias. (c) Even studies of high quality according to the current criteria show a significant bias. This observation could be explained by the fact that the high validity of prospective randomised trials is based on ensuring blinding and the un-influenced decision of the examiner. These objectives can well be realised in testing pharmaceuticals; for surgical interventions, however, this is associated with considerable restrictions.
8
N. Böhler and G. Labek
In summary, sample base studies are subject to a clear bias, the value of comprehensive data collections is significantly higher. Four questions are of prime importance to assess the validity of comprehensive datasets: 1. Are the data specifically collected for the purpose the evaluations are going to be made for? If this is not the case, as for instance with discharge records used for outcome-associated purposes, this leads to a decrease in the validity of statements. 2. In which geographic area are the data collected? 3. Are the data complete? Particular importance should be accorded to the question whether patients can undetectedly pass the borders of the areas of collection, e.g. whether the primary operation has been recorded in the dataset while revisions remain undetected. 4. Are the datasets relevant for the purpose of the evaluation? A structured representation of these results can be provided by means of a matrix. The basic aim of the issue can be indicated in the first vertical line, the values referring to the individual dimension can be given in the following lines, with 1 being the highest qualitative value.
Description of Dimension Aim/purpose
Outcome (A)
Process (B)
Structure (C)
Conformity between aim of data collection and aim of evaluation
Data collection performed for the specific purpose of evaluation (1)
Data collection not performed for the specific purpose of evaluation (2)
Coverage
Nationwide (1)
Regional (2)
Local (3)
Data collection
Comprehensive (1)
Incomprehensive (2)
Sample based (3)
Conformity dataset for assessment
Representative (1)
Not representative (2)
For questions referring to the outcome of an implant in a certain country a complete National arthroplasty register of the same country would be described: A.1.1.1.1 If the same dataset was used for the evaluation of another country, the description would read: A.1.1.1.2 If the basic dataset for the same question was taken from incomplete discharge records of a certain region of another country, the description would be: A.2.2.1.2
Discussion The quality of national arthroplasty registers is welldocumented. However, the complex structure of a register makes it very difficult for individuals or small groups to introduce these valuable instruments. Putting them into practice can be positively influenced by forming a network for mutual support enabling the participants to take advantage of the experiences, results, and learning processes in other countries. Even concentrating on adapting successful attempts to one’s National health system is an extremely difficult task. For those responsible for the project it will be essential to receive support from the National experts association. The co-operation with public health authorities will also substantially decide on the success of arthroplasty registers, even if organisational details may differ greatly. Moreover, integrating Orthopaedic expertise is not only essential for data interpretation. Orthopaedists are also the main target group for the results as they are chiefly responsible for implementing the findings in practice. This strong position within the register organisation should be made clear to the other partners and requires an engaged group of physicians supported by the mandate from their National professional association. This group should be stable for a longer period of time in order to gain the necessary detailed expertise, and it should consist of accepted specialists willing to spend a lot of time and energy on the project. It has proven worthwhile to have both in the team, experienced and generally accepted orthopaedists as well as young colleagues. Register staff have access to raw data of high quality and significance. The greatest importance must thus be attached to the fact that any evaluation, communication, and publication must be independent and sufficiently detached from all partners. Manipulative statements have to be avoided at all cost, as they could do great harm to the register as a valid instrument. Critical examination should precede any decision about which contents should be made available to the public and which part of the information should be discussed within a closed circle of experts. Evaluating results without considering the circumstances under which they have been obtained may lead to misinterpretation. The training of physicians or the complexity of the operation based on the diagnosis influences revision rates. Departments with a higher proportion of training tasks and, on average, more difficult initial situations will therefore implicitly have to expect a worse outcome in register data; however, it would be wrong to automatically conclude from this that their performance is generally worse. Being authorised by their professional association places those responsible for a register under an obligation to act
Current Status of Arthroplasty Registers in Europe
independently and thus represents a control mechanism which is exerted by the specialists as a whole. It is an essential advantage of register results that the bias – which in clinical studies carried out on the basis of samples can be reduced but can never be totally avoided – is significantly lower through referencing to the entire population. However, this advantage is only valid in full if you are working within the closed system. Transferring results to other countries may lead to misinterpretation. The development of National registers over the last decade will change the quality of information available to the individual physician as a basis for his decisions. Register publications will increase. From a global view, the precise description of the circumstances under which the results have been obtained will be difficult because of the variety of factors of influence. Efforts to simplify the comparison of National register results are most advisable. In co-operation with all National Registers and by fostering and developing arthroplasty registers, the European Arthroplasty Register project of EFORT will do its best to make a contribution to an improved treatment of patients.
Acknowledgements We thank all surgeons participating in arthroplasty registers. The success of every register depends on the willingness to collaborate in documentation and quality improvement. We thank the members of all National Registers for their cooperation and their support of colleagues in all European countries. We thank EFORT for supporting our work through the large network of orthopaedists, their comprehensive knowledge, and the variety of ideas initiating fruitful discussion. We thank those scientists, such as Prof. Heino Kienapfel and Dr. Ingeborg Lang, who have been trying with great commitment to build up registers and have also reappraised and published problems and set-backs in a most serious scientific way. In doing so they have made a major contribution to the further development of registers in general and have helped to avoid mistakes.
References 1. Robertsson, O. Knee arthroplasty registers. JBJS-B 2007; 89-B:1–4. 2. Herberts P, Malchau H. Long-term registration has improved the quality of hip replacement: A review of the Swedish THR Register comparing 160,000 cases. Acta Orthop Scand 2000;71–2:111–21.
9 3. Herberts P, Malchau H. How outcome studies have changed total hip arthroplasty practices in Sweden. Clin Orthop 1997; 344:44–60. 4. Malchau H, Garrellick G, Eisler T, Karrholm J, Herberts P. Presidential guest address: The Swedish hip registry: Increasing the sensitivity by patient outcome data. Clin Orthop 2005;441:19–29. 5. Havelin LI, Engesaeter LB, Espehaug B, Furnes O, Lie SA, Vollset SE. The Norwegian arthroplasty register: 11 years and 73,000 arthroplasties. Acta Orthop Scand 2000;71(4): 337–53. 6. Robertsson O, Dunbar MJ, Knutson K, Lewold S, Lidgren L. The Swedish knee arthroplasty register. 25 years experience. Bull Hosp Jt Dis 1999;58(3):133–8. 7. Lucht U. The Danish hip arthroplasty register. Acta Orthop Scand 2000;71(5):433–9. 8. Puolakka TJ, Pajamaki KJ, Halonen PJ, Pulkinen PO, Paavolainen P, Nebelainen JK. The Finnish arthroplasty register: Report of the hip register. Acta Orthop Scand 2001; 72(5):433–41. 9. Furnes A, Lie SA, Havelin LI, Engesaeter LB, Vollset SE. The economic impact of failures in total hip replacement surgery. The Norwegian arthroplasty register 1987–1993. Acta Orthop Scand 1996;67:115–21. 10. Robertsson O, Lewold S, Knutson K, Lidgren L. The Swedish knee arthroplasty project. Acta Orthop Scand 2000; 71(1):7–18. 11. Furnes O, Lie SA, Havelin LI, Vollset SE, Engesaeter LB. Exeter and Charnley arthroplasties with boneloc or high viscosity cement. Comparison of 1127 arthroplasties followed for 5 years in the Norwegian arthroplasty register. Acta Orthop Scand 1997;68:515–20. 12. Espehaug B, Halelin LI, Engesaeter L, Vollset S. The effect of hospital-type and operating volume on the survival of hip replacements – A review of 39,505 primary total hip replacements reported to the Norwegian arthroplasty register, 1988–1996. Acta Orthop Scand 1999;70(1):12–18. 13. Pitto RP, Lang I, Kienapfel H, Willert HG. The German arthroplasty register. Acta Orthop Scand Suppl 2002;73(305): 30–3. 14. Pedersen AB, Johnsen SP, Overgaard S, Soballe K, Sorensen HT, Lucht U. Registration in the Danish Hip arthroplasty registry: Completeness of total hip arthroplasties and positive predictive value of registered diagnosis and postoperative complications. Acta Orthop Scand 2004;75(4):434–41. 15. Arthursson AJ, Furnes O, Espehaug B, Havelin LI, Soreide JA. Validation of data in the Norwegian arthroplasty register and the Norwegian patient register: 5,134 primary total hip arthroplasties and revisions operated at a single hospital between 1987 and 2003. Acta Orthop 2005;76(6):823–8. 16. Espehaug B, Furnes O, Havelin LI, Engesaeter LB, Vollset SE, Kindseth O. Registration completeness in the Norwegian arthroplasty register. Acta Orthop 2006;77(1):49–56. 17. Robertsson O, Dunbar M, Knutson K, Lewold S, Lidgren L. Validation of the Swedish knee arthroplasty register: A postal survey regarding 30,376 knees operated on between 1975 and 1995. Acta Orthop Scand 1999;70(5):467–72. 18. Sodermann P, Malchau H, Herberts P, Johnell O. Are the findings in the Swedish National total hip arthroplasty register valid? A comparison between the Swedish National total hip
10 arthroplasty register, the National discharge register, and the National death register. J Arthroplasty 2000;15(7):884–9. 19. Garrelik G, Malchau H, Herberts P. Survival of hip replacements. A comparison of a randomized trial and a registry. Clin Ortho 2000;(375):157–67. 20. Nikolajsen L, Brandsborg B, Lucht U, Jensen TS, Kehlet H. Chronic pain following total hip arthroplasty: A nationwide questionnaire study. Acta Anaesthesiol Scand 2006;50:495–500. 21. Robertsson O, Dunbar MJ, Knutson K, Lidgren L. Patient satisfaction after knee arthroplasty: A report on 27,372 knees operated on between 1981 and 1995 in Sweden. Acat Orthop Scand 2000;71(3):262–7. 22. Robertsson O, Ranstanm JP. No bias of ignored bilaterality when analysing the revision risk of knee prostheses: Analysis of a population based sample of 44,590 patients with 55,298 knee prostheses from the national Swedish knee arthroplasty register. BMC Musculoskelet Disord 2003;4:1.
N. Böhler and G. Labek 23. Espehaug B, Havelin LI, Engesaeter LB, Langeland N, Vollset SE. Patient satisfaction and function after primary and revision total hip replacement. Clin Orthop 1998; 351: 135. 24. Havelin LI, Espehaug B, Lie SA, Engesaeter LB, Furnes O, Vollset SE. Prospective studies of hip prostheses and cements. A presentation of the Norwegian arthroplasty register 1987–1999. Scientific exhibition presented at the 67th Annual Meeting of the American Academy of Orthopaedic Surgeons, March 15–19, 2000, Orlando, USA. 25. Annual Report 2005. http://www.jru.orthop.gu.se/ (accessed 29/01/2007). 26. Lohmander LS, Engesaeter LB, Herberts P, Ingvarsson T, Lucht U, Puolakka TJ. Standardized incidence rates of total hip replacement for primary hip osteoarthritis in the 5 Nordic countries: Similarities and differences. Acta Orthop 2006; 77(5):733–40.
National Registration of Hip Fractures in Sweden Karl-Göran Thorngren
Development of the National Registration RIKSHÖFT In Sweden there has been developed registers for conditions which have large socio-economic importance both concerning high number of patients as well as a great need for use of resources. The first national registers were created within the area of orthopaedics initiated by Professor Göran Bauer in Lund. He started the Swedish Knee Arthroplasty Register 1975 and then the Swedish Hip Arthroplasty Register was started 1979. In the beginning it registered only reoperations and from 1992 onwards also person linked information about primary hip arthroplasties was collected. The Swedish National Hip Fracture Registry called RIKSHÖFT [1] was started by the author in 1988. The arthroplasty registers deal with information concerning a procedure whereas the hip fracture register in addition to the fracture type and type of operation also deals with information about the patient, function and social conditions, making it a disease register. Based on the experience of the orthopaedic registers successively more registers have been introduced within other medical fields. Swedvasc, the registry for peripheral vascular surgery, was started 1987 as the first non-orthopaedic register. During the 1990s several registers have been started such as RiksStroke, the national quality register for stroke, which was started in 1994. Other examples of registers are the Swedish coronary angiography and angioplasty register as well as the registry on cardiac intensive care, RIKS-HIA. During the last decade the national quality registers have after application received grants yearly from the Swedish National Board of Health and Welfare together with the Swedish Association of Local Authorities and Regions. The latter has taken over the central administration of the quality
Karl-Göran Thorngren Department of Orthopaedics, Lund University Hospital, SE-221 85 Lund, Sweden e-mail:
[email protected]
registers since 1 January 2007. All applications are evaluated by a Scientific Advisory Committee to guide the decisions of the Executive Committee composed by representa tives from the Swedish Association of Local Authorities and Regions, the National Board of Health and Welfare, the Swedish Society of Medicine and the Swedish Society of Nursing. In 2008 in total 64 national quality registers received economic support in this way. There are also 18 different national cancer registers usually supported by grants from the Swedish cancer foundation. Areas with more rare diseases and smaller volumes to register are usually covered by research registers supported by specific research grants. These often have higher level of details in the registration with many parameters. To continuously register disease groups on a national level or to register procedures with large patient volumes, demands a small amount of well chosen parameters, so the registration can be complete. One particular factor that facilitates registration in Sweden is the system with national personal identification numbers, which makes it possible to trace patients through the medical system from birth to death. Supported by law the Epidemiological Centre at the National Board of Health and Welfare has registers for statistical use such as the patient register for all in hospital care with diagnoses and operative procedures according to ICD 10, the medical birth register, the cancer register and the pharmaceutical register. They are also responsible for the register concerning dates and causes of death. Since 2006 the Swedish Association of Local Authorities and Regions is publishing a yearly report with open comparisons at regional or hospital level of some key factors from the National Quality Registers. The National Quality Registers have been created by the medical profession which continues to handle the development and analyses of the registers. Within the sector of health care administration there has been a development of systems to follow the activity from economical and personnel administrative aspects. They have not developed registration systems concerning the work with the patients. The traditional patient filing systems have not made it possible
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to compile and analyse data easily. Thus, there is a need for special diagnose related registers.
Hip Fracture Demographics The treatment of elderly patients with orthopaedic problems is dominated by the demand both from the elderly and from the society that they should be able to live an independent, mobile and pain free life [2–5]. In Sweden at the age of 50 years the risk to sustain a hip fracture is 23% for women and 11% for men during the remaining life time. Hip fracture belongs to the most resource consuming groups within health care. All these patients need operation and hospital treatment. They consume 25% of all bed days in hospital for orthopaedic diseases. Due to the increasing amount of elderly in the population the amount of hip fractures is increasing. At present the hip fracture care in Sweden costs 1.5 billions Swedish Crowns yearly. The RIKSHÖFT aims at optimising all aspects of patient treatment. The aim is to create a high and evenly distributed quality of care all over the country. RIKSHÖFT is also a basis for local development projects. Also the reorganisations after administrative decisions with changed patient flow between hospitals and cities find through RIKSHÖFT a form to be evaluated. The awareness of results leads to improved treatment and more effective cost utilisation. During 1995–1998 RIKSHÖFT was spread in Europe with a project supported by grants from the European Commission. This registration was called SAHFE (standardised audit of hip fractures in Europe) [6]. Also other international registration has started [7–9].
Karl-Göran Thorngren
years has now risen to 83 years. Half (48%) of the patients are living alone. There is a slight tendency to diminished living alone since 1999 (Fig. 1). Continuing during the 1980s and the beginning of 1990s the mean hospital treatment time in the operating departments has successively decreased. In 1988 the mean hospitalisation time was 19 days for hip fractures in Sweden. Since 1996 it has been around 11 days with only small changes over the years for the mean hospitalisation time whereas the median hospitalisation time has been constant. In 2007 the mean hospitalisation time was 10.7 days and the median hospitalisation time 9 days. The waiting time from admittance to the hospital until performance of the operation was in 2007 mean 1.2 days and median 1 day (Fig. 2). The lowered mean hospitalisation time during the last years has been possible without lowering the percentage of patients admitted from the acute hospital to their original form of living as they had before the fracture. It has been fairly constant around 50% during the last 10 years. Shortened time in the hospital has previously been related to a greater amount of patients being sent to secondary rehabilitation in some institution instead of primary rehabilitation in the form of living they had before the fracture. Thus, during the last 15 years the hip fracture care in Sweden has been optimised through diminished mean hospitalisation times in the acute hospital combined with a high number of patients possible to return to original place of living (Fig. 3). This evolution is obvious when separate departments in Sweden are compared. In the diagrams below each dot 100 90 80 70
National Data 2007 Hip fractures are predominant in elderly persons due to increasing osteoporosis and falling tendency by age. A hip fracture below 50 years of age is unusual (less than 3% of the total in RIKSHÖFT) and usually caused by severe trauma, like traffic accidents or fall from heights. The elderly person is usually falling on the floor when walking or raising from a chair. In the figures below therefore only patients of age 50 years and above are included. Osteoporosis is very common among the elderly patients. The small number of patients with other pathological change of the skeleton, e.g. metastatic fractures, have been excluded in the analysis. In 2007 in Sweden the patients consisted of 70% women and 30% men. Mean age which in the middle of 1990s was 81
60 50 40 30 20
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Fig. 1 Mean age, percentage of women and living alone before the hip fracture
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Fig. 3 Mean time in acute hospital (orthopaedic department) and percentage of patients discharged from there directly to original place of living
represents a hospital. During the years 1988–1990 no hospital had mean hospitalisation time below 10 days and there was a broad range of values up to 27 days (Fig. 4). In 2007 no department has a mean hospitalisation time over 20 days and the majority had a mean hospitalisation time between 6 and 12 days. One department with an
extremely short mean hospitalisation time of 1.2 days combine this by sending 100% of the patients to rehabilitation or other type of institutional care. The policy in Sweden for the departments is to send as many patients as possible to their original place of living with as short hospitalisation time in acute care as possible. Some few hospitals are primarily treating the hip fracture patients directly in a geriatric ward with the orthopaedic surgeon more as a consultant. They have a mean hospitalisation time and percent of patients directly returning home to original living equal to the majority of the orthopaedic departments. In total the comparison of the two periods shows a considerable reduction of the amount of bed days needed to treat the hip fracture patients. The fracture types have shown a stable pattern during the last years. From the medical point of view this is natural as no sudden changes in the falling tendency or grade of osteoporosis is to be expected among the patients. It also shows that the classification system is reproducible on a large scale with
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Fig. 5 Types of hip fracture
well defined groups. In 2007 there were registered in Sweden 15% undisplaced cervical hip fractures, 36% displaced cervical, 3% baso-cervical, 24% trochanteric two-fragment fractures, 14% trochanteric multi-fragment fractures and 8% subtrochanteric hip fractures (Fig. 5). The type undisplaced cervical (femoral neck) fractures comprises Garden types I + II. The type displaced cervical hip fractures comprises Garden types III + IV. Two types of primary operations for cervical (femoral neck) fractures are predominating. One is osteosynthesis with two hook pins or screws. The other is to substitute the proximal end of the femur with an arthroplasty. In Sweden beginning 1999 there has been performed a successively increasing amount of primary hemi/bipolar hip arthroplasties for the displaced cervical fractures. The number of total hip arthroplasties is comparatively constant. For per-trochanteric fractures screw plate is still the most common operation method. A small fraction of intramedullarly nails is increasing since the millennium change (Fig. 6). For all hip fractures comparing 1996–2007 the primary hemi-arthroplasties have increased from 2.1 to 25%. If also the total hip arthroplasties are included the increase of arthroplasties from 1996 to 2007 is from 5.4 to 30%. At the
2002
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Year Total hip arthroplasty Screw, pin or nail with sideplate Intramedullary nail Other operation Not operated
Fig. 6 Operation methods used for all hip fractures
same time the use of two hook pins/screws have diminished from 45.2% in 1996 to 20% in 2007. The use of three screws has ceased. There is a small increase in the number of total hip arthroplasties from 3.3% 1996 to 5% 2007. During the last 4 years the change seems to have levelled off. There is an optimal balance between primary osteosynthesis and primary arthroplasty if consideration is taken to the stress by the operation on the patient and the resource utility at the different types of primary operations as well as the amount of complications and reoperations needed. The future will show when this level has been achieved. For the undisplaced cervical hip fractures (Garden I–II) osteosynthesis is the predominant primary method in accordance with the good healing prognosis for these fractures. They have no or very little displacement which has given little damage to the blood circulation to the femoral head. The use of arthroplasty 1998 was for these fractures 0.4% hemi-prostheses and this had increased to 8% in 2007. The summarized use of arthroplasty including hemi-prostheses and total hip prostheses was 1.5% in 1998 and had increased to 11% in 2007. For the displaced cervical hip fractures (Garden III–IV) the use of hemi-prostheses was 3% in 1998 and in 2007 it had increased to 63%. The use of total hip arthroplasty for
National Registration of Hip Fractures in Sweden
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% 50 40 30 20 10 0 1998 1999 2000 2001 2002 2003 2004 2005 2006 2007
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Hemi or bipolar arthroplasty
Total hip arthroplasty
Fig. 7 Operation methods used for displaced, cervical (femoral neck) fractures. The top unmarked area comprises other osteosynthesis types 100 90 80 70 60 % 50 40 30 20 10 0 1996
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Walked alone out of doors Walked out of doors only if accompanied Walked alone indoors but not out of doors Walked indoors only if accompanied Unable to walk Unknown
Fig. 8 Walking ability before the hip fracture
the displaced cervical fractures has been fairly constant around 10%. In 2007 it amounted to 13%. The summarized use of hip arthroplasty including hemi- and total was 12% in 1998 and had increased to 76% in 2007 (Fig. 7). For the trochanteric hip fractures a screw plate is the dominating operation method. In 1998 the trochanteric two-fragment fractures were in 91% operated with a sliding screw and plate and this has slowly diminished to 84% in 2007. The trochanteric multi-fragment fractures were operated with screw plate in 86% of the cases in 1998 and this had diminished to 57% in 2007. Arthroplasty is not the first hand choice for the trochanteric hip fractures unless in some extreme exceptional case. Intramedullarly nails have increased successively since the millennium change. In 2002 for the trochanteric two-fragment fractures they amounted to 3% and for the multi-fragment fractures 15%. In 2007 12% of the two-fragment fractures and 39% of the multi-fragment fractures were operated with a proximal femoral nail. The baso-cervical fractures constitute a transition form between cervical and trochanteric hip fractures. From the stabilisation aspect they are usually operated with a screw plate. Some times the vascular damage to the femoral head leads to pseudarthrosis or femoral head necrosis which makes them more similar to cervical hip fractures. In 2007 11% of the baso-cervical hip fracture patients were operated with two pins/screws, 68% with a screw plate, 3% with other type of osteosynthesis, 12% with hemi-arthroplasty and 4% with total hip arthroplasty. Subtrochanteric hip fractures go by definition as far as 5 cm below the minor trochanter. If they go further they are considered a femoral shaft fracture. The sub-trochanteric fractures are often more multi-fragmented and unstable. In 2007 they were operated with a screw plate in 27%, with a intra medullarly nail in 67%, with other osteosynthesis in 2%, hemi-arthroplasty in 1% and with total hip arthroplasty in 1%. The walking ability for the hip fracture patients shows mainly the same pattern during the last couple of years. More than half of the patients (58%) could before the fracture walk alone outdoors with a slight tendency of increase during recent years. A further 7% could walk outdoors if somebody accompanied them. The rest of the patients could walk indoors except 3% who could not walk at all before the fracture (Fig. 8). The patient’s general walking ability gives a picture of the stability of the hip and the lack of pain as well as the general condition of the patient. The change in choice of
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Fig. 10 Walking aids normally used before the hip fracture occurred
Fig. 9 Walking ability at 4 months after hip fracture 100 90
operations has consequently not in any major way influenced this functional level. There is however a tendency that somewhat more patients can walk alone outdoors at 4 months after the hip fracture with a slight increase from 31% in 1996 to 39% in 2007 (Fig. 9). To evaluate walking ability the walking aids are commonly used as indicator. Before the fracture there is a trend from 1996 until 2000 that an increasing amount of elderly are using rollator whereas the fraction who did not use any walking aids or only one stick have diminished. To use two sticks or walkers before the hip fracture is unusual. The percentage of patients using a wheel chair or not walking at all before the fracture was unchanged around 5% during this period (Fig. 10). At 4 months after the operation the use of walking aids for the hip fracture patients when they walk indoors has shown mainly the same pattern during the last years. There is a tendency to increased use of rollators from 2000 which has then levelled off mirroring the prefracture increased use of rollators. At the same time the group with good walking capacity i.e. walking without aids or with only one stick as well as the group who cannot walk at all have diminished somewhat (Fig. 11).
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Fig. 11 Walking aids normally used at 4 months after the hip fracture occurred
National Registration of Hip Fractures in Sweden
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Motivation
Computing and Feed Back
It is necessary to build up registers that can be prospectively used over many years and that will facilitate the daily work. Motivating the different departments to participate is of vital importance [10–12]. Motives differ in different places and times. The first major motive is the facilitation of everyday routine medical work. The audit form can be used as a standardised party of the patient’s file, thereby simplifying routines. Less unstructured type-written text and thereby less secretarial work is needed. It is also easier to find the information in the file at a later date, e.g. at outpatient follow up visits. It can also be retrieved by computers. The second main motive is its usefulness for administrative purposes, e.g. yearly activity reports, to support resource claims in discussions with administrative authorities and to receive funding. The third motive is scientific. Centrally, the large amount of prospective standardised material provides possibilities for the analysis of the overall panorama of hospitals, diagnoses and modes of treatment. It also provides unique possibilities for studying special rare indications that need the multi-centre approach to collect enough material. Locally, it is possible to use the audit forms as a basis for a study, e.g. comparison between two operation methods, introduction of new types of rehabilitation and so forth. The motivation is especially strong when someone can use the register for his/her thesis work.
The use of PC programs and handling of data on desk top computers, were early used by the Swedish Hip Fracture Register RIKSHÖFT which is now using direct on line web registration accessible through its home-page www.rikshoft.se. The possibility for the participating centres to make their own calculations on their data is important. Permits for the registration from the Swedish Data Inspection have been given. Access to the data is limited on several levels of aggregation to protect individual patients. Feedback to the participants with regular reports containing their own data as well as comparative mean values for the whole country is necessary. The hip fracture register makes a yearly report. To keep the enthusiasm for the project on a high level, regular discussion meetings are required, e.g. in connection with the Swedish Orthopaedic Societies meetings.
Performance In RIKSHÖFT detailed functional parameters are registered, as this is important in the short-term perspective of these elderly patients. Previous studies have shown that over 80% of the complications needing reoperation occur within 2 years after the hip fracture. The registered hip fracture patients also have a considerable mortality with time due to high mean age and concomitant diseases [13–15]. In Sweden all persons have a social security number e.g. 050315-1649. This person was born as child number 164 in Sweden on the 15th of March 1905. The last digit is a control based on the other digits. Due to this social security number, which is unique to the person, it is possible to trace the patient. The number is generally used for all kinds of identification in Sweden. This is a great advantage when checking data with files from different departments and when patients change their address.
Funding Great amounts of energy and idealism are necessary to start a large-scale registration project. Furthermore, economic resources are necessary to print forms, to communicate with the other centres and to register data on computer, as well as to do calculations and print reports. The Swedish Medical Research Council has funded this project during the initial years. From 1990 the Swedish Government has decided to fund the national registers, which are still to be run at the original centres. It has been decided to be advantageous that the profession itself outlines the guidelines for a register and keeps it running. The goodwill and enthusiasm of the orthopaedic community has been the basis for managing the Swedish audit projects.
References 1. Thorngren K-G. Experience from Sweden. In: Medical Audit. Rationale and Practicalities. Cambridge University Press, New York, 1993, pp 365–75. 2. Berglund-Rödén M, Swierstra B, Wingstrand H, Thorngren K-G. Prospective comparison of hip fracture treatment, 856 cases followed for 4 months in the Netherlands and Sweden. Acta Orthop Scand 1994;65:287–94. 3. Thorngren K-G. Epidemiology of fractures of the proximal femur. In: J Kenwright, J Duparc and P Fulford (Ed.), European Instructional Course Lectures 1997;3:144–53.
18 4. Thorngren K-G. Standardisation of hip fracture audit in Europe. J Bone Joint Surg 1998;80-B(Suppl 1):22. 5. Kitamura S, Hasegawa Y, Suzuki S, Ryuichiro S, Iwata H, Wingstrand H, Thorngren K-G. Functional outcome after hip fracture in Japan. Clin Orthop Rel Res 1998;348:29–36. 6. Parker MJ, Currie CT, Mountain JA, Thorngren K-G. Standardized audit of hip fracture in Europe (SAHFE). Hip Int 1998;8:10–15. 7. Tolo ET, Bostrom MPG, Simic PM, Lyden JP, Cornell CM, Thorngren K-G. The short term outcome of elderly patients with hip fractures. Int Orthop (SICOT) 1999;23:279–82. 8. Heikkinen T, Wingstrand H, Partanen J, Thorngren KG, Jalovaara P. Hemiarthroplasty or osteosynthesis in cervical hip fractures: matched-pair analysis in 892 patients. Arch Orthop Trauma Surg 2002;122(3):143–7. 9. Cserhati P, Fekete K, Berglund-Rödén M, Wingstrand H, Thorngren K-G. Hip fractures in Hungary and Sweden – differences in treatment and rehabilitation. Int Orthop (SICOT) 2002; 26(4):222–8.
Karl-Göran Thorngren 10. Thorngren KG, Hommel A, Norrman PO, Thorngren J, Wingstrand H. Epidemiology of femoral neck fractures. Injury 2002;33(Suppl 3):C1–7. 11. Thorngren K-G, Norrman P-O, Hommel A, Cedervall M, Thorngren J, Wingstrand H. Influence of age, sex, fracture type and pre-fracture living on rehabilitation pattern after hip fracture in the elderly. Disabil Rehabil 2005;27(18–19): 1091–7. 12. Thorngren K-G. National registration of hip fractures. Acta Orthop 2008;79(5):580–2. 13. Thorngren M, Nilsson LT, Thorngren K-G. Prognosis-determined rehabilitation of hip fractures. Compr Gerontol 1988;2A(1):12–7. 14. Holmberg S, Kalen R, Thorngren K-G. Treatment and outcome of femoral neck fractures. An analysis of 2418 patients admitted from their own homes. Clin Orthop Rel Res 1987;(218):42–52. 15. Holmberg, S, Thorngren K-G. Rehabilitation after femoral neck fracture. 3053 patients followed for 6 years. Acta Orthop Scand 1985;56(4):305–8.
Current Status of Articular Cartilage Repair Emmanuel Thienpont
Introduction Articular cartilage injury is a common problem that is frequently encountered by practising Orthopaedic Surgeons [1]. Following a retrospective review of 31,516 knee arthroscopies, Curl et al., reported that cartilage lesions were present in 63% of the procedures [2]. More recently, Widuchowski et al., reported similar results, with chondral lesions found in 60% of 25,124 patients who underwent knee arthroscopies [3]. Importantly, both studies reported that patients with lesions had a mean age of approximately 40 years [2, 3]. As it is widely accepted that patients who experience a traumatic cartilage injury when they are young, have a high risk of developing osteoarthritis later in life, effective early treatment of symptomatic cartilage defects is vital to minimise the risk of degeneration of the damaged joint [4–6]. The treatment goals of articular cartilage defects in the knee include replacement, regeneration, or repair methods that result in hyaline tissue that integrates with native host tissue and functions durably under load and over time, and most importantly provides an asymptomatic joint [7–9]. The treatment of chondral defects is challenging, with repair techniques rapidly evolving. Due to its avascular nature and extracellular matrix structure, articular cartilage has a limited intrinsic capacity for healing after injury [1]. A variety of methods have been developed for cartilage repair, with the most recent treatments focussing on tissue regeneration [9]. These regenerative treatments aim to resurface the joint with new tissue that has the structural and mechanical properties of physiological hyaline cartilage [10]. Repair techniques routinely used in clinical practice include reparative or marrow stimulation techniques (MSTs) [9]. Autologous grafting procedures such as osteo-
chondral autologous transplantation system (OATS) and mosaicplasty can be considered as biologic replacements [9]. And more recently, autologous chondrocyte transplantation (ACT)/autologous chondrocyte implantation (ACI) could be seen as a first-generation regeneration technique [9]. In addition to these techniques, arthroscopic lavage, with or without debridement, is also common [9]. A number of factors, including the size and depth of the lesion, as well as patient characteristics such as age and activity level, influence the most appropriate choice of treatment [1, 9]. Several key components have been proposed as essential to optimize the production of new articular cartilage tissue [9]. The first component is a chondroprogenitor cell source for replication, biologic turnover and extracellular matrix production. Sources of chondroprogenitor cell lines include mesenchymal stem cells (MSCs), juvenile chondrocytes or differentiated chondrocytes (as in ACI) [9]. The second component is a porous scaffold to act as a delivery vehicle for the selected chondroprogenitors and to provide a unique 3D structure [9]. Scaffolds may be purely biological in nature (collagen, hyaluronate, alginate,…) whereas others are mineral-based (tricalcium phosphate, hydroxyapatite, calciumsulphate) and still others are carbohydrate-based (polylactide, polyglycolide,…) [9]. A final third component would include the use of bioactive factors that may be used to amplify cell expansion, strengthen phenotype, improve extracellular matrix production (anabolic agents and growth factors), and also reduce cell breakdown and catabolic degradation (catabolic inhibitors) [9, 11].
Arthroscopic Debridement Emmanuel Thienpont University Hospital Saint Luc, U.C.L., Avenue Hippocrate 10, 1200 Brussels, Belgium e-mail:
[email protected]
Arthroscopic debridement is employed to remove loose cartilage that can mechanically impede joint function and cause inflammation [12–15].
G. Bentley (ed.), European Instructional Lectures. European Instructional Course Lectures 9, DOI: 10.1007/978-3-642-00966-2_3, © 2009 EFORT
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Mechanical overloading results in increased matrix metalloproteinase production which has a damaging effect on the surrounding cartilage [16, 17]. While the procedure provides symptomatic relief from pain, the missing cartilage is not replaced and clinical outcome significantly deteriorates by 5 years [18, 19]. Thus, in clinical practice, joint debridement is often combined with reparative techniques, such as drilling or microfracture (MF) [20]. A Cochrane review shows no benefit of arthroscopic debridement for undiscriminated osteoarthritis [21].
Reparative Techniques Reparative techniques, or MST, include subchondral drilling [22], abrasion arthroplasty [23] and MF [24]. The MF technique was developed in the 1980s by Steadman, and is now widely used [25–28]. MF involves perforating the subchondral bone with a number of holes, thereby triggering the release of bone marrow components such as stem cells, growth factors and cytokines into the defect [27, 29]. These components form a “superclot”, providing an enriched environment in which new fibrocartilaginous repair tissue is generated [27]. Published literature supports favourable outcomes for MF [30]; however, few randomised controlled trials (RCTs) comparing MF to other surgical techniques have been reported and limited long-term outcome data are available. Short-term clinical efficacy (i.e. 2–4 years after MF) has been demonstrated in several clinical trials, particularly in younger patients (age < 30–40 years) [24, 25, 29–31], active or athletic patients [24, 30, 32], patients with a low body mass index (BMI; <30 kg/m2) [30, 32, 33], short duration of symptoms (<1 year) [30, 32, 33], no history of previous knee surgery [32, 34], and in patients with defects that are small (<2–4 cm2) [32, 33] or affect the femoral condyle [33]. However, concerns over the long-term efficacy of MF include the fibrous nature of the repair tissue, which does not have the elastic properties of hyaline cartilage and degrades over time [35–38]. It has been estimated that MF repair tissue has a durability of only 2–5 years in patients with high functional demand (e.g. athletes and labourers) [1]. In addition, magnetic resonance imaging (MRI) suggests that bony overgrowth may occur, which may contribute to subsequent cartilage loss [36]. Moreover, the use of MSTs may reduce the success of secondary surgical treatments. Recently, Gomoll et al. [39] reported that failure of ACI was threefold higher in patients who had previously been treated with MF, abrasion chondroplasty or drilling compared to those with no significant prior treatment. Complete and partial failures
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were each reported in 25% of the 121 patients who underwent MSTs, compared to 9 and 8%, respectively, of the 208 patients with no significant prior treatment [39]. An adaptation of the MF technique would be the AMIC (autologous matrix induced chondrogenesis) where a collagene membrane is sutured over the microfractured defect [40]. This seems an option if ACI is too expensive or for the patella where classic MF seems less favourable [40]. Recently the use of a new resorbable matrix scaffold would allow faster weight bearing [9]. The TruFit Plug (Smith & Nephew, San Antonio, TX) is a resorbable tissue regeneration scaffold made of polylactide-coglycolide copolymer, calcium sulphate and polyglycolide [9, 11]. The implant is intented to serve as a scaffold for native marrow elements and matrix ingrowth in chondral defect repair [11].
Restorative Techniques Restorative surgical techniques aim to restore function through the regeneration of tissue that has the biomechanical and physiological functions of hyaline cartilage. These techniques involve harvesting autologous tissue and include cartilage grafting (mosaicplasty and OATS) and implantation of chondrocytes (ACI).
Autologous Osteochondral Grafting Mosaicplasty or the OATS was first described in 1993 [41, 42]. and is now used for treating both chondral and osteochondral defects. In this technique, a number of small osteochondral cylinders harvested from a low-weight-bearing area of the knee are used to fill the chondral defect, thereby allowing the curvature of the articular surface to be maintained [17, 20]. Often, integration of the transplanted cylinders with the adjacent hyaline cartilage occurs via the formation of fibrocartilage between implants [17, 20]. Positive results have been obtained using mosaicplasty to treat small and medium-sized defects [43–47]. However, poor results have been reported by Bentley et al. in the treatment of femoral and patellar defects [48]. A recent paper by Williams et al. showed however promising results in OATS of the patella, if patellar mal-alignment was addressed adequately [49]. In addition, limitations relating to donor site surface area and morbidity, as well as problems in achieving satisfactory surface congruence, thickness and filling, restrict the use of this technique [17]. Furthermore, the lack of integration between the mosaic plugs and the surrounding native
Current Status of Articular Cartilage Repair
cartilage may result in synovial fluid leakage and cyst formation, making healing unlikely [17, 20].
Autologous Chondrocyte Transplantation/Implantation Developed in the late 1980s as a novel approach to the treatment of cartilage defects, this technique was first performed in 1987 by Peterson in Gothenburg [17, 50] and described by Brittberg et al. [51]. The ACI technique involves two surgical procedures [51, 52]. In the first step, cells are harvested from a cartilage biopsy taken during an initial arthroscopy. The harvested cells are then cultured in vitro and injected into the defect during a second procedure. A periosteal flap is sutured over the defect in order to keep the cell suspension in place [51, 52]. A variety of studies investigating ACI have reported good results for a number of different aspects of treatment, including defect filling, adherence to bone, cartilage integration, mechanical properties of the repair tissue, and long-term clinical outcome [10, 48, 50, 52–54]. ACI was reported to be more efficient than debridement for full-thickness chondral defects of the knee at 3 year follow-up [55]. Both ACI and MF were effective in terms of functional improvement and pain after 2 years in one RCT [30], with clinical improvement still apparent at 5 years post-surgery [56]. Defect size did not appear to affect the outcome following ACI [56]. Over the mid- to long-term (3–5 years), however, ACI performed better than MST for functional outcomes, pain and swelling in another multi-centre, nonrandomised study [57]. Compared to MF, ACI resulted in better defect filling and repair cartilage was less likely to be depressed relative to adjacent cartilage based on MRI data at 1–2 years [36]. In addition, histological examinations after 2 years suggest that ACI results in more hyaline cartilage than MF [30, 56]. If ACI is used as a second-stage procedure, after debridement or MF, 76% treatment success has been published [58]. Conflicting results have been reported for studies comparing ACI and mosaicplasty. In a prospective RCT of patients with a symptomatic lesion of the articular cartilage in the knee excellent or good macroscopic and histological repair after 1 year was observed in 82% of patients treated with ACI compared with only 34% of those treated with mosaicplasty [48]. In a different study of patients with an articular cartilage lesion of the femoral condyle, Horas et al. reported, that while symptoms decreased at 2 years post-surgery following both ACI and mosaicplasty, recovery was significantly slower in patients treated with ACI [59]. In contrast to results
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reported in other studies, histological assessments in the study by Horas et al. indicated that defects treated with ACI were primarily filled with fibrocartilage [59]. However, while the mosaicplasty implants retained their hyaline character, a persistent interface with the surrounding cartilage remained [59]. Recent modifications to the conventional ACI technique include a number of developments designed to address limitations associated with use of a periosteal flap, cell leakage, and de-differentiation of cells cultured in vitro [9]. Use of a periosteal flap to seal the injected suspension in the defect is associated with additional morbidity at the donor site and a risk of later hypertrophy [9, 40, 60–62]. Consequently, the use of collagen membranes has been investigated, with promising results [40, 60, 61]. Steinwachs et al. reported that the use of a collagen I/III membrane is associated with good and excellent results in 87% of patients, and showed no evidence of symptomatic hypertrophy [40]. In another study, Gooding et al. found that there was no statistically significant difference in clinical outcome at 2 years between periosteal and collagen membranes, but 36.4% arthroscopic shavings in the periosteal membrane group [61]. Rosenberger published that additional arthroscopic procedures were necessary in 43% of his over 45 years patients group [62]. Collagen-covered ACI (ACI-C) showed good results in treatment of symptomatic osteochondritis dissecans of the knee [63]. Whether using a periosteal flap or collagen membrane, cell leakage remains a potential problem in conventional ACI [9]. Due to the loading and shearing forces resulting from joint movement, sutures must be very stable and additional fibrin glue is often employed to ensure a good seal is maintained [9]. Thus, recent developments designed to minimise the risk of cell leakage include the implantation of chondrocytes using a range of scaffolds, including synthetic polymers and biological matrices [9]. The use of injectable mediums has been suggested as an alternative to the solid scaffolds as they can be implanted in a less invasive manner, but still provide bulk and could potentially be moulded in situ [64]. In vitro studies have shown that fibrin glue alone or in combination with other polymers promotes cell proliferation and maintains good cell viability when used as a chondrocyte carrier [64, 65]. Other modifications that minimise the risk of cell leakage include matrix-guided autologous chondrocyte implantation (MACI®; Genzyme, Cambridge, MA) and Hyalograft C (Fidia, Albano Terme, Italy), which are “third generation” procedures that are becoming increasingly popular [1]. MACI involves the implantation of a collagen type I/III membrane seeded with autologous chondrocytes harvested
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from the initial biopsy, rather than a suspension of cultured cells [1]. The MACI membrane is easy to handle and can be fixed in place using fibrin glue with a small number of stabilising sutures or even without [1]. The chondrocytes have been found back on the membrane [66]. Short-term results appear promising, with one study reporting the formation of cartilage-like tissue as early as 21 days, and 75% hyaline-like cartilage regeneration at 6 months post-surgery [67, 68]. The Hyalograft C implant uses a hyaluronic acid-based scaffold for the delivery of the autologous chondrocytes [1]. Clinical results using this scaffold also appear positive, with improvement in 91.5% of patients according to the International Knee Documentation Committee subjective evaluation, normal or nearly normal cartilage repair in 96.4% of the scored knees, and the majority of the second-look biopsies assessed as hyaline-like at 2–5 years follow-up [47]. While both MACI and Hyalograft C techniques have shown promising results in the short-term, long-term prospective randomised trials of both techniques are required before broader use can be advocated [69]. A positive correlation between the hyaline content of repair tissue and clinical outcome has been reported, and one of the main aims of ACI is the regeneration of tissue with hyaline-like characteristics [52]. However, the formation of fibrocartilage or mixed hyaline/fibrocartilage has also been reported following ACI [48, 59]. In vitro expansion of harvested cells in conventional ACI can result in loss of phenotype and thus, chondrogenic capacity [70, 71]. To overcome this issue, characterised chondrocyte implantation (CCI) has recently been developed (ChondroCelect, Tigenix, Belgium). In this technique, expanded cells are “characterised” using a gene marker profile to identify phenotypically stable chondrocytes, thus ensuring greater homogeneity in the cartilage-forming capability of the implanted cell populations [72]. In a RCT of CCI (n = 57) vs. MF (n = 61) in the repair of single symptomatic cartilage defects of the femoral condyle, the repair tissue generated following CCI was superior to that generated following MF 1 year after treatment; however, short-term clinical outcome was similar in both groups [10]. Traditional ACI has been modified in recent years by implantation of chondrocytes onto a range of scaffolds and the use of injectable mediums. Currently, different scaffolds are being investigated for their suitability to restore articular cartilage. MACI® and Hyalograft C are becoming increasingly popular, with promising short-term results reported in the literature [47, 67, 73, 74]. Especially for patellofemoral problems [73–77]. Fixation to bone immediately after surgery has been proven by MRI studies [78]. Similarly, positive short-term data have been reported for
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CCI, but no long-term follow-up evaluations are currently available [10]. The techniques based on ACI all involve two surgical procedures (i.e. harvesting autologous chondrocytes and subsequent re-implantation). Recently, Lu et al. reported a novel approach for cell-based cartilage repair involving the use of a cartilage autograft implantation system (CAIS) [79]. By using minced cartilage placed onto a bioabsorbable scaffold and then stapling the construct into the focal chondral defect, the system only requires one surgical procedure [28, 79].
Fresh Allograft Transplantation Full cartilage resurfacing is possible with fresh allografts [80–84]. This can be a mega OATS [85] or biologic replacements with different parts of osteochondral tissue [80–84]. These can include meniscal tissue, ligaments or the extensor mechanism [80–84].
Treatment Selection Although a variety of options are available for the treatment of articular cartilage defects, to date, no generally accepted treatment algorithm exists. The most appropriate surgical technique should be selected on a patient-by-patient basis, taking into account numerous factors, including the size and depth of the lesion, patient characteristics such as age, BMI and activity level [30]. Based on a review of recent European and US literature on cartilage repair a treatment algorithm can be composed, which recommends that lavage and debridement are mostly indicated in the treatment of degenerative arthritis with mechanical symptoms (meniscal lesions, cartilage flaps, loose bodies) [18, 19]. MF is the most widely used treatment method [17]. Indeed, since ACI currently necessitates a concomitant arthrotomy, which has associated morbidity, most surgeons treat isolated lesions of <2 cm2 with MF, reserving ACI for more extensive lesions that cause greater functional deficits [86]. MF can be used on bigger lesions if a concomitant anterior cruciate ligament tear is treated [17]. OATS is considered to be a viable alternative to MF for smaller lesions on the femoral condyles (one plug), particularly in young active patients; however, it is not advised for the treatment of patellar lesions [17, 48]. ACI is recommended for larger lesions (i.e. >2 cm2) [17]. ACI can be used to effectively treat chondral lesions of the
Current Status of Articular Cartilage Repair
femur, trochlea, patella and tibia, either a first- or second-line treatment, as well as for large cartilage lesions in patients who have failed other treatment modalities [1]. The ideal candidates for ACI appear to be high-demand patients aged 15–55 years who are highly motivated and likely to comply with the postoperative rehabilitation programme [1, 86]. A number of factors are predictive of a favourable outcome from ACI, including youth (age £ 40 years, although <20 years is ideal), high preoperative modified Cincinnati score, short duration of symptoms (<2 years), a single defect on the trochlea or lateral femoral condyle, and fewer than two previous procedures on the affected knee [87]. However Minas et al. have showed 72% good or excellent patients if they rated themselves, in an age group over 45 years [62]. However additional arthroscopic procedures were necessary in 43% of patients for graft hypertrophy and adhesions [62]. In most review articles no clear difference between the most frequently used techniques is observed, often due to bad design of the studies [88]. The cost effectiveness of ACI has not been proven yet. If we compare it to MF at 2 years the quality of life gain should be between 70 and 100% better at 2 years to be costeffective [54].
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Growth Factors Growth factors combined with tissue engineering seems to be one of the promising therapies for the future [90]. Growth factors are cytokines with regulatory functions for healing in tissues. They can affect the metabolism of chondrocytes and influence cartilage healing [90, 91]. Available data show that IGF-1 and TGF-B modulate the synthesis of cartilage matrix, bFGF is a mitogenic factor that stimulates the differentiation of chondrocytes and BMP-2 seems to be involved in the growth and differentiation of mesenchymal cells to chondroblasts and osteoblasts [92, 93]. For the moment administration of growth factors and the right carrier seems to be the problem [94].
Gene Therapy With gene therapy, genes encoding for therapeutic growth factors can be expressed at a high level in the injured site for an extended period of time [9]. Recent studies have suggested the presence of pluripotent stem cells in musclederived cells [9].
Mesenchymal Stem Cell Regeneration
Future Developments Cartilage repair is a rapidly emerging field. A variety of techniques have been described for the treatment of articular cartilage lesions, each with benefits and limitations, however no standard of care has yet been established. Future directions in cartilage repair technology should focus on optimising current techniques, as well as the development of novel procedures. Furthermore, research efforts should be directed towards obtaining long-term safety and efficacy data, so that promising therapeutic approaches can progress from experimental use to widespread clinical practice. Emerging techniques focus on delivering autologous or allogenic chondrocytes, or stem cells, to the defect [28]. Scaffolds should be implanted easily, reduce surgical morbidity, require no harvesting of other tissues, exhibit enhanced cell proliferation and maturation, have easier phenotype maintenance and allow complete integration with surrounding articular cartilage [89]. Future research endeavours are likely to involve genetic manipulation of donor and recipient cells using gene or growth factor therapies, with the aim of developing tissueengineering technologies capable of fully restoring the articular cartilage in focal chondral defects [28].
MSC’s are relatively undifferentiated, embryonic-like cells with the potential to develop into various types of cells [95, 96]. They are found in adult bone marrow and in the periosteum [95, 96]. They are easily harvested through a bone marrow aspiration, could be placed in a gel which could be placed in the cartilage lesion [95–97].
Biomaterials The use of innovative 3D biomimetic composite materials to induce in vivo tissue regeneration seems the new challenge [9]. These new scaffolds must be able to guide new tissue formation by providing support for the osteoprogenitor cells as well as providing mechanical resistance [98].
Conclusions Articular cartilage defects are common and are recognised to play a significant role in the development of degenerative joint disease. Due to its avascular nature and extracellular matrix structure, articular cartilage has limited intrinsic
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capacity for healing after injury. Thus, a variety of treatment methods have been developed with the aim of repairing and resurfacing the joint with new tissue that has the structural and mechanical properties of physiological hyaline cartilage. Current surgical options include arthroscopic lavages, with and without debridement, reparative techniques or MSTs, and autologous grafting or implantation procedures, such as OATS, mosaicplasty and ACI. These procedures are generally regarded as effective in restoring knee function after injury; however, there is no accepted treatment algorithm for articular cartilage defects. Decisions regarding the best surgical approach for articular cartilage injuries are based on a number of factors, including features of the lesion such as size and depth, and patient characteristics such as age, BMI and activity level. Although lesion size is of primary concern when deciding upon the most appropriate treatment option, other pertinent factors should also be considered in order to increase the patients’ chances of good, long-term clinical outcome. A meta-analysis performed by Jakobsen et al. concluded that caution was necessary when interpreting results after surgical cartilage repair. This because of the generally low methodological quality found in most studies [99]. Limited long-term clinical efficacy and safety data are available for a number of the newer cartilage repair techniques, with some of the most recent developments still regarded as experimental [56, 100]. Future research efforts should focus on obtaining long-term outcome data in order for these initially promising techniques to gain widespread acceptance within the orthopaedic community. Further research into novel techniques is necessary in order to develop effective tissue-engineering technologies that are capable of fully restoring the articular cartilage in chondral defects.
References 1. Williams RJ. Articular cartilage repair: clinical approach and decision making. Oper Tech Orthop 2006;16(4):218–226. 2. Curl W, Krome J, Gordon ES, Rushing J, Smith BP, Poehling GG. Cartilage injuries: a review of 31516 knee arthroscopies. Arthroscopy 1997;13:456–460. 3. Widuchowski W, Lukasik P, Kwiatkowski G, Faltus R, Szyluk K, Widuchowski J, Koczy B. Isolated full thickness chondral injuries: prevalence and outcome of treatment. A retrospective study of 5233 knee arthroscopies. Acta Chir Orthop Traumatol Cech 2008;75:382–386. 4. Arøen A, Løken S, Heir S, Alvik E, Ekeland A, Granlund OG, Engebretsen L. Articular cartilage lesions in 993 consecutive knee arthroscopies. Am J Sports Med 2004;32(1):211–215.
E. Thienpont 5. Gelber AC, Hochberg MC, Mead LA, Wang NY, Wigley FM, Klag MJ. Joint injury in young adults and risk for subsequent knee and hip osteoarthritis. Ann Intern Med 2000; 133(5):321–328. 6. Buckwalter JA, Saltzman C, Brown T. The impact of osteoarthritis: implications for research. Clin Orthop Relat Res 2004; (427 Suppl):S6–S15. 7. Vangsness CT Jr, Kurzweil PR, Lieberman JR. Restoring articular cartilage in the knee. Am J Orthop 2004;33(2 Suppl): 29–34. 8. Poole R. What type of cartilage repair are we attempting to attain? J Bone Joint Surg Am 2003;85(Suppl 2):40–44. 9. Sgaglione NA. Biologic approaches to articular cartilage surgery: future trends. Orthop Clin North Am 2005;36:485–495. 10. Saris DB, Vanlauwe J, Victor J, Haspl M, Bohnsack M, Fortems Y, Vandekerckhove B, Almqvist KF, Claes T, Handelberg F, Lagae K, van der Bauwhede J, Vandenneucker H, Yang KG, Jelic M, Verdonk R, Veulemans N, Bellemans J, Luyten FP. Characterized chondrocyte implantation results in better structural repair when treating symptomatic cartilage defects of the knee in a randomized controlled trial versus microfracture. Am J Sports Med 2008;36(2):235–246. 11. Williams RJ, Gamradt SC. Articular cartilage repair using a resorbable matrix scaffold. Instr Course Lect 2008;57:563–571. 12. Day B. The indications for arthroscopic debridement for osteoarthritis of the knee. Orthop Clin North Am 2005;36: 413–417. 13. Stuart MJ, Lubowitz JH. What, if any, are the indications for arthroscopic debridement of the osteoarthritic knee? Arthroscopy 2006;22:238–239. 14. Siparsky P, Ryzewicz M, Peterson B, Bartz R. Arthroscopic treatment of osteoarthritis of the knee: are there any evidencebased indications? Clin Orthop Relat Res 2007;455:107–112. 15. van den Bekerom MP, Patt TW, Rutten S, Raven EE, van de Vis HM, Albers GH. Arthroscopic debridement for grade III and IV chondromalacia of the knee in patients older than 60 years. J Knee Surg 2007;20:271–276. 16. Blain EJ, Gilbert SJ, Wardale RJ, Capper SJ, Mason DJ, Duance VC. Up-regulation of matrix metalloproteinase expression and activation following cyclical compressive loading of articular cartilage in vivo. Arch Biochem Biophys 2001;396:49–55. 17. Smith GD, Knutsen G, Richardson JB. A clinical review of cartilage repair techniques. J Bone Joint Surg 2005;87-B: 445–449. 18. Hubbard MJ. Articular debridement versus washout for degeneration of the medial femoral condyle. A five-year study. J Bone Joint Surg Br 1996;78(2):217–219. 19. Shah MR, Kaplan KM, Meislin RJ, Bosco JA. Articular cartilage restoration of the knee. Bull NYU Hosp Jt Dis 2007; 65(1):51–60. 20. Bhosale AM, Richardson JB. Articular cartilage: structure, injuries and review of management. Br Med Bull 2008;87: 77–95. 21. Laupattarakasem W, Laopaiboon M, Laupattarakasem P, Sumananont C. Arthroscopic debridement for knee osteoarthritis. Cochrane Database Syst Rev 2008;23:CD005118. 22. Pridie KH. A method of resurfacing osteoarthritic knee joints. J Bone Joint Surg Br 1959;41-B:618–619.
Current Status of Articular Cartilage Repair 23. Johnson LL. Arthroscopic abrasion arthroplasty: a review. Clin Orthop 2001;391:S306–S317. 24. Steadman JR, Miller BS, Karas SG, Schlegel TF, Briggs KK, Hawkins RJ. The microfracture technique in the treatment of full-thickness chondral lesions of the knee in National Football League players. J knee Surg 2003;16:83–86. 25. Steadman JR, Briggs KK, Rodrigo JJ, Kocher MS, Gill TJ, Rodkey WG. Outcomes of microfracture for traumatic chondral defects of the knee: average 11-year follow-up. Arthroscopy 2003;19(5):477–484. 26. Steadman JR, Rodkey WG, Singleton SB, Briggs KK. Microfracture technique for full-thickness chondral defects: technique and clinical results. Oper Tech Orthop 1997;7: 300–304. 27. Steadman JR, Rodkey WG, Rodrigo JJ. Microfracture: surgical technique and rehabilitation to treat chondral defects. Clin Orthop Rel Res 2001;(391 Suppl):S362–S369. 28. Lattermann C, Kang RW, Cole BJ. What’s new in the treatment of focal chondral defects of the knee? Orthopedics 2006;29(10):898–903. 29. Gudas R, Stankevičius E, Monastyreckien? E, Pranys D, Kalesinkas RJ. Osteochondral autologous transplantation versus microfracture for the treatment of articular cartilage defects in the knee joint in athletes. Knee Surg Sports Traumatol Arthrosc 2006;14:834–842. 30. Knutsen G, Engebretsen L, Ludvigsen TC, Drogset JO, Grøntvedt T, Solheim E, Strand T, Roberts S, Isaksen V, Johansen O. Autologous chrondrocyte implantation compared with microfracture in the knee. A randomised trial. J Bone Joint Surg Am 2004;86-A:455–464. 31. Kreuz PC, Erggelet C, Steinwachs MR, Krause SJ, Lahm A, Niemeyer P, Ghanem N, Uhl M, Südkamp N. Is microfracture of chondral defects in the knee associated with different results in patients aged 40 years or younger? Arthroscopy 2006;22(11):1180–1186. 32. Mithoefer K, Williams RJ III, Warren RF, Potter HG, Spock CR, Jones EC, Wickiewicz TL, Marx RG. The microfracture technique for the treatment of articular cartilage lesions in the knee. A prospective cohort study. J Bone Joint Surg (Am) 2005;87-A(9):1911–1920. 33. Kreuz PC, Steinwachs MR, Erggelet C, Krause SJ, Konrad G, Südkamp N. Results after microfracture of full-thickness chondral defects in different compartments in the knee. Osteoarthritis Cartilage 2006;14(11):1119–1125. 34. Mithoefer K, Williams RJ III, Warren RF, Potter HG, Spock CR, Jones EC, Wickiewicz TL, Marx RG. Chondral resurfacing of articular cartilage defects in the knee with the microfracture technique. Surgical technique. J Bone Joint Surg Am 2006;878:294–304. 35. Hunziker EB. Articular cartilage repair: basic science and clinical progress. A review of the current status and prospects. Osteoarthritis Cartilage 2002;10(6):432–463. 36. Brown WE, Potter HG, Marx RG, Wickiewiicz TL, Warren RF. Magnetic resonance imaging appearance of cartilage repair in the knee. Clin Orthop 2004;422:214–223. 37. Buckwalter JA, Mankin HJ. Articular cartilage: degeneration and osteoarthritis, repair, regeneration, and transplantation. Instr Course Lect 1998;47:487–504.
25 38. Minas T, Nehrer S. Current concepts in the treatment of articular cartilage defects. Orthopedics 1997;20(6):525–538. 39. Gomoll AH, Rosenberger R, Bryant T, Minas T. Marrow stimulation techniques increase the failure rate of subsequent autologous chondrocyte implantation. Presented at AAOS, San Franciso, CA, 2008. 40. Steinwachs MR, Guggi T, Kreuz PC. Marrow stimulation techniques. Injury 2008;39:S26–S31. 41. Hangody L, Kish G, Karpati Z, Szerb I, Udvarhelyi I. Arthroscopic autogenous osteochondral mosaicplasty for the treatment of femoral condylar reticular defects: a preliminary report. Knee Surg Sports Traumatol Arthrosc 1997;5:262–267. 42. Matsusue Y, Yamamuro T, Hama H. Arthroscopic multiple osteochondral transplantation to the chondral defect in the knee associated with anterior cruciate ligament disruption. Arthroscopy 1993;9:318–321. 43. Jakob RP, Franz T, Gautier E, Mainil-Varlet P. Autologous osteochondral grafting in the knee: indication, results, and reflections. Clin Orthop Relat Res 2002;(401):170–184. 44. Hangody L, Feczko P, Bartha L, Bodo G, Kish G. Mosaicplasty for the treatment of articular defects of the knee and ankle. Clin Orthop 2001;391:S328–S336. 45. Hangody L, Füles P. Autologous osteochondral mosaicplasty for the treatment of full-thickness defects of weight-bearing joints: ten years of experimental and clinical experience. J Bone Joint Surg (Am) 2003;85-A(Suppl 2):25–32. 46. Hangody L, Ráthonyi GK, Duska Z, Vásárhelyi G, Füles P, Módis L. Autologous osteochondral mosaicplasty. Surgical technique. J Bone Joint Surg (Am) 2004;86-A(Suppl 1): 65–72. 47. Marcacci M, Berruto M, Brocchetta D, Delcogliano A, Ghinelli D, Gobbi A, Kon E, Pederzini L, Rosa D, Sacchetti GL, Stefani G, Zanasi S. Articular cartilage engineering with Hyalograft C: 3-year clinical results. Clin Orthop Relat Res 2005;(435):96–105. 48. Bentley G, Biant LC, Carrington RW, Akmal M, Goldberg A, Williams AM, Skinner JA, Pringle J. A prospective, randomised comparison of autologous chondrocyte implantation versus mosaicplasty for osteochondral defects in the knee. J Bone Joint Surg (Br) 2003;85-B(2):223–230. 49. Nho SJ, Foo LF, Green DM, Shindle MK, Warren RF, Wickiewicz TL, Potter HG, Williams RJ. Magnetic resonance imaging and clinical evaluation of patellar resurfacing with press-fit osteochondral autograft plugs. Am J Sports Med 2008;36:1101–1109. 50. Peterson L, Minas T, Brittberg M, Lindahl A. Treatment of osteochondritis dissecans of the knee with autologous chondrocyte transplantation: Results at two to ten years. J Bone Joint Surg Am 2003;85(Suppl 2):17–24. 51. Brittberg M, Lindahl A, Nilsson A, Ohlsson C, Isaksson O, Peterson L. Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation. N Engl J Med 1994;331(14):889–895. 52. Peterson L, Minas T, Brittberg M, Nilsson A, SjögrenJansson E, Lindahl A. Two- to 9-year outcome after autologous chondrocyte transplantation of the knee. Clin Orthop 2000;5:212–234.
26 53. Peterson L, Brittberg M, Kiviranta I, Akerlund EL, Lindahl A. Autologous chondrocyte transplantation. Am J Sports Med 2002;30(1):2–12. 54. Clar C, Cummins E, McIntyre L, Thomas S, Lamb J, Bain L, Jobanputra P, Waugh N. Clinical and cost-effectiveness of autologous chondrocyte implantation for cartilage defects in knee joints: systematic review and economic evaluation. Health Technol Assess 2005;9(47):iii–iv; ix–x; 1–82. 55. Fu FH, Zurakowski D, Browne JE, Mandelbaum B, Erggelet C, Moseley JB Jr, Anderson AF, Micheli LJ. Autologous chondrocyte implantation versus debridement for treatment of full-thickness chondral defects of the knee: an observational cohort study with 3-year follow-up. Am J Sports Med 2005;33:1658–1666. 56. Knutsen G, Drogset JO, Engebretsen L, Grøntvedt T, Isaksen V, Ludvigsen TC, Roberts S, Solheim E, Strand T, Johansen O. A randomized trial comparing autologous chondrocyte implantation with microfracture. Findings at five years. J Bone Joint Surg Am 2007;89(10):2105–2112. 57. Browne JE, Moseley B, Erggelet C, Fu FH, Mandelbaum BR, Arciero RA, Micheli LJ, Anderson AF. Marrow stimulation techniques versus autologous chondrocyte implantation for treatment of full-thickness chondral defects of the knee: comparison of patient outcomes at 3–5 years. Arthroscopy 2003;19(6 Suppl):65–66. 58. Zaslav K, Cole B, Brewster R, Deberardino T, Farr J, Fowler P, Nissen C. A prospective study of autologous chondrocyte implantation in patients with failed prior treatment for articular cartilage defect of the knee: results of the study of the treatment of articular repair (STAR) clinical trial. Am J Sports Med 2008;37:42–55. 59. Horas U, Pelinkovic D, Herr G, Aigner T, Schnettler R. Autologous chondrocyte implantation and osteochondral cylinder transplantation in cartilage repair of the knee joint: a prospective, comparative trial. J Bone Joint Surg 2003; 85-A:185–192. 60. Cherubino P, Grassi FA, Bulgheroni P, Ronga M. Autologous chondrocyte implantation using a bilayer collagen membrane: a preliminary report. J Orthop Surg (Hong Kong) 2003;11(1):10–15. 61. Gooding CR, Bartlett W, Bentley G, Skinner JA, Carrington R, Flanagan A. A prospective, randomised study comparing two techniques of autologous chondrocyte implantation for osteochondral defects in the knee: periosteum covered versus type I/III collagen covered. Knee 2006;13(3):203–210. 62. Rosenberger RE, Gomoll AH, Bryant T, Minas T. Repair of large chondral defects of the knee with autologous chondrocyte implantation in patients 45 years or older. Am J Sports Med. 2008;36:2336–2344. 63. Krishnan SP, Skinner JA, Carrington RW, Flanagan AM, Briggs TW, Bentley G. Collagen-covered autologous chondrocyte implantation for osteochondritis dissecans of the knee: two- to seven-year results. J Bone Joint Surg Br 2006;88:203–205. 64. Kim JK, Lee JS, Jung HJ, Cho JH, Heo JI, Chang YH. Preparation and properties of collagen/modified hyaluronic acid hydrogel for biomedical application. J Nanosci Nanotechnol 2007;7:3852–3856.
E. Thienpont 65. Visna P, Pasa L, Cizmar I, Hart R, Hoch J. Treatment of deep cartilage defects of the knee using autologous chondrograft transplantation and by abrasive techniques – a randomized controlled study. Acta Chir Belg 2004;104:709–714. 66. Gigante A, Bevilacqua C, Ricevuto A, Mattioli-Belmonte M, Greco F. Membrane-seeded autologous chondrocytes: cell viability and characterization at surgery. Knee Surg Sports Traumatol Arthrosc 2007;15:88–92. 67. Zheng MH, Willers C, Kirilak L, Yates P, Xu J, Wood D, Shimmin A. Matrix-induced autologous chondrocyte implantation (MACI): biological and histological assessment. Tissue Eng 2007;13(4):737–746. 68. Behrens P, Bitter T, Kurz B, Russlies M. Matrix-associated autologous chondrocyte transplantation/implantation (MACT/MACI) – 5 year follow-up. Knee 2006;13:194–202. 69. Vanlauwe J, Almqvist F, Bellemans J, Huskin JP, Verdonk R, Victor J. Repair of symptomatic cartilage lesions of the knee: the place of autologous chondrocyte implantation. Acta Orthop Belg 2007;73(2):145–158. 70. Dell’Accio F, De Bari C, Luyten FP. Microenvironment and phenotypic stability specify tissue formation by human articular cartilage-derived cells in vivo. Exp Cell Res 2003; 287(1):16–27. 71. Kang SW, Yoo SP, Kim BS. Effect of chondrocyte passage number on histological aspects of tissue-engineered cartilage. Biomed Mater Eng 2007;17(5):269–276. 72. Dell’Accio F, De Bari C, Luyten FP. Molecular markers predictive of the capacity of expanded human articular chondrocytes to form stable cartilage in vivo. Arthritis Rheum 2001;44:1608–1619. 73. Gobbi A, Kon E, Berruto M, Francisco R, Filardo G, Marcacci M. Patellofemoral full-thickness chondral defects treated with Hyalograft-C: a clinical, arthroscopic, and histologic review. Am J Sports Med 2006;34:1763–1773. 74. Gigante A, Enea D, Greco F, Bait C, Denti M, Schonhuber H, Volpi P. Distal realignment and patellar autologous chondrocyte implantation: mid-term results in a selected population. Knee Surg Sports Traumatol Arthrosc. 2009;17(1):2–10. 75. Farr J. Autologous chondrocyte implantation and anteromedialization in the treatment of patellofemoral chondrosis. Orthop Clin North Am 2008;39:329–335. 76. Farr J. Autologous chondrocyte implantation improves patellofemoral cartilage treatment outcomes. Clin Orthop Relat Res 2007;463:187–194. 77. Minas T, Bryant T. The role of autologous chondrocyte implantation in the patellofemoral joint. Clin Orthop Relat Res 2005;436:30–39. 78. Marlovits S, Striessnig G, Kutscha-Lissberg F, Resinger C, Aldrian SM, Vecsei V, Trattnig S. Early postoperative adherence of matrix-induced autologous chondrocyte implantation for the treatment of full-thickness cartilage defects of the femoral condyle. Knee Surg Sports Traumatol Arthrosc 2005;13:451–457. 79. Lu Y, Dhanaraj S, Wang Z, Bradley DM, Bowman SM, Cole SJ, Binette F. Minced cartilage without cell culture serves as an effective intraoperative cell source for cartilage repair. J Ortop Res 2006;24(6):1261–1270.
Current Status of Articular Cartilage Repair 80. Hennig A, Abate J. Osteochondral allografts in the treatment of articular cartilage injuries of the knee. Sports Med Arthrosc 2007;15:126–132. 81. Williams RJ, Ranawat AS, Potter HG, Carter T, Warren RF. Fresh stored allografts for the treatment of osteochondral defects of the knee. J Bone Joint Surg Am 2007;89:718–726. 82. Emmerson BC, Görtz S, Jamali AA, Chung C, Amiel D, Bugbee WD. Fresh osteochondral allografting in the treatment of osteochondritis dissecans of the femoral condyle. Am J Sports Med 2007;35:907–914. 83. Davidson PA, Rivenburgh DW, Dawson PE, Rozin R. Clinical, histologic, and radiographic outcomes of distal femoral resurfacing with hypothermically stored osteoarticular allografts. Am J Sports Med 2007;35:1082–1090. 84. Gross AE, Shasha N, Aubin P. Long-term follow-up of the use of fresh osteochondral allografts for posttraumatic knee defects. Clin Orthop Relat Res 2005;435:79–87. 85. Karataglis D, Learmonth DJ. Management of big osteochondral defects of the knee using osteochondral allografts with the MEGA-OATS technique. Knee 2005;12:389–393. 86. Jones DG, Peterson L. Autologous chondrocyte implantation. J Bone Joint Surg (Am) 2006;88-A(11):2502–2520. 87. Krishnan SP, Skinner JA, Bartlett W, Carrington RW, Flanagan AM, Briggs TW, Bentley G. Who is the ideal candidate for autologous chondrocyte implantation? J Bone Joint Surg (Br) 2006;88-B(1):61–64. 88. Magnussen RA, Dunn WR, Carey JL, Spindler KP. Treatment of focal articular cartilage defects in the knee: a systematic review. Clin Orthop Relat Res 2008;466:952–962. 89. Safran MR, Kim H, Zaffagnini S. The use of scaffolds in the management of articular cartilage injury. J Am Acad Orthop Surg 2008;16:306–311. 90. O’Connor WJ, Botti T, Khan SN, Lane JM. The use of growth factors in cartilage repair. Orthop Clin North Am 2000;31:399–410. 91. Trippel SB. Growth factors as therapeutic agents. Instr Course Lect 1997;46:473–476.
27 92. Van Beuningen HM, Glansbeek HL, van der Kraan PM, van den Berg WB. Differential effects of local application of BMP-2 or TGF-beta on both articular cartilage composition and osteophyte formation. Osteoarthritis Cartilage 1998;6:306–317. 93. Hunziker EB. Growth-factor-induced healing of partial thickness defects in adult articular cartilage. Osteoarthritis Cartilage 2001;9:22–32. 94. Evans CH, Ghivizzani SC, Smith P, Shuler FD, Mi Z, Robbins PD. Using gene therapy to protect and restore cartilage. Clin Orthop 2000;379:S214–S219. 95. Wakitani S, Imoto K, Yamamoto T, Saito M, Murata N, Yoneda M. Human autologous culture expanded bone marrow mesenchymal cell transplantation for repair of cartilage defects in osteoarthritic knees. Osteoarthritis Cartilage 2002;10:199–206. 96. Biant LC, Bentley G. Stem cells and debrided waste: two alternative sources of cells for transplantation of cartilage. J Bone Joint Surg Br 2007;89:1110–1114. 97. Wakitani S, Nawata M, Tensho K, Okabe T, Machida H, Ohgushi H. Repair of articular cartilage defects in the patello-femoral joint with autologous bone marrow mesenchymal cell transplantation: three case reports involving nine defects in five knees. J Tissue Eng Regen Med 2007; 1:74–79. 98. Marcacci M, Kon E, Zaffagnini S, Giardino R, Rocca M, Corsi A, Benvenuti A, Bianco P, Quarto R, Martin L, Muraglia A, Cancedda R. Reconstruction of extensive long bone defects in sheep using porous hydroxyapatite sponges. Calcif Tissue Int 1999;64:83–90. 99. Jakobsen RB, Engebretsen L, Slauterbeck JR. An analysis of the quality of cartilage repair studies. J Bone Joint Surg Am 2005;87:2232–2239. 100. Blevins FT, Steadman JR, Rodrigo JJ, Silliman J. Treatment of articular cartilage defects in athletes: an analysis of functional outcome and lesion appearance. Orthopedics 1998; 21(7):761–767.
Thromboprophylaxis After Major Orthopaedic Surgery: State of the Art Alexander G.G. Turpie
Introduction Venous thromboembolism (VTE), consisting of deep vein thrombosis (DVT) and pulmonary embolism (PE), is estimated to affect over one million people in the EU each year. With over 540,000 VTE-related deaths estimated per year in Europe, VTE represents a significant health concern. A study carried out in six European countries (France, Germany, Italy, Spain, Sweden and the UK) estimated the occurrence of over 460,000 cases of DVT and nearly 300,000 cases of non-fatal PE each year [1]. Two large community-based studies carried out in France and Sweden estimated the incidence of VTE to be approximately 160–180 per 100,000 population [2, 3]. Although slightly lower incidences have been reported in the United States [4, 5], it remains the third leading cause of cardiovascular death after myocardial infarction and stroke [6]. An estimated two million patients develop DVT each year in the United States and an estimated 600,000 develop PE, 10% of which are fatal [7]. As well as the short-term consequences, VTE is also associated with longer-term consequences such as recurrent events and the post-thrombotic syndrome (PTS). A prospective cohort study assessing the clinical course of 528 patients with symptomatic DVT in Italy found that nearly one-fifth of patients experienced a recurrent event. The cumulative incidence of recurrent VTE after 2, 5 and 8 years was 17.2, 24.3 and 29.7%, respectively, and the cumulative incidence of PTS after 2, 5 and 8 years was 24.5, 29.6 and 29.8%, respectively [8]. Similar rates of the PTS have been reported in patients with venographically detected VTE in the postoperative period [9]. Although VTE occurs frequently, it is often clinically silent and death can often be the first presentation of DVT.
A. G. G. Turpie McMaster University, 237 Barton Street East, Hamilton, Canada ON L8L 2X2 e-mail:
[email protected]
Between 60 and 80% of post-operative DVTs are asymptomatic and are only detected post mortem [1, 10, 11]. Undiagnosed VTE may predispose patients to long-term morbidity from the PTS and future recurrent events [9]. The seriousness of potential consequences and long-term complications, in addition to the often silent nature of VTE, mean that it is inappropriate to wait for symptoms before action is taken. Guidelines recommend the appropriate use of anticoagulants for the treatment of VTE and for the prevention of VTE in surgical patients, acutely ill non-surgical patients and cancer patients [12, 13]. Despite this, studies have shown that adherence to established guidelines is relatively low [14–17]. The reasons for this will be detailed in this review.
Venous Thromboembolism After Major Orthopaedic Surgery There is an increased risk of VTE after surgery, particularly total hip replacement (THR), total knee replacement (TKR) and hip fracture surgery (HFS). Without thromboprophylaxis, the incidence of hospital-acquired DVT is approximately 10–40% among medical or general surgical patients, but this percentage increases to approximately 40–60% after major orthopaedic surgery [13]. VTE is the most serious and most frequent complication after major orthopaedic surgery, with the risk for an event increasing with the duration of surgery and period of immobility. It also carries a considerable healthcare cost burden, both in the short and long term. A study in France has estimated the total annual cost of VTE associated with major orthopaedic surgery to be approximately 60€ million, of which 28€ million was attributable to inpatient care and 30€ million to recurrent events and the PTS [18]. In the United States, the mean total costs of in-patient care for patients with VTE after major orthopaedic surgery were almost double those for patients without VTE. This was due to a tenfold longer time in intensive care and a doubling in the length of hospital stay [19].
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The average total VTE cost per patient after major orthopaedic surgery (including initial therapy, follow-up care, recurrent VTE and the PTS) is estimated to be between US$12,000 and US$18,000 [20, 21]. The cumulative incidence of symptomatic VTE within 3 months of THR and TKR surgery was found to be 2.8 and 2.1%, respectively [22]. In this study of nearly 44,000 patients, the incidence of DVT or PE was reviewed from a hospital discharge database. The mean length of hospital stay was 7 ± 4 days, and in-hospital thromboprophylaxis (subcutaneous heparin, warfarin, pneumatic compression or a combination) was given in 88% of these patients. Only 32% were given thromboprophylaxis (with warfarin) after discharge, with an average duration of 4 weeks. However, the diagnosis of VTE was made after discharge in 76% and 47% of patients who had undergone THR and TKR, respectively [22]. After HFS, symptomatic VTE has been reported in 1.3–8.2% of patients receiving routine thromboprophylaxis within 3 months of surgery [23, 24]. One study has shown that, with a median hospital stay of 8 days after HFS, the in-hospital incidence of VTE was 1.6% compared with a 3-month rate of 8.2%. The incidence of in-hospital nonfatal PE was 0.5% compared with a 3-month rate of 2.6% [24]. These findings suggest that, to reduce VTE further, thromboprophylaxis needs to be extended beyond the length of hospital stay.
Guideline Recommendations American College of Chest Physicians Guidelines [13] After THR and TKR, thromboprophylaxis is recommended for at least 10 days (grade 1A). For patients undergoing THR, thromboprophylaxis is recommended for up to 35 days after surgery (grade 1A). Routine use of one of the following is recommended: low molecular weight heparin (LMWH; at a usual high-risk dose, started 12 h before surgery or 12–24 h after surgery, or 4–6 h after surgery at half the usual high-risk dose and then increasing to the usual highrisk dose the following day), fondaparinux (2.5 mg started 6–24 h after surgery) or adjusted-dose vitamin K antagonist (VKA; started pre-operatively or the evening before surgery with a target international normalized ratio [INR] of 2.5, INR range 2.0–3.0) (all grade 1A) [13]. For patients undergoing TKR, the guidelines suggest that thromboprophylaxis be extended beyond 10 days and be considered for up to 35 days after surgery (grade 2B). The recommended options are LMWH (at the usual high-risk
A.G.G. Turpie
dose), fondaparinux or adjusted-dose VKA (INR target 2.5, INR range 2.0–3.0) [13]. The American College of Chest Physicians (ACCP) guidelines recommend against the use of acetylsalicylic acid (ASA), dextran, low-dose unfractionated heparin (UFH), graduated compression stockings or a venous foot pump (VFP) as sole methods of thromboprophylaxis after orthopaedic surgery (all grade 1A) [13]. For patients undergoing HFS, guidelines recommend routine use of fondaparinux (grade 1A), LMWH (grade 1B), adjusted-dose VKA (INR target 2.5, INR range 2.0–3.0; grade 1B) or low-dose UFH (grade 1B). The guidelines recommend against the use of ASA (grade 1A) as a sole method of thromboprophylaxis [13].
Current Options for Thromboprophylaxis Currently available options for prophylaxis include the VKAs (including warfarin), UFH, LMWHs, ASA, mechanical methods and, more recently, fondaparinux. Dabigatran etexilate and rivaroxaban have also recently been approved in some countries. The VKAs, of which warfarin is the most frequently used, are among the recommended agents for VTE prevention in patients undergoing major orthopaedic surgery. However, they have unpredictable pharmacokinetics and pharmacodynamics, which leads to considerable inter- and intra-patient variability in the dose–response relationships. They have a narrow therapeutic window and are associated with multiple drug–drug and food–drug interactions [25]. This can prove problematic in certain patient groups, especially the elderly, who frequently receive concomitant medications. Regular costly and inconvenient coagulation monitoring is therefore required to ensure that the INR is within the required range. Studies have shown that a considerable number of patients are often not within the required INR [26, 27] for a number of reasons, ranging from the setting and quality of anticoagulation management to patient-specific factors [28, 29]. UFH has largely been replaced by the LMWHs, which are effective, have a low risk of bleeding and do not require regular coagulation monitoring [30]. LMWHs have several other advantages over UFH, including lower levels of binding to plasma proteins and endothelium, higher bioavailability, a predictable dose response and a long half-life. Furthermore, there is no potential for developing heparin resistance associated with the use of LMWHs, as observed with UFH. However, LMWHs need to be administered subcutaneously and are also associated with a risk of heparin-induced thrombocytopenia (HIT) [30]. They have
Thromboprophylaxis After Major Orthopaedic Surgery: State of the Art
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only been shown to be cost-effective if self-administered beyond the hospital stay, particularly after major orthopaedic surgery [31–33]. Their subcutaneous route of administration means that patients often need to attend daily appointments or receive daily nurse visits to administer their medication. ASA is an antiplatelet agent. The evidence for the efficacy of ASA in the prevention of VTE is limited [5, 34, 35] and no direct comparison studies between ASA, LMWHs and VKAs in prolonged use are available [36]. While the ACCP guidelines advise against ASA alone for thromboprophylaxis after major orthopaedic surgery [13], the American Academy of orthopaedic Surgeons (AAOS) guidelines recommend its use to prevent PE in those at standard risk of PE and/or major bleeding [37]. However, by disregarding DVT, the AAOS guidelines do not consider the long-term sequelae of DVT, including recurrent DVT, the PTS and proximal DVTs, which are more likely to embolize, causing PE. Mechanical prophylaxis methods include VFPs, intermittent pneumatic compression (IPC) devices and graduated compression stockings. IPC devices are recommended by the ACCP guidelines in patients undergoing TKR, but VFPs are not recommended as a sole method of prophylaxis (Group 1B). After THR, mechanical methods are only recommended as a sole method in those with a high risk of bleeding (grade 1A). However, there is evidence
that mechanical prophylaxis may not be as effective as drug prophylaxis for DVT prevention [38]. The synthetic pentasaccharide fondaparinux is indicated for the prevention of VTE in patients undergoing major orthopaedic surgery. However, the use of fondaparinux remains limited in this indication, which may be due to the reported increased incidence of major bleeding with fondaparinux compared with enoxaparin [39]. Additional factors that may explain this include the need for subcutaneous administration, the fact that caution is recommended when it is used in the elderly (due to an increased risk of bleeding) and that it is contra-indicated in patients with severe renal impairment (creatinine clearance < 30 ml/min) [40]. The limitations of the currently available prophylaxis options mean that prophylaxis is often underused or inappropriately administered [14–17].
New Developments in Prophylaxis: Targeted Anticoagulants In the development of novel anticoagulants, there are many potential targets in the coagulation pathway (Fig. 1), including Factor Xa (FXa) and thrombin (Factor IIa). The binding of tissue factor pathway inhibitor to FXa inactivates the
ORAL
PARENTERAL TF/VIIa
TFPI (tifacogin)
TTP889
X
IX APC (drotrecogin alpha) sTM (ART-123)
IXa VIIIa Rivaroxaban Apixaban YM150 DU-176b Betrixaban
Fig. 1 The coagulation pathway and the targets of anticoagulant agents. APC activated protein C; AT antithrombin; TF tissue factor; TFPI tissue factor pathway inhibitor; sTM soluble thrombomodulin
Va AT Xa
II Dabigatran Ximelagatran
DX-9065a
IIa
Fibrinogen
Fondaparinux Idraparinux
Fibrin
32
A.G.G. Turpie
tissue factor–Factor VIIa complex, preventing initiation of coagulation. Activated protein C degrades Factors Va and VIIIa, and thrombomodulin converts thrombin from a procoagulant to a potent activator of protein C (a natural anticoagulant). Of the new anticoagulants in development, dabigatran and AZD0837 are oral, direct thrombin inhibitors, and the oral, direct FXa inhibitors include YM150, betrixaban, DU-176b, apixaban and rivaroxaban.
Thrombin Inhibitors Dabigatran etexilate is an oral, direct thrombin inhibitor that has been approved in the EU and Canada for the prevention of VTE in adult patients who have undergone elective THR or TKR. Dabigatran etexilate is a prodrug of dabigatran, developed for oral administration. Dabigatran has a fast onset of action, relatively low bioavailability and does not require routine coagulation monitoring (Table 1) [51]. In the phase III RE-NOVATE and RE-MODEL studies, dabigatran 150 and 220 mg once daily (o.d.) were both non-inferior to enoxaparin 40 mg o.d. for the prevention of VTE in patients undergoing elective THR and TKR, respectively [52, 53]. Dabigatran had a similar safety profile to enoxaparin in both trials. The RE-MOBILIZE trial compared dabigatran with enoxaparin 30 mg twice daily (b.i.d.; the commonly used North American regimen) for the prevention of VTE after TKR [54]. Dabigatran, although effective compared with enoxaparin o.d., failed to demonstrate non-inferiority to the enoxaparin b.i.d. regimen, perhaps due to the more intense and prolonged dosing of the b.i.d. regimen [54]. AZD0837 is a prodrug, which is bioactivated into the direct thrombin inhibitor AR-H067637. It has been shown to significantly reduce thrombin formation in venous and
arterial animal models [55, 56]. Ongoing phase II trials are currently focussing on the prevention of stroke and systemic embolic events after atrial fibrillation.
Factor Xa Inhibitors FXa may be a more attractive target for novel anticoagulants than thrombin for several reasons. The primary functions of FXa are as a procoagulant or pro-inflammatory agent, whereas thrombin has many functions in addition to coagulation, including activating protein C, a natural anticoagulant. In vitro and kinetic studies have demonstrated that FXa activates coagulation over a much wider concentration range than thrombin [57]; suggesting this might result in a greater separation of efficacy and bleeding with a FXa inhibitor. The phenomenon of “rebound” ischaemia has been associated with direct and indirect thrombin inhibitors [58, 59], but has not been reported with FXa inhibitors. Focussing on the efficacy of heparin-based drugs, there is a suggestion that, as they become more specific for FXa, their efficacy increases [60]. For example, fondaparinux is more effective than LMWHs, which, in turn, are more effective than UFH. These reasons, in addition to there being no risk of HIT, suggest that the inhibition of FXa activity may be superior to thrombin inhibition.
Indirect Factor Xa Inhibitors Fondaparinux is an indirect inhibitor of FXa, which selectively binds to antithrombin, causing it to rapidly inhibit FXa [61], and has provided proof of principle for the inhibition of FXa activity in the development of new anticoagulants.
Table 1 Comparison of vitamin K antagonists, dabigatran, apixaban and rivaroxaban [25, 41–50] Property
a
Vitamin K antagonists
Dabigatran
Apixaban
Rivaroxaban
Route of administration
Oral
Oral
Oral
Oral
Target
Thrombin (Factor IIa)
Factor Xa
Factor Xa
Dosing Monitoring required Drug–drug interactions
Vitamin K-dependent clotting factors Once daily Yes Multiple
Once or twice dailya No Proton pump inhibitors
Twice daily No Potent inhibitors of CYP3A4
Bioavailability (%) Half-life (h) Mode of elimination
Approximately 100 36–42 Renal
6.5 14–17 Renal (80% after i.v. administration)
43–46 8–15 Faecal (56%), renal (25%)
Once daily No Potent inhibitors of CYP3A4 or P-glycoprotein Approximately 80 5–9 (11–13 in elderly) Renal (66%), hepatic (28%)
Depending on indication; i.v. intravenous
Thromboprophylaxis After Major Orthopaedic Surgery: State of the Art
Direct Factor Xa Inhibitors YM150 is an oral, direct inhibitor of FXa in the early stages of development. A phase II dose-escalation study (n = 174) showed that o.d. doses (10–60 mg) are as safe as enoxaparin o.d. for VTE prevention after THR, with a clear dose-proportional efficacy [62]. Betrixaban is an oral, direct FXa inhibitor that has shown antithrombotic activity in animal models of thrombosis [63]. A phase II VTE prevention trial in patients undergoing TKR provided proof of principle for the efficacy and safety of betrixaban 15 or 40 mg b.i.d. compared with enoxaparin 30 mg b.i.d. (n = 215) [64]. Another oral, direct FXa inhibitor in development is DU-176b, which has shown potent inhibition of arterial and venous thrombosis in animal models [65]. A recent study investigating the safety and efficacy of four doses of DU-176b vs. the LMWH dalteparin after THR has shown that it reduced the incidence of VTE with a significant dose response in efficacy (p < 0.01) and low rates of major bleeding across both groups [66]. It has also been indicated that the use of this agent might be associated with a lower risk of bleeding than UFH, LMWHs and warfarin [67], and recombinant Factor VIIa has been shown to reverse bleeding induced by DU-176b [68]. Additional phase II and III trials are ongoing in each of these three agents. Apixaban is an oral, highly selective, direct FXa inhibitor that has shown similar efficacy and safety to enoxaparin followed by a VKA in a phase II dose-ranging study [69]. A study of apixaban after TKR found apixaban 2.5 mg b.i.d. to has a benefit–risk profile similar to the current standards of care with enoxaparin and warfarin [70]. This was the basis for the dosing regimen applied in the ongoing phase III studies, which evaluate the safety and efficacy of apixaban in patients undergoing major orthopaedic surgery (ADVANCE-1 and -2 in TKR patients and ADVANCE-3 in THR patients). In ADVANCE-1, the rate of the primary efficacy endpoint (composite of symptomatic or asymptomatic DVT, PE and all-cause mortality) was similar to that of enoxaparin (9.0 vs. 8.9%; p = 0.064), but this did not meet the pre-specified statistical criteria for non-inferiority compared with the dosing regimen of enoxaparin in the United States (30 mg b.i.d.) [71]. Rivaroxaban is an oral, direct FXa inhibitor that has been approved in Canada and the EU for the prevention of VTE in patients undergoing elective THR and TKR. It has a fast onset of action, high oral bioavailability and a predictable pharmacological profile (Table 1) [41, 42]. It therefore does not require routine coagulation monitoring and can be administered in a fixed dose. RECORD (REgulation of Coagulation in ORthopaedic Surgery to prevent Deep vein
33
thrombosis and pulmonary embolism) was a large phase III programme comprising four clinical trials (RECORD1–4) investigating rivaroxaban for the prevention of VTE after elective THR and TKR. RECORD2 was designed to compare short-term thromboprophylaxis with enoxaparin with extended thromboprophylaxis for up to 5 weeks with rivaroxaban after THR [72]. Patients received either subcutaneous enoxaparin 40 mg o.d., beginning the evening before surgery and continuing for 10–14 days (short-term prophylaxis), followed by placebo until day 35 ± 4, or oral rivaroxaban 10 mg o.d. beginning 6–8 h after surgery and continuing for 35 ± 4 days (extended prophylaxis). Mandatory, bilateral venography was conducted at the end of the extended treatment period. The primary efficacy endpoint, total VTE, was the composite of any DVT, non-fatal PE and all-cause mortality. The results of this study demonstrated that extended prophylaxis with rivaroxaban 10 mg o.d. was superior to short-term prophylaxis with enoxaparin 40 mg o.d. for the prevention of VTE, including symptomatic events, after THR (Table 2) [72]. The RECORD1 and 3 studies were designed to compare rivaroxaban 10 mg o.d. (starting 6–8 h after surgery) with enoxaparin 40 mg o.d. (starting the evening before surgery) given for 31–39 days after THR (RECORD1) [73] and 10–14 days after TKR (RECORD3) [74]. In both studies, rivaroxaban was significantly more effective than enoxaparin for the prevention of VTE (Table 2) [73, 74]. RECORD 3 also showed a significant reduction in symptomatic VTE, and whereas RECORD1 showed a general trend for reduction in symptomatic VTE, this was not significant. RECORD4 compared rivaroxaban 10 mg o.d. with the common North American regimen of enoxaparin 30 mg b.i.d. (starting the evening before surgery) given for 10–14 days after TKR [75]. This study demonstrated the superior efficacy of rivaroxaban for the primary efficacy endpoint of total VTE, with a lower rate of major and symptomatic VTE compared with enoxaparin regimens. Across all four studies, the rate of major bleeding was similar for both rivaroxaban and enoxaparin regimens (Table 2). The incidence of cardiovascular events, including myocardial infarction, ischaemic stroke and cardiovascular death, was similar for both rivaroxaban and enoxaparin regimens. A comparison of VKAs, apixaban, dabigatran and rivaroxaban is shown in Table 1.
Discussion Due to an ageing population, the number of THR and TKR procedures is predicted to increase significantly worldwide. In Europe, the number of THR procedures is expected to
34
A.G.G. Turpie
Table 2 Incidence of venous thromboembolism and bleeding events across the RECORD1, 2 and 3 studiesa [72–74] Endpoint
RECORD1 (THR) Enoxaparin 40 mg o.d.
Rivaroxaban 10 mg o.d. 5 weeks
RECORD2 (THR) Enoxaparin 40 mg o.d.
Rivaroxaban 10 mg o.d.
10–14 days
5 weeks
9.3 (81/869)
2.0 (17/864)
RECORD3 (TKR) Enoxaparin 40 mg o.d.
Rivaroxaban 10 mg o.d.
10–14 days
Efficacy endpoints Total VTE, % (n/N) (primary endpoint) RRR Major VTE, % (n/N) RRR Symptomatic VTE, % (n/N) RRR
3.7 (58/1,558) 70% p < 0.001b 2.0 (33/1,678) 88% p < 0.001b 0.5 (11/2,206)
1.1 (18/1,595)
0.2 (4/1,686)
0.3 (6/2,193)
45% p = 0.22b
79% p < 0.0001b 5.1 (49/962) 88% p < 0.0001b 1.2 (15/1,207)
0.6 (6/961)
0.2 (3/1,212)
80% p = 0.0040b
18.9 (166/878) 9.6 (79/824) 49% p < 0.001b 2.6 (24/925) 62% p = 0.01b 2.0 (24/1,217)
1.0 (9/908)
0.7 (8/1,201)
66% p = 0.005b
Bleeding endpoints Major bleeding, % (n/N) Clinically relevant non-major bleeding, % (n/N)
0.1 (2/2,224)
0.3 (6/2,209)
<0.1 (1/1,229)
<0.1 (1/1,228)
0.5 (6/1,239)
0.6 (7/1,220)
2.4 (54/2,224)
2.9 (65/2,209)
2.7 (33/1,229)
3.3 (40/1,228)
2.3 (28/1,239)
2.7 (33/1,220)
a
RECORD4 has been completed and is currently being prepared for publication All p-values for efficacy calculated from absolute risk reduction o.d. once daily; RRR relative risk reduction; THR total hip replacement; TKR total knee replacement; VTE venous thromboembolism b
increase by 20–50% over the next 20 years [76–78], and TKR procedures by approximately 30% [79]. In the United States, THR and TKR procedures are predicted to increase twofold and over fivefold, respectively, in the next 20 years [80, 81]. Because VTE is the most frequently occurring serious complication after these procedures, the burden of VTE is therefore predicted to increase considerably. New anticoagulants could help to address the limitations of the currently available agents, with the potential to reduce this burden. New oral anticoagulants have the potential to benefit patients, physicians and health-care systems. Their relatively easy mode of administration, compared with currently available therapies, could simplify thromboprophylaxis after hospital discharge. Recommended guidelines could therefore be more easily adhered to, which could potentially help prevent death from PE, reduce morbidity from acute events, prevent short-term recurrences of DVT and PE, and avoid the long-term consequences of VTE (i.e. the PTS). In addition, there is no need for routine coagulation
monitoring with these new anticoagulants, which should make the management of anticoagulation more convenient and cost-effective, and improve adherence to the recommended guidelines. Importantly, the new agents in development do not significantly increase the risk of bleeding compared with enoxaparin, a current standard of care. Of the new agents in development, the oral, direct FXa inhibitors show considerable promise for the prevention of VTE. Rivaroxaban has recently been approved in the EU and Canada for the prevention of VTE after elective TKR and THR. It has demonstrated superior efficacy and a similar safety profile to enoxaparin after both TKR and THR. Dabigatran has also been approved in the EU and Canada for the primary prevention of venous thromboembolic events after elective THA or TKA, and has shown similar efficacy and safety to the EU regimen of enoxaparin (40 mg o.d.) after both TKR and THR. As oral, once-daily agents, their use could potentially be more convenient for both physicians and patients than the currently available options.
Thromboprophylaxis After Major Orthopaedic Surgery: State of the Art Acknowledgement The author would like to acknowledge Elizabeth Ng, who provided editorial support with funding from Bayer Schering Pharma AG.
References 1. Cohen AT, Agnelli G, Anderson FA, Arcelus JI, Bergqvist D, Brecht JG, Greer IA, Heit JA, Hutchinson JL, Kakkar AK, Mottier D, Oger E, Samama MM, Spannagl M, VTE Impact Assessment Group in Europe (VITAE). Venous thromboembolism (VTE) in Europe. The number of VTE events and associated morbidity and mortality. Thromb Haemost 2007;98:756–64. 2. Oger E. Incidence of venous thromboembolism: A community-based study in Western France. EPI-GETBP Study Group. Groupe d’Etude de la Thrombose de Bretagne Occidentale. Thromb Haemost 2000;83:657–60. 3. Nordstrom M, Lindblad B, Bergqvist D, Kjellstrom T. A prospective study of the incidence of deep-vein thrombosis within a defined urban population. J Intern Med 1992;232: 155–60. 4. Silverstein MD, Heit JA, Mohr DN, Petterson TM, O’Fallon WM, Melton LJ III. Trends in the incidence of deep vein thrombosis and pulmonary embolism: A 25-year populationbased study. Arch Intern Med 1998;158:585–93. 5. Tsai AW, Cushman M, Rosamond WD, Heckbert SR, Polak JF, Folsom AR. Cardiovascular risk factors and venous thromboembolism incidence: The longitudinal investigation of thromboembolism etiology. Arch Intern Med 2002;162: 1182–9. 6. Jaffer AK. An overview of venous thromboembolism: Impact, risks, and issues in prophylaxis. Cleve Clin J Med 2008;75(Suppl 3):S3–6. 7. Hirsh J, Hoak J. Management of deep vein thrombosis and pulmonary embolism. A statement for healthcare professionals. Council on thrombosis (in consultation with the council on cardiovascular radiology), American Heart Association. Circulation 1996;93:2212–45. 8. Prandoni P, Villalta S, Bagatella P, Rossi L, Marchiori A, Piccioli A, Bernardi E, Girolami B, Simioni P, Girolami A. The clinical course of deep-vein thrombosis. Prospective longterm follow-up of 528 symptomatic patients. Haematologica 1997;82:423–8. 9. Siragusa S, Beltrametti C, Barone M, Piovella F. [Clinical course and incidence of post-thrombophlebitic syndrome after profound asymptomatic deep vein thrombosis. Results of a Transverse Epidemiologic Study]. Minerva Cardioangiol 1997;45:57–66. 10. Sandler DA, Martin JF. Autopsy proven pulmonary embolism in hospital patients: Are we detecting enough deep vein thrombosis? J R Soc Med 1989;82:203–5. 11. Stein PD, Henry JW. Prevalence of acute pulmonary embolism among patients in a general hospital and at autopsy. Chest 1995;108:978–81. 12. Kearon C, Kahn SR, Agnelli G, Goldhaber S, Raskob GE, Comerota AJ. Antithrombotic therapy for venous thromboem-
35 bolic disease: American college of chest physicians evidencebased clinical practice guidelines (8th Edition). Chest 2008; 133:S454–545. 13. Geerts WH, Bergqvist D, Pineo GF, Heit JA, Samama CM, Lassen MR, Colwell CW, American College of Chest Physicians. Prevention of venous thromboembolism: American college of chest physicians evidence-based clinical practice guidelines (8th Edition). Chest 2008;133:S381–453. 14. Yu HT, Dylan ML, Lin J, Dubois RW. Hospitals’ compliance with prophylaxis guidelines for venous thromboembolism. Am J Health Syst Pharm 2007;64:69–76. 15. Friedman RJ, Gallus AS, Cushner FD, Fitzgerald G, Anderson FA Jr. Physician compliance with guidelines for deep-vein thrombosis prevention in total hip and knee arthroplasty. Curr Med Res Opin 2008;24:87–97. 16. Warwick D, Friedman RJ, Agnelli G, Gil-Garay E, Johnson K, Fitzgerald G, Turibio FM. Insufficient duration of venous thromboembolism prophylaxis after total hip or knee replacement when compared with the time course of thromboembolic events: Findings from the global orthopaedic registry. J Bone Joint Surg Br 2007;89:799–807. 17. Devine EB, Hopefl AW, Wittkowsky AK. Adherence to guidelines for the management of excessive warfarin anticoagulation. J Thromb Thrombolysis 2008. 18. Tilleul P, LaFuma A, Colin X, Ozier Y. Estimated annual costs of prophylaxis and treatment of venous thromboembolic events associated with major orthopedic surgery in France. Clin Appl Thromb Hemost 2006;12:473–84. 19. Ollendorf DA, Vera-Llonch M, Oster G. Cost of venous thromboembolism following major orthopedic surgery in hospitalized patients. Am J Health Syst Pharm 2002;59:1750–4. 20. Edelsberg J, Ollendorf D, Oster G. Venous thromboembolism following major orthopedic surgery: Review of epidemiology and economics. Am J Health Syst Pharm 2001;58(Suppl 2): S4–13. 21. Oster G, Ollendorf DA, Vera-Llonch M, Hagiwara M, Berger A, Edelsberg J. Economic consequences of venous thromboembolism following major orthopedic surgery. Ann Pharmacother 2004;38:377–82. 22. White RH, Romano PS, Zhou H, Rodrigo J, Bargar W. Incidence and time course of thromboembolic outcomes following total hip or knee arthroplasty. Arch Intern Med 1998;158:1525–31. 23. Rosencher N, Vielpeau C, Emmerich J, Fagnani F, Samama CM. Venous thromboembolism and mortality after hip fracture surgery: The ESCORTE Study. J Thromb Haemost 2005;3: 2006–14. 24. Hitos K, Fletcher JP. Venous thromboembolism and fractured neck of femur. Thromb Haemost 2005;94:991–6. 25. Ansell J, Hirsh J, Hylek E, Jacobson A, Crowther M, Palareti G. Pharmacology and management of the vitamin K antagonists: American college of chest physicians evidence-based clniical practice guidelines (8th Edition). Chest 2008;133: S160–98. 26. Verhovsek M, Motlagh B, Crowther MA, Kennedy C, Dolovich L, Campbell G, Wang L, Papaioannou A. Quality of anticoagulation and use of warfarin-interacting medications in long-term care: A chart review. BMC Geriatr 2008;8:13.
36 27. Levi M. Self-management of anticoagulation. Expert Rev Cardiovasc Ther 2008;6:979–85. 28. Garwood CL, Dumo P, Baringhaus SN, Laban KM. Quality of anticoagulation care in patients discharged from a pharmacist-managed anticoagulation clinic after stabilization of warfarin therapy. Pharmacotherapy 2008;28:20–6. 29. Platt AB, Localio AR, Brensinger CM, Cruess DG, Christie JD, Gross R, Parker CS, Price M, Metlay JP, Cohen A, Newcomb CW, Strom BL, Laskin MS, Kimmel SE. Risk factors for nonadherence to warfarin: Results from the IN-RANGE Study. Pharmacoepidemiol Drug Saf 2008;17:853–60. 30. Hirsh J, Raschke R. Heparin and low-molecular-weight heparin: The seventh ACCP conference on antithrombotic and thrombolytic therapy. Chest 2004;126: S188–203. 31. Detournay B, Planes A, Vochelle N, Fagnani F. Cost effectiveness of a low-molecular-weight heparin in prolonged prophylaxis against deep vein thrombosis after total hip replacement. Pharmacoeconomics 1998;13:81–9. 32. Sarasin FP, Bounameaux H. Antithrombotic strategy after total hip replacement. A cost-effectiveness analysis comparing prolonged oral anticoagulants with screening for deep vein thrombosis. Arch Intern Med 1996;156:1661–8. 33. Sarasin FP, Bounameaux H. Out of hospital antithrombotic prophylaxis after total hip replacement: Low-molecularweight heparin, warfarin, aspirin or nothing? A cost-effectiveness analysis. Thromb Haemost 2002;87:586–92. 34. Glynn RJ, Ridker PM, Goldhaber SZ, Buring JE. Effect of low-dose aspirin on the occurrence of venous thromboembolism: A randomized trial. Ann Intern Med 2007;147: 525–33. 35. Collins R, Scrimgeour A, Yusuf S, Peto R. Reduction in fatal pulmonary embolism and venous thrombosis by perioperative administration of subcutaneous heparin. Overview of results of randomized trials in general, orthopedic, and urologic surgery. N Engl J Med 1988;318:1162–73. 36. Hovens MM, Snoep JD, Tamsma JT, Huisman MV. Aspirin in the prevention and treatment of venous thromboembolism. J Thromb Haemost 2006;4:1470–5. 37. American Academy of Orthopaedic Surgeons. American Academy of Orthopaedic Surgeons clinical guideline on prevention of symptomatic pulmonary embolism in patients undergoing total hip or knee arthroplasty, 2007. www.aaos. org/Research/guidelines/PE_guideline.pdf. 38. Blanchard J, Meuwly JY, Leyvraz PF, Miron MJ, Bounameaux H, Hoffmeyer P, Didier D, Schneider PA. Prevention of deepvein thrombosis after total knee replacement. Randomised comparison between a low-molecular-weight heparin (nadroparin) and mechanical prophylaxis with a foot-pump system. J Bone Joint Surg Br 1999;81:654–9. 39. Bauer KA, Eriksson BI, Lassen MR, Turpie AG. Fondaparinux compared with enoxaparin for the prevention of venous thromboembolism after elective major knee surgery. N Engl J Med 2001;345:1305–10. 40. Arixtra (fondaparinux sodium) – Prescribing Information, 2005. http://us.gsk.com/products/assets/us_arixtra.pdf (accessed 24/10/08). 41. Kubitza D, Becka M, Wensing G, Voith B, Zuehlsdorf M. Safety, pharmacodynamics, and pharmacokinetics of BAY
A.G.G. Turpie 59-7939 – an oral, direct factor Xa inhibitor – after multiple dosing in healthy male subjects. Eur J Clin Pharmacol 2005; 61:873–80. 42. Weinz C, Schwartz T, Pleiss U, Schmeer K, Kubitza D, Mueck W, Condol D, Atken H. Metabolism and distribution of [14C] BAY 59–7939 – an oral, direct factor Xa inhibitor – in rat, dog and human. Drug Metab Rev 2004;36(Suppl 1): Abstract 196. 43. Stangier J, Rathgen K, Stahle H, Gansser D, Roth W. The pharmacokinetics, pharmacodynamics and tolerability of dabigatran etexilate, a new oral direct thrombin inhibitor, in healthy male subjects. Br J Clin Pharmacol 2007;64:292–303. 44. Stangier J, Eriksson BI, Dahl OE, Ahnfelt L, Nehmiz G, Stahle H, Rathgen K, Svard R. Pharmacokinetic profile of the oral direct thrombin inhibitor dabigatran etexilate in healthy volunteers and patients undergoing total hip replacement. J Clin Pharmacol 2005;45:555–63. 45. Shantsila E, Lip GY. Apixaban, an oral, direct inhibitor of activated factor Xa. Curr Opin Investig Drugs 2008;9: 1020–33. 46. Raghavan N, Frost CE, Yu Z, He K, Zhang H, Humphreys WG, Pinto D, Chen S, Bonacorsi S, Wong PC, Zhang D. Apixaban metabolism and pharmacokinetics following oral administration to humans. Drug Metab Dispos 2009;37: 74–81. 47. Eikelboom JW, Weitz JI. A replacement for warfarin. The search continues. Circulation 2007;116:131–3. 48. Gross PL, Weitz JI. New anticoagulants for treatment of venous thromboembolism. Arterioscler Thromb Vasc Biol 2008;28:380–6. 49. Kubitza D, Becka M, Voith B, Zuehlsdorf M, Wensing G. Safety, pharmacodynamics, and pharmacokinetics of single doses of BAY 59–7939, an oral, direct factor Xa inhibitor. Clin Pharmacol Ther 2005;78:412–21. 50. Kubitza D, Becka M, Roth A, Mueck W. Dose-escalation study of the pharmacokinetics and pharmacodynamics of rivaroxaban in healthy elderly subjects. Curr Med Res Opin 2008;24:2757–65. 51. Stangier J. Clinical pharmacokinetics and pharmacodynamics of the oral direct thrombin inhibitor dabigatran etexilate. Clin Pharmacokinet 2008;47:285–95. 52. Eriksson BI, Dahl OE, Rosencher N, Kurth AA, van Dijk CN, Frostick SP, Prins MH, Hettiarachchi R, Hantel S, Schnee J, Buller HR. Dabigatran etexilate versus enoxaparin for prevention of venous thromboembolism after total hip replacement: A randomised, double-blind, non-inferiority trial. Lancet 2007;370:949–56. 53. Eriksson BI, Dahl OE, Rosencher N, Kurth AA, van Dijk CN, Frostick SP, Kalebo P, Christiansen AV, Hantel S, Hettiarachchi R, Schnee J, Buller HR, E-MODEL Study Group. Oral dabigatran etexilate vs. subcutaneous enoxaparin for the prevention of venous thromboembolism after total knee replacement: The RE-MODEL randomized trial. J Thromb Haemost 2007;5:2175–7. 54. Ginsberg JS, Vidson BL, Comp PC. The oral thrombin inhibitor dabigatran etexilate vs the North American enoxaparin regimen for the prevention of venous thromboembolism after knee arthroplasty surgery. J Arthroplasty 2009;24:1–9.
Thromboprophylaxis After Major Orthopaedic Surgery: State of the Art 55. Hockings PD, Adler G, Palmer M, Andreasson AC, Elg M. The oral direct thrombin inhibitor AZD0837 reduces thrombus formation in a rat model. J Thromb Haemost 2007;5(Suppl 2): Abstract P-S-697. 56. Pehrsson S, Elg M. The antithrombotic effect of AR-HO67637, the active form of the novel oral direct thrombin inhibitor AZDO837, in rat models of arterial and venous thrombosis. J Thromb Haemost 2007;5(Suppl 2):Abstract P-W-637. 57. Bauer KA. New anticoagulants: Anti IIa vs anti Xa − is one better? J Thromb Thrombolysis 2006;21:67–72. 58. Gold HK, Torres FW, Garabedian HD, Werner W, Jang IK, Khan A, Hagstrom JN, Yasuda T, Leinbach RC, Newell JB. Evidence for a rebound coagulation phenomenon after cessation of a 4-hour infusion of a specific thrombin inhibitor in patients with unstable angina pectoris. J Am Coll Cardiol 1993;21:1039–47. 59. Theroux P, Waters D, Lam J, Juneau M, McCans J. Reactivation of unstable angina after the discontinuation of heparin. N Engl J Med 1992;327:141–5. 60. Turpie AG. Oral, direct factor Xa inhibitors in development for the prevention and treatment of thromboembolic diseases. Arterioscler Thromb Vasc Biol 2007;27:1238–47. 61. Turpie AG, Gallus AS, Hoek JA. A synthetic pentasaccharide for the prevention of deep-vein thrombosis after total hip replacement. N Engl J Med 2001;344:619–25. 62. Eriksson BI, Turpie AG, Lassen MR, Prins MH, Agnelli G, Kalebo P, Gaillard ML, Meems L. A dose escalation study of YM150, an oral direct factor Xa inhibitor, in the prevention of venous thromboembolism in elective primary hip replacement surgery. J Thromb Haemost 2007;5:1660–5. 63. Abe K, Siu G, Edwards S, Lin PH, Zhu BY, Marzec U, Hanson S, Pak Y, Hollenbach S, Sinha U. Animal models of thrombosis help predict the human therapeutic concentration of PRT54021, a potent oral factor Xa inhibitor. Blood 2006;108:Abstract 901. 64. Turpie AG, Gent M, Bauer K, Davidson BL, Fisher WD, Huo M, Borow K. Evaluation of the factor Xa (FXa) inhibitor, PRT054021 (PRT021), against enoxaparin in a randomized trial for the prevention of venous thromboembolic events after total knee replacement (EXPERT). J Thromb Haemost 2007;5:Abstract P-T-652. 65. Furugohri T, Isobe K, Honda Y, Kamisato-Matsumoto C, Sugiyama N, Nagahara T, Morishima Y, Shibano T. DU-176b, a potent and orally active factor Xa inhibitor: In vitro and in vivo pharmacological profiles. J Thromb Haemost 2008;6: 1542–9. 66. Raskob G, Cohen A, Eriksson B, MacDonald, Puskas, Shi J, Verho, Weitz J. Randomized double-blind multi-dose trial of the oral factor-Xa inhibitor DU-176b versus LMW heparin (Dalteparin) for prevention of venous thromboembolism after total hip replacement. Eur Heart J 2008;29:609. 67. Furugohri T, Isobe K, Honda Y, Matsumoto C, Sugiyama N, Morishima Y, Shibano T. Pharmacological characterization, antithrombotic and bleeding effects of DU-176b, a novel, potent and orally active direct inhibitor of factor Xa: A wider safety margin of antithrombotic and bleeding effects compared to heparin, LMWH and warfarin. J Thromb Haemost 2005; 3(Suppl 1) P1110.
37 68. Morishima Y, Honda Y, Matsumoto C, Fukuda T, Isobe K, Kumada T, Shibano T. Recombinant factor VIIa reverses the prolonged bleeding time induced by a high dose of DU-176b, a novel direct factor Xa inhibitor, in rats. J Thromb Haemost 2005;3(Suppl 1) P0512. 69. Buller H, Deitchman D, Prins M, Segers A. Efficacy and safety of the oral direct factor Xa inhibitor apixaban for symptomatic deep-vein thrombosis. The Botticelli DVT Dose-Ranging Study. J Thromb Haemost 2008;6:1313–8. 70. Lassen MR, Davidson BL, Gallus A, Pineo G, Ansell J, Deitchman D. The efficacy and safety of apixaban, an oral, direct factor Xa inhibitor, as thromboprophylaxis in patients following total knee replacement. J Thromb Haemost 2007;5:2368–75. 71. Bristol-Myers Squibb and Pfizer. Bristol-Myers Squibb and Pfizer Provide Update on Apixaban Clinical Development Program, 2008. http://newsroom.bms.com/article_display. cfm?article_id = 5371. 72. Kakkar AK, Brenner B, Dahl OE, Eriksson BI, Mouret P, Muntz J, Soglian AG, Pap AF, Misselwitz F, Haas S. Extended duration rivaroxaban versus short-term enoxaparin for the prevention of venous thromboembolism after total hip arthroplasty: A double-blind, randomised controlled trial. Lancet 2008;372:31–9. 73. Eriksson BI, Borris LC, Friedman RJ, Haas S, Huisman MV, Kakkar AK, Bandel TJ, Beckmann H, Muehlhofer E, Misselwitz F, Geerts W. Rivaroxaban versus enoxaparin for thromboprophylaxis after hip arthroplasty. N Engl J Med 2008;358:2765–75. 74. Lassen MR, Ageno W, Borris LC, Lieberman JR, Rosencher N, Bandel TJ, Misselwitz F, Turpie AG. Rivaroxaban versus enoxaparin for thromboprophylaxis after total knee arthroplasty. N Engl J Med 2008;358:2776–86. 75. Turpie AGG, Bauer KA, Davidson BL, Gent M, Kwong LM, Lassen MR, Cushner FD, Lotke PA, Bandel TJ, Misselwitz F, Fisher WD. Comparison of rivaroxaban – an oral, direct factor Xa inhibitor – and subcutaneous enoxaparin for thromboprophylaxis after total knee replacement (RECORD4: A Phase III Study). European Federation of National Associations of Orthopaedics and Traumatology 2008 Annual Meeting, 29 May–1 June, 2008. Nice, France, Abstract F85. 76. Ostendorf M, Johnell O, Malchau H, Dhert WJ, Schrijvers AJ, Verbout AJ. The epidemiology of total hip replacement in the Netherlands and Sweden: Present status and future needs. Acta Orthop Scand 2002;73:282–6. 77. Birrell F, Johnell O, Silman A. Projecting the need for hip replacement over the next three decades: Influence of changing demography and threshold for surgery. Ann Rheum Dis 1999;58:569–72. 78. Pedersen AB, Johnsen SP, Overgaard S, Soballe K, Sorensen HT, Lucht U. Total hip arthroplasty in Denmark: Incidence of primary operations and revisions during 1996–2002 and estimated future demands. Acta Orthop 2005;76:182–9. 79. Robertsson O, Dunbar MJ, Knutson K, Lidgren L. Past incidence and future demand for knee arthroplasty in Sweden: A report from the Swedish knee arthroplasty register regarding the effect of past and future population changes on the
38 number of arthroplasties performed. Acta Orthop Scand 2000; 71:376–80. 80. Iorio R, Robb WJ, Healy WL, Berry DJ, Hozack WJ, Kyle RF, Lewallen DG, Trousdale RT, Jiranek WA, Stamos VP, Parsley BS. Orthopaedic surgeon workforce and volume assessment for total hip and knee replacement in the United
A.G.G. Turpie States: Preparing for an epidemic. J Bone Joint Surg Am 2008;90:1598–605. 81. Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J Bone Joint Surg Am 2007;89: 780–5.
DDH: Diagnosis and Treatment Strategies R. Graf
Introduction Congenital hip dysplasia (CDH) has been known since early times and its characteristics have already been described by Hippocrates. The efforts to establish the earliest possible diagnosis and adequate early-stage therapy as well as recommendations for their accomplishment are predominant throughout the history of Paediatrics and Orthopaedics. The consequences of an undiagnosed dislocated hip are horrendous for the babies. In spite of adequate therapy a late diagnosis usually leads to lasting damage and in many cases to severe pain and disability, including osteoarthritis. It has been estimated that 10% of inserted hip joint prostheses which are currently being implanted are for treatment of disorders of hip maturation [1] including hip dislocation and hip dysplasia. Although clinical instability examinations according to Ortolani [2] have been introduced and are widely used in practice, it was established at a crucial symposium in Vienna in 1971 that 47% of completely dislocated hip joints were only diagnosed at the end of the first year of age [3]. At that time the authors expressed with resignation: “this development hardly leaves hope that under the given circumstances diagnosis and therapy of hip dysplasia can be mastered to some extent”. Only since the introduction of hip sonography and its increasing standardisation [1, 4] has the situation decisively improved, due to its excellent transparency and expressiveness in respect of pathological divergencies of the infant hip joint in comparison with clinical and x-ray examinations. The recommendation for using ultrasound as a screening method for early diagnosis of pathological hip joints has
R. Graf Allgemeines u. Orthopädisches Landeskrankenhaus, 8852 Stolzalpe, Austria e-mail:
[email protected]
received much support in Central-Europe [5–9] On the other hand Anglo-American authors are less impressed with sonographic screening [10]. They approve of it only if there is a clear indication due to a suspect history or suspect clinical signs and symptoms [11–13]. For countries with an excellent functioning social health scheme which have a high incidence of hip dysplasia and dislocation, the introduction of ultrasonic screening is only a supplement or a substitute for already existing means of screening [1]. On the other hand in countries where the means are not available, the introduction of sonographic hip screening presents a considerable organisational and financial burden. Thus sonographic hip screening must give way to other medical priorities. On the other hand the value and outcome of hip sonography is discussed controversially in Europe and USA. The technique developed in early 1980 [1] classifies the bony and cartilaginous roof according the age of the baby and quantifies also instability. The technique is independent of the experience and skill of the examiner. The USA-technique [14] employs the dynamic technique visualizing instability without quantification and has no standard plane for quantification of the bony and cartilaginous roof.
Method For the examination a special holding device for the baby and a probe guide system is mandatory. The probe guide system avoids tilting effects which may lead to wrong diagnosis (Fig. 1). The examination is done tomogram-like. In order to be reproducible always the same sonographic section through the hip joint must be used. To define a plane one requires three points in space to be defined. For ultrasound purposes the lower limb of the os ilium is the centre of the acetabulum and must always be seen except in
G. Bentley (ed.), European Instructional Lectures. European Instructional Course Lectures 9, DOI: 10.1007/978-3-642-00966-2_5, © 2009 EFORT
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R. Graf
Fig. 1 Correct scanning technique with cradle and probe-guiding system (sonoguide)
a
b
c
Fig. 2 (a) Checking the landmarks. (1) Lower limb of the os ilium, (2) Standard sectional plane, (3) Acetabular labrum. (b) The standard plane, see Fig. 2a. (c) Image with posterior-tilting error, compared with the correct image in (a)
de-centred hip joints. The posterior part of the bony acetabulum roof is better developed than middle or anterior parts. For sonography the middle portion of the acetabular roof is essential. To avoid tilting effects the labrum as the third landmark is essential. The standard plane is defined through (Fig. 2a): 1. The lower limb of the os ilium 2. The middle of bony acetabular roof 3. The acetabular labrum
“Static” or “Dynamic”? Hip sonography is always a dynamic examination (tomogram!) To make it reproducible a standard plane is necessary. Additional a stress test can be performed (“dynamic examination”). The stress test is performed by pushing the leg and observing the movement or dislocation of the femoral head.
Problems and Questions The hip joint must only be evaluated and measured in the standard plane (Fig. 2b). Incorrect Sonograms with wrong planes or tilted sonograms must not be accepted (Fig. 2c).
1. How much movement is the femoral head allowed within the joint when the femur is put under pressure?
DDH: Diagnosis and Treatment Strategies
2. When does the degree of movement exceed the line of tolerance and become harmful to the hip joint? In principle it is necessary to differentiate between normal, physiological movement (elasticity, “elastic whipping”) and true pathological instability. By quantification of the bony and the hyaline cartilaginous pre-formed acetabular roof with and without stress and measuring the dislocation and deformation of the hyaline cartilage under stress harmless “elastic whipping” can be separated from real pathological instability which needs immediate treatment and has no chance for spontaneous recovery.
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published in the world literature. Also pelvic osteotomy and acetabuloplasty had been reduced dramatically (Table 2).
Costs of Treatment Regarding total costs including it’s many aspects a tendency to cost reduction can be ascertained (Table 3). The decrease of surgical interventions (and ensuing hospitalisation), through the reduction by half of conventional cases, has produced an overall lowering of costs. Comparing costs of screening and therapy in relation to costs of treatment in the pre-sonographic era a reduction of 1/3 of
Results
Table 1 Decrease of open reduction to 0.13/1000 in 2004 Black columns: Unscreened in foreign country-born babies
Screening Results of Hip Sonography in Babies from Austria
Results Late Cases (Open Reduction per 1000 @ ICD 9 754.3 / ICD 10 Q65.0-8) 0.35 0.3 0.25 0.2 0.15 0.1 0.05 0
foreign born
0,13
2004 2003 2002 2001 2000 1999 1998 1997 1996 1995 1994 1993 1992 1991
Table 2 Decrease of surgical interventions from 1991 to 2004 (pelvic osteotomies, acetabuloplasty)
Results Surgical procedures@ Diagnosis ICD-9 754.3 / ICD-10 Q65.0-8 per 1000 (in first two years of life) 4 3.5 3
Pelvic Osteotomy Acetabuloplasty
2.5 2 1.5 1 0.5
2004
2003
2002
2001
2000
1999
1998
1997
1996
1995
1994
1993
1992
0
1991
Nationwide results are available from Austria which introduced screening in 1991 and from Germany which introduced screening in 1996. Screening is also performed in Poland and the Czech-Republic. In a report of 1997 by Grill and Muller [15] the main statistics were published a year after the introduction of hip screening in Austria. In 1985, in the pre-sonographic era, the proportion of infants treated with conventional methods was still 13.6%. In 1992 the rate was only 6.57%. Thus the preliminary concern that hip screening could lead to excess therapy was clearly discredited. This rate of therapy however is 2% higher than the average quota of dysplasia of 4.69% in large Central European studies [15]. The explanation for this seemingly discrepancy lies in the fact that the dysplasia rate of 4.69% applied only to infants diagnosed by means of X-ray and clinical evaluation, whereas “silent” cases of dysplasia diagnosed exclusively by sonographic screening remained primarily undiscovered. They become suspect only in adolescence and are then submitted to surgical intervention (acetabuloplasty, osteotomies etc.). Sonoscreening of the hip also diagnoses “silent” dysplasias – thus the initially higher treatment rate. Consequently, however as experience shows, surgical intervention in adolescence has been considerably reduced. Even more impressive is the number of surgical interventions in hips of infants, which were effectively reduced to 0.24/1,000 live births. The last evaluation in Austria in 2006 [12] confirmed the trend: in 2004 only 0.13/1,000 needed an open reduction (Table 1). This is the lowest number, that has ever been
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R. Graf
Table 3 Treatment costs of DDH/1000 for newborns in Austria. Dramatic decrease of costs till 2004 Austrian treatment costs for DDH per 1000 newborns in € beyond age of two remains incalculable ! 25.000 20.000 15.000 10.000 5.000 0 1991
1998
2004
total costs [12, 15] can be expected. Not included are the follow up costs for coxarthrosis of the hip with sick leave, convalescent homes, early retirement pay, etc.
Screening Results from Germany In Germany the proof of the efficiency of general sonographic screening of the hip is published [16] (Hufeland Award 2004). During the period 1997–2002 using registration forms and questionaires all hospitalised children needing treatment, were assessed. 66% having primary surgical intervention underwent a closed and 11% an open reduction. 23% underwent also an osteotomy of the pelvis or femur. Therefore the incidence of “first surgical intervention” is 0.26/1,000 live births for the 1997 age-group. During the period of assessment the number of registered children with “primary surgical intervention”, decreased yearly by 31%. The allocated percentage of operations did not alter. Through the ultrasonic hip screening in Germany the rate of surgical interventions was reduced to 1/3 in comparison to the pre-screeening era [16]. Eighty one percnet of the children needing surgery who were examined on time, presented a pathological diagnosis at the first ultrasonic screening. However 19% were classified as “without pathological findings”. If at the latest by the 6th week examination, the children did not undergo ultrasonic hip screening but at a later date, the diagnosis of hip dysplasia was confirmed on an average with a delay of 167 days: without screening there was an average of 276 days. If children were mis-diagnosed with no pathological findings the correct diagnosis became apparent after 277 days. The fact of the matter is that the final diagnosis by sonographic mis-diagnosis was established just as late as by those children who never underwent hip screening.
This emphasises the demand for hip sonography also at the “final examination”. In the case of a faulty diagnosis the patient returns only when the damages are irreparable.
Preliminary Résumé The exceptional value of hip sonography in comparison with clinical or X-ray examination is evident. The rate of hospitalisation, the days spent in hospital and the incidence of surgical intervention has been considerably reduced. The tendency to cost reduction is apparent. Infants “at-risk” or showing suspect clinical findings should be examined immediately post-partum. The routine screening should occur in the fourth up to the beginning of the sixth week of age. Delayed ultrasonic examinations lead to an increase of open reductions and osteotomies. Screening results are significant in many aspects: The results of the Austrian and German screening are almost identical [12, 16]. The main concern is that the results are nationwide and not the achievement of individual groups [11, 14, 17]. Thus the results are of considerable importance for health scheme policies. The hip sonography was carried out by Orthopaedists, Paediatricians and Radiologists with different professional aptitudes. The quality standard therefore can not be matched with that of hip sonography experts.
Treatment Strategies The quality of results is indicated by the in-patient treatments e.g. the frequency of surgical open or closed reductions, osteotomy of the acetabulum or the proximal femur. The problem is summarized in a single formula: Final result = Diagnosis + therapy Hip sonography is only responsible for the diagnosis but not for treatment. It is simply alarming, if 47% of the examined children are later in life in need of surgery in spite of adequate diagnostic and initiated therapy [16]. Apart from a few exceptions current therapeutic procedures were not challenged. According to our experience it would be of paramount importance to adapt and improve historic standards of treatment which are basically correct. Uncritical splinting which is not adapted to the pathoanatomical situation of the hip joint as classified by sonogram, must often end in disaster i.e. the need for surgery even when early diagnosed.
DDH: Diagnosis and Treatment Strategies
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show that besides historical tradition, the surgeon is willing to take risks at the patient’s expense but little readiness to use the reliable consistent course of treatment. The most critical phase during treatment is the phase of retention. Independent of co-operative parents the foolproof retention by means of a cast in the squatting position; (not to be confounded with the old Lorenz-cast) is preferably the method to be applied in place of all other appliances (Fig. 3).
Conclusion and Recommendation Fig. 3 Modern cast in “human position” in the step of retention: flexion about 100°, abduction 50°
Hip sonography depicts a quasi virtual antibiogramme guiding to the most effective and cheapest antibiotic with the least side-effects for the given situation. Each sonographic type can be assigned to a specific phase of treatment correlated with a specific procedure effective in the given pathoanatomical situation [1] (Table 4). Missing the best time for diagnosis and treatment (up to the beginning of the 6th week of life) is just as disastrous as the wrong choice of treatment. Acetabular dysplasia needing maturation does not need extension. A de-centric hip, primarily needing reduction, cannot be treated with a splint or simple abduction device. Remarks like “it also works” “or it was done so always”
Hip- screening is highly efficient. The method of performing hip ultrasound must be standardized to make it reproducible and reliable. The technique is independent of the examiner’s experience and skill. Quantification of the bony and cartilaginous roof according the age of the baby is mandatory. Timing and method of screening presently illustrate the best possible compromise between organisation, feasibility and cost efficiency. Hip sonography is a final examination. Sonographic evaluation of the hip must be attained by proper teaching. Autodidacticism is disastrous. Courses meanwhile are offered by qualified teachers in many countries. Bed-side teaching must be rejected since it promotes habitual faults being passed on. The continuous advancement of hip sonography necessitates extra tuition of instructors. Criteria concerning quality and controls of quality are well established.
Table 4 Therapeutic consequences: standardized system according the biomechanical situation (=types) Phase
Hip type
Therapy
Alternative
Phase of preparation
III and IV
Phase of reduction
D, III and IV
Overhead extension; medical gymnastics; if necessary tenotomy of adductors Manual reduction
Phase of retention
II c unstable (exception: newborn), reducted D, III and IV
Necessary in cases of limited movement or shortening of adductor muscles Reduction orthosis Dynamic hip examina(for example according tion monitored by to Pavlik, Hanausek, …) ultrasound can show whether normal reduction is possible or phase of preparation is necessary Retention orthosis (for Compliance of the example according to parents? Pavlik or Fettweisorthosis, …)
Phase of maturity
II a (-), II b and II c stable
Modified plaster cast according to Fettweis in human position; newborns for 2 weeks, others for 4 weeks Abduction device according to Mittelmeier-Graf (size 1–3)
Maturity orthosis (abduction device for example according to Pavlik, Bernau)
Annotation
Compliance of the parents? Sonographic follow up till type I
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Quality controls in medicine have become commonplace and should not precipitate reservations. Correct technical equipment, an adequate ultra-sound machine, fixation device and sonoguide to avoid tilting effects, which lead to mis-diagnosis, are mandatory. Historically unsystematic, splinting-abduction devices have to be re-considered. Changing to well- established classifications of therapeutic intervention is essential if the benefits of earliest diagnoses are not to be lost through inadequate therapy.
Acknowledgments Figure 1–2 are taken from [1]. We thank also Prof. F. Grill Vienna Speising for Table 1–3 [12].
References 1. Graf R. Hip Sonography. Diagnosis and Management of Infant Hip Dysplasia. Springer, Heidelberg. 2006 2. Ortolani M. Un segno poco noto e sua importanza per la diagnosis precoce de prelussazione congenita dell’anca. Pediatric 1937; 45: 129–36 3. Meznik F, Slancar P. Ursachen für den verspäteten Behandlungsbeginn bei angeborenen Hüftdysplasien. Österr Ärztezeitung 1971; 26/4: 356–58 4. Graf R. Sonographie der Säuglingshüfte und therapeutische Konsequenzen. Thieme, Stuttgart. 2000 5. Exner GU. Ultrasound screening for hip dysplasie in neonates. J Pediatr Orthop 1988; 8: 656–60 6. Ganger R, Grill F, Leodolter S. Ultrasound screening of the hip in newborns: results and experience. J Pediatr Orthop 1990; 1: 45–9
R. Graf 7. Joller R, Waespe B. Sonographie der Säuglingshüfte – erste Ergebnisse eines Screeningprogramms im Kanton Uri. In: Schilt M (Hrsg.), Angeborene Hüftdysplasie und –Luxation vom Neugeborenen zum Erwachsenen. SGUMB-SVUPPEigenverlag, Zürich. 1993, pp. 163–9 8. Katthagen BD, Mittelmeier H, Becker D. Häufigkeit und stationärer Behandlungsbeginn kindlicher Hüftgelenksluxationen in der Bundesrepublik Deutschland. U Orthop 1988; 126: 475–83 9. Wirth T, Hinrichs F, Stratmann L. Verlaufsbeobachtungen der Inzidenz der Hüftdysplasie nach 14-jähriger Anwendung eines sonographischen Neugeborenenscreenings. In: Reichel H und Krauspe R (Hrsg.), Langzeitergebnisse in der Kinderorthopädie, Steinkopff Darmstadt. 2003, pp. S111–22 10. Caterall A. The early diagnosis of congenital dislocation of the hip. J Bone Joint Surg B 1994; 76-B: 515–6 11. Castelein RM, Sauter AJM. Ultrasound screening for congenital dysplasiea of the hip in newborns its value. J Pediatr Orthop 1988; 8: 666–70 12. Grill F, Müller D, Hübl M, Hexel M. Presentation at training course for pediatric orthopedic surgeons, Speising orthopedic hospital Vienna 2006; June, 30th 13. Lewis K, Jones DA, Powel N. Ultrasound and neonatal hip screening: the five-year results of a prospective study in high risk babies. J Pediatr Orthop 1999; 19(6): 760–2 14. Harke HT. Screening newborns for developmental dysplasia of the hip: the role of sonography. Am J Roentgenol 1994; 162: 399–400 15. Grill F, Müller D. Ergebnisse des Hüftultraschallscreenings in Österreich. Orthopadie 1997; 26: 25–32 16. Kries v R, Ihme N, Oberle D, Lorani A, Stark R, Altenhofen L, Niethard FU. Universal ultrasound screening programme for developmental dysplasia of the hip in Germany: impact on the rate of first operative procedures. Lancet 2003; 362: 1883–7 17. Holen KH, Tegnaander A, Bredland T, Johansen OJ, Saether OD, Eik-Nes SH, Terjesen T. Universal or selective screening of the neonatal hip using ultrasound. A prospective, randomised trial of 15529 newborn infants. J Bone Joint Surg Br 2002; 84-B: 886–90
Slipped Capital Femoral Epiphysis C. Zilkens, M. Jäger, Y-J. Kim, M.B. Millis, and R. Krauspe
Introduction Most osteoarthritis (OA) of the young adult hip is secondary to paediatric or developmental hip disorders. Besides Developmental Dysplasia of the hip and Perthes disease, slipped capital femoral epiphysis (SCFE), the displacement of the epiphysis from the metaphysis, is amongst the most common disorders of the young and adolescent hip. There is a correlation between the severity of slippage and the longterm outcome in affected patients with less favourable outcome for the more severe slips [1–3]. The aetiology of SCFE is complex and multi-factorial. Affected patients are generally between the ages of 11 and 15 years. There is evidence that the mean age of onset has decreased during the last part of the twentieth century, possibly because of a decrease in the age of puberty. Boys are affected almost twice as often as girls and at a later age and approximately in the same pubertal period. The incidence is reported to be about 4–5 per 1,00,000 for all patients in pre-puberty and puberty with a significant variation among different populations. There is a higher incidence in groups with higher mean body-weight with the left hip slightly more often affected than the right [4]. A possible hereditary factor in the etiology of SCFE remains controversial [5–7]. Several endocrine, systemic and immunological factors lead to an alteration of the cellular components and matrix at the growth-plate resulting in physeal biomechanical instability of the femoral head [8–10]. In addition to obesity, there are other mechanical factors that may to contribute to the development of SCFE: the angle of the epiphysis during puberty has an oblique
R. Krauspe (*) Department of Orthopaedic Surgery, University Hospital of Düsseldorf, Moorenstrasse 5, 40225 Düsseldorf, Germany e-mail:
[email protected]
plane which leads to higher shear forces at the epiphysealmetaphyseal junction. These shear forces can be further increased by a reduced anteversion of the femoral neck [11], a decreased neck-shaft angle and a deep acetabulum [12, 13].
Classification Clinically, SCFE is classified according to the duration of symptoms (acute, acute-on-chronic, chronic), the ability to bear weight (stable, unstable) and radio-morphologically according to the severity of the slip (Table 1). The distinction between mechanically stable and unstable slips is most important, since the risk of osteonecrosis is much higher in the unstable group. Acute slips are those with sudden onset of severe symptoms which prevent walking or bearing weight on the affected leg. Radiographs show variable epiphyseal displacement with no evidence of bone healing or remodelling. Chronic slips are characterized by a gradual or intermittent onset and symptoms of more than 3 weeks duration. Radiographs show some bone healing and remodelling of the femoral neck. The acute-on-chronic slip is defined as having a sudden onset of severe symptoms with radiographic signs of remodelling of the proximal femur and, if reducible, only the degree of the acute slip can be reduced by gentle closed manipulation. Our own data suggest that the chronic form is found in about 75% of cases, the acute slip in about 10% and the acute-on-chronic slip is observed in nearly 15% [14]. Loder et al. [15] proposed a classification of stable and unstable SCFE by clinical parameters, mainly the ability to bear weight. If the femoral physis is grossly unstable or if the patient is unable to weight-bear then this is considered an unstable SCFE, which is associated with a high rate of avascular necrosis (AVN). Currently, this is the preferred method of clinically classifying SCFE.
G. Bentley (ed.), European Instructional Lectures. European Instructional Course Lectures 9, DOI: 10.1007/978-3-642-00966-2_6, © 2009 EFORT
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48 Table 1 Classifications of SC FE
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Temporal
Acute Acute-on-chronic Chronic Clinical Stable Unstable Radio-morphological Mild (grade I) Moderate (grade II) Severe (grade III)
Radiologically, a slip of less than 30° is considered to be grade I, between 30 and 60° grade II and of more than 60° grade III [16]. Some authors prefer to differentiate between grade II and III at an angle of 50° [17]. The severity of the condition may also be determined by measuring the percentage of the slip in relation to the width of the femoral neck [18]. There are inter- and intra-observer errors as well as differences in measured angles because the radiographic technique and projection which are significantly dependent on the positioning of the leg.
Clinical Signs and Symptoms The most frequently presenting complaint is groin, thigh or knee pain associated with a limp. The pain associated with stable SCFE may be due to any or all of the following: (a) Intracapsular hematoma, (b) Effusion, (c) Ischemia “compartment syndrome of the bone”, (d) Synovitis and muscular imbalance depending on the pathological biomechanics. Although most SCFE patients have groin pain, symptoms may also be referred to the
Symptoms <3 weeks, abrupt displacement Initially chronic afterwards acute symptoms Symptoms >3 weeks, pain exacerbation and remission Able to walk, no effusion, metaphyseal remodeling Unable walk, effusion, no metaphyseal remodeling 0–30° of slip 30–50° (60°) of slip More than 50° (60°) of slip
knee, and either isolated knee pain or a painless limp may be the only presenting symptom. Green et al. report a 2½ month delay and a 52% incidence of apparent missed diagnosis for SCFE in a review of 102 patients [19]. Pain is usually intermittent and gradual in onset. Some patients describe episodes of trauma in the recent past. Physical examination most often reveals mild pain on movement with limited internal rotation and abduction. Flexion of the hip usually results in obligatory external rotation of the hip because of anterior metaphyseal impingement on the acetabular rim. This phenonmenon is referred to as Drehmann’s sign (Fig. 1). In severe slips the flexion may be limited to 60° or less because of impingement caused by the anterior prominence of the femoral neck. The incidence of bilateral SCFE has been reported as 79% by Hägglund et al. [5] and as 59% by Jerre [20] at follow-up. Both groups, however, found bilateral SCFE at the time of the first clinical presentation in only 23% and 8–27%, respectively. These data underline the importance of frequent follow-up examination of the contralateral hip or simultaneous prophylactic treatment of the unaffected hip.
Fig. 1 Drehmann’s sign: while the non-affected hip can be flexed normally (a), flexion of the affected hip (b, c) results in obligatory external rotation because of anterior metaphyseal impingement on the acetabular rim
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Radiological Appearances Antero-posterior and lateral radiographs of BOTH hips on the same film are the primary (and, most of the time, the only) imaging modality needed to diagnose and to initially evaluate the disease. On the antero-posterior film the physis may be widened with indistinct margins; the epiphysis may appear rather normal even if there is considerable displacement posteriorly and inferiorly. The classic deformity of variable posterior displacement and tilt of the epiphysis is much more easily seen in the lateral view (Fig. 2). In long-standing slips a rim of new bone may be found at the posterior aspect of the neck adjacent to the femoral head. In addition, the femoral neck becomes uncovered anteriorly, producing the characteristic prominence of its superior and anterior aspects. An epiphysis that doesn’t intersect Klein’s line [21] is suspicious of being slipped (Figs. 2 and 6). A true lateral view can help to determine the extent of posterior displacement of the epiphysis and a frog-leg lateral view detects minor slips. The radiographic technique described by Imhäuser [22] allows for diagnosis, measurement and classification in a reproducible manner. We therefore prefer to perform a standard antero-posterior radiograph of the pelvis and a lateral projection using this method which is performed with the hip in 90° of flexion
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and as much abduction as the measured result of the projected caput-collum-diaphysis angle −90°. CT scans have been used for pre-operative planning and for the post-operative assessment of a possible hardware penetration into the joint [23]. MRI-findings in SCFE are well described [24–26] and have been used in patients with normal X-rays for the detection of a “pre-slip” [27, 28] and as a tool for decisionmaking and prognosis [29, 30].
Treatment Early diagnosis and surgical treatment are widely recommended [8, 20, 31]. The aim is to stabilize the epiphysis, to prevent further slipping and to avoid complications. Since, all other factors being equal, the best results are obtained in stable mild slips it is clear that diagnosis and treatment should be established as early as possible to prevent a progression to either more severe deformity or to an unstable slip. Details of treatment are shown in Table 2.
Treatment of Acute SCFE Unstable SCFE is one of the few non-traumatic emergencies in Children’s Orthopaedics since the blood supply of the epiphysis is in danger. There is some controversy on the timing of reduction (emergent, urgent or elective) [32, 33] of the unstable slip, though most authors suggest reduction as soon as is practical. The surgical approach for reduction, the amount of reduction (partial or complete), the role of decompression of the joint (puncture or open decompression) and the method of fixation (single or double screw, K-wires) also remains controversial.
Treatment of Chronic SCFE Treatment options for stable SCFE include in-situ-fixation, neck osteochondroplasty, and different corrective osteotomies. Bone graft epiphyseodesis and cast immobilization are historical methods now rarely employed. Fig. 2 On the antero-posterior film (a) the physis may be widened but the epiphysis does not seem grossly displaced but does not intersect Klein’s line. The displacement is easily seen on Lateral views (b). The importance of obtaining lateral X-rays for the evaluation of SCFE cannot be overemphasized
Treatment of Acute-on-Chronic SCFE The acute-on-chronic slip is defined as having a sudden onset of severe symptoms, but radiographs show signs of
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Table 2 Treatment of SCFE Acute SCFE/unstable SCFE Acute on chronic/unstable SCFE Chronic SCFE/stable SCFE Degree of slip <30°, grade I Degree of slip 30–60°, grade II Degree of slip >60°, grade III
Reduction and fixation with pins (K-wires), screws Reduction of the acute part and fixation with pins or screws. If indicated one- or two-stage surgery with deformity correction osteotomy, Ganz-procedure Fixation with pins (K-wires) or screws and in functionally impaired patients (moderate/ severe slips), Imhäuser-Osteotomy or Ganz-procedure Fixation in situ with pins (K-wires), screws Fixation in situ with pins (K-wires) or screws, if indicated (functionally impaired patients) osteotomy Imhäuser-Osteotomy or Ganz-procedure Fixation with pins (K-wires) and Imhäuser-Osteotomy or Ganz-procedure
remodelling of the proximal femur, If reducible only the degree of the acute slip can be reduced by gentle closed re-positioning. However, it may be difficult to determine the degree of the acute slip and therefore how much reduction is safe. The remaining deformity defines the need for further corrective procedures. For decision-making on the optimal treatment option and consideration of risks and benefits, the following algorithm may be helpful:
Treatment of Unstable, Mild SCFE With a low risk of AVN and a low long-term risk of OA, in-situ-pinning is indicated. If cam impingement seems present after stabilization of the unstable physis, then procedures to eliminate the impingement should be considered.
Treatment of Unstable, Moderate to Severe SCFE With a high risk of AVN and a high risk of OA the treatment options are in-situ-pinning without reduction, in-situpinning after gentle closed reduction and/or some sort of (sub-) capital reduction procedure.
Stable, Mild SCFE As in unstable, mild SCFE, with a low risk of AVN and a low long-term risk of OA, in-situ-pinning is indicated.Again, femoro-acetabular impingement has to be diagnosed and treated as soon as possible to prevent further joint damage [34].
Stable, Moderate to Severe SCFE The associated risk of AVN is low while the risk of developing OA is higher. After in-situ-pinning, only symptomatic patients should be treated: early safe reconstruction
(Imhäuser, Southwick), leaving some anatomic deformity or early Ganz procedure with most anatomic reconstruction but a higher risk of AVN is indicated. In patients with mild symptoms due to femoro-acetabular impingement, corrective surgery must be done skillfully and without complications.
Prophylactic Treatment The indications for prophylactic treatment of the undisplaced contra-lateral side are controversial. The risk of developing a slip of the contra-lateral hip is reported to be 2–3 times higher than the risk of an initial SCFE [35]. In Central Europe prophylactic fixation of the contralateral hip is the standard while in the USA, perhaps partly for medico-legal reasons, surgery of a “healthy” hip is more controversial and not commonly done [14, 35–37]. In our series published by Seller et al. [14] no major complications occurred in hips pinned prophylactically in 109 patients treated with K-wires bilaterally at the first presentation.
In-Situ-Fixation There is remaining controversy regarding the best surgical procedure for in-situ-fixation which may involve percutaneous or open pinning and internal fixation of the epi- and metaphysis by nails, one or two screws or three or more pins/Kirschner- (K-) wires (Fig. 3). The stabilization of the epiphysis with a gliding screw has been advocated recently [38] and preliminary results are promising [39] since the procedure combines the advantages of K-wires and screws in terms of stability and the potential of growing. Figure 4 depicts the principle of the sliding screw with the threads lying only in the epiphysis while the unthreaded part of the screw bridges the physis. Each surgical technique has its advantages and disadvantages and the choice of treatment must be individualized
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Fig. 3 Pre- (a) and post-operative (b) anteroposterior x-rays of a 12-years old boy with mild stable SCFE of the left hip. Fixation of the epiphysis by K-wire pinning and prophylactic pinning of the contralateral hip
for each case and should be based at least to some degree on the experience of the surgeon with the method applied. Screws are appropriate to guarantee a stable fixation. However, based on their large diameter compared with pins and the thread, screws may damage the growth-plate and restrict further growth of the femoral head. In North America, the effect of screws in hastening physeal closure is usually viewed as advantageous. Titanium screws have the disadvantage of solid osteo-integration, are difficult to remove and may result in complications such as fractures [40, 41]. They are therefore not recommended for transphyseal stabilization. König et al. [42] reported that fixation with K-wires showed the best results in the short and long-term with the lowest complication rates, compared with stabilization by screws or Smith-Peterson nails. After fixation by K-wires significantly better long-term results were found with regard to pain and objective parameters such as the Harris
Hip Score, the development of OA, sphericity of the femoral head, differences in leg-length and the neck/shaft ratio of the proximal femur. Patients who needed a second or even a third operation because of relative shortening of the wires while the femoral neck grew further, were a mean of 11 years of age at the time of initial treatment, which was significantly lower compared with other series. We estimate that the advantages of fixation with K-wires are greater in these young patients despite the risk of further surgery because of the remaining growth of the proximal femur and the maintenance of the sphericity of the femoral head by this method of fixation. Careful placement and radiological intra-operative control are mandatory to detect any perforation of the joint and to place the wires or screws in a correct position (Fig. 5). De Sanctis et al. [43] favoured a single percutaneous screw and argued that fixation with pins has a higher rate of complications of 18% compared with other methods, but reported minor complications, such as superficial wound infection in the pin group and severe complications such as AVN or chondrolysis in the group treated with screws. In the case of severe slip, after a few days in traction, if partial reduction is achieved Hansen et al. [44] preferred bilateral pinning without further reduction.
Osteotomies
Fig. 4 Sliding screw (adapted from [38]) with the threads lying only in the epiphysis while the unthreaded part of the screw bridges the physis
Re-alignment osteotomies for moderate to severe slips have been described for subcapital, basi-cervical, intertrochanteric and subtrochanteric regions (Fig. 6) [16, 45–52]. While AVN is absent or rare in stable SCFE pinned in situ [2, 46, 53, 54], the risk of necrosis after re-alignment procedures has been described as being almost reciprocally proportional to the distance of the osteotomy from the physis [53, 55–58]. However, only osteotomies at the level of the deformity, i.e., on the subcapital level will allow for restoring an almost normal hip anatomy, theoretically minimizing the risk of OA [46, 47, 59–68].
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Fig. 5 Possible pin penetration of the femoral epiphysis which may be undetected due to the projection (a). Withdrawal-Manoeuvre: rotating the leg or changing the direction of the X-raybeam reveals the incorrect position of the K-wire (b)
The rationale of subcapital osteotomy is the reduction of the capital femoral epiphysis on the femoral neck, minimizing the tension on the vessels in the posterior periosteum, either by resecting a wedge of the superior femoral neck, by resecting any posterior callus, or both [62]. Fish described the removal of the physeal cartilage while the deformity is corrected, thus removing the natural barrier of blood supply from metaphysis to epiphysis, enhancing bone union and revascularization [64]. Among other authors, the recommended surgical approach, size and location of wedge resection and the type of hardware varies [47, 58–60, 69, 70]. There is also a wide variety in the amount of the reported onset of AVN after subcapital wedge osteotomy ranging from virtual absence to 100% [32, 46, 47, 50, 57, 58, 60–63, 66–68, 70–91]. Ganz combined the Dunn subcapital re-alignment osteotomy with the surgical dislocation approach [92]
1
2
3 4
Fig. 6 The levels of osteotomy for deformity correction: (1) subcapital: Dunn, Fish, Ganz; (2) femoral neck: Kramer, Barmada; (3) intertrochanteric: Imhäuser, Southwick; (4) Klein’s line: SCFE is suspected if the epiphysis does not intersect Klein’s
which allows the development of an extended retinacular soft tissue flap and offers an extensive subperiosteal exposure of the circumference of the femoral neck before reducing the slipped epiphysis anatomically [93, 94]. In the hands of the experienced surgeon, the “Ganz procedure” seems to be a safe procedure with promising shortand medium-term results and no reported AVN in 40 consecutive SCFE with open physes in two institutions (Fig. 7a–d) [95–97].
Complications Specific disease and treatment related complications of SCFE include chronic loss of range of movement, secondary degenerative OA, AVN of the femoral head, chondrolysis and surgery-related complications such as metal failure or migration, infections and fractures. The risk of AVN depends on the degree and the acuitness of slip and the treatment [98]. It is rare in untreated patients, especially in chronic SCFE and probably results from an interruption of the retrograde blood supply by the initial injury in acute cases. In treated patients, forceful repetitive manipulation, open reduction and/or osteotomy could be the major cause of AVN. The risk is higher with moderate or severe displacement than with mild slips. Overall, AVN has been reported in 20% of all cases of SCFE. With repetitive manipulation the risk increases up to 47% [15]. If AVN becomes evident salvage procedures like intertrochanteric valgus and flexion osteotomies may be indicated, rotating the area of AVN away from the main weight-bearing area and allowing for at least some remodeling of the affected area (Fig. 8). In some AVN-cases with total head involvement, an arthrodesis or early total joint arthroplasty may be required as a salvage procedure to keep the patient pain-free and mobile.
Slipped Capital Femoral Epiphysis
The curative and symptomatic efficiency of the prostaglandin analogue iloprost for bone marrow oedema and early AVN has been demonstrated recently [99] and might lead to its prophylactic application in hips at risk for AVN after SCFE. Maussen et al. [100] reported that in a long-term study only one of ten hips with a slip of less than 40° showed signs of OA, compared with 15 of 16 hips with a slip of more than 40°. All patients had been treated by an intertrochanteric osteotomy. The higher the degree of slip the higher is the risk of OA. Therefore they postulated that it is not the treatment which is the main factor for developing secondary OA but the degree of the initial slip. This again supports the requirement for early diagnosis and treatment of the condition. The most frequent cause of chondrolysis is penetration of the joint by the pins. The diagnosis of chondrolysis requires a joint space of less than 3 mm wide and a restricted range of movement of the hip. Treatment is bed rest, intensive physiotherapy, traction and control of pain. If a pin is left penetrating the joint it must be replaced immediately. The rate of success, however, with this type of treatment is not very high and if severe narrowing of the joint space persists with a limited range of movement and pain, salvage procedures such as arthrodesis or arthroplasty may be indicated.
After-Treatment After the operation of pinning-in-situ in chronic SCFE we recommend treatment by continuous passive motion and partial weight-bearing according to symptoms. Physiotherapy should aim to improve the range of movement of the hip and to build up the muscle strength and co-ordination in the leg. After wound healing we allow partial weight-bearing of 20 kg beginning in week three after operation. If the patient is free of pain and the range of movement is adequate full weight-bearing is allowed after 6 weeks. If there is any sign of pain or effusion in the joint, partial weight-bearing for another 6 weeks is recommended. Clinical and radiological follow-up is at 2, 6 and 12 weeks and 6 and 12 months after surgery. In acute SCFE we recommend bed-rest and no weightbearing pre-operatively and continuous passive motion immediately post-operatively. The patient is mobilized on crutches with non-weight-bearing for 14 days and 20 kg of partial weight-bearing for a total of 6–12 months after operation. The movement of the hip should be commensurate with the result of the reduction or the persistent angle of slip, and the patient should be free from pain when full weight-bearing is
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allowed. Any sign or symptom which may indicate AVN or chondrolysis should influence the regimen and we then recommend further partial weight-bearing using crutches until relief of symptoms, with or without further therapy or surgery. In patients who have had an intertrochanteric osteotomy as described by Imhäuser [101] we recommend bed-rest with continuous passive movement and physiotherapy for 2–3 days, followed by non-weight-bearing mobilization for 14 days. The patient is then mobilized on crutches for another 3 months of partial weight-bearing with 20 kg. Full weightbearing is allowed after healing of the osteotomy.
Prognosis The study of Hägglund et al. [5] showed that 25% of the initially unaffected and untreated hips developed secondary OA before the age of 50 years. No degenerative joint disease was found in contra-lateral hips, which were simultaneously stabilized prophylactically. In patients with untreated SCFE the reduced range of movement results in the contraction of the external rotators with a persistent Drehmann’s sign which is related to the degree of the slip. Secondary OA develops late, usually not before the fifth decade. In cases of severe slip the restriction of flexion can also lead to loss of function and secondary problems in the lumbar spine. In more than 80% of patients with a slip of less than 40° the results are good. If the degree of slip is more than 60° OA is likely to occur in more than 50% of the cases after 20 or 30 years. It remains uncertain whether or not and in what extent subclinical SCFE contributes to the development of early OA and whether or not “pre-arthrotic deformity”, “tilt deformity” or “pistol grip deformity” are due to SCFE or degenerative changes [83, 102–106]. In addition to the slip angle, the femoral head-neck junction morphology should be used as a criterion for reconstructive surgery and should be taken into account when planning a surgical procedure [107–109]. If an anterior femoro-acetabular impingement develops, surgical hip dislocation or arthroscopy for restoration of the femoral head-neck-offset might be necessary and should be performed before severe cartilage damage occurs [34, 92, 110]. In any cases of a necessary osteotomy it should be remembered that later in life an arthroplasty may become necessary. The risk-benefit-balance for high-neck cuneiform and lateral neck osteotomies indicates these procedures if the slip is moderate to severe with significant functional impairment.
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(a)
(b)
(c)
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(d)
Fig. 7 Ganz-procedure: Figures reprinted from [95] with permission. (a) Proximal femur after surgical dislocation and trochanterflip-osteotomy. The femoral physis is stabilized with two threaded K-wires before dislocation (A). TP trochanteric physis, TB trochanteric basis. The proximal third (R) of the trochanteric basis is removed to help free up the posterior periosteal flap (B). (b) Trochanteric basis is removed and the periosteum of the femoral neck exposed (A). Once the periosteal sleeve has been mobilized, the pins are removed and the epiphysis is gently lifted free of the femoral neck (N) (B, C). (c) Now, the neck is trimmed of the posterior callus, slightly shortended and thinned until the femoral epiphysis can easily be reduced (A, B, C). An antegrade threaded pin and then a retrograde threaded pin are inserted fixing the epiphysis anatomically on the neck. (d) Case report of a severe unstable SCFE (A) Documentation of absent perfusion of the epiphysis: arrow points at a drill hole in the epiphysis without bleeding after in-situ-fixation. (B) After freeing from femoral neck periosteum and reposition of the epiphysis, there was bleeding from the same drill hole. (C) Anatomic reposition of the femoral head
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Fig. 8 Development of AVN in a 12-year-old boy after operative treatment of an acute on chronic SCFE. (a) Postoperative X-ray after pinning in situ of the affected left side and prophylactic pinning of the contralateral side. (b) Development of AVN 8 months afterwards. (c) Imhäuser-Osteotomy as salvage procedure with valgus, flexion and rotation. (d) Seven years after osteotomy with favourable clinical and radiological outcome
The long-term results after the intertrochanteric osteotomy are favourable to satisfactory in more than 80% [111]. It is mandatory that consultation is held with the patient and his or her family as to the choice of their profession in life and the risks and benefits of the different types of treatment.
Summary SCFE is a common hip disorder in adolescence and should be diagnosed and treated surgically as soon as possible with transfixation of the epiphysis with K-wires, screws or gliding screws. Concerning the etiology, biomechanical, biochemical and hereditary factors are still under investigation. The typical patient is a tall, obese, pubertal boy of 12 years. The clinical presentation ranges from sudden disability of standing and walking to complete lack of symptoms. Pain in the knee without trauma in the pre-disposed patient always requires clinical examination of the knee and hip joint, usually with appropriate radiographs including a lateral view of the hip. The classification of SCFE can be
temporal (acute, acute-on- chronic, chronic) clinical (stable, unstable) and radio-morphological (mild <30°, moderate 30–50° or 60° and severe >50° or 60°). AVN and chondrolysis occur more often in operated than in non-operated patients. Medium and long-term sequelae of SCFE are loss of function and degenerative joint disease due to femoro-acetabular impingement or consequences from complications such as AVN and chondrolysis. For mild slips, long-term prognosis is significantly better than for moderate and severe slips. The contra-lateral side is affected in up to 60–80% of patients and is often treated prophylactically in Europe. After-treatment has to be regular until completion of growth since K-wires as well as screws will become relatively too short if the epiphysis grows away proximally. Recent developments like gliding screws are promising in this context. Higher grade unstable SCFE may benefit from a reduction while in chronic slips corrective osteotomies may be indicated. Traditional osteotomies such as Imhäuser or Southwick intertrochanteric osteotomies are safe but correct the deformity remote from the site of deformity. The
Slipped Capital Femoral Epiphysis
Ganz procedure with surgical dislocation and modified Dunn osteotomy allows for the development of an extended retinacular soft tissue flap and offers an extensive subperiosteal exposure of the circumference of the femoral neck before reducing the slipped epiphysis anatomically. This procedure seems to be safe with promising short- and medium-term results and no reported AVN in 40 consecutive SCFE with open physes in two institutions. In cases of femoro-acetabular impingement due to mild deformitiy, restoration of the head-neck-offset via hip arthroscopy or surgical dislocation should be considered before higher grade cartilage damage occurs.
References 1. Carney BT, Weinstein SL, Noble J. Long-term follow-up of slipped capital femoral epiphysis. J Bone Joint Surg Am 1991;73(5):667–74. 2. Engelhardt P. Juvenile Hueftkopfloesung und Koxarthrose. Stuttgart: Ferdinand Enke, 1984. 3. Oram V. Epiphysiolysis of the head of the femur: a followup examination with special reference to end results and the social prognosis. Acta Orthop Scand 1953;23(2):100–20. 4. Loder RT. The demographics of slipped capital femoral epiphysis. An international multicenter study. Clin Orthop Relat Res 1996;322:8–27. 5. Hägglund G, Hansson LI, Sandstrom S. Familial slipped capital femoral epiphysis. Acta Orthop Scand 1986;57(6): 510–2. 6. Moreira JF, Neves MC, Lopes G, Gomes AR. Slipped capital femoral epiphysis. A report of 4 cases occurring in one family. Int Orthop 1998;22(3):193–6. 7. Gunal I, Ates E. The HLA phenotype in slipped capital femoral epiphysis. J Pediatr Orthop 1997;17(5):655–6. 8. Weiner D. Pathogenesis of slipped capital femoral epiphysis: current concepts. J Pediatr Orthop B 1996;5(2):67–73. 9. Krauspe R. Epiphyseolysis Capitis Femoris. In: Tschauner C, ed. Die Hüfte. Stuttgart: Enke, 1997, pp. 135–7. 10. Wells D, King JD, Roe TF, Kaufman FR. Review of slipped capital femoral epiphysis associated with endocrine disease. J Pediatr Orthop 1993;13(5):610–4. 11. Stanitski CL, Woo R, Stanitski DF. Acetabular version in slipped capital femoral epiphysis: a prospective study. J Pediatr Orthop B 1996;5(2):77–9. 12. Kordelle J, Millis M, Jolesz FA, Kikinis R, Richolt JA. Three-dimensional analysis of the proximal femur in patients with slipped capital femoral epiphysis based on computed tomography. J Pediatr Orthop 2001;21(2):179–82. 13. Kitadai HK, Milani C, Nery CA, Filho JL. Wiberg’s centeredge angle in patients with slipped capital femoral epiphysis. J Pediatr Orthop 1999;19(1):97–105. 14. Seller K, Raab P, Wild A, Krauspe R. Risk-benefit analysis of prophylactic pinning in slipped capital femoral epiphysis. J Pediatr Orthop B 2001;10(3):192–6.
57 15. Loder RT, Richards BS, Shapiro PS, Reznick LR, Aronson DD. Acute slipped capital femoral epiphysis: the importance of physeal stability. J Bone Joint Surg Am 1993;75(8):1134–40. 16. Southwick WO. Osteotomy through the lesser trochanter for slipped capital femoral epiphysis. J Bone Joint Surg Am 1967;49(5):807–35. 17. Boyer DW, Mickelson MR, Ponseti IV. Slipped capital femoral epiphysis. Long-term follow-up study of one hundred and twenty-one patients. J Bone Joint Surg Am 1981;63(1): 85–95. 18. Jacobs B. Diagnosis and natural history of slipped capital femoral epiphysis. Instr Course Lect 1972;21:167–73. 19. Green DW, Reynolds RA, Khan SN, Tolo V. The delay in diagnosis of slipped capital femoral epiphysis: a review of 102 patients. Hss J 2005;1(1):103–6. 20. Jerre R, Billing L, Hansson G, Karlsson J, Wallin J. Bilaterality in slipped capital femoral epiphysis: importance of a reliable radiographic method. J Pediatr Orthop B 1996; 5(2):80–4. 21. Klein A, Joplin RJ, Reidy JA, Hanelin J. Slipped capital femoral epiphysis: early diagnosis and treatment facilitated by normal roentgenograms. J Bone Joint Surg Am 1952; 34-A-1:233–9. 22. Imhäuser G. Pubertäre Hüfterkrankungen. In: Witt A, Rettig H, Schlegel K, eds. Orthopädie in Praxis und Klinik, 2nd ed. Stuttgart: Thieme, 1987. 23. Kamegaya M, Saisu T, Ochiai N, Moriya H. Preoperative assessment for intertrochanteric femoral osteotomies in severe chronic slipped capital femoral epiphysis using computed tomography. J Pediatr Orthop B 2005;14(2):71–8. 24. Futami T, Suzuki S, Seto Y, Kashiwagi N. Sequential magnetic resonance imaging in slipped capital femoral epiphysis: assessment of preslip in the contralateral hip. J Pediatr Orthop B 2001;10(4):298–303. 25. Umans H, Liebling MS, Moy L, Haramati N, Macy NJ, Pritzker HA. Slipped capital femoral epiphysis: a physeal lesion diagnosed by MRI, with radiographic and CT correlation. Skeletal Radiol 1998;27(3):139–44. 26. Strange-Vognsen H, Wagner A, Dirksen K, Rabol A, Folke M, Hede A, Christensen S. The value of scintigraphy in hips with slipped capital femoral epiphysis and the value of radiography and MRI after 10 years. Acta Orthop Belg 1999; 65(1):33–8. 27. Lalaji A, Umans H, Schneider R, Mintz D, Liebling MS, Haramati N. MRI features of confirmed “pre-slip” capital femoral epiphysis: a report of two cases. Skeletal Radiol 2002;31(6):362–5. 28. Schittich I. [MRI in the diagnosis and treatment of Perthes disease and epiphysiolysis of the head of the femur]. Orthopade 2001;30(8):519–27. 29. Tins B, Cassar-Pullicino V, McCall I. The role of pre-treatment MRI in established cases of slipped capital femoral epiphysis. Eur J Radiol 2008. 30. Tins B, Cassar-Pullicino V, McCall I. Slipped upper femoral epiphysis: imaging of complications after treatment. Clin Radiol 2008;63(1):27–40. 31. Krauspe R, Eulert J. Differentialdiagnose des Hüftschmerzes im Kindes- und Jugendalter. Z Allg Med 1991;67:1741–8.
58 32. Exner GU, Schai PA, Notzli HP. [Treatment of acute slips and clinical results in slipped capital femoral epiphysis]. Orthopade 2002;31(9):857–65. 33. Krauspe R, Seller K, Westhoff B. [Epiphyseolysis capitis femoris]. Z Orthop Ihre Grenzgeb 2004;142(5):R37–52; quiz R3–6. 34. Leunig M, Casillas MM, Hamlet M, Hersche O, Notzli H, Slongo T, Ganz R. Slipped capital femoral epiphysis: early mechanical damage to the acetabular cartilage by a prominent femoral metaphysis. Acta Orthop Scand 2000;71(4):370–5. 35. Schultz WR, Weinstein JN, Weinstein SL, Smith BG. Prophylactic pinning of the contralateral hip in slipped capital femoral epiphysis: evaluation of long-term outcome for the contralateral hip with use of decision analysis. J Bone Joint Surg Am 2002;84-A-8:1305–14. 36. Kocher MS, Bishop JA, Hresko MT, Millis MB, Kim YJ, Kasser JR. Prophylactic pinning of the contralateral hip after unilateral slipped capital femoral epiphysis. J Bone Joint Surg Am 2004;86-A-12:2658–65. 37. Plotz GM, Prymka M, Hassenpflug J. The role of prophylactic pinning in the treatment of slipped capital femoral epiphysis–a case report. Acta Orthop Scand 1999;70(6):631–4. 38. Hackenbroch MH, Kumm DA, Rutt J. [Dyamic screw fixation for slipped capital femoral epiphysis. Treatment results]. Orthopade 2002;31(9):871–9. 39. Bertram C, Kumm DA, Michael JW, Rutt J, Hackenbroch MH, Eysel P. Stabilization of the femoral head with a gliding screw in slipped capital femoral epiphysis. Oper Orthop Traumatol 2007;19(4):358–67. 40. Maus U, Ihme N, Niedhart C, Abeler E, Kochs A, Gravius S, Ohnsorge JA, Andereya S. [Comparison of the treatment of slipped capital femoral epiphysis with K-wires and cannulated titanium screws]. Z Orthop Unfall 2008;146(2):251–5. 41. Ilchmann T, Parsch K. Complications at screw removal in slipped capital femoral epiphysis treated by cannulated titanium screws. Arch Orthop Trauma Surg 2006;126(6):359–63. 42. König A, Krauspe R, Fella E, Eulert J. Die Entwicklung des koxalen Femurendes nach operativer Therapie der Epiphyseolysis Capitis Femoris. Orthop Praxis 1996;32:515–20. 43. de Sanctis N, Di Gennaro G, Pempinello C, Corte SD, Carannante G. Is gentle manipulative reduction and percutaneous fixation with a single screw the best management of acute and acute-on-chronic slipped capital femoral epiphysis? A report of 70 patients. J Pediatr Orthop B 1996;5(2):90–5. 44. Hansson LI, Hagglund G, Ordeberg G. Slipped capital femoral epiphysis in southern Sweden 1910–1982. Acta Orthop Scand Suppl 1987;226:1–67. 45. Barmada R, Bruch RF, Gimbel JS, Ray RD. Base of the neck extracapsular osteotomy for correction of deformity in slipped capital femoral epiphysis. Clin Orthop Relat Res 1978;132:98–101. 46. Carlioz H, Vogt JC, Barba L, Doursounian L. Treatment of slipped upper femoral epiphysis: 80 cases operated on over 10 years (1968–1978). J Pediatr Orthop 1984;4(2):153–61. 47. Fish JB. Cuneiform osteotomy of the femoral neck in the treatment of slipped capital femoral epiphysis. A follow-up note. J Bone Joint Surg Am 1994;76(1):46–59. 48. Imhäuser G. [Pathogenesis and therapy of hip dislocation in youth.]. Z Orthop Ihre Grenzgeb 1956;88(1):3–41.
R. Krauspe et al. 49. Kramer WG, Craig WA, Noel S. Compensating osteotomy at the base of the femoral neck for slipped capital femoral epiphysis. J Bone Joint Surg Am 1976;58(6):796–800. 50. Pearl AJ, Woodward B, Kellyrp. Cuneiform osteotomy in the treatment of slipped capital femoral epiphysis. J Bone Joint Surg Am 1961;43-A:947–54. 51. Sugioka Y. Transtrochanteric rotational osteotomy of the femoral head. In: Riley LH Jr., ed. The Hip. Proceedings of the Eighth Open Scientific Meeting of the Hip Society. St. Louis: CV Mosby, 1980, pp. 3. 52. Wiberg G. Considerations on the surgical treatment of slipped epiphysis with special reference to nail fixation. J Bone Joint Surg Am 1959;41-A-2:253–61. 53. Crawford AH. Osteotomies in the treatment of slipped capital femoral epiphysis. Instr Course Lect 1984;33:327–49. 54. Zilkens J, Löer F, Zilkens K-W. [Long-term results after conservatively treated SCFE]. In: Blauth/Ulrich, ed. Spätergebnisse in der Orthopädie. Berlin: Springer, 1986. 55. Abraham E, Garst J, Barmada R. Treatment of moderate to severe slipped capital femoral epiphysis with extracapsular base-of-neck osteotomy. J Pediatr Orthop 1993;13(3):294–302. 56. Diab M, Hresko MT, Millis MB. Intertrochanteric versus subcapital osteotomy in slipped capital femoral epiphysis. Clin Orthop Relat Res 2004;427:204–12. 57. Gage JR, Sundberg AB, Nolan DR, Sletten RG, Winter RB. Complications after cuneiform osteotomy for moderately or severely slipped capital femoral epiphysis. J Bone Joint Surg Am 1978;60(2):157–65. 58. Hall JE. The results of treatment of slipped femoral epiphysis. J Bone Joint Surg Br 1957;39-B-4:659–73. 59. Clarke HJ, Wilkinson JA. Surgical treatment for severe slipping of the upper femoral epiphysis. J Bone Joint Surg Br 1990;72(5):854–8. 60. Compere CL. Correction of deformity and prevention of aseptic necrosis in late cases of slipped femoral epiphysis. J Bone Joint Surg Am 1950;32A-2:351–62. 61. DeRosa GP, Mullins RC, Kling TF, Jr. Cuneiform osteotomy of the femoral neck in severe slipped capital femoral epiphysis. Clin Orthop Relat Res 1996–322:48–60. 62. Dunn DM. The treatment of adolescent slipping of the upper femoral epiphysis. J Bone Joint Surg Br 1964;46-B-4:621–9. 63. Dunn DM. Severe slipped capital femoral epiphysis treated by cervical osteotomy and open replacement. In: The Hip Society. St. Louis: CV Mosby, 1975:115–26. 64. Fish JB. Cuneiform osteotomy in treatment of slipped capital femoral epiphysis. J Bone Joint Surg Am 1974;56-A:1301. 65. Fish JB. Cuneiform osteotomy of the femoral neck in the treatment of slipped capital femoral epiphysis. J Bone Joint Surg Am 1984;66(8):1153–68. 66. Martin PH. Slipped capital femoral epiphysis in the adolescent hip: a reconsideration of open reduction. J Bone Joint Surg Am 1948;30-A-1:9–19. 67. Schnute WJ. Slipped capital femoral epiphysis. Clin Orthop 1958;11:63–80. 68. Green WT. Slipping of the upper femoral epiphysis. Diagnostic and therapeutic considerations. Arch Surg 1945;50: 19–32. 69. Mueller ME. Die Hueftnahen Osteotomien. Stuttgart: Thieme, 1971:100–13.
Slipped Capital Femoral Epiphysis 70. Nishiyama K, Sakamaki T, Ishii Y. Follow-up study of the subcapital wedge osteotomy for severe chronic slipped capital femoral epiphysis. J Pediatr Orthop 1989;9(4):412–6. 71. Lehman WB, Grant A, Rose D, Pugh J, Norman A. A method of evaluating possible pin penetration in slipped capital femoral epiphysis using a cannulated internal fixation device. Clin Orthop Relat Res 1984;186:65–70. 72. Arnold P, Jani L, Scheller G, Herrwerth V. [Results of treating slipped capital femoral epiphysis by pinning in situ]. Orthopade 2002;31(9):880–7. 73. Badgley E, Isaacson A, Wolgamot J, Miller J. Operative therapy for slipped capital femoral epiphysis. J Bone Joint Surg Am 1948;30:19. 74. Bianco AJ, Jr. Treatment of slipping of the capital femoral epiphysis. Clin Orthop Relat Res 1966;48:103–10. 75. Lefort G, Cottalorda J, Bouche-Pillon MA, Lefebvre F, Daoud S. [Open reduction by the Dunn technique in upper femoral epiphysiolysis. Report of 14 cases]. Chir Pediatr 1990;31(4–5):229–34. 76. Haase M, Fengler F, Hein W. [Previous experience with subcapital femoral neck osteotomy in severe cases of epiphysiolysis capitis femoris]. Beitr Orthop Traumatol 1989;36(10–11): 530–4. 77. Cleveland M, Bosworth DM, Daly JN, Hess WE. Study of displaced capital femoral epiphyses. J Bone Joint Surg Am 1951;33-A-4:955–67. 78. Wiberg G. [Osteotomy of the femur neck in advanced cases of epiphyseolysis of the femur head.]. Z Orthop Ihre Grenzgeb 1962;95:456–65. 79. Ballmer PM, Gilg M, Aebi B, Ganz R. [Results following sub-capital and Imhauser-Weber osteotomy in femur head epiphyseolysis]. Z Orthop Ihre Grenzgeb 1990;128(1):63–6. 80. Adorjan I. On the treatment of advanced slipping of the upper femoral epiphysis. Acta Orthop Scand 1961;30:286–93. 81. Broughton NS, Todd RC, Dunn DM, Angel JC. Open reduction of the severely slipped upper femoral epiphysis. J Bone Joint Surg Br 1988;70(3):435–9. 82. Fron D, Forgues D, Mayrargue E, Halimi P, Herbaux B. Follow-up study of severe slipped capital femoral epiphysis treated with Dunn’s osteotomy. J Pediatr Orthop 2000;20(3): 320–5. 83. Howorth B. Slipping of the capital femoral epiphysis. Treatment. Clin Orthop Relat Res 1966;48:53–70. 84. Rey JC, Carlioz H. [Severely slipped femoral epiphyses treated by the D. Dunn open reduction method]. Rev Chir Orthop Reparatrice Appar Mot 1975;61(4):261–73. 85. Velasco R, Schai PA, Exner GU. Slipped capital femoral epiphysis: a long-term follow-up study after open reduction of the femoral head combined with subcapital wedge resection. J Pediatr Orthop B 1998;7(1):43–52. 86. Szypryt EP, Clement DA, Colton CL. Open reduction or epiphysiodesis for slipped upper femoral epiphysis. A comparison of Dunn’s operation and the Heyman-Herndon procedure. J Bone Joint Surg Br 1987;69(5):737–42. 87. Balensweig I. Femoral osteochondritis of adolescents and sequelae. Epiphyseal separation of the hip. Surg Gynec Obstet 1926;43:604–14. 88. Boyd HB, Ingram AJ, Bourkard HO. The treatment of slipped capital femoral epiphysis. South Med J 1949;42: 551–60.
59 89. Frymoyer JW. Chondrolysis of the hip following Southwick osteotomy for severe slipped capital femoral epiphysis. Clin Orthop Relat Res 1974;99:120–4. 90. Crawford HB. Ten cases of marked slipping of the upper femoral epiphysis. Clin Orthop Relat Res 1966;48:129–38. 91. Wilson PD, Jacobs B, Schecter L. Slipped capital femoral epiphysis: an end-result study. J Bone Joint Surg Am 1965; 47:1128–45. 92. Ganz R, Gill TJ, Gautier E, Ganz K, Krugel N, Berlemann U. Surgical dislocation of the adult hip a technique with full access to the femoral head and acetabulum without the risk of a vascular necrosis. J Bone Joint Surg Br 2001;83(8):1119–24. 93. Leunig M, Slongo T, Ganz R. Subcapital realignment in slipped capital femoral epiphysis: surgical hip dislocation and trimming of the stable trochanter to protect the perfusion of the epiphysis. Instr Course Lect 2008;57:499–507. 94. Leunig M, Slongo T, Kleinschmidt M, Ganz R. Subcapital correction osteotomy in slipped capital femoral epiphysis by means of surgical hip dislocation. Oper Orthop Traumatol 2007;19(4):389–410. 95. Zilkens C, Spencer S, Millis MB, Kim Y-J. [Treatment of SCFE by surgical dislocation and subcapital osteotomy]. Orthop Praxis 2008;44(6):299–305. 96. Ziebart K, Zilkens C, Spencer S, Leunig M, Ganz R, Kim Y-J. Capital realignment for moderate and severe SCFE using a modified Dunn procedure. Clin Orthop Relat Res 2009; 467(3):704–16. 97. Rebello G, Spencer S, Millis MB, Kim YJ. Surgical dislocation in the management of pediatric and adolescent hip deformity. Clin Orthop Relat Res 2009;467(3):724–31. 98. Lubicky JP. Chondrolysis and avascular necrosis: complications of slipped capital femoral epiphysis. J Pediatr Orthop B 1996;5(3):162–7. 99. Jäger M, Tillmann FP, Thornhill TS, Mahmoudi M, Blondin D, Hetzel GR, Zilkens C, Krauspe R. Rationale for prostaglandin I2 in bone marrow oedema - from theory to application. Arthritis Res Ther 2008;10(5):R120. 100. Maussen JP, Rozing PM, Obermann WR. Intertrochanteric corrective osteotomy in slipped capital femoral epiphysis. A long-term follow-up study of 26 patients. Clin Orthop Relat Res 1990;259:100–10. 101. Imhäuser G. [Late results of Imhauser’s osteotomy for slipped capital femoral epiphysis (author’s transl)]. Z Orthop Ihre Grenzgeb 1977;115(5):716–25. 102. Murray RO. The aetiology of primary osteoarthritis of the hip. Br J Radiol 1965;38(455):810–24. 103. Solomon L. Patterns of osteoarthritis of the hip. J Bone Joint Surg Br 1976;58(2):176–83. 104. Stulberg SD. Unrecognized childhood hip disease: a major cause of idiopathic osteoarthritis of the hip. In: Cordell LD, Harris WH, Ramsey PL, MacEwen GD, eds. The Hip: Proceedings of the Third Open Scientific Meeting of the Hip Society. St. Louis, MO: CV Mosby; 1975:212–228. 105. Resnick D. The ‘tilt deformity’ of the femoral head in osteoarthritis of the hip: a poor indicator of previous epiphysiolysis. Clin Radiol 1976;27(3):355–63. 106. Jäger M, Wild A, Westhoff B, Krauspe R. Femoroacetabular impingement caused by a femoral osseous head-neck bump deformity: clinical, radiological, and experimental results. J Orthop Sci 2004;9(3):256–63.
60 107. Mamisch TC, Richolt JA, Kim J-Y, Zilkens C, Kikinis R, Millis MB, Kordelle J. Range of motion after CT based simulation of intertrochanteric corrective osteotomy in cases of Slipped Capital Femoral Epiphysis (SCFE): Comparison of uni-planar flexion osteotomy and multi – planar flexion-, valgisation and rotational osteotomy. J Pediatr Orthop 2009 (in press). 108. Mamisch TC, Kim YJ, Richolt JA, Millis MB, Kordelle J. Femoral morphology due to impingement influences the range of motion in slipped capital femoral epiphysis. Clin Orthop Relat Res 2008;467(3):692–8.
R. Krauspe et al. 109. Richolt JA, Teschner M, Everett PC, Millis MB, Kikinis R. Impingement simulation of the hip in SCFE using 3D models. Comput Aided Surg 1999;4(3):144–51. 110. Spencer S, Millis MB, Kim YJ. Early results of treatment of hip impingement syndrome in slipped capital femoral epiphysis and pistol grip deformity of the femoral headneck junction using the surgical dislocation technique. J Pediatr Orthop 2006;26(3):281–5. 111. Schai PA, Exner GU, Hansch O. Prevention of secondary coxarthrosis in slipped capital femoral epiphysis: a longterm follow-up study after corrective intertrochanteric osteotomy. J Pediatr Orthop B 1996;5(3):135–43.
Major Joint Contractures in Children Deborah M. Eastwood
Joint contractures, defined as a chronic loss of joint movement secondary to changes in the non-osseous structures of the joint, are common in all branches of Orthopaedics and, indeed, the principles of management of such contractures form part of the basic workload of all Orthopaedic surgeons. Although many people may think of contractures in terms of a tight or short muscle-tendon unit there are other soft tissues that can be implicated such as the skin and subcutaneous tissues, the ligaments and the joint capsule itself. Often there is a combination of problems either due to the aetiology of the condition or due to its long-standing nature. Changes in bone shape are also common and may influence prognosis and management. In children, joint contractures pose a particular problem. On the one hand children are often able to cope with a significant degree of contracture and develop and maintain a functional level surprisingly well but on the other hand the process of growth often acts against them making contractures more problematic with time. A major contracture may be thought of as one that affects a large joint rather than small joint or one that affects even a small joint but with a significant loss of movement. If a single joint is involved, the impact on the child’s quality of life is often not marked and hence treatment may not be necessary. If the contracture affects the lower limb, functional difficulties are more likely but the problem can often be improved significantly by appropriate treatment. Treatment must always improve on the natural history of the condition in order to be worthwhile and in children with multiple joint contractures a holistic approach to the patient is essential.
Deborah M. Eastwood Department of Paediatric Orthopaedics, Great Ormond St Hospital for Children and the Royal National Orthopaedic Hospital, London, UK e-mail:
[email protected]
Make the Diagnosis As with all medical problems it is essential to make a diagnosis when faced with a young patient with joint contractures by taking a full history, performing a complete examination and arranging the appropriate investigations. The probable aetiology of the contracture may be clear from a history of trauma or infection of a single joint and in the reverse situation the involvement of a single joint must raise the possibility of unrecognised trauma or infection at some stage, often in early infancy. When considering the possible causes of the contracture it can be helpful to think in terms of intra- and extra-articular causes (Table 1). A full history is essential: it is impossible to list all the questions that a skilful clinician will need to ask but certain factors are important: 1. Was the child born with contractures? 2. What has happened since then? 3. Are the contractures progressive or are they resolving? 4. Is this change spontaneous or in response to treatment? 5. What is the response of the tissues/contractures to treatment? To injury? 6. Is there a dynamic component to the joint deformity? 7. Is there a family history of a similar problem and what has been the natural history of the condition in other family members? Table 1 Possible causes of a joint contracture Inside the joint
Outside the joint
Infection Inflammation Haemophilia
Neuromuscular problems – balanced or not? Vascular malformations Soft tissue fibrosis secondary to trauma, congenital malformation etc Additional tissue such as occurs with popliteal webs, and possibly in syndromes such as Proteus syndrome
Trauma
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Examination of the child must be complete and thorough and repeated, particularly if there is a neuromuscular component to it, to ensure that an accurate picture of the child is achieved. All children (and of course adults too) may become tense and stiff when faced with a formal examination by strangers in an unfamiliar environment. It is very important to observe the child throughout the consultation: from when they walk into the room to the minute they leave and to note how functional they are and how much help is offered to them from family members. Is the help appropriate to the age of the child and to their difficulties? It is always important to relate the position of one joint to its neighbouring joints and determining the relationship, for example, of forefoot to hindfoot and then to knee joint and most proximally the hip. This is essential for understanding gait patterns and predicting the effects of treatment. Whilst the Orthopaedic surgeon understandably concentrates on the musculo-skeletal system in the management of complex cases where multi-system involvement is likely it is often essential to ask for help and these children are often seen by a variety of specialists. An assessment of general development is important. Many children with musculoskeletal disabilities are very versatile and determined: their functional level may be surprisingly good. However, some children also have significant learning difficulties and lack the ability and/or the motivation to cope with physical difficulties. These factors must be considered when planning treatment. Investigations may be directed to understanding the aetiology of the problem or to determining the nature of the individual contracture. Plain radiographs and MRI scans are used most frequently but care must be taken to ensure that the radiographs are taken in the plane of the contracted joint in order to gain the most information.
D. M. Eastwood
fied who will be important in helping the family understand differing priorities for treatment and the balance between risks and benefits of treatment plans. The aim of treatment must be clearly understood: usually treatment improves the quality of life for the child but in some circumstances the treatment may indirectly improve the care of the child by increasing the ease with which the parents and primary carers can look after the child. For example, releasing a painless adduction contracture of the hip may help with toileting and dressing. In general, with conditions that are causing progressive contractures, the aim of treatment is to prevent progression, pain and loss of function. In static contractures, treatment may aim to improve limb position and hence function and reduce pain. In some circumstances the most appropriate treatment plan is to accept the situation and improve quality of life by providing suitable mobility and communication aids such as electric wheelchairs and laptop computers, with adapted controls if necessary.
Physiotherapy Physiotherapy is a mainstay of treatment and is designed to obtain or maintain joint movement and/or an improved resting position of the joint. Maintaining muscle length is always important particularly in childhood during bone growth and helps normalise muscle forces acting across the joints. A stretching and strengthening programme needs to become part of the daily routine of the child.
Splints and Orthotics Planning Treatment As emphasised previously, before planning treatment the natural history of the joint contracture must be understood. The influence of other co-morbidities on the child’s health must be known and in the case of the child with multiple difficulties there are often moral and philosophical arguments to be discussed as to how much treatment the family are willing to consider and whether or not aggressive treatment plans are acceptable. In complex cases, where many physicians are involved in the child’s care, it is important that a lead clinician is identi-
Positioning of the joint and the limb is important to help maintain joint position and prevent progression of the contracture. Function may also be improved by a change in position of the affected joint or limb. Overall, too many splints and orthotic devices are supplied to children with joint contractures without the indication for treatment being established or the aim of treatment and its likely outcome being discussed with the child and their family. Such a lack of discussion would be unacceptable if an operation was planned and hence it is similarly unacceptable when commencing treatment with splints or orthotics particularly as patient/family compliance is a major factor in the success of the treatment. Splints and orthotics must fit
Major Joint Contractures in Children
well and be comfortable: they must be monitored closely and altered for growth and for changing deformity. The weight of some splints or caliper devices is also an important factor in children whose overall muscle power is poor.
Tone-Reducing Medication In patients in whom the joint contractures are secondary to neuromuscular problems, the alteration of muscle tone may be very beneficial in preventing contractures and maintaining function. Medication affecting neurotransmission may be taken orally, for example, baclofen or administered by intramuscular injection as with botulinum toxin injections. In both situations a degree of titration of muscle relaxation vs. side effects can be achieved by altering the dose and/or the frequency of administration. A better titration effect can sometimes be achieved by using an implantable intra-thecal baclofen pump where the pump is placed in the abdomen (Fig. 1). A dorsal rhizotomy is a more permanent method of reducing high tone.
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Soft Tissue Releases Carefully planned and appropriately performed releases of contracted muscles and/or joint capsules may improve joint position. The new position must then be maintained and the post-operative rehabilitation in both the short and medium term is essential in achieving a good outcome. The predicted effect of surgery on the soft tissues must be considered: will excessive scarring or recurrent contracture occur? Following major soft tissue releases of a joint contracture, the joint may become unstable and uncontrolled movement may give pain and may lead to a loss of function. This risk must be anticipated and discussed with the family prior to surgery. In neuromuscular conditions, unbalanced muscle pulls across a joint often lead to contractures; thus following a release of the contracted muscle-tendon unit recurrence may be predicted even in the presence of a good physiotherapy and splinting regime. Tendon transfers may be useful in maintaining the corrected position but if the transferred tendon is expected to work against gravity it needs to be strong (MRC grade 4) before it is transferred and often the effect of the transfer needs to be supplemented by the use of a splint (for function rather than for position).
Correction of Limb Alignment
Fig. 1 Plain pelvic radiograph showing joint contractures affecting both hips. An intra-thecal baclofen pump has been implanted and is shown in the right iliac fossa
The use of osteotomies or the principles of guided growth with physeal staples or systems such as the 8-plate can improve limb alignment and hence function even if the joint contracture persists. For example, the use of an anterior 8-plate on the distal femur has proved helpful in improving a knee flexion contracture in children with cerebral palsy. In patients with multiple joint contractures, great care must be taken when planning such surgery as, for example, even a small change in lower limb alignment may not be tolerated in the presence of stiff joints distally. In the upper limb, a change in wrist position may decrease finger function or prevent the hand from reaching the mouth. A change in position in one arm may prevent the child using both arms for bimanual activities thus a gain in function for one activity may be negated by the loss of many other functions.
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Arthrodesis A well-planned and performed arthrodesis can often improve function and relieve pain but such procedures should be delayed until towards the end of growth when possible. Commonly the most distal joints are managed in this way but more proximal joints such as the hip and the shoulder can be treated very effectively this way as long as the position and mobility of neighbouring joints is considered carefully.
Arthroplasty Traditionally, excision arthroplasty has been recommended for some joint contractures to improve position, as for example when performing a talectomy for a severe deformity in an arthrogryphotic foot, or to improve movement and relieve pain when an proximal femoral excision is considered in cases of a severely contracted and painful hip dislocation in cerebral palsy. The role of joint replacement is increasing but only in a highly selected group of patients with severe joint contracture. Some aetiologies are more suited for this form of treatment and obviously joint replacement in the skeletally-mature teenager may be the treatment of choice in patients with endstage juvenile inflammatory arthritis.
D. M. Eastwood
Overall the complication rates may be high particularly in conditions where there is low muscle tone and poor muscle control. The joint replacement itself may not function well but the reduction in pain following joint arthroplasty may lead to an overall improvement in function. In patients with a neuromuscular conditon there may be a general improvement in muscle tone and a reduction in the mass effect of muscle contraction.
Decision Making Overall what to do, when, and in which patients and for what reason are very complex questions for which there are no easy answers. A multidisciplinary approach is needed to assess the child on several occasions and looking at the child from many points of view. Do not be afraid to delay your decision regarding the need for surgery but also, as a surgeon, do not be afraid of taking the decision that in any individual case, surgical management is NOT the appropriate option. Some of the most common generalised joint contracture cases are associated with neuromuscular conditions such as cerebral palsy and spina bifida. Less common contracture syndromes include arthrogryposis and Larsen’s syndrome or patients with popliteal webs or pterygia. The management approach outlined above should help the clinician and the patient devise a suitable treatment plan to enable the young adult to be comfortable and independently mobile be that walking, with or without aids, or by using a wheelchair.
Damage-Control Orthopaedic Surgery in Polytrauma: Influence on the Clinical Course and Its Pathogenetic Background Hans-Christoph Pape
Decision Making for the Treatment of Major Fractures: Evidence for the Benefits of Tapered Treatment to According to the Patient Condition The standard of care for major extremity fractures in patients with multiple injuries foresees early definitive fixation of all major fractures. Recently controversial results were gathered from studies [1–7], and observations were made about certain patient sub-groups that developed unexpectedly high complication rates, when early definitive stabilization was performed. It was suggested that potential deleterious effects of internally fixing long-bone fractures in the acute setting, where systemic hypo-perfusion and inflammation occurred, increases susceptibility to end-organ injury. In summary, three factors appeared to play a role that are pathogenetically connected: 1. Additional severe injuries (such as chest trauma) 2. Prolonged surgeries 3. The pre-operative condition [8, 9] Several observational studies and one randomized study have suggested clinical benefits from early stabilization of major long-bone fractures in reducing the incidence of pulmonary complications and mortality. Differences in treatment definition, time cut-offs and type of fixation used, small samples limited to single institutions and inadequate control of confounding variables, all serve to limit the validity and general application of prior findings. One of the problems of previous studies was the lack of focus on those patient sub-groups that did appear to be at high risk for complications and take into
Hans-Christophe Pape, MD, FACS Chairman, University of Aachen, Department of Orthopaedics Pauwelstreet 30 52074 Aachen, Germany e-mail:
[email protected]
account the three factors listed above. Recently, two studies have become available that investigate the effect of fracture fixation depending on the pre-operative clinical condition of the patient and take into account that additional severe injuries and hypo-perfusion may influence the course. 1. A prospective randomized multi-center study summarized 165 multiply-injured patients from ten different centres between 1, Jan 2000 and 28, Feb 2006 [10]. This study is different from other retro- or prospective studies because no patients with isolated fractures were included. Moreover, patients were excluded if they had severe head and chest injuries, as well as exsanguinating conditions. Thereby, a better focus on the potential impact of the fixation of the femoral shaft fracture was obtained. Of the 165 patients in the study, 71 (43.0%) were randomized to the external fixation treatment group and 94 (56.9%) were randomized to the intra-medullary nailing treatment group. Comparisons between the two groups on demographic characteristics and initial injury severity demonstrated a similar pattern, except for a higher head trauma score in the external fixation group when compared with patients undergoing initial intra-medullary nailing of the femur. Analyses documenting differences between patients in a clinically stable or uncertain (borderline) condition in terms of initial injury severity and post-operative outcomes validated the notion that borderline patients have significantly worse injuries and post-operative outcomes than stable patients. In terms of initial injury, borderline patients demonstrated higher scores on the revised trauma index, injury severity index, and head and thorax injury indices in comparison to stable patients. Borderline patients were also more likely to have a bilateral femoral fracture, a hemothorax, and require a blood transfusion within 24 h of admission in comparison to stable patients. In terms of post-operative outcomes, borderline patients spent more hours in the ICU and more hours on ventilation in comparison with
G. Bentley (ed.), European Instructional Lectures. European Instructional Course Lectures 9, DOI: 10.1007/978-3-642-00966-2_8, © 2009 EFORT
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stable patients. Borderline patients were also more likely than stable patients to experience clinical complications such as acute lung injury, systemic inflammatory response, sepsis, and multiple organ failure. The analyses examined the influence of treatment group status on post-operative clinical course and complications separately for stable patients and those in uncertain condition (see Table 1). Again, regression analyses statistically controlled for differences between the two treatment groups in terms of initial injury severity (i.e., revised trauma score, new injury severity index, head injury score) when examining group differences. For patients who presented in stable condition, those who underwent intra-medullary nailing experienced a shorter duration on a ventilator in comparison to those with external fixation. In contrast, borderline patients that underwent initial nailing of the femur had a higher incidence of acute lung injury in comparison to those who underwent external fixation. After adjusting for initial injury severity, the odds of developing acute lung injury were 6.69 times greater in borderline patients who underwent intra-medullary nailing in comparison to those who underwent external fixation. The authors concluded that the type of surgical procedure for fixation of a femoral shaft fracture should be carefully selected, according to the initial assessment of the clinical condition. In patients who present in an uncertain (borderline)
condition, an external fixator should be applied for temporizing purposes. 2. The second study used the National Trauma Databank (NTDB) from the United States [10] between 1, January 2000 and 31, December 2004 [12]. In this study, the inclusion criteria encompassed: (a) The presence of a closed or open fracture(s) of the femoral shaft (b) An injury severity score greater than or equal to 15 (c) Sixteen years of age or older (d) Those who underwent a internal fixation of the femur This study is different from many other studies because it tried to provide clinically relevant categories for treatment beyond a simple dichotomy at 12 or 24 h. Five time periods were selected a priori, based on commonly used cut-points from the literature [11–13]: t0 ≤ 12h, 24 < t2 ≤ 48 h, 12 < t1 ≤ 24 h, 48 < t3 ≤ 120 h, It is also different because the authors hypothesize that an additional physiologic stress from definitive fracture surgery could activate an adverse systemic response leading to end-organ injury and a higher mortality rate. The authors used an inverse-probability-of-treatment-weighted (IPTW) analysis to estimate the risk of mortality for a defined treatment time. Their results document that definitive fixation in all but one (24–48 h) of four delayed treatment categories
Table 1 Treatment group differences in clinical course and complications for patients in stable and uncertain (borderline) condition (data from [58]) Stable condition
Uncertain (borderline) condition
s−I°ExFix (N = 50)
s−I°IMN (N = 71)
Regression analyses
Outcomes
M ± SD
M ± SD
HR
ICU (h)
212.4 ± 167.93
133.52 ± 193.49
1.06
0.84−1.86
0.290
476.95 ± 284.50
399.14 ± 404.13
1.28
0.67−2.44
0.445
Ventilator (h)
142.2 ± 121.32
66.54 ± 108.45
1.55
1.04−2.33
0.030
360.48 ± 245.47
313.81 ± 359.77
1.36
0.74−2.53
0.325
%
%
OR
95% C.I.
p
%
%
OR
95% C.I.
p 0.995
95% C.I.
p
b−I°ExFix (N = 21)
b−I°IMN (N = 23)
Regression analyses
M ± SD
M ± SD
IRR
95% C.I.
p
Pneumonia
23.8
6.5
0.40
0.11−1.50
0.176
38.9
45.0
1.00
0.22−4.59
ALI
28.6
12.9
0.39
0.14−1.08
0.170
16.7
52.4
6.69
1.01−44.08
0.048
ARDS SIRS
9.5 30.2
6.3 30.8
0.73 1.49
0.15−3.53 0.62−3.57
0.700 0.367
11.1 50.0
16.7 52.6
2.01 0.73
0.13−31.91 0.17−3.24
0.618 0.684
Sepsis MOF
11.9 0.0
6.3 0.0
0.60
0.15−2.36
0.469
11.1 16.7
36.8 22.2
3.86 0.78
0.46−32.52 0.13−4.75
0.214 0.791
Regression analyses represent the relation between treatment condition (0 = external fixation, 1 = intramedullary nailing) and each outcome after controlling for initial treatment group differences on the revised trauma score, new injury severity score, and AIS head score. Cox regression with robust standard errors was used for number of hours until release from ICU and hours until taken off the ventilator. Logistic regression with robust standard errors was used for binary outcomes ALI acute lung injury; ARD acute respiratory distress; SIR systemic inflammatory response; MOF multiple organ failure; HR hazard ratio; OR odds ratio; C.I. confidence interval
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was associated with a significantly lower risk of mortality to about 50% of that expected with early treatment (less than 12 h). Also, patients with serious associated injuries demonstrated greater risk reductions from delayed fixation when compared with those with less serious or no abdominal injury. Their data was consistent with the results of multivariate standardized risk ratios when the early treatment group was used as the standard population Table 2. The authors conclude from this study that a cautious approach to early definitive femoral shaft fracture fixation among multi-trauma patients should be performed and re-inforce this for patients who present with serious associated abdominal injuries. These two studies appear to present strong evidence in favour of a tapered approach toward the multiply-injured patient. They show that a close relationship exists between the duration of surgery, the degree of initial injuries and the state of resuscitation, or the general condition. It appears that current end-points used to guide resuscitation, such as blood pressure, urine output, heart rate, base deficit and serum lactate may underestimate occult tissue hypo-perfusion. The clinical status was graded for decades by using only cardiovascular parameters. General surgeons have then considered several other factors to be important to describe changes observed in exsanguinating injuries caused by penetrating trauma: these include hypothermia, acidosis, and coagulopathy induced by hemorrhagic shock, and have been named the “triade of death” [14]. Orthopaedic surgeons have then tried to adapt these to the population of blunt trauma patients with predominant extremity injuries. As a fourth element, they have added “soft tissue injuries” summarizing all muscular and subcutaneous injuries of the extremities, lung, abdomen,
and pelvis. It should be noted that this fourth entity summarizes a number of clinical diagnoses rather than a single cascade system. These four pathophysiological entities – hemorrhagic shock, hypothermia, coagulopathy, and soft tissue injuries/ inflammation – were named the “four pathophysiological cycles of blunt polytrauma”. Moreover, many authors ask for more sensitive measures of tissue oxygenation measured by polarographic or nearinfrared technologies and markers of inflammation and coagulation that better reveal the physiologic condition of a patient and these are likely to replace simple temporal distinctions. The following paragraph summarizes why there are similarities in the pathogenesis of post-traumatic organ dysfunction and the changes induced by major surgical procedures.
Pathogenesis of Organ Failure Following Trauma Induced by Multiple Fractures, Soft-Tissue Damage and Acute Haemorrhage In those subsets of polytrauma patients who present with severe haemorrhage, severe soft tissue trauma, severe pelvic disruptions or sustained head trauma [11], clinical studies documented that an over-activated immune response pre-determines these complications [12, 15, 16]. The following pathogenetic changes after trauma and the influence of fracture fixation applies. Within the first hours, the most important physiologic changes are induced by local and systemic hypoxia [17]. Blood loss and tissue damage caused by fractures and soft tissue crush injuries induce
Table 2 Comparison of crude, regression, and marginal structural model estimates of effect of treatment time on mortality (data from [59]) Estimate
12–24 h
24–48 h
48–120 h
>120 h
Crude relative risk
0.50 [0.06] (0.18, 1.01) 0.45 [0.03] (0.15, 0.98) 0.47 [0.07] (0.14, 1.11)
1.13 [0.69] (0.58, 2.05) 0.83 [0.49] (0.43, 1.44) 0.94 [0.85] (0.44, 1.76)
1.19 [0.52] (0.67, 2.03) 0.58 [0.03] (0.28, 0.93) 0.58 [0.09] (0.21, 1.09)
1.17 [0.77] (0.24, 2.65) 0.43 [0.03] (0.10, 0.94) 0.43 [0.05] (0.09, 0.94)
IPTWa relative risk Standardized risk ratiob
Point estimates are given with p values in square brackets and 95% confidence intervals in parentheses. All analyses use t0 (£12 h) as the referent treatment group a Inverse-probability-of-treatment-weighted (IPTW) population relative risk was derived using model for treatment assignment controlling for Wm (NISS, GCS, Northeast region, age, arrival time, number of serious extremity/pelvis or head injuries, number of femur fractures, presence of cardiac or cerebrovascular comorbidities, teaching status, and ACS Level 1 designation) b Standardized risk ratio (SRR) using same treatment model as IPTW analysis but modified weights to give the estimated proportionate risk had those subjects treated early (t0) received treatment at a later time
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generalized hypoxemia in the entire vascular bed of the body [18]. Hypoxemia is the leading cause of damage as it causes all endothelial membranes to alter their shape. Subsequently, the circulating immune system, namely the neutrophil and macrophage defence systems, identify these altered membranes. The first immunologic reaction is the adhesion of neutrophils to the altered endothelial cell walls. They subsequently release their proteolytic enzymes that cause additional damage to the cell walls. This auto-destructive reaction occurs because of a lack of external pathogens that usually are a target for these mediators. Proteolytic enzymes and oxygen radicals are liberated into the bloodstream and aggravate the degree of endothelial damage [19]. Circulating neutrophils also adhere directly to tissue damaged from contusions, which may be located in the extremities, the muscles, or the lungs. Fracture haematoma is known to produce a manifold increase in cytokines, which may subsequently produce systemic effects [20]. Subsequently, the damaged endothelial cell walls, by trying to seal the damaged tissue, induce activation of the coagulatory system. This explains why these patients develop a drop in the platelet count. Further cascade mechanisms, such as the complement system, the prostaglandin system, the specific immune system and others, are activated [21]. Two prominent theories explain the pathogenesis of organ failure: The first concept is based on the on-going inflammatory process. The early neutrophil response described above is followed by a later response initiated by macrophages [22]. While the neutrophils exert their activity inside the vascular bed, macrophages have been well described cross the endothelium and act inside the interstitium [13]. If the reaction is part of an on-going inflammatory reaction, the classical signs of inflammation are clinically measurable. Generalized tissue swelling occurs, including in the extremities, a negative fluid balance is observed, and sometimes vasopressors are required in addition to increased fluid uptake. The subsequent chronic tissue hypoxemia caused by the interstitial swelling later results in the deterioration of several internal organs, a condition known as multiple organ dysfunction. It is represented by rubor (increased microvascular perfusion), calor (fever >38.5°C), tumour (generalized tissue swelling), dolor (pain and requirement for analgesia) and functio laesa(loss of function) of all organs [23, 24]. The main causes of late death following trauma are adult respiratory distress syndrome (ARDS) and multiple organ failure (MOF) and the immunologic response is closely associated with the development of these complications. Longstanding inflammation can convert the neutrophils and macrophages into a state of exhaustion and anergy. Anti-inflammatory mediators are liberated along with pro-
Hans-Christoph Pape
inflammatory mediators and weaken the defence, a state summarized as counter-activity-response syndrome, CARS [25]. Clinically, this period usually develops following the first week after trauma and is associated with an increased risk of infection, a decrease in wound healing capacity and the development of organ dysfunction [26]. Since the largest endothelial space is located in the lungs, which represent a special focus, it explains why the lungs are usually the first organ to deteriorate in the sequence of organ failure (requirement of high PEEP, high FiO2, and inverse inspiration-vs.-expiration ratio) [22, 27, 28]. Postmortem analyses demonstrated an increase in tissue oedema in various organs, and accumulation of inflammatory cells, namely neutrophils and macrophages in these organs [29, 30]. Neutrophils are regarded as mediators of the early phase and the increase in systemic Interleukin 6 levels after trauma is thought to be mediated by neutrophils. A parallel process occurs in the intestine and leads to activation and exhaustion of the stationary immune system, the reticulo-endothelial system: The centralization induced by blood loss causes intestinal hypoxemia and an alteration in intestinal permeability [31], which enables the crossing of intestinal pathogens through intestinal barriers and the permeation of pathogens in surrounding lymphatic tissues. It has been clearly proven that pathogens proceed to the liver through the portal vein break down [32, 33]. The most important effect of the exposure to endotoxins deriving from these pathogens is the induction of an inflammatory stimulus. This systemic inflammation occurs in the lymphatic tissues, followed by the reticulo-endothelial system of the liver. This can act as a buffer system [34] against pathogens and immunologic stimuli. Its protective effect fails when the endotoxin-induced inflammatory stimulus is on-going and overwhelming. Then, pathogens can spill over into the lung and accentuate the pre-existing inflammatory reaction. This spill-over is another reason why the lung is the first organ to show organ dysfunction in severely-injured trauma patients. The pivotal importance of the intestinal theory of posttraumatic organ dysfunction is widely accepted [35].
Interaction Between Acute Surgery After Trauma and the Pathophysiological Responses Induced by Trauma Many clinical studies have revealed that operations cause similar changes of the immunologic response to those induced by acute trauma. Among these, pro-inflammatory cytokines are most specific for trauma patients [2, 36]. Their
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levels usually remain elevated for more than 5 days after trauma in patients with a high injury-severity score, and early elevated levels discriminate trauma patients who later develop organ failure [3]. They also have been demonstrated to be closely related with the magnitude of the injury (burden of trauma) and with the operative procedure [37]. The degree of surgery has also been determined by changes in the specific immune system [38–40]. These and other studies reveal that the immuno-modulatory mechanisms after elective surgery and after primary surgery in trauma patients are well described [41]. Also, the inflammatory response induced by femoral nailing is biochemically comparable to that induced by other Orthopaedic operations. Moreover, in polytrauma patients, an additional impact due to primary surgery could be determined that occurs in addition to the one induced by the initial trauma. Clinical studies have clearly documented an exaggerated inflammatory response in which the duration of surgery and the amount of blood and temperature loss [28, 42, 43] play a role [38, 44]. A clinical prospective randomized study has shown that patients in uncertain conditions have a higher incidence of acute lung injuries, if longer surgical procedures are performed [10]. These factors may be induced by major surgery when a pre-activated immune response is present, such as in severe haemorrhage and soft tissue damage. In patients who present with very severe injuries, these factors outweigh the positive effects from the definitive stabilization of fractures described above [45]. Therefore, in these cases many Level I trauma centres have preferred to use a temporizing approach by using external fixation of the femoral shaft in selected patients, and named this approach “damage control orthopaedics” [45, 46]. Prior to the introduction of this approach, the most frequent treatment of major fractures in these situations was traction. The advantage of using an external fixator over traction lies in the fact that the fracture is stabilized which allows the patient to
move for nursing manoeuvres and to sit up in the ICU, which improves pulmonary toilet [47].
Factors for Grading Patient Assessment The damage-control concept of limiting the initial surgical time in patients with severe exsanguinating injuries was used for abdominal shotgun victims in Philadelphia. Packing of the major sources of haemorrhage, followed by ICU treatment and definitive repair in the following days was found to improve survival rates [48, 49]. For Orthopaedic injuries, the potential benefits of the damage control approach are more difficult to detect. Several aspects must be considered, such as slower progress of haemorrhage, existence of severe soft tissue injuries, and longer duration of the Orthopaedic repair. For patients with abdominal trauma the most important clinical factors are blood loss, coagulopathy and loss of temperature (triade-of-death); likewise in Orthopaedic patients, it is important to account for soft tissue injuries as well [50, 51]. Orthopaedic surgeons added a new patient category to the three existing classifications (stable, unstable, in extremis), which was named the “borderline” patient [52] (Table 3). Existing parameters for the classification of the patient condition have been for assessment. The abbreviated injury scale, Moore’s organ injury score and ATLS criteria of severe haemorrhage have all proven to be effective and have therefore been incorporated. Three out of the four criteria should be present to qualify a patient for a specific category. Fortunately, most patients fall into the stable or borderline category and among the latter, resuscitation can lead to improvement of the clinical condition to allow early fracture fixation [53]. Critical parameters can be summarized as follows: soft tissue injuries (major extremity fractures, crush injuries, severe pelvic fractures, lung
Table 3 Inverse-probability-of-treatment-weighted estimates of the relative risk of mortality for treatment delay (> 12 h) by severity of associated injury (data from [59]) Associated injury
Low severity (AIS <3)
n
Relative risk (95% confidence interval) Extremity/pelvis fractures Abdomen Chest Head
High severity (AIS ≥3)
n
p value
Relative risk (95% confidence interval)
0.58 (0.33, 1.20)
1,846
0.73 (0.39, 1.36)
1,223
0.63
0.82 (0.54, 1.35) 0.67 (0.32, 1.37) 0.71 (0.37, 1.77)
2,261 1,373 1,923
0.36 (0.13, 0.87) 0.64 (0.39, 1.11) 0.62 (0.40, 0.99)
808 1,696 1,146
0.09 0.90 0.74
Reported p values test the equality of treatment effects between low and high severity associated injury sub-groups AIS abbreviated injury score
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Hans-Christoph Pape
Table 4 Incorporation of existing classification systems (data from [53]) for clinical patient assessment to assess patients that are stable or can be stabilized to undergo definitive fracture fixation (modified according to [47])
Shock
Coagulation
Temperature Soft-tissue injuries
Parameter
Stable (Grade I)
Borderline (Grade II)
Unstable (Grade III)
In extremis (Grade IV)
Blood pressure (mmHg) Blood units (2 h) Lactate levels Base deficit (mmol/L) ATLS classification Platelet count (µg/mL) Factor II and V (%) Fibrinogen (g/dL) D-dimer
100 or more 0–2 Normal range Normal range I >110,000 90–100 >1 Normal range <33°C 350–400
80–100 2–8 Around 2.5 No data II–III 90,000–110,000 70–80 Around 1 Abnormal 33–35°C 300–350
60–90 5–15 >2.5 No data III–IV <70,000–90,000 50–70 <1 Abnormal 30–32°C 200–300
<50–60 >15 Severe acidosis >6–8 IV <70,000 <50 DIC DIC 30°C or less <200
Lung function; PaO2/FiO2 Chest trauma scores; AIS Chest trauma score; TTS Abdominal trauma (Moore) Pelvic trauma (AO class.) External (AIS)
AIS I or II AIS 2 or more (e.g., AIS 3 or more (e.g., (e.g., abrasion) 2–3 rib fractures) serial rib fx. >3) 0 I–II II–III £ or = II < or = III III
AIS 3 or more (e.g., unstable chest) IV III or >III
A type (AO)
B or C
C
AIS I–II (e.g., abrasion)
AIS II–III (e.g., mult. >20 cm tears)
AIS III–IV (e.g., <30% burn)
C (crush, rollover abd.) (Crush injury, >30 % burn)
Three out of the four categories should be met to classify for a certain category. It is of note, that patients who respond to resuscitation qualify for early definitive fracture care, as long as prolonged surgeries are avoided
contusions AIS >2), coagulopathy (platelets <90,000) and shock (systolic BP <90 mmHg, requirement of vasopressors) contribute to hypothermia (core temp <33°C) and are dangerous. The term “borderline”, referred to above, was coined to describe a fourth category of patients who are in an apparently stable condition pre-operatively, but deteriorate unexpectedly and may develop organ dysfunction [54]. Some of the criteria used to identify this patient population appeared to derive from clinical experience only, whereas others were the result of clinical studies undertaken to evaluate the impact of initial surgery on outcome. This assessment is made on the basis of overall injury severity, presence of specific injuries and current haemodynamic status [55, 56]. Any deterioration in the clinical state or physiological parameters should prompt rapid re-assessment and adjustment of management approach as appropriate [57] (Table 4 [53]). Based on the current understanding of pathophysiological principles, we feel that the initial polytrauma patient assess-
ment can be structured according to the “four pathophysiological cycles of polytrauma” described above. Patients may be categorized into one of the four different classes (stable, borderline, unstable, in extremis), if they meet the criteria in at least in three out of the four categories. In addition, it is important to note that individual variations exist.
Summary Damage-control appears to be a viable alternative in severely polytraumatized patients who are in a borderline or unstable condition. In these, it is important to perform a thorough pre-operative clinical assessment of physiologic parameters. In those patients at severe risk for systemic complications, the staged repair of Orthopaedic injuries is advised, while stable polytrauma patients benefit from early definitive fracture treatment.
Damage-Control Orthopaedic Surgery in Polytrauma
References 1. Patrick DA, Moore EE, Moore FA, Biffl WL, Barnett CC. Release of anti-inflammatory mediators after major torso trauma correlates with the development of post injury multiple organ failure. Am J Surg 1999;178:564–568. 2. Roumen R, Hendrijks T, ven der Ven-Jongekrijk, et al. Cytokine patterns in patients after major vascular surgery, hemorrhagic shock, and severe blunt trauma. Ann Surg 1993;218(6):769–776. 3. Partrick DA, Moore FA, Moore EE, et al. The inflammatory profile of Il-6, Il-8, and soluble intercellular adhesion molecule-1 in postinjury MOF. Am J Surg 1996;172:425–429. 4. Dunham CM, Bosse MJ, Clancy TV, Cole FJ Jr, Coles MJ, Knuth T, Luchette FA, Ostrum R, Plaisier B, Poka A, Simon RJ; EAST Practice Management Guidelines Work Group. Practice management guidelines for the optimal timing of long-bone fracture stabilization in polytrauma patients: The EAST Practice Management Guidelines Work Group. J Trauma 2001;50:958–967. 5. Olson S. Pulmonary aspects of treatment of long bone fractures in the polytrauma patient. CORR 2004;422:66–70. 6. Pryor JP, Reilly PM. Initial care of the patient with blunt polytrauma. Clin Orthop Relat Res 2004;422:30–36. 7. Talucci RC, Manning J, Lampard S, Bauch A, Carrico CJ. Early intramedullary nailing of femoral shaft fractures: A cause of fat embolism syndrome. Am J Surg 1983;46:107–111. 8. Roberts CS, Pape HC, Jones AL, Malkani AL, Rodriguez JL, Giannoudis PV. Damage control orthopaedics: Evolving concepts in the treatment of patients who have sustained orthopaedic trauma. Instr Course Lect 2005;54:447–462. 9. Townsend RN, et al. Timing fracture repair in patients with severe brain injury (Glasgow Coma Scale score <9). J Trauma 1998;44:977–982; discussion 982–983. 10. American College of Surgeons. National trauma data bank reference manual. 2005. http://www.facs.org/trauma/ntdb/ ntdbannualreport2005.pdf. Accessed 2008 Sept 11. Nast-Kolb D, Waydhas C, Gippner-Steppert C, Schneider I, Trupka A, Ruchholtz S, Zettl R, Schweiberer L, Jochum M. Indicators of the posttraumatic inflammatory response correlate with organ failure in patients with multiple injuries. J Trauma 1997;42:446–55. 12. Meduri GU, Kohler G, Headley S, Tolley E, Stentz F, Postlethwaite A. Inflammatory cytokines in the BAL of patients with ARDS. Persistent elevation over time predicts poor outcome. Chest 1995;108:255–259. 13. Pape H-C, Remmers D, Kleemann W, Goris, JA, Regel G, Tscherne H. Posttraumatic multiple organ failure – a report on clinical and autopsy findings. Shock 1994;1:228–234. 14. Rotondo MF, Zonies DH. The damage control sequence and underlying logic. Surg Clin North Am 1997;77:761–777. 15. Pellegrini JD, Puyana JC, Lapchak PH, Kodys K, MüllerGraziano CL. A membrane TNF-alpha/TNFR ratio correlates to MODS score and mortality. Shock 1996;6:389–396. 16. Napolitano LM, Ferrer T, McCarter RJ Jr, Scalea TM. Systemic inflammatory response syndrome score at admis-
73 sion independently predicts mortality and length of stay in trauma patients. J Trauma 2000;49:647–653. 17. Pape H-C, Giannoudis PV. The care of the multiply injured patient. In: RB Bucholz, JD Heckman, C Court Brown (eds). Rockwood and Green’s Fractures in adults, 6th edition. Lippincott Williams and Wilkins, Philadelphia, 2005. 18. Rotondo MF, Zonies DH. The damage control sequence and underlying logic. Surg Clin North Am 1997;77:761–777. 19. Dwenger A, Regel G, Schweitzer G. Pathomechanisms of the adult respiratory distress syndrome (ARDS) – Chemiluminescence analysis of polymorphonuclear leukocytes. Fresenius Z Anal Chem 1986;324:360–365. 20. Hauser CJ, Zhou X, Joshi P, Cuchens MA, Kregor P, Devidas M, Kennedy RJ, Poole GV, Hughes JL. The immune microenvironment of human fracture/soft-tissue hematomas and its relationship to systemic immunity. J Trauma 1997;42:895–903. 21. Faist E, Mewes A, Strasser TH. Alteration of monocyte function after major injury. Arch Surg 1987;123:287–292. 22. Chaudry IH, Ayala A, Ertel W, Stephan R. Hemorrhage and resuscitation: Immunological aspects. Am J Physiol 1990; 259:R28, 663–678. 23. Meakins JL, Marshall JC. The gastrointestinal tract: The motor of multiple organ failure. Arch Surg 1986;121:197–201. 24. Deitch EA. The role of intestinal barrier failure and bacterial translocation in the development of systemic infection and multiple organ failure. Arch Surg 1990;125:403–409. 25. Faist E, Kupper TS, Backer CC. Depression of cellular immunity after major injury. Arch Surg 1986;125:1000–1006. 26. Tate RM, Repine JE. Neutrophils and the adult respiratory distress syndrome. Am Rev Resp Dis 1983, 128:552 27. Horovitz JH, Carrico CH, Shires T. Pulmonary response to major injury. Arch Surg 1974;108:349. 28. Hildebrand F, Giannoudis PV, van Griensven M, Chawda M, Pape H-C. Pathophysiologic changes and effects of hypothermia on outcome in elective surgery and trauma patients. Am J Surg 2004;187(3):363–371. 29. Pape H-C, Kleemann W, Regel G, Goris RJA, Tscherne H. Organ response after severe trauma – a comparison between clinical and morphological patterns. J Eur Urgency Resuscitation 1994;7:13–20. 30. Pape H-C, Remmers D, Kleemann W, Goris, JA, Regel G, Tscherne H. Posttraumatic multiple organ failure – a report on clinical and autopsy findings. Shock 1994;1:228–234. 31. Pape H-C, Dwenger A, Regel G, Auf` M, Kolck M, Gollub F, Wisner D, Sturm JA, Tscherne H. Increased gut permeability after multiple trauma. Br J Surg 1994;81:850–852. 32. Meakins JL, Marshall JC. The gastrointestinal tract: The motor of multiple organ failure. Arch Surg 1986;121:197–201. 33. Deitch EA, Winterton J, Li Ma, Berg A. The gut as a portal entry for bacteria. Ann Surg 1987;205:681–685. 34. Pape H-C, Remmers D, Grotz M, Kotzerke J, Glinski S, van Griensven M, Dahlweid M, Sznidar S, Tscherne H. Reticuloendothelial system activity and organ failure in multiply injured patients. Arch Surg 1999;134:421–427. 35. Deitch EA. The role of intestinal barrier failure and bacterial translocation in the development of systemic infection and multiple organ failure. Arch Surg 1990;125:403–409.
74 36. Roumen R, Redl H, Schlag G. Inflammatory mediators in relation to the development of multiple organ failure in patients after severe blunt trauma. Crit Care Med 1995;23:474–480. 37. Giannoudis PV, Hildebrand F, Pape H-C. Inflammatory serum markers in multiple trauma patients – can they predict outcome ? J Bone Joint Surg (Br) 2004;86(3):313–323B. 38. Brune IB, Wilke W, Hensler T, et al. Downregulation of T helper type I immune response and altered pro-inflammatory and antiinflammatory T-cell cytokine balance following conventional but not laparoscopic surgery. Am J Surg 1999;177:55–60. 39. Hensler T, Heidecke CD, Hecker H, Heeg K. Increased susceptinbility to postoperative sepsis in patients with impaired monocyte Il-12 production. J Immunol 1998;161:2655–2659. 40. Hensler T, Hecker H, Heeg K, Heidecke C. Distinct mechanisms of immunosuppression as a consequence of major surgery. Infect Immun 1997;65:2283–2291. 41. Hoch RC, Rodruiguez R, Manning T. Effects of accidental trauma on cytokine and ET production. Crit Care Med 1993;1:839–845. 42. Pryor JP, Reilly PM. Initial care of the patient with blunt polytrauma. Clin Orthop Relat Res 2004;422:30–6. 43. Giannoudis PV, Abbott C, Stone M, Bellamy MC, Smith RM. Fatal systemic inflammatory response syndrome following early bilateral femoral nailing. Intensive Care Med 1998;24:641–642. 44. Porter JM, Ivatury RR, Nassauoura ZE. Extending the horizons of damage control in unstable patients beyond the abdomen and the gastrointestinal tract. J Trauma 1997;42:559–561. 45. Scalea TM, et al. External fixation as a bridge to intramedullary nailing for patients with multiple injuries and with femur fractures: Damage control orthopedics. J Trauma 2000;48: 613–621;discussion 621–623. 46. Nowotarski PJ, Turen CH, Brumback RJ, Scarboro JM. Conversion of external fixation to intramedullary nailing for fractures of the shaft of the femur in multiply injured patients. J Bone Joint Surg Am 2000;82:781–788. 47. Border JR. Death from severe trauma: Open fractures to multiple organ dysfunction syndrome. J Trauma 1995;39:12–22. 48. Rotondo MF, Schwab CW, McGonigal MD, et al. “Damage Control”: An approach for improved survival in exsanguinating penetrating abdominal injury. J Trauma 1993;35:375–382.
Hans-Christoph Pape 49. Moore EE, Thomas G. Memorial lecture: Staged laparotomy for the hypothermia, acidosis, and coagulopathy syndrome. Am J Surg 1996;172:405–410. 50. Asensio JA, Petrone P, O’Shanahan G, Kuncir EJ. Managing exsanguination: What we know about damage control/bailout is not enough. Proc (Bayl Univ Med Cent) 2003;16:294–296. 51. Keel M, Trentz O. Pathophysiology of polytrauma. Injury 2005;36:691–709. 52. Pape H-C, Regel G, Tscherne H. Pulmonary complications after intramedullary stabilization of the femur. In: B Browner (ed). The science of intamedullary nailing. Williams & Wilkins, Philadelphia, 1996, pp. 77–88. 53. Pape HC, Giannoudis PV, Krettek C, Trentz O. Timing of fixation of major fractures in blunt polytrauma: Role of conventional indicators in clinical decision making. J Orthop Trauma 2005;19:551–562. 54. Pape HC, Giannoudis P, Krettek C. The timing of fracture treatment in polytrauma patients: Relevance of damage control orthopedic surgery. Am J Surg 2002;183:622–629. 55. Bone LB, Johnson KD, Weigelt J, Scheinberg R. Early versus delayed stabilization of femoral fractures. A prospective randomized study. J Bone Joint Surg Am 1989;71:336–340. 56. Behrman SW, Fabian TC, Kudsk KA, Taylor JC. Improved outcome with femur fractures: Early vs. delayed fixation. J Trauma 1990;30:792–798. 57. Crowl AC, Young JS, Kahler DM, Claridge JA, Chrzanowski DS, Pomphrey M. Occult hypoperfusion is associated with increased morbidity in patients undergoing early femur fracture fixation. J Trauma 2000;48:260–267. 58. Pape HC, Rixen D, Morley J, Husebye EE, Mueller M, Dumont C, Gruner A, Oestern HJ, Bayeff-Filoff M, Garving C, Pardini D, van Griensven M, Krettek C, Giannoudis P; EPOFF Study Group. Impact of the method of initial stabilization for femoral shaft fractures in patients with multiple injuries at risk for complications (borderline patients). Ann Surg 2007;246: 491–499. 59. Morshed S, Miclau T, III, Bembom O, Cohen MM, Knudson M, Colford J. Delayed internal fixation of femoral shaft fracture reduces mortality among multi-system trauma patients. JBJS-A 2009;91:3–13.
Fractures and Non-Unions of the Clavicle Patrick Simon
Fractures of the clavicle are common, accounting for 3–5% of all fractures in adults, most often caused by a simple fall on the outstretched hand or a direct impact on the shoulder. They usually affect active and healthy people during sports activities (bicycle, ski, ball-sports) or road traffic accidents: these demanding patients are asking for a quick and full recovery. Until now treatment was usually conservative for mid-clavicle fractures (“they all heal and do fine”) whilst surgical treatment was usually preferred for lateral-end fractures. However, many papers in the last decade pointed out long-term deficits following conservative treatment for clavicle fractures, leading more Surgeons to propose surgical treatment to their patients. So this article will present the recent literature concerning the non-operative treatment of clavicle fractures, the various methods of surgical fixation and the treatment of malunions and non-unions.
1. Group I including middle third fractures (accounting for 70–80% from all clavicle fractures) 2. Group II lateral third fractures 3. Group III medial third fractures Neer [2] proposed dividing group II into three types: 1. Type I including fractures with coraco-clavicular ligaments intact 2. Type II fractures with coraco-clavicular ligaments detached from the proximal fragment 3. Type III intra-articular fractures For mid-clavicle fractures it is necessary to consider separately minimally-displaced fractures from those with severe deformity, shortening or comminution. From this point of view the classification proposed by Robinson [3] is logical even if type I from Allman becomes a type II in that classification detailed below:
Surgical Anatomy and Classification The clavicle has an S-shaped configuration with medial and distal flat ends, a tubular middle and a very small medullary canal. These considerations explain that plates or rigid nails are relative unsuitable implants. The clavicle acts as a bone strut to maintain the width of the shoulder and therefore provides power and stability to the arm-trunk mechanism: so shortening or mal-union after clavicle fractures may have an effect on shoulder function. The most commonly used classification is that of Allman [1] who separated clavicle fractures into three groups:
Type 1-medial fractures
B-displaced Type 2-middle fractures
A-cortical alignment B-displaced
Type 3-distal fractures Pr Patrick Simon Centre Hospitalier Saint Joseph Saint Luc, Lyon (France) 20 quai Claude Bernard 69365 Lyon Cedex e-mail:
[email protected]
A-non-displaced
A-non-displaced
B-displaced
G. Bentley (ed.), European Instructional Lectures. European Instructional Course Lectures 9, DOI: 10.1007/978-3-642-00966-2_9, © 2009 EFORT
A1-extra-articular A2-intra-articular B1-extra-articular B2-intra-articular A1-non-displaced A2-angulated B1-simple or butterfly fragment B2-comminuted or segmental A1-extra-articular A2-intra-articular B1-extra-articular B2-intra-articular
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Up-Date on Conservative Treatment for Mid-Clavicular Fractures Modalities of Conservative Treatment Non-operative treatment involves most often in a single arm sling or a figure-of-eight harness: there are no controlled studies that demonstrate a difference in bone healing between these two types of immobilization. In a prospective study Andersen et al. [4] compared a figure-of-eight bandage and a simple sling. The only difference was a higher rate of dissatisfaction in the figure-of-eight group (93% vs.74%; relative chance of satisfaction, 1.3; p = 0.09). The figure-ofeight splint may be preferred for the dominant limb as the hand remains free for writing, keyboarding or other activities of daily living. The duration of the treatment is usually 4–6 weeks whatever the kind of immobilization.
Outcomes After Conservative Treatment Until the mid-1990s many authors reported on good outcomes for fracture healing and restoration of function after non-operative treatment of clavicle fractures while the patients’ complaints were thought to be of cosmetic concern only. Nordqvist [5] reported on non-surgically treated midclavicular fractures at Malmö University Hospital: from 225 fractures reviewed with an average follow-up of 17 years, 53 were mal-united (23.5%) and 7 were non-unions (3.1%). For the authors the only indications for surgical treatment of isolated clavicle fractures were initial neurovascular interference and skin jeopardy. However there were 50% lost from review in this retrospective study. In one of the first papers to highlight the limits of conservative treatment Hill and colleagues [6] showed a high rate of non-union (15%) and unsatisfactory results (31%). Initial shortening at the fracture site of 20 mm or more had a highly significant association with non-union in this retrospective study of 52 patients. In a retrospective study of 132 patients Lazarides and Zafriopoulos [7] found that final clavicular shortening of more than 18 mm in male patients and of more than 14 mm in female patients was significantly associated with an unsatisfactory result. Of the patients, 34 (25.8%) were dissatisfied with the result of their management. McKee et al. [8] evaluated 30 patients at a mean of 55 months from the date of injury and showed that after conservative treatment strength of the involved shoulder was reduced to 75% compared to the uninjured shoulder
P. Simon
and the mean DASH (disabilities of the arm shoulder and hand) was 24.6 points indicating substantial residual dysfunction. In a prospective study Nowak et al. [9] showed that after 6 months 57% from 222 patients had completely recovered while 42% were not fully recovered and 7% presented a non-union (13% of the women, 3% of men). Moreover as many as 46% of 208 patients seen at long-term of 9–10 years did not consider themselves fully recovered: 9% complained from pain at rest, 29% from pain during activity, 27% had cosmetic defects. Comminuted fractures with transverse fragments had an increased risk for remaining symptoms while shortening itself did not predict outcome [10]. The prospective study of Robinson et al. [11] included 581 diaphyseal fractures, 263 lateral fractures and 24 medial fractures; the prevalence of non-union at 24 weeks was 4.5% of diaphyseal fractures, the non-union risk being significantly increased by advancing age, female gender, displacement of the fracture and the presence of comminution; the rate of non-union was 11.5% for lateral fractures.
Initial Radiographic Evaluation Shortening and over-riding of the fracture are often obvious on initial X-rays. Optimized X-rays may be necessary in some cases: an oblique antero-posterior view is then usually performed. Sharr and Mohammed [12] published in 2003 a study to assess the accuracy and utility of the postero-anterior 15° caudad view of the clavicle. This simple, reliable method of imaging the clavicle reduces the magnification by reducing the film to object distance. It is important to consider that often emergency radiographs are performed with a patient in a supine position. Before considering clavicle fracture minimally-displaced, it is necessary to obtain at least true clavicle A-P radiographs with and without a 20° cephalic tilt, the patient in a standing position.
In summary, non-operative treatment of acute midshaft clavicle fractures results in an overall non-union rate of 5.9%. The non-union rate for displaced fractures is 15.1%. Factors associated with non-union are displacement (relative risk = 2.3), comminution (relative risk = 1.4), female gender (relative risk = 1.4). Factors associated with long-term sequelae are fracture displacement (odds ratio = 1.9–3.4 for various measures), fracture comminution (odds ratio = 2), number of fracture fragments (odds ratio = 1.4), advancing age [13].
Fractures and Non-Unions of the Clavicle
Modalities of Plate Fixation of Mid-Clavicular Fractures Advocates for plating mid-clavicular fractures point out the quality of the reduction, and the rigid fixation while detractors criticize soft tissue stripping, length of scars and discomfort with such superficial plates. The gold standard is the open anatomical reduction and plate fixation. Spiral or oblique fractures are easily reduced and maintained by a reduction forceps; if necessary a lagcrew is inserted to stabilize a wedge fragment. A 7-or 8-hole LC-DCP plate 3.5 is usually used. A reconstruction plate which allows adequate contouring may also be used. Some authors are using smaller plates such as semi-tubular plates but the risk for failure is important to consider. Pre-contoured plates save operative time and minimize soft tissue irritation at the proximal and distal ends due to their low profile [14]. In complex comminuted fractures bridging plates are used to protect vascularisation of small fragments. The approach for plate fixation is superior, direct or inferior to the bone: anterior-inferior plate placement is associated with fewer post-operative symptoms. It is also possible to use a sabre cut incision to minimize cosmetic problems. In order to facilitate the bone union, mini-invasive approach has been proposed. This is possible with LCP plates which don’t need anatomic reduction due to their inherent stability [15]. However Brouwer published four cases of failure of superior locking clavicle plates by axial pull-out: from these one was a fresh fracture which presented partial pull-out and delayed union while the three others were non-unions with numerous previous surgeries which developed persistent non-union [16]. One disadvantage of plate fixation is that the hardware is always extremely prominent: therefore secure wound closure is of major importance.
Intra-Medullary Fixation Advocates for intra-medullary fixation point out the easy procedure, the limited exposure, the good cosmetic results and the satisfactory union rate. However it is interesting to note that in a cadaveric biomechanical study plate constructs showed superior performances to intra-medullary fixation [17]. Whatever the implant used a full access for the C arm is mandatory to obtain cephalic and caudal tilt intra-operative views of the entire length of the clavicle. Knowles pins or Kirchsner wires were used for a long time with good results. Chu et al. [18] noted a 100% union rate and a Constant score of 97% from 73 cases treated with Knowles pins reported at 1 year F-U.
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Similarly 2.0–3.5 mm elastic titanium nails introduced by a hole on the ventral cortex of the medial clavicle 1 cm distal to the sternoclavicular joint are more and more used, especially in Germany. An open reduction is sometimes necessary. In the series from Jubel et al. [19] all fractures united and the Constant score was 98% one year post-surgery. However the authors proposed the nail only for transverse or oblique fractures or for wedge fractures; whenever comminution is present at fracture site they proposed plating rather than nailing. Parsons [20] proposed an intra-medullary screw fixation which can be performed through a small incision with a cannulated 6.5 partially-threaded cancellous screw inserted from lateral to medial.
Results of Operative Treatment The multi-centre prospective study of Altamani supports primary plate fixation relative to improved functional outcome and lower mal-union and non-union rates compared with conservative treatment [14]. In a large series Shen et al. [21] showed a 3% non-union rate and a risk of refracture after plate removal (2 cases from 171). Conversely, Böstman et al. [22] reported a 23% complication rate and a 7% infection rate after plate fixation of fresh displaced mid-clavicular fractures. In the meta-analysis of Zlowodzki et al. [13] the nonunion rate is 5.9% for fractures treated non-operatively, 2.5% for fractures treated with a plate and 1.6% for fractures treated with an intra-medullary pin. For displaced fractures the non-union rate was 15.1% for fractures treated non-operatively vs. 2.2% and 2% for fractures treated with a plate or intra-medullary pin. The results must be interpreted with caution as the majority of the identified studies were retrospective and either had no control group or did not use any randomization if there was a control group. In a prospective non-randomised study Lee et al. [23] compared 56 patients treated with Knowles pin and 32 patients treated by plate: shoulder score, union rate and healing time were not significantly different between the two groups, leading the authors to propose pinning rather than plating.
Indications for Surgery in Mid-Clavicular Fractures It is clear that until now most clavicle fractures are still treated conservatively. This is a good option indeed for nondisplaced or minimally-displaced fractures. Initial X-rays are to be done as previously mentioned.
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Indications for surgery are listed below: absolute indications are limited. Vascular injuries are rare: they maybe lifethreatening but most often the injury is an intimal tear and the diagnosis may be late. Floating shoulder is usually an indication for fixation in order to restore the adequate length of the shoulder compass, even if satisfactory results may be obtained without fixation [24]. Open clavicle fracture is a rare injury, often associated with pulmonary injury (pneumothorax or contusion), vascular or neurologic lesions [25]. Relative indications are to be approached on a caseby-case basis. Indications for fixation are: Multiple trauma Neurovascular injuries Open fracture or impending perforation of the skin Ipsilateral scapular neck fracture (displaced floating shoulder injury) Relative indications for fixation are: Grossly-displaced mid-shaft fractures Intolerance to immobilization, intolerable pain Patients who need quick and full recovery: sportsmen, active workers Associated lower-extremity fractures that require crutches Ipsilateral serial rib fractures
Mal-Union of Midshaft Clavicle Fractures Surgical treatment of clavicle mal-unions is unusual. Indications may be severe shortening (>15 mm), angular deformity, substantial disability, dissatisfaction with the appearance or asymmetry of the shoulders: reasonable indications may be severe local pain or neurovascular impairment. An intercalary bone graft is usually necessary to compensate for bone loss; an osteotomy must be performed through the remodelled fracture site; the initial butterfly fragments are to be resected and the medullary cavity opened. The mal-rotation especially of the distal fragment is corrected by re-directing superiorly the flat surface, which is typically rotated anteriorly. In these cases plate fixation is the best option while rigid plate fixation maintains the restored length and rotation. There are few papers on this specific problem, most of them relating small series of cases. Mc Kee et al. [26] reported on 15 clavicle mal-unions treated by corrective osteotomy and limited contact-plate osteosynthesis; 11 of the 15 patients presented pre-operatively a thoracic outlet syndrome. It is
P. Simon
interesting to note that in a recent paper patients remain functionally impaired even if solid union is achieved [27].
Non-Union of Mid-Clavicle Fractures They induce dysfunction of the upper limb in more than half cases; restoration of the length and rigid fixation are required. the need for bone grafting depends on the type of non-union. Most often the fracture site is atrophic: in these situations where clavicular ends are sclerotic some degree of resection and intercalary bone graft are required. The incision is carried out directly to the bone providing thick flaps without dissection of the suprascapular nerves. Clavicle ends are freed from surrounding tissues. Vascular channels are drilled in both cortical ends and a medullary canal is created. If there is some obliquity to the fracture extremities it’s easy to place a lag screw. If required a cortico-cancellous graft is fashioned in either a parallelogram or a keystone shape. Plate fixation may be preferred because of improved rotational stability, ability to incorporate bone graft, and prevention of implant displacement. To decrease the risk of screw pull-out and prominence of the instrumentation, Kloen et al., proposed antero-inferior plating using a 3.5-mm pelvic reconstruction plate with a lag-screw and bone graft [28]. A simple sling is used for 3 weeks and then active assisted forward elevation is allowed. Pendulum exercises are contra-indicated because downward traction is a risk for displacement. O’Connor et al. [29] reported on 24 clavicle non-unions treated by open reduction, internal fixation and autologous bone grafting. At a mean follow-up of 42 months the DASH scores did not show any significant difference when compared with normative data for the general population. The use of bone morphogenetic proteins, low-intensity pulsed ultrasound or pulsed electromagnetic fields in clavicle non-union is not very common and no paper clearly established whether these methods are useful or not. Free vascularized cortico-periosteal bone graft has been used for the treatment of persistent non-union of the clavicle [30].
Fractures of the Lateral Third of the Clavicule Type 1 or 3 distal clavicle fractures are usually treated non-operatively by a simple sling. Type 2 fractures require surgery due to the high rate of non-union if conservative treatment is chosen (up to 40%). This is related to the
Fractures and Non-Unions of the Clavicle
displacing forces: weight of the arm, pulling forces of pectoralis major and minor, latissimus dorsi and trapezius muscle. However the best surgical method is still in debate. Standard techniques involving trans-articular or extra-articular K wire fixation, coraco-clavicular screw fixation and tensionband wiring have considerable risks for complications, especially loss of reduction, pin migration, screw pulling out and acromio-clavicular joint degeneration. Coraco-clavicular dacron tape, coraco-clavicular screw and tension-band suture over the fracture site may be used in a combined procedure. It is important to understand that in order to neutralize displacing forces coraco-clavicular screwing is useful to protect the direct fixation of the fracture. Specialized distal clavicular plates are helpful because they match the shape of the distal clavicle. Plating with a hook-plate is the more recent method; careful operative technique is necessary to prevent complications including sub-acromial impingement, rotator cuff damage, acromion fracture and hook cut-out. It is best to remove the plate after bony union. Lee et al. [31] in a recent retrospective study considered that hook-plate had more advantages than tension-band wires.
Conclusions Surgical treatment of adult displaced clavicle fractures should be considered in order to lower non-union rate and to minimize cosmetic and functional sequelae. While the two most popular methods of fixation (plate or intra-medullary fixation) lead to higher union rates and better shoulder function, operative treatment must be discussed seriously as a treatment option for the young, high-demand patient with a fracture at risk of non-union or mal-union.
References 1. Allman FL. Fractures and ligamentous injuries of the clavicle and its articulation. J Bone Joint Surg [Am] 1967;49: 774–784. 2. Neer CS. Fractures of the distal third of the clavicle. Clin Orthop 1968;58:43–50. 3. Robinson CM. Fractures of the clavicle in adults. Epidemiology and classification. J Bone Joint Surg [Br] 1998; 80:476–484. 4. Andersen K, Jensen PO, Lauritzen J. Treatment of clavicular fractures. Figure-of-eight bandage versus a simple sling. Acta Orthop Scand 1987;58:71–74.
79 5. Nordqvist A, Petersson CJ, Redlung-Johnell I. Mid-clavicle fractures in adults: End result study after conservative treatment. J Orthop Trauma 1998;12:572–576. 6. Hill J, McGuire M, Crosby L. Closed treatment of displaced middle third fractures of the clavicle gives poor results. J Bone Joint Surg [Br] 1997;79:537–539. 7. Lazarides S, Zafiropoulos G. Conservative treatment of fractures of the middle third of the clavicle: The relevance of shortening and clinical outcome. J Shoulder Elbow Surg 2006;15:191–194. 8. McKee MD, Pedersen EM, Jones C, et al. Deficits following nonoperative treatment of displaced midshaft clavicular fractures. J Bone Joint Surg [Am] 2006;88A:35–40. 9. Nowak J, Holgersson M, Larsson S. Sequelae from clavicular fractures are common. A prospective study of 222 patients. Acta orthopaedica 2005;76:496–502. 10. Nowak J, Holgersson M, Larsson S. Can we predict long term sequelae after fractures of the clavicle based on initial findings? A prospective study with nine to ten years of follow-up. J Shoulder Elbow Surg 2004;13:479–486. 11. Robinson CM, Court-Brown MC, McQueen M, Wakefield A. Estimating the risk of non-union following nonoperative treatment of a clavicular fracture. J Bone Joint Surg [A] 2004;86:1359–1365. 12. Sharr RP, Mohammed KD. Optimizing the radiographic technique in clavicular fractures. J Shoulder Elbow Surg 2003;12:170–172. 13. Zlowodzki M, Zelle BA, Cole PA, Jeray K, McKee MD. Treatment of acute midshaft clavicle fractures: Systematic review of 2144 fractures on behalf of the evidence-based Orthopaedic Trauma Working Group. J Orthop Trauma 2005;19:504–507. 14. Altamimi SA, McKee MD; The Canadian Orthopaedic Trauma Society. Nonoperative treatment compared with plate fixation of displaced midshaft clavicular fractures. Surgical technique. J Bone Joint Surg [Am] 2008;90(suppl 2):1–8. 15. Andermahr J, Faymonville C, Rehm KE, Jubel A. Percutaneous plate osteosynthesis for clavicular fractures. Initial description. Unfallchirurg 2008;111:43–45. 16. Brouwer KM, Wright TC, Ring DC. Failure of superior locking clavicle plate by axial pull-out of the lateral screws: a report of four cases. J Shoulder Elbow Surg 2008;18: e22–e25. 17. Golish SR, Oliviero JA, Francke EI, Miller MD. A biomechanical study of plate versus intramedullary devices for midshaft clavicle fixation. J Orthop Surg 2008;16:28. 18. Chu CM, Wang SJ, Lin LC. Fixation of mid-third clavicular fractures with Knowles pins: 78 patients followed for 2–7 years. Acta Orthop Scand 2002;73:134–139. 19. Jubel A, Andermahr J, Schiffer G, et al. Elastic stable intramedullar nailing of midclavicular fractures with a titanium nail. Clin Orthop Relat Res 2003;408:279–285. 20. Parsons M, Blitzner CM. Small-incision,intramedullary compression osteosynthesis of acute and non-united midshaft clavicle fractures. Tech Shoulder Elbow Surg 2005;6:218–225. 21. Shen WJ, Liu TJ, Shen YS. Plate fixation of fresh displaced midshaft clavicle fractures. Injury 1999;30:497–500.
80 22. Bostman O, Manninen M, Pihlajamaki H. Complications of plate fixation in fresh displaced midclavicular fractures. J Trauma 1997;43:778–783. 23. Lee YS, Huang HL, Lo TY, Hsieh YF, Huang CR. Surgical treatment of midclavicular fractures: A prospective comparison of Knowles pinning and plate fixation. Int Orthop 2008;32:541–545. 24. Edwards SG, Whittle AP, Wood GW. Non operative treatment of ipsilateral fractures of the scapula and clavicle. J Bone Joint Surg 2000;82-A:774–780. 25. Taitsman LA, Nork SE, Coles CP, Barei DP, Agel J. Open clavicle fractures and associated injuries. J Orthop Trauma 2006;20(6):396–399. 26. McKee MD, Wild LM, Schemitsch EH. Midshaft malunions of the clavicle. J Bone Joint Surg 2003;85-A:790–797. 27. Rosenberg N, Neumann L, Wallace AW. Functional outcome of surgical treatment of symptomatic non-union and malunion
P. Simon of midshaft clavicle fractures. J Shoulder Elbow Surg 2007; 16:510–513. 28. Kloen P, Sorkin AT, Rubel IF, Helfet DL. Anteroinferior plating of midshaft clavicular nonunions. J Orthop Trauma 2002;16:425–430. 29. O’Connor D, Kutty S, McCabe J. Long-term functional outcome assessment of plate fixation and autogenous bone grafting for clavicular non-union. Injury Int J Care Injured 2004;35:575–579. 30. Fuchs B, Steinmann SP, Bishop AT. Free vascularized corticoperiosteal bone graft for the treatment of persistent nonunion of the clavicle. J Shoulder Elbow Surg 2005;14: 264–268. 31. Lee YS, Lau MJ, Tseng YC, Chen WC, Kao HY, Wei JD. Comparison of the efficacy of hook plate versus tension band wire in the treatment of unstable fractures of the distal clavicle. Int Orthop 2008, epub ahead of print.
Proximal Humeral Fractures C. Torrens
Introduction Despite more than 3,000 articles published proximal humeral fractures remain difficult to define and classify, natural evolution has been poorly defined and the best treatment option is yet to be established. Current trends in management of these complex fractures are analyzed and rationale decisionmaking is presented.
Epidemiology Analysis of fracture distribution shows that proximal humeral fractures are osteoporotic fractures with a unimodal distribution in older men and women [1]. Women are likely to present a proximal humeral fracture three times more frequently than men and the average age of women sustaining a proximal humeral fracture is significantly older than that in men (70 years old in women vs. 56 years in men) [2]. Proximal humeral fractures are the third most frequent fracture in elderly people after hip and Colles’ fractures and are exponentially increasing. Palvanen et al., reported that the total number of Finnish adults 60 years and older hospitalized with a proximal humeral fracture rose during their study period from 208 in 1970 to 1,120 in 2002. The overall incidence of these fractures also increased 63% and the mean age of patients with proximal humeral fractures increased from 72 years old (1970) to 77 years old (2002).They concluded that if these trends continue, the current number of fractures in the elderly will triple during the next three decades [3].
C. Torrens Orthopaedic Department, Hospital del Mar, Passeig Marítim 25-29, 08003 Barcelona, Spain e-mail:
[email protected]
The vast majority of fractures are produced by falls from standing height (87%), while sports injuries and road accidents constitute a small proportion of proximal humeral fractures (8%) and represent the younger population (33 years-old for sport injuries and 46 years for road accidents) whose fracture patterns and treatment considerations are not the same as the common osteoporotic proximal humeral fracture [2]. An increase in the rate of falls, independent of the average rate, may be associated with a higher risk of humeral fractures [4]. Fall-related risk factors included previous falls, diabetes mellitus, difficulty walking in dim light, seizure medication use, depression, using a hearing-aid and left-handedness [5]. Conversely, patients who present a proximal humeral fracture are much fitter than those who present with proximal femoral fractures, and pre-fracture functional status reveals that nine-tenths live at home [2]. When planning treatment options, this condition has to be taken into account to preserve pre-operative functional status. Although the majority of the proximal humeral fractures are considered to be non-displaced the mortality after shoulder fracture is considered to be higher than that of the general population immediately after the fracture and this condition is maintained until 5 years after fracture when mortality is not significantly different from mortality of the general population [6]. Even more, at the age of 60 years old, a prior shoulder fracture is associated with an immediate risk of hip, forearm or spine fracture that is significantly higher than that of the age and sex-matched population [7].
Imaging Studies Traditionally, proximal humeral fractures have been studied by the so called “trauma series” including a true antero-posterior view, lateral projection in the scapular plane and axillary view as described by Neer [8]. In acute fractures good axillary views are not always easy to obtain because of the pain induced by arm mobilization and because most of these X-rays are done
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in the emergency room scenario. Recently, the axillary view has been progressively substituted by CT studies. It has been demonstrated that CT scans provide clinically-useful information for the treatment of complex proximal humeral fractures when radiographs provide inadequate information [9]. The rationale may be to obtain from each projection what can be obtained instead of trying to allocate an image to a rigid classification system. The antero-posterior view clearly defines the relationship between humeral head and humeral shaft (Fig. 1) and some articular and greater tuberosity fractures (Fig. 2), but fails to inform about the posterior displacement of the greater tuberosity fragment and gives little information about the lesser tuberosity. Multiple radiographic views are needed to evaluate displacement of the greater tuberosity appropriately [10]. Lateral projection provides good information about anterior or posterior dislocation (Fig. 3) and the relationship between the humeral head and humeral shaft (Fig. 4) but gives
Fig. 3 Humeral head anteriorly dislocated seen in lateral projection
Fig. 1 A-P view showing gross displacement between humeral head and diaphysis
Fig. 2 Greater tuberosity fracture on A-P view
Fig. 4 Lateral projection showing displacement between humeral head and diaphysis
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Fig. 5 Posteriorly displaced greater tuberosity as seen in CT scan
Fig. 6 Lesser tuberosity fracture in CT scan
a
a
unclear information of the position of the tuberosities. CT scan is helpful in the analysis of greater and lesser tuberosity fracture pattern as well as displacement (Figs. 5 and 6) and gives also information of the quality of the subchondral bone of the humeral head. Recently, different sequential image analysis systems have been proposed to rationally-analyze the fracture patterns and obtain a better understanding of the fracture itself by answering simple questions [11–13].
Classifications Systems Codman first pointed out that fracture lines in the proximal humerus tend to occur between 4 major fragments: the head, the greater tuberosity, the lesser tuberosity, and the shaft, and composed a scheme of all possible fracture patterns [14]. Later on, Neer defined the four-segment classification of proximal humeral fractures, and arbitrarily established the criteria of displacement of 1.0 cm or 45° of angulation [8]. The AO group has also developed a classification system, which differentiates between articular and
b
b
extra-articular fractures [15]. Both systems have failed to obtain reasonable reliability and reproducibility even after the inclusion of CT scans to analyze fracture pattern [16–21]. Moreover, the Neer classification system does not include all possible fracture patterns [22], and also fails to differentiate specific types of fractures with substantially different prognoses such as the four-part valgus-impacted fracture [23]. Recently, Neer has redefined the purpose and use of the four-segment classification system restating the criteria for some of the categories (two-part shaft displacement divided into impacted, un-impacted and comminuted) and including a specific comment on the four-part valgusimpacted fracture. It also has been observed that analyses of reliability have been performed in most of the studies without using the trauma series views, including inexperienced interpreters with low scores and without applying the regular four-segment classification rather than five or six categories or lists of questions [24]. As Shrader et al. have stated, the problem is understanding the image of complex fractures, not the classification system [12]. Anyway, the Neer classification system remains the most used world-wide and has contributed to better understanding of these complex fractures.
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Current Trends of Treatment The best surgical treatment of proximal humeral fractures is yet to be defined if any surgical treatment is needed at all. The first unanswered question arises to whether proximal humeral fractures should be managed non-operatively or operatively. Lanting et al., have stated in a recent systematic review of primary intervention of proximal humeral fractures that there is a wide variation in recommended treatments and that the quality of the evidence is low and does not support any specific treatment choice [25].
General Considerations The main end-points to consider when planning proximal humeral fracture treatment are the functional outcome, development of aseptic necrosis and complication rate. Edelson et al., have recently studied the natural history of complex displaced fractures of the proximal humerus in a series of 63 patients non-operatively treated. They have stated that after conservative treatment motion is considerably compromised but pain is minimal and functional status is acceptable to most individuals in this older patient population, obtaining a mean forward flexion of 112°, lateral rotation with the elbow at the side of 37° and internal rotation of level L1 [26]. Zyto also considers non-operative treatment of three-part fractures after following a series of 15 patients conservatively-treated after more than 10 years and obtaining a mean forward elevation of 120°, lateral rotation of 45° and internal rotation of 60° [27]. The same author in a previously-reported series randomized 40 elderly patients with displaced three-part and four-part fractures to either conservative treatment or tension-band osteosynthesis and found no functional differences between the two groups. Anatomical reduction had little effect on improved function and complications were found to occur mainly in the surgically-treated group [28]. Conversely, Gerber et al., found that the operative treatment of complex fractures of the proximal humerus gives good results if anatomical reduction is obtained and that it is possible to obtain this if the bone quality, as judged by the thickness of the cortex of the proximal humerus diaphysis, is good [29]. Resch et al. also found strong correlation between the functional result and the quality of reduction in a series of 22 patients with valgus-impacted fractures operatively-treated [30]. The avascular necrosis rate depends on the fracture pattern, the treatment applied and the follow-up accomplished, and has been reported from 20 to 90%. Despite this, ana-
C. Torrens
tomical studies determine that some fracture patterns strongly correlate with blood-supply disruption of the humeral head [31, 32], Hertel et al. in a series of 100 intra-capsular fractures of the proximal humerus treated by open surgery stated that the most relevant predictors of ischemia were: 1. The length of the dorso-medial metaphyseal extension (shorter than 8 mm in all ischaemic heads). 2. The integrity of the medial hinge (also previously described by Resch et al. [30]. 3. The basic fracture type determined with the binary description system with an anatomic neck component, also stating that besides the disruption of the medial hinge, all other directions of fracture displacement did not strongly correlate with the vascular status [33]. Later on, the same group published the longer follow-up of those patients considered to be at risk of developing necrosis of the humeral head, and surprisingly eight of the ten initially ischemic humeral heads did not collapse over time indicating that revascularization may occur and 4 of the 30 initially perfused heads developed avascular necrosis with no clear explanation for that phenomenon [34]. Complications seem to be more frequent in operated patients and can vary widely depending on what is to be considered a complication but can be reported to be as high as 42 shoulders with complications out of 82 operated on if incomplete reduction, loss of anatomic fracture fixation, delayed healing, infection and cuff failure are included as reported by Smith et al. [35].
Treatment Outcomes One-part or non-displaced proximal humeral fractures have shown an acceptable range of good and excellent functional results (77–88%) after non-operative treatment, but significant limitation in internal and external rotation may be expected, age being the main determinant of outcome. Starting physical therapy less than 14 days after injury also contributes to best results [36–38]. If non-operative treatment is decided upon in impacted proximal humeral fractures, early mobilization seems to be safe and more effective for quickly restoring the physical capability of the injured arm, although differences tend to disappear at 6 months follow-up [39]. Many different surgical treatments have been proposed for the management of severely displaced proximal humeral fractures, including osteosutures [40], Ender-nails together with osteosutures [41], plate fixation [42], extra-medullary pinning [30] and intra-medullary nailing [43]. All of them achieve reasonable functional results and also in most of
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the cases a pain-free shoulder. Commonest complications include loss of reduction, need for a second operation to remove implant material, avascular necrosis of the humeral head, stiffness and infection at different rates depending on the populations selected, the fracture pattern and the treatment choice. Recently-developed locked plates have change the treatment map of proximal humeral fractures and their use has widely spread over the last years. Specially developed to obtain strength fixation in osteoporotic bone, locked plates were expected to improve older designs. Early published results are not so encouraging as expected and numerous complications have also been reported. Fankhauser et al., reported in a series of 29 fractures at a follow-up of 1 year a final mean Constant Score result of 74.6, and despite early mobilization, there was a slow functional recovery of the patients evaluated at 1.5, 3, 6 and 12 months. Age and complexity of the fracture also influenced end result [44]. Koukakis et al., in a small series of 20 patients also obtained a mean final Constant Score of 76.1% in a relatively young population with a mean age of 61.7 years [45]. Moonot et al., have reported in a series of 32 patients with a mean age of 59.9 years-old a mean final Constant Score of 66.5 in a short follow-up of 11 months [46]. Handschin et al., in a series of 31 patients presented a mean final adjusted Constant Score of 80% and compared the results with a historical control group of 60 patients operated for the same fracture types using two one-third tubular plates finding no differences in complication rate, return to work and functional outcome. Differences were noted in the total cost, being 684 Euros for angular-stable plate and of 158 for the one-third tubular plate [47]. On the other hand, several complications have been published associated with the use of locked plates. Egol et al., reported in a series of 51 patients the development of 16 complications in 12 patients, including screw penetration, necrosis, non-union, infection and early failure of the implant [48]. Owsley et al., in a series of 53 patients reported in 36% of the patients the presence of radiographic signs of complications, including 23% of screw cut-outs, 25% of varus displacement and 4% of necrosis. They also reported a 13% of revision surgery, and considered that complications tended to affect elderly people being significant in patients older than 60 years [49]. Neer reported in 1970 early results of prosthetic replacement in severely-displaced proximal humeral fractures, and although his excellent results have never been reached again, hemiarthroplasty still remains as the treatment of choice in those more complex fractures [50]. Antuña et al., have reported the results of 57 patients with a long follow-up (minimum of 5 years) treated with a shoulder hemi-arthroplasty for acute fractures of the proximal humerus with a mean age of 66 years. There were 27 patients satisfied and 30 unsatisfied. 16%
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referred moderate or severe pain and range of motion averaged 100° for anterior elevation (20–180°) and 30° for external rotation (0–90°). They concluded that hemi-arthroplasty gives good pain relief but unpredictable functional results [51]. Looking closer to the results presented, the average movement may not be representative of the general status due to the wide range observed, with patients moving from 20 to 180° of anterior elevation. Grönhagen et al., also found in a series of 46 patients a mean Constant score of 42 but ranging from 11 to 83 with primary hemi-arthroplasty for comminuted proximal humerus fractures. Constant score decreased significantly in 24 prostheses that had migrated superiorly [52]. Boileau et al., in a series of 66 patients tried to find out the reasons for poor outcomes after hemi-arthroplasty. There were 27% of initially badly-positioned tuberosities and 23% of tuberosity detachments and migration. Final tuberosity mal-position was observed in 50% of the patients and correlated with unsatisfactory results, superior migration of the prosthesis, stiffness or weakness and persistent pain. The factors associated with failure of tuberosity osteosynthesis were poor initial position of the prosthesis, poor position of the greater tuberosity and women over the age of 75 years [53]. Poor initial positioning of the prosthesis is related to the lack of landmarks in acute fractures with distorted anatomy. Different attempts have been made to find anatomical references to properly position the prosthesis in acute fractures. The bicipital groove has been considered helpful for some author’s to reproduce accurate retroversion [54, 55] while others believe that a significant internal rotation occurs along the course of the bicipital groove (15.9°) that has clinical implications if it is used as a landmark for humeral head replacement in acute fractures [56]. Recently the upper insertion of the pectoralis major has been proposed as a landmark for proper restoration of the humeral height [57–59] as well as to determine retroversion of humeral head [59] It has been stated that placing the humeral head at 5.6 cm from upper pectoralis major insertion and locating the posterior prosthesis fin 1.06 cm posterior to upper pectoralis insertion will result in anatomical height and version restoration. Frankle et al., have studied how to improve tuberosity reattachment and configuration of the sutures in a cadaveric model, concluding that circumferential cerclage reduced interfragmentary motion and strain and maximized fracture stability [60]. De Wilde et al., have proposed a new concept of trauma shoulder prosthesis allowing an anatomic reconstruction of the rotator cuff insertions around the prosthetic head through specially-designed holes in the humeral head, but clinical results are still to be reported [61]. Due to the unpredictable functional outcome of hemiarthroplasty in complex humeral fractures, reversed designs
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have increasingly become part of the therapeutic choice. Avoiding the need of cuff function by improving the deltoid, the reversed prostheses were thought to be the solution for such osteoporotic comminuted fractures. Once again recent results are not so encouraging as expected and in a series of 43 patients with a short mean follow-up of 22 months, the mean active elevation was 97° (35–160°) and mean external rotation was 30° (0–80°). The mean Constant Score was 44 (16–69). Peri-prosthetic calcification was observed in 90% of the patients, displacement of the tuberosities in 53% and a scapular notch in 25% [62].
Author’s Rationale Elderly patients sustaining a proximal humeral fracture can initially be allocated in two groups; 1. The first one includes elderly fit patients in good mental condition and willing to restore their previous functional level. 2. The second one includes elderly unfit patients in fair mental condition and not motivated to follow rehabilitation programmes. Fig. 7 Two-part surgical neck fracture
In the second group, almost all proximal humeral fractures can be properly managed conservatively since non-operative treatment has been proven to obtain good pain relief and functional level which is good enough for this selected population [26]. In the first group, pros. and cons. of surgical treatment have to be discussed with the patient taken into account that surgery may almost only be indicated in patients willing to restore good function. The Surgeon also has to be aware that elderly people may mostly use their arms in a below-shoulder level but that active external rotation is present in almost every single daily activity and must be preserved. Patients also have to be aware that acute treatment of proximal humeral fractures is relatively easy and report good results meanwhile late treatment is complex and often has limited results. If non-operative treatment is chosen on the basis of the initial X-ray exam., no further displacement of the fracture is to be expected, so there is no need for a 1-week second radiolograph and the patient can start an early rehabilitation program. Two-part surgical neck fractures with less than 30% contact between the humeral head and the diaphysis can be properly managed with two Ender nails together with a tension-band suture followed by 3-weeks immobilization (Figs. 7 and 8). They can also be treated with a locked plate
Fig. 8 Two-part surgical neck fracture reduced and stabilized with two Ender nails plus tension-band suture
but extensive surgical exposure is needed, a higher rate of complications can be expected and the functional benefit remains unclear. Two-part greater tuberosity fractures are commonly associated with poor results if there is a displacement greater than 5 mm and can be easily managed by open reduction and
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Fig. 9 Three-part greater tuberosity fracture
Fig. 10 Per-operative view of the reduction and stabilization with trans-osseous sutures
stabilization with simple sutures through a delto-pectoral or antero-superior approach. Three-part greater tuberosity fractures with the head impacted in valgus position and four-part valgus fractures can also be properly managed by open elevation of the humeral head, restoring anatomical neck-diaphysis angle and then reducing the greater and lesser tuberosities to their position and securing them with trans-osseous sutures (Figs. 9–11). Special training is required to percutaneously elevate the humeral head, reduce the tuberosities and pin the fragments but constitutes a good alternative for this selected fractures. Three-part greater tuberosity fractures with the head impacted in a varus position produce severe impaction
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Fig. 11 One-year follow-up with the fracture consolidated without losing reduction
of the cancellous bone of the humeral head compromising the stability of reduction. If anatomical reduction is employed, a locked plate together with bone graft filling humeral head defect is required, but most of the times varus impactation can be assumed and surgery may be limited to properly replace the greater tuberosity if any surgery is needed at all. Four-part fractures and four-part fracture-dislocations can be treated with open reduction and stabilization with a locked plate if reasonable reduction and stability is achieved, otherwise arthroplasty is to be considered. If arthroplasty is considered, “young-elderly” patients under 80 years, with a “one-piece” greater tuberosity, no signs of cuff disruption and males, are the best candidates for hemi-arthroplasty. Conversely, “elderly-elderly” patients over 80 years, with a comminuted greater tuberosity, severe osteoporosis and female are the best candidates for reverse prostheses if any treatment is needed at all.
Conclusions The total number and complexity of humeral fractures is increasing. There is a current trend to a more conservative management of these fractures. Patient selection for operative treatment should consider physical and mental status, willingness of the patient to restore function under a long rehabilitation program, fracture pattern and associated osteoporosis.
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References 1. Court-Brown CM, Caesar B. Epidemiology of adult fractures: a review. Injury 2006;37:691–7. 2. Court-Brown CM, Garg A, McQueen MM. The epidemiology of proximal humeral fractures. Acta Orthop Scand 2001; 72:365–71. 3. Palvanen M, Kannus P, Niemi S, Parkkari J. Update in the epidemiology of proximal humeral fractures. Cin Orthop 2006; 442:87–92. 4. Schwartz AV, Nevitt MC, Brown BW, Kelsey JL. Increased falling as a risk factor for fracture among older women. Am J Epidemiol 2005;161:180–5. 5. Chu SP, Kelsey JL, Keegan THM, Sternfeld B, Prill M, Quesenberry CP, Sidney S. Risk factors for proximal humeral fracture. Am J Epidemiol 2004;160:360–7. 6. Johnell O, Kanis JA, Odén A, Sernbo I, Redlund-Johnell I, Petterson C, De Laet C, Jönsson B. Mortality after osteoporotic fractures. Osteoporos Int 2004;15:38–42. 7. Johnell O, Kanis JA, Odén A, Sernbo I, Redlund-Johnell I, Petterson C, De Laet C, Jönsson B. Fracture risk following an osteoporotic fracture. Osteoporos Int 2004;15:175–9. 8. Neer CS II. Displaced proximal humeral fractures. Part I. Classification and evaluation. J Bone Joint Surg Am 1970;52: 1077–89. 9. Castagno AA, Shuman WP, Kilcoyne RF, Haynor DR, Morris ME, Matsen FA. Complex fractures of the proximal humerus: role of CT in the treatment. Radiology 1987;165: 759–62. 10. Parsons BO, Klepps SJ, Miller S, Bird J, Gladstone J, Flatow E. Reliability and reproducibility of radiographs of greater tuberosity displacement. A cadaveric study. J Bone Joint Surg Am 2005;87:58–65. 11. Hertel R, Hempfing A, Stiehler M, Leuning M. Predictors of humeral head ischemia after intracapsular fracture of the proximal humerus. J Shoulder Elbow Surg 2004;13:427–33. 12. Shrader MW, Sanchez-Sotelo J, Sperling JW, Rowland CM, Cofield R. Understanding proximal humerus fractures: image analysis, classification, and treatment. J Shoulder Elbow Surg 2005;14:497–505. 13. Mora JM, Sanchez A, Vila J, Cañete E, Gamez F. Proposed protocol for reading images of humeral head fractures. Clin Orthop 2006;448:225–33. 14. Codman EA. The Shoulder, 2nd ed. Malabar: RE Krieger, 1984, pp 313–31. 15. Müller ME, Allgöwer M, Schneider R, Willenegger H. Manual of Internal Fixation: Techniques Recommended by the AO-ASIF Group, 3rd ed. Berlin: Springler, 1991, pp 118–25. 16. Siebenrock KA, Gerber C. The reproducibility of classification of fractures of the proximal end of the humerus. J Bone Joint Surg Am 1993;75:1751–5. 17. Sidor ML, Zuckerman JD, Lyon T, Koval K, Cuomo F, Schoenberg N. The Neer classification system for proximal humeral fractures. J Bone Joint Surg Am 1993;75:1745–50. 18. Sidor ML, Zuckerman JD, Lyon T, Koval K, Schoenberg N. Classification of proximal humerus fractures: the contribution
C. Torrens of the scapular lateral and axillary radiographs. J Shoulder Elbow Surg 1994;3:24–7. 19. Bernstein J, Adler LM, Blank JE, Dalsey RM, Williams GR, Iannotti JP. Evaluation of the Neer system of classification of proximal humeral fractures with computerized tomographic scans and plain radiographs. J Bone Joint Surg Am 1996;78:1371–5. 20. Sjödén GO, Movin T, Günter P, Aspelin P, Ahrengart L, Ersmark H, Sperber A. Poor reproducibility of classification of proximal humeral fractures. Acta Orthop Scand 1997;68: 239–42. 21. Sjödén GO, Movin T, Aspelin P, Günter P, Shalabi A. 3D-radiographic analysis does not improve the Neer and AO classifications of the proximal humeral fractures. Acta Orthop Scand 1999;70:325–8. 22. Torrens C, Melendo E, Solano A, Caceres E. Two-part bituberosity proximal humeral fracture. A case report. J Trauma 2008. 23. Jakob RP, Miniaci A, Anson PS, Jaberg H, Osterwalder A, Ganz R. Four-part valgus impacted fractures of the proximal humerus. J Bone Joint Surg Br 1991;73:295–8. 24. Neer CS II. Four-segment classification of proximal humeral fractures: purpose and reliable use. J Shoulder Elbow Surg 2002;11:389–400. 25. Lanting B, MacDermid J, Drosdowech D, Faber KJ. Proximal humeral fractures: a systematic review of reatment modalities. J Shoulder Elbow Surg 2008;17:42–54. 26. Edelson G, Safuri H, Salami J, Vigder F, Militianu D. Natural history of complex fractures of the proximal humerus using a three-dimensional classification system. J Shoulder Elbow Surg 2008;17:399–409. 27. Zyto K. Non-operative treatment of comminuted fractures of the proximal hmerus in elderly patients. Injury 1998;29:349–52. 28. Zyto K, Ahrengart L, Sperber A, Törnkvist H. Treatment of displaced proximal humeral fractures in elderly patients. J Bone Joint Surg Br 1997;79:412–7. 29. Gerber C, Werner CML, Vienne P. Internal fixation of complex fractures of the proximal humerus. J Bone Joint Surg Br 2004;86:848–55. 30. Resch H, Beck E, Bayley I. Reconstruction of the valgusimpacted humeral head fracture. J Shoulder Elbow Surg 1995; 4:73–80. 31. Gerber C, Schneeberger AG, Vinh JS. The arterial vascularization of the humeral head. An anatomical study. J Bone Joint Surg Am 1990;72:1486–94. 32. Brooks CH, Revell WJ, Heatley FW. Vascularity of the humeral head after proximal humeral fractures. J Bone Joint Surg Br 1993;75:132–6. 33. Hertel R, Hempfing M, Stiehler M, Leunig M. Predictors of humeral head ischemia after intracapsular fracture of the proximal humerus. J Shoulder Elbow Surg 2004;13:427–33. 34. Bastian JD, Hertel R. Initial post-fracture humeral ischemia does not predict development of necrosis. J Shoulder Elbow Surg 2008;17:2–8. 35. Smith AM, Mardones RM, Sperling JW, Cofield RH. Early complications of operatively treated proximal humeral fractures. J Shoulder Elbow Surg 2007;16:14–24.
Proximal Humeral Fractures 36. Koval K, Gallagher MA, Marsicano JG, Cuomo F, McShinany A, Zuckerman JD. Functional outcome after minimally displaced fractures of the proximal part of the humerus. J Bone Joint Surg Am 1997;79:203–7. 37. Gaebler C, McQueen MM, Court-Brown CM. Minimally displaced proximal humeral fractures. Acta Orthop Scand 2003;74:580–5. 38. Tejwani NC, Liporace F, Walsh M, France MA, Zuckerman JD, Egol KA. Functional outcome following one-part proximal humeral fractures: a prospective study. J Shoulder Elbow Surg 2008;17:216–9. 39. Lefevre-Colau MM, Babinet A, Fayad F, Fermanian J, Anract P, Roren A, Kansao J, Revel M, Poiraudeau S. Immediate mobilization compared with conventional immobilization for the impacted nonoperatively treated proximal humeral fracture. J Bone Joint Surg Am 2007;89:2582–90. 40. Dimakopoulos P, Panagopoulos A, Kasimatis G. Transosseous suture fixation of proximal humeral fractures. J Bone Joint Surg Am 2007;89:1700–9. 41. Cuomo F, Flatow EL, Maday MG, Miller SR, McIlveen SJ, Bigliani LU. Open reduction and internal fixation of twoand three-part displaced surgical neck fractures of the proximal humerus. J Shoulder Elbow Surg 1992;1:287–95. 42. Esser RD. Treatment of three- and four-part fractures of the proximal humerus with a modified cloverleaf plate. J Orthop Trauma 1994;8:15–22. 43. Lin J, Hou S-M, Hang Y-S. Locked nailing for displaced surgical neck fractures of the humerus. J Trauma 1998;45:1051–7. 44. Fankhauser F, Boldin C, Schippinger G, Haunschmid C, Szyszkowitz R. A new locking plate for unestable fractures of the proximal humerus. Clin Orthop 2005;430:176–81. 45. Koukakis A, Apostolou CD, Taneja T, Korres DS, Amini A. Fixation of proximal humerus fractures using the Philos plate. Clin Orthop 2006;442:116–20. 46. Moonot P, Ashwood N, Hamlet M. Early results for treatment of three- and four-part fractures of the proximal humerus using the Philos plate system. J Bone Joint Surg Br 2007; 89:1206–9. 47. Handschin AE, Cardell M, Contaldo C, Trentz O, Wanner GA. Functional results of angular-stable plate fixation in displaced proximal humeral fractures. Injury 2008;39:306–13. 48. Egol KA, Ong CC, Walsh M, Jazrawi LM, Tejwani NC, Zuckerman JD. Early complications in proximal humerus fractures (OTA types 11) treated with locked plates. J Orthop Trauma 2008;22:159–64. 49. Owsley KC, Gorczyca JT. Displacement/screw cutout after open reduction and locked plate fixation of humeral fractures. J Bone Joint Surg Am 2008;90:233–40.
89 50. Neer CS II. Displaced proximal humeral fractures. Part II. Treatment of three-part and four-part displacement. J Bone Joint Surg Am 1970;52:1090–103. 51. Antuña SA, Sperling JW, Cofield RH. Shoulder hemiarthroplasty for acute fractures of the proximal humerus: a minimum five-year follow-up. J Shoulder Elbow 2008;17:202–9. 52. Grönhagen CM, Abbaszadegan H, Révay SA, Adolphson PY. Medium-term results after primary hemiarthroplasty for comminute proximal humerus fractures: a study of 46 patients followed up for an average of 4.4 years. J Shoulder Elbow Surg 2007;16:766–73. 53. Boileau P, Krishnan SG, Tinsi L, Walch G, Coste JS, Mole D. Tuberosity malposition and migration: reasons for poor outcomes after hemiarthroplasty for displaced fractures of the proximal humerus. J Shoulder Elbow Surg 2002;11:401–12. 54. Hempfing A, Leunig M, Ballmer FT, Hertel R. Surgical landmarks to determine humeral head retrotorsion for hemiarthroplasty in fractures. J Shoulder Elbow Surg 2001;10:460–3. 55. Angibaud L, Zuckerman JD, Flurin PH, Roche C, Wright T. Reconstructing proximal humeral fractures using the bicipital groove as a landmark. Clin Orthop 2007;458:168–74. 56. Itamura J, Dietrick T, Roidis N, Shean C, Tibone J. Analysis of the bicipital groove as a landmark for humeral head replacement. J Shoulder Elbow Surg 2002;11:322–6. 57. Murachovsky J, Ikemoto RY, Nascimento LGP, Fujiki EN, Milani C, Warner JJP. Pectoralis major tendon reference (PMT): a new method for accurate restoration of humeral length with hemiarthroplasty for fracture. J Shoulder Elbow Surg 2006;15:675–8. 58. Greiner SH, Kääb MJ, Kröning I, Scheibel M, Perka C. Reconstruction of humeral length and centering of the prosthetic head in hemiarthroplasty for proximal humeral fractures. J Shoulder Elbow Surg 2008;17:709–14. 59. Torrens C, Corrales M, Melendo E, Solano A, RodríguezBaeza A, Caceres E. Pectoralis major tendon as a reference for restoring humeral length and retroversion with hemiartroplasty for fracture. J Shoulder Elbow Surg 2008;17:947–50. 60. Frankle MA, Ondrovic LE, Markee BA, Harris ML, Lee WE III. Stability of tuberosity reattachment in proximal humeral hemiarthroplasty. J Shoulder Elbow Surg 2002;11:413–20. 61. De Wilde LF, Berghs BM, Beutler T, Ferguson SJ, Verdonk RC. A new prosthetic design for proximal humeral fractures: reconstructing the glenohumeral unit. J Shoulder Elbow Surg 2004;13:373–80. 62. Bufquin T, Hersan A, Hubert L, Massin P. Reverse shoulder arthroplasty for the treatment of three- and four-part fractures of the proximal humerus in the elderly. J Bone Joint Surg Br 2007;89:516–20.
Fixation of Intertrochanteric Femoral Fractures Vilmos Vécsei and Stefan Hajdu
Introduction During the past 30 years a large change in operative treatment of intertrochanteric femoral fractures has occurred, caused by a rapid development of new and biomechanically more stress-resistant fixation devices. For nearly 40 years (1950–1990), the sliding hip screw and plate has been the standard treatment for intertrochanteric fractures of the femur. In patients with stable fractures, the implant produces excellent results. The absence of medial support of the lesser trochanter in the fracture area and dorso-medial comminution in unstable fractures increases the mechanical overload of extramedullary implants leading to system failure, particularly cut-out and subsequent loss of reduction. This demonstrated the necessity to reduce the lever-arm of the implant and bring the vertical part as near as possible to the physiological mechanical axis. Thus, interest arose in intra-medullary implants for the treatment of intertrochanteric femoral fractures. The shortened lever-arm of intra-medullary devices provides better load-sharing and, above all, can be inserted through small incisions. Although an obvious improvement in patient care intra-medullary stabilization in intertrochanteric femoral fractures is still frequently and controversially discussed in the literature.
Treatment Methods 1940, Kuentscher and Maatz started working with the Y-nail and recommended use of this intra-medullary device for stabilization of peritrochanteric fractures in 1945 [1].
Stefan Hajdu (*) Department of Trauma Surgery, Vienna Medical University, Währinger Gürtel 18-20, 1090-Wien, Austria e-mail:
[email protected]
Condylocephalic nails, such as those designed by Kuentscher, Ender and Harris, are inserted from the condyles up into the femoral head without opening the fracture site. The Ender method of intra-medullary fixation in fractures of the proximal femur gained popularity in the 1970s [2]. Advantages were said to include decreased operative mortality, minimal surgical trauma secondary to not opening the fracture site, decreased blood loss, decreased operating time and the patient returns to an ambulatory status within a few days. Although initial reports were encouraging, subsequent investigations have demonstrated significant complications. Chapman et al., reported as complications nails backing out of the medullary canal, perforation of the nails through the femoral head, and rotation deformity at the fracture site [2]. In 100 Patients Vécsei et al. [3] reported distal nail migration in 39%, cut-out in 4%, femoral neck perforation in 2% and rotational deformity in 25.5% (in 8.5% more than 20°). Raugstad et al. [4] and Kuderna et al. [5] found that 70 and 50% of patients, respectively, had a rotational deformity after fixation with Ender nailing. In addition to mal-rotation, knee pain, stiffness and supracondylar fractures have been reported as significant complications of the Ender nails. Multiple studies have documented complications with Ender nailing, including frequent mal-union in external rotation, as well as knee stiffness and local irritation from migration of the flexible nails. We use Ender nailing in exceptional indications, e.g. if skin conditions at the lateral aspect of the hip prohibit the use of surgery in this area.
Cephalomedullary Nailing The unstable intertrochanteric fracture is the most common indication for cephalomedullary nailing in this area. The goals and advantages of the cephalomedullary nail systems are as follows: 1. To provide proximal fixation in the femoral neck by nails or screws. 2. To allow the femoral head and neck to collapse and impact the fracture to increase stability.
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3. To lie within the medullary canal of the femur, thereby decreasing the lever-arm on the proximal fragment; and to allow early full weight-bearing. Many different modern reconstruction nail designs, which are currently available, include the gamma nail, proximal femoral nail (PFN), sliding nail, intra-medullary hip screw, the Russell–Taylor reconstruction nail, trochanteric nail, Fi nail, etc. Three of the most controversial discussed application problems of the intra-medullary fixation methods will be considered in this paper: the cut-out phenomenon, the shaft fracture at the tip of the nail and the learning curve. Because most patients with intertrochanteric fractures have considerable osteopenia, with the quality of bone for the purchase of fixation within the femoral head and neck less than desirable, it is important that the internal fixation device be placed in that part of the head and neck where the quality of bone is best. The bone of poorest quality is in the antero-superior aspect of the head and neck. Although the optimal position of femoral neck screw is somewhat controversial, all agree that it should be central or slightly inferior and posterior. Kukla et al. [6] and Hesse et al. [7, 8] reported cut-out rate in their gamma nail studies of 2,1%, respectively 3,8% in unstable fractures. Similar or higher cut-out rate [9, 10] was observed by the PFN. Because of the double-T profile of the femoral neck screw by the sliding nail, the risk of dislocation can be diminished [11]. The new blade design, by the new proximal femoral nail (PFNA™), is supposed to compress the surrounding cancellous bone in the femoral neck during insertion to prevent cut-out (Fig. 1a–f). Since June 2006 we stabilized 140 unstable intertrochanteric fractures by this new device in our level 1 Trauma centre. The first results showed technical problems in three patients: lateral migration of the blade, locking of the blade and disconnection of the blade (handling or product failure?), but so far cut-out was not observed. The shaft fracture caused by intra-medullary fixation of intertrochanteric fractures has been associated with multiple factors, involving implant design and surgical procedure. With the standard gamma nail, peri-operative fractures occurred between 1 and 4% of cases [6–8, 11–16]. The causes may be due to the geometric mismatch between the nail and the proximal medullary canal, inadequate or eccentric proximal reaming, too forceful an insertion of the nail with a hammer, excessive medio-lateral curvature of the standard nail (10°), and failure of the target device and distal double-locking of the nail. Heinz and Vécsei [17] described a misplacement of the distal locking bolts in 14.5% (67 of 440 patients), which was because of loosening of the, originally, non-radiolucent aiming device. In our level 1 Trauma centre routine double-locking has been left in 1992 – only in exceptional
V. Vécsei and S. Hajdu
cases rectified. The problems detected in the gamma nail due to the need for reaming and its somewhat excessively-valgus design have led the manufacturers to change the design of the system, with the appearance of the new trochanteric range nail, which does not require reaming before insertion and has a valgus angle of only 4°. At present, this new gamma nail (Gamma 3™) has substituted the regular gamma nail in our routine with satisfactory results. A new development, the U-blade, is designed to reduce the cut-out rate (Fig. 2a–f). At the present time, this new device will be used in our level 1 Trauma centre in fractures with secondary rotational tendency in the implant, e.g. in “basocervical” fractures AO/ ASIF 31-A1.2 (fractures with the highest cut-out rate). The learning curve has been the cause of the low popularity of the use of intra-medullary stabilization of intertrochanteric femoral fractures in the past. In a comparative study on the compression hip screw and the gamma nail, Goldhagen et al. [18] noted a significant learning curve in the use of the gamma nail. In a retrospective study over 8 years Hesse et al. [7] reported 387 patients treated by gamma nail between 1992 and 2000. A significant learning curve was noted with a decrease of complications from 29% during the first 4 years to 9% in the second half of the study. In their critical analysis of 1,000 gamma nails Kukla et al. [6] found a highly significant association of the incidence of intra-operative complications and the increasing clinical experience of the surgeons. The patient’s risk of sustaining an intra-operative complication was reduced by 50% each year. An internationally-acceptable complication rate of <4% was achieved at the end of the third year of the study.
Treatment of Intertrochanteric Fractures in Austria In 2001, a standardized questionnaire was sent to 20 out of 54 trauma units in Austria to evaluate the treatment modalities of proximal femoral fractures. In intertrochanteric fractures the survey showed following operative treatment: stable fractures were treated by using a dynamic hip screw (DHS) in 80%, in 20% by utilising intra-medullary stabilization (10% Gamma-Nail, 5% Sliding Nail, 5% PFN). However unstable fractures were treated by using intra-medullary stabilization in 90% (60% Gamma-Nail, 5% Sliding Nail, 25% PFN).
Discussion Fractures in the trochanter region occur particularly at an advanced age, resulting in the need for the least invasive technique possible [19]. The gold standard has not yet been discovered, particularly for unstable fractures.
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Fig. 1 Unstable intertrochanteric fracture AO/ASIF 31-A2.2 fixed by the proximal femoral nail (PFNA™). Radiographs of a 94-yearold man: pre-operative (a, b), post-operative (c, d), and healing 8 months post-operative (e, f )
The 2000 Cochrane database [20] looked at the gamma nail, Kuntscher Y-nail, intra-medullary hip screw in comparison with the DHS for extra-capsular hip fractures. It concluded that the DHS was the implant of choice and recommended further studies, in particular on the best implant for subtrochanteric fractures. In 2005 Parker and Handoll [21] reported that the DHS is superior for trochanteric fractures in comparison with
extra-medullary implants and proposed further studies to determine if different types of intra-medullary nail produce similar results, or if intra-medullary nails have advantages for selected fracture types (for example, subtrochanteric fractures). Parker and Handoll [22] proposed in 2006 not comparing different designs of intra-medullary nails, but that any new design should be evaluated in comparison with the sliding hip
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f d b
Fig. 2 Unstable intertrochanteric fracture AO/ASIF 31-A1.2 stabilized by the new gamma nail with the U-blade (Gamma 3™). The new blade design is supposed to reduce the cut-out rate. Images of a 76-year-old woman: pre-operative (a, b), post-operative (c, d), and after full weight-bearing (e, f)
screws. Our opinion, in consideration of these metanalysis and similar studies is that they don’t differ specifically between complications after stable or unstable fractures. In contrast to these and numerous published results showing the advantages of sliding hip screw devices with overall complications of
22% (3.9% infections) using [23, 24], is the study from Kukla et al. [6] with a complication rate of 12.7% (1.7% infections) using gamma nailing in unstable fractures. The preliminary results by the stabilization of unstable intertrochanteric fractures with the new generations of
Fixation of Intertrochanteric Femoral Fractures
intra-medullary implants (Gamma3™ with U-blade, PFNA™) are very satisfactory.
Conclusions ● In patients with stable fractures extra-medullary implants produce excellent results. ● Intra-medullary implants are in unstable fractures superior compared with extra-medullary devices. ● The complication rate has been diminished. ● Further improvements of the results due to technical developments can be expected. ● The operative rules should be followed carefully. Nevertheless, intra-medullary implants are not the definitive solution for every situation because the problem of instability, within an unstable fracture, persists unchanged, on the one hand together with the bone structure-related mechanical defect. On the other hand, osteoporosis, reducing the bone substance, is the situation to be dealt with. The lack of substance causes a displacement of mechanical forces towards the implant and is followed by a biomechanical deficit, which leads to a possible consecutive implant failure. The question of the best implant is summed up in the best way by Schipper and associates: “A skilled Surgeon may treat the demanding unstable trochanteric fractures with any type of fixation device, as long as he or she remembers that the fixation device will never make up for surgical failures. Therefore, improvement of treatment of the unstable trochanteric fractures will predominantly be in the hands of Surgeons, rather than in those of industry” [25].
References 1. Küntscher G, Maatz R. Technik der Marknagelung. Leipzig: Georg Thieme, 1945. 2. Chapman MW, Bowman WE, Csongradi JJ, Day LJ, Trafton PG, Bovill EG Jr. The use of Ender’s pins in extracapsular fractures of the hip. J Bone Joint Surg Am 1981;63(1):14–28. 3. Vécsei V. [Ender nailing–pro and contra]. Chirurg 1985; 56(1):16–24. 4. Raugstad TS, Molster A, Haukeland W, Hestenes O, Olerud S. Treatment of pertrochanteric and subtrochanteric fractures of the femur by the Ender method. Clin Orthop Relat Res 1979; 138:231–7. 5. Kuderna H, Bohler N, Collon DJ. Treatment of intertrochanteric and subtrochanteric fractures of the hip by the Ender method. J Bone Joint Surg Am 1976;58(5):604–11.
95 6. Kukla C, Heinz T, Gaebler C, Heinze G, Vecsei V. The standard gamma nail: A critical analysis of 1,000 cases. J Trauma 2001;51(1):77–83. 7. Hesse B, Lampert C, Remiger A, Ebert T, Gachter A. [Treatment of trochanteric fractures with the gamma nail]. Unfallchirurg 2003;106(4):281–6. 8. Hesse B, Gachter A. Complications following the treatment of trochanteric fractures with the gamma nail. Arch Orthop Trauma Surg 2004;124(10):692–8. 9. Banan H, Al-Sabti A, Jimulia T, Hart AJ. The treatment of unstable, extracapsular hip fractures with the AO/ASIF proximal femoral nail (PFN) – our first 60 cases. Injury 2002;33(5):401–5. 10. Simmermacher RK, Bosch AM, Van der Werken C. The AO/ASIF-proximal femoral nail (PFN): A new device for the treatment of unstable proximal femoral fractures. Injury 1999;30(5):327–32. 11. Fritz T, Hiersemann K, Krieglstein C, Friedl W. Prospective randomized comparison of gliding nail and gamma nail in the therapy of trochanteric fractures. Arch Orthop Trauma Surg 1999;119(1–2):1–6. 12. Baumgaertner MR, Curtin SL, Lindskog DM. Intramedullary versus extramedullary fixation for the treatment of intertrochanteric hip fractures. Clin Orthop Relat Res 1998;348: 87–94. 13. Gaebler C, Stanzl-Tschegg S, Tschegg EK, Kukla C, MenthChiari WA, Wozasek GE, Heinz T. Implant failure of the gamma nail. Injury 1999;30(2):91–9. 14. Leung KS, So WS, Shen WY, Hui PW. Gamma nails and dynamic hip screws for peritrochanteric fractures. A randomised prospective study in elderly patients. J Bone Joint Surg Br 1992;74(3):345–51. 15. Forthomme JP, Costenoble V, Soete P, Docquier J. [Treatment of trochanteric fractures of the femur using the gamma nail (apropos of a series of 92 cases)]. Acta Orthop Belg 1993; 59(1):22–9. 16. Adams CI, Robinson CM, Court-Brown CM, McQueen MM. Prospective randomized controlled trial of an intramedullary nail versus dynamic screw and plate for intertrochanteric fractures of the femur. J Orthop Trauma 2001;15(6): 394–400. 17. Heinz T, Vécsei V. [Complications and errors in use of the gamma nail. Causes and prevention]. Chirurg 1994;65(11): 943–52. 18. Goldhagen PR, O’Connor DR, Schwarze D, Schwartz E. A prospective comparative study of the compression hip screw and the gamma nail. J Orthop Trauma 1994;8(5):367–72. 19. Kukla C, Heinz T, Gabler C. [Acute management of para-articular hip fractures in geriatric patients]. Wien Klin Wochenschr 1995;107(5):169–74. 20. Parker MJ, Handoll HH. Gamma and other cephalocondylic intramedullary nails versus extramedullary implants for extracapsular hip fractures. Cochrane Database Syst Rev 2000; 2:CD000093. 21. Parker MJ, Handoll HH. Gamma and other cephalocondylic intramedullary nails versus extramedullary implants for extracapsular hip fractures in adults. Cochrane Database Syst Rev 2005;4:CD000093.
96 22. Parker MJ, Handoll HH. Intramedullary nails for extracapsular hip fractures in adults. Cochrane Database Syst Rev 2006;3:CD004961. 23. Bridle SH, Patel AD, Bircher M, Calvert PT. Fixation of intertrochanteric fractures of the femur. A randomised prospective comparison of the gamma nail and the dynamic hip screw. J Bone Joint Surg Br 1991;73(2):330–4.
V. Vécsei and S. Hajdu 24. Wolfgang GL, Bryant MH, O’Neill JP. Treatment of intertrochanteric fracture of the femur using sliding screw plate fixation. Clin Orthop Relat Res 1982;163:148–58. 25. Schipper IB, Steyerberg EW, Castelein RM, van der Heijden FH, den Hoed PT, Kerver AJ, van Vugt AB. Treatment of unstable trochanteric fractures. Randomised comparison of the gamma nail and the proximal femoral nail. J Bone Joint Surg Br 2004;86(1):86–94.
Surgical Management of Distal Tibial Fractures in Adults Mathieu Assal and Richard Stern
Introduction Fractures of the distal tibia involve the diaphyse al-metaphyseal area of the bone, and may be either extra-articular or intraarticular, the latter known as pilon or plafond fractures. They are one of the most challenging injuries in orthopaedic traumatology [8, 17, 28, 30, 36, 52, 58, 68]. These fractures are considered severe injuries because of the elevated risk of complications which may result from the nature of the injury itself, secondary to surgery, or both. For the past 20 years there have been a number of guidelines published as to the management of these injuries [1, 2, 4–7, 12, 15, 20, 21, 26, 51]. In addition, several surgical incisions in the operative management of these fractures have been recently described [2, 15, 26, 45]. The development of anatomically-contoured plates, along with angular stability, has helped considerably in obtaining stable fixation in these difficult fractures. In spite of all this progress the clinical results are not always successful, and it is quite difficult to predict the final outcome [3, 40, 52, 68]. Fractures of the distal tibia account for less than 10% of all fractures of the lower extremity, and occur more frequently in men than women [18, 41]. Although these fractures occur in all age groups, they are rare in children and the elderly, and occur most frequently between 35 and 40 years of age [41]. These fractures occur most often following a high energy mechanism of injury usually secondary to a motor vehicle accident, and the incidence has risen during the past decade because airbags and seatbelts are protecting automobile occupants from injuries that previously would have been lethal [14].
Mathieu Assal () Orthopaedic Surgery Service, University Hospital of Geneva, Switzerland e-mail:
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As opposed to malleolar fractures which are secondary to a rotational injury, pilon fractures are secondary to axial compression of high energy. Morphologically, pilon fractures are differentiated from ankle fractures by the fact that the line of the fracture passes through the horizontal weightbearing surface of the distal tibia. These two fractures have different mechanisms of injury and their treatment and outcome vary considerably. Thus, it is very important that they are classified and treated appropriately.
Classification Several classification systems have been described since 1960 [18, 43, 55, 56, 68]. These different classifications have points in common: they describe fractures that are entirely extra-articular, those that are intra-articular but only involve part of the articular surface, and those that involve the complete articular surface (in this latter case no part of the articular surface remains in contact with the rest of the tibia). One of the earliest classifications of these fractures was described by Rüedi and Allgöwer [55, 56], which divided them into three groups: non-displaced, low-energy mildlydisplaced, and high-energy comminuted fractures. The most commonly-used classification system today is that described by the Arbeitsgemeinschaft für Osteosynthesefragen (AO) [43]. With this system, fractures of the distal tibia are designated as 4 for the tibia and 3 for the distal end segment (Fig. 1). The extra-articular fractures are type A, partial articular fractures type B, and complete articular fractures are type C. Each type is divided into three groups based upon the amount of comminution, and each group is further sub-divided into three sub-groups based upon various features such as direction of displacement, degree of comminution, location of fracture lines, etc. There are 24 sub-groups which makes the classification difficult to work with in daily clinical practice.
G. Bentley (ed.), European Instructional Lectures. European Instructional Course Lectures 9, DOI: 10.1007/978-3-642-00966-2_12, © 2009 EFORT
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Fig. 1 Classification of fractures of the distal tibia according to the AO. There are three types: 43-A, extra-articular metaphyseal; 43-B, partial articular pilon fracture where a part of the articular surface remains in contact with the shaft; and 43-C, complete articular pilon fracture where no part of the articular surface remains in contact with the shaft. Each type is divided into three groups (1, 2, and 3), and then each group into subgroups (not illustrated here)
Radiology The AO classification of distal tibia fractures is based upon conventional radiographs. These include anterior-posterior, lateral and mortise views of the ankle, as well as radiographs of the entire tibia and foot. Computed tomography (CT) is necessary for a clear appreciation of the fracture in all its aspects, especially for pre-operative planning [62]. This examination gives an understanding of the individual fracture lines and impaction of osteochondral fragments at the articular surface. It is better to perform the CT scan after application of an ankle-bridging external fixator to evaluate the effect of ligamentotaxis on fragments of the articular surface [12]. Three-dimensional reconstruction offers the possibility of a more precise analysis, and is accomplished by means of two
methods: (1) Multiplanar reconstruction allows the surgeon to manipulate the images in real-time and make the specific cuts in the preferred planes (Fig. 2); and (2) Volume-rendering or 3-D reconstruction permits for visualisation in three dimensions of the involved surfaces (Fig. 3). Careful analysis of the imaging studies is a key step in the surgical planning of these fractures, and should comprise a certain number of points in their evaluation. These 14 points include: (1) Intra-articular extension (present/absent) (2) Diaphyseal extension(present/absent) (3) Metaphyseal impaction (present/absent) (4) Articular surface impaction (present: central, anterior, other/absent) (5) Simple split (present: sagittal, coronal, oblique/absent)
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Fig. 2 CT images with MPR (Multiplanar Reconstruction)
(6) Number of articular fragments (7) Involved columns (medial, lateral, posterior) (8) Fracture of Tillaux-Chaput fragment isolated from the lateral column (present/absent) (9) Medial malleolar fracture isolated from the medial column (present/absent) (10) Posterior malleolar fragment isolated from the posterior column (present/absent) (11) Fibular fracture (present/absent) (12) Alignment (frontal, sagittal, transverse) (13) Shortening (present/absent) and (14) Air in the soft tissues (present/absent)
Soft Tissue Injuries
Fig. 3 CT images with Volume Rendering
An important characteristic of fractures of the distal tibia, particularly those of high energy, is that the bony injury cannot be separated from injury to the surrounding soft tissues. The thin tissue envelope covering the distal tibia is subject to a trauma that requires careful physical examination for assessment as to its thickness, superficial or deep. The time for delineation of the status of the soft tissues may take up to 10–15 days, and thus early surgical intervention should be avoided.
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Soft Tissue Injuries with Closed Fractures Tscherne and Oestern [64, 65] proposed a classification system for soft tissue injuries with closed fractures, divided into four categories: (Grade 0) Negligible soft tissue injury; (Grade 1) Superficial abrasions or contusions of the skin and subcutaneous tissue; (Grade 2) Deep abrasions and contusions of skin and muscle; risk of compartment syndrome; (Grade 3) Extensive de-gloving of the subcutaneous tissue; severe muscular injury; established compartment syndrome; arterial injury. The value of this classification is debated in the literature and suffers from lack of validation and intra- and interobserver reliability. In addition, the classification system has not been specifically designed for distal tibial fractures. In spite of that its message remains essential in treating these injuries. To quote Professor H. Tscherne [65], “Soft tissue injuries accompanying closed fractures are especially troublesome and often are insufficiently appreciated on account of their occult nature. Even a simple skin contusion over a closed fracture can pose a more complex range of therapeutic and prognostic problems than skin which has been broken by a fractured bone”. In this setting, as soon as the patient arrives the physical examination should include a detailed description of the soft tissues, including abrasions, contusions, oedema, skin tension, and presence of blisters. Blisters are frequently observed and can be divided into two groups, the clear fluid-filled and the blood-filled types (Fig. 4). Histologically both types are secondary to a separation at the epidermaldermal junction. However, the blood-filled blisters are indicative of a deeper soft tissue injury [66]. There are more reported wound healing complications when the surgical incision is performed through a previous blood-filled blister [24, 66].
Soft Tissue Injuries in Open Fractures The Gustilo-Anderson system [27] is the standard classification for all open fractures. However, its use in the distal tibia is limited by the fact that the soft tissue coverage is severely limited, and what may appear as a simple Grade I according to this classification because of a wound less than 1 cm, is really a more severe injury based upon contusion to the local soft tissues. However, this is the most widespread system and is useful with an understanding of its limitations.
Fig. 4 Photograph of an ankle post-injury. There are blisters and areas of contusion with a closed pilon fracture, type 43-C
Initial Management As soon as the patient arrives in the emergency department the limb should be stabilised to avoid further compromise to the soft tissues. This can be done with a simple radiolucent splint before the patient is sent to radiology. Once clinical and radiological examination has been performed, there are three possible scenarios. The first, although unlikely, is that the patient proceeds directly to the operating room for definitive open reduction internal fixation (ORIF). The patients that would perhaps fall into this group are those with simple extra-articular fractures, classified as 43-A, which can be treated with minimally-invasive techniques. But for most patients, immediate surgery is not usually done out of concern for the soft tissues and the need for further imaging studies and pre-operative planning. The more usual second scenario for these patients with extra-articular fractures is for them to be immobilized in a full-leg plaster splint and definitive surgery delayed until soft tissues permit. The third very common situation is the patient with a high energy
Surgical Management of Distal Tibial Fractures in Adults
pilon fracture who goes to the operating room for provisional fracture stabilisation with an ankle-bridging external fixator.
Provisional Surgical Stabilisation: External Fixation ± ORIF of Fibula Provisional external fixation with an ankle-bridging frame (tibio-calcaneal) will allow for re-establishment of correct length, reduce the inflammatory response, improve local venous drainage, permit additional imaging studies, mobilize the patient, and most importantly allow for soft tissue recovery before proceeding to definitive fracture fixation. Perhaps the most important advancement in the surgical treatment of high energy pilon fractures has been the recognition of the need to delay primary surgery. The goal is to have an external fixation frame that is simple, with pins well away from the site of future planned surgery (Fig. 5). A trans-calcaneal pin is utilized distally, and
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two pins are placed well proximal in the tibia. The pins are connected in a box-like frame with medial and lateral bars. If possible, one should try and keep the clamps away from the fracture site and ankle joint line for better imaging studies. The objective is to re-establish length and place the talus underneath the axis of the tibia in frontal and sagittal planes. Originally the AO Group had advocated primary ORIF of the fibula at the same time as placing the provisional external fixator [61]. The idea was that it would help to reduce any antero-lateral fragment(s) and facilitate the later ORIF of the articular surface. However, experience has shown primary fixation of the fibula is difficult and may lead to an imperfect reduction which will make definitive fixation of the pilon actually more difficult. Additionally, a mobile fibula during reconstruction of the pilon fracture may be advantageous. Furthermore, the presence of a lateral or postero-lateral incision performed during the primary surgery will preclude the option of an antero-lateral approach for definitive fixation of the pilon fracture [26]. Thus we do not perform an ORIF of the fibula prior to definitive fixation of the pilon fracture.
Definitive Management External Fixation with or without Limited Internal Fixation
Fig. 5 Photograph of a leg 10 days after application of ankle bridging external fixator (tibiocalcaneal), for a closed pilon fracture. One can see how far the pins are proximally from the fracture site, and the resolution of initial skin lesions in this 43-C fracture
In the decade from 1980 to 1990 numerous publications favoured an approach to distal tibial fractures that included external fixation as primary stabilisation, with or without some form of limited internal fixation. This was in reaction to the numerous complications that were observed previously following ORIF [4, 19, 22, 23, 34, 39, 42, 44, 57, 64, 67, 69]. In spite of adjunctive indirect reduction techniques, such as pointed reduction forceps and/or percutaneous screw or wire fixation, definitive external fixation failed to allow for anatomic and stable joint reconstruction [6, 47, 52, 53]. Furthermore, prolonged tibio-calcaneal external fixation requires prolonged immobilization of both the ankle and subtalar joints [1, 9, 10, 13, 32, 37, 59]. This led to the concept of a non-bridging external fixator, either with the use of the original Ilizarov frame, or with the socalled “hybrid” fixator with fine wires in the distal tibial segment connected to the two pins proximally [4, 19, 22, 23, 34, 42, 57, 63, 69]. The minimum distance between the most distal fracture line and the ankle joint allowing a stable tibio-tibial frame has not been established, although some advocate a minimum of 2 cm [25]. If the fragment is very small and one cannot follow the above suggested guidelines, then it appears preferable to place a tibio-calcaneal frame. Technically, the tibio-tibial montage should start with the placement of a ring at a level just above the ankle joint.
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The percutaneous insertion of the fine wires requires knowledge of the local anatomy to avoid iatrogenic lesions [39, 42]. Although definitive treatment with external fixation offers obvious safety with regards to the soft tissues, a number of complications have been reported with the fine wires, including infection and neurovascular and tendon injuries affecting up to 37% of patients, loss of reduction and non-union [25, 33, 39, 42, 48, 49, 53]. The risk of septic arthritis secondary to fine wires which pierce the joint capsule has also been described [38]. Thus, because of the difficulty in obtaining an anatomic reduction, achieving stable fixation, and the risk of the above-mentioned complications, few trauma centres favour this approach.
Open Reduction Internal Fixation Only open reduction can permit satisfactory restoration of the articular surface. Therefore, this surgical step is necessary if one has that as its objective. The fear of iatrogenic complications following ORIF should be reconsidered in light of the now accepted delay between injury and definitive surgery, newly described surgical approaches, and more anatomically-contoured, less bulky implants. These developments have considerably improved the peri-operative safety and diminished the associated complication rate. For these reasons external fixation should remain a temporary stabilisation in the majority of cases. Recognition of the importance of the interval between injury and definitive ORIF is probably the most important factor in obtaining good results without major soft tissue complications [2, 21, 32, 50, 61]. Between the first step of external fixation and the later ORIF the traumatic oedema which has infiltrated the soft tissues decreases and the areas of possible necrosis demarcate. The mean duration of this interval has been reported to be from 7 to 24 days [2, 13, 21, 26, 32, 50, 61]. During this time it is advisable to repeat conventional radiographs and perform a CT scan, for images after ligamentotaxis can provide worthwhile information. This time is also essential to allow for good pre-operative planning.
Surgical Techniques Extra-Articular Fractures, AO 43-A These are basically extra-articular metaphyseal fractures (Fig. 6), but for the purpose of type of osteosynthesis we include those with a simple articular split and no joint
Fig. 6 Anterior-posterior and lateral radiographic views of a distal tibia extra-articular fracture, type 43-A
compression. These fractures may have extension into the diaphysis. The more recent improvement of implants, both nails and plates, has changed their management and prognosis. Intra-medullary (IM) nails with very distal and multiple locking options have permitted us to extend our indications for IM nailing of these fractures, and satisfy the need for minimally-invasive surgery [45]. More recently the advent of newer anatomically-shaped plates with angle stable fixation have made possible plate osteosynthesis of these fractures while respecting the soft tissues and the principles of minimally invasive surgery. This has been called minimally invasive plate osteosynthesis (MIPO) and has decreased the surgical insult from previous types of plates which were more bulky and with bigger screws [11, 16, 29, 31, 35, 46, 54]. Most Type A fractures can be treated with either of these two methods of fixation, nails or plates, and this depends mostly upon surgeon preference. In all cases a certain number of points must be discussed during the pre-operative planning. These include: (1) Is there intra-articular extension, and if so is this a simple split or articular impaction? (2) Is it necessary to apply a provisional external fixator? (3) Does the size of the metaphyseal fragment allow the placement of two or preferably three locking screws when using a nail? (4) What type of peri-operative reduction (manual traction, peri-operative external fixation, ORIF of any associated fibula fracture) should be utilized in those cases where there has not been a provisional ankle bridging external fixator? (5) Is fixation of the fibula necessary?
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To each of these questions the literature suggests the following answers: (1) The presence of a simple articular split vs. articular compression will be visible on the CT scan, which should be performed even with these extra-articular-appearing fractures. By definition the presence of an intra-articular split will change the AO classification to Types B or C, but from a surgical viewpoint the simple split (which can be frontal, sagittal, or oblique) can be treated by means of the above mini-invasive techniques. Therefore we include those fractures in this discussion. (2) The application of a temporary external fixator is usually not necessary in these types of fractures since they can be approached by minimally-invasive techniques with limited soft tissue dissection. Delay to definitive surgery may not be necessary, but if chosen a simple splint will provide sufficient stability for the soft tissues. (3) If the distal fragment is small so as to preclude satisfactory locking with an IM nail, other fixation techniques such as the use of an angular stable locking plate should be considered. (4) In those cases where a provisional external fixator has been applied it can be left in place to maintain alignment during ORIF. In other cases where there is no preoperative fixator, the choice of reduction aids depends upon surgeon preference. It can be carried out with simple manual traction, but in the more complex fractures an ankle bridging fixator can help to obtain and maintain alignment during the osteosynthesis. Additionally fixation of an associated fibular fracture can help to achieve alignment and provide stability during nailing or plating. (5) In a cadaveric biomechanical study [60] in the setting of 43-A fractures with either full or no contact of the fracture fragments (43-A1 vs. 43-A3), an IM nail was compared to a locking plate. The results demonstrated that fibular fixation associated with tibial nailing in 43-A3 fractures offered the same stability as a locking plate
Fig. 7 Anterior-posterior and lateral radiographic views pre-operative and post-operative of a type 43-A fracture treated with an IM nail and ORIF of the distal fibula
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without fibula fixation. On the basis of this study it is recommended to fix the fibula when IM nailing is considered for the comminuted fractures.
Technique of Intramedullary Nailing Cannulated IM nails utilized for these distal fractures offer the possibility of at least two locking bolts within 20 mm from the articular surface (Fig. 7). The patient is placed in the supine position and installed on the operating table in one of two possible ways. One technique is to use a fracture table with a calcaneal pin which offers the advantage of obtaining the reduction prior to nailing and maintaining stability. Or secondly, the leg is draped free which offers the additional advantage of approaching any simple articular fractures. We prefer the latter technique. An image intensifier (C-arm) is positioned on the opposite side of the leg to be operated upon. A single intravenous dose of antibiotic (second generation cephalosporin) and low molecular weight heparin for anticoagulation are administered 1 h before skin incision. In case of any doubt as to the status of the compartments in the leg or foot, compartment pressures should be measured. The use of a tourniquet is not recommended due to the potential for generating excess heat during reaming. The first part of the procedure concerns determining the correct entry point in two planes and opening the tibia into the medullary canal. The reaming guide-rod is then passed across the fracture under C-arm control. The guiderod should be positioned in line with the centre of the talar dome in the frontal plane, and at the junction of anterior and middle thirds of the metaphysis in the sagittal plane. In addition to the previous described techniques for reduction of the fracture (manual traction, external fixator, ORIF of fibula) one can use a threaded pin as a “joystick”, placed from the lateral side and very distal and parallel to the articular
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surface of the distal tibia, to manipulate a small distal fragment. The foot must be maintained in 15–20° of external rotation with respect to the tibial tuberosity. After achieving satisfactory reduction the guide-rod is impacted into the distal fragment. The size of the nail (length and diameter) is then chosen using the C-arm to be sure that there will not be either shortening or distraction at the fracture site. Reaming is carried out just past the isthmus with the objective to have the dense cancellous metaphyseal bone augment the hold of the nail in the small distal fragment. As the nail is inserted its position is controlled by the C-arm to assure correct frontal and sagittal plane alignment. The nail is carefully impacted into the distal fragment. Rotation must be carefully controlled clinically, and still can be modified at this point. The nail is locked in a static fashion. It is important to be sure that the distal locking bolts do not interfere with the tibio-fibular joint. As necessary, compartment pressures are re-evaluated. Ankle and syndesmosis stability must be determined by a stress test in valgus and external rotation. Any instability must be noted and stabilised. For the more comminuted A3 fractures it is advisable to perform ORIF of the fibula [60].
Technique of Minimally-Invasive Plate Osteosynthesis (MIPO) The implant utilized is an anatomically-shaped, angle stable, stainless steel or titanium medial metaphyseal plate with locking screws of 3.5, 4.5, and 5.0 mm. The plate provides for four locking screws within the most distal 2 cm of the tibia (Fig. 8). For use as a bridge-plate with this technique,
Fig. 8 Anterior-posterior and lateral radiographic views pre-operative and postoperative of a type 43-A fracture with extension into the diaphysis treated by MIPO through a medial incision and ORIF of the fibula
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it is generally accepted that the plate should be three times the length of the fracture and no more than 50% of the holes filled with screws. This provides for relative stability and secondary healing with callus. The patient is placed supine on a radio-lucent operating table. Prophylactic antibiotics and anticoagulation are administered 1 h prior to surgery. If one suspects a compartment syndrome of the leg or foot, compartment pressure measurements must be obtained. If there is a compartment syndrome one has the option of performing an ankle-bridging external fixation along with fasciotomies and after wound healing perform definitive fixation of the fracture, or performing primary IM nailing along with the fasciotomies. It is inadvisable to perform MIPO in the setting of fasciotomy incisions. A tourniquet is placed at the level of the thigh and the C-arm is positioned on the contra-lateral side. Typically one can reduce the fracture by manual traction and proceed directly to fixing the tibia. In cases where the fibula is fractured and relatively non-comminuted, one can consider first performing ORIF of the fibula to help re-align and stabilise the tibia prior to MIPO. For the fibula, an incision is made at the level of the fracture and fixation is achieved with a one-third tubular plate. Regarding the tibia, an oblique 30 mm long incision is made at the tip of the medial malleolus extending from proximal anterior to distal posterior (Fig. 9a). The obliquity permits the incision to be prolonged towards the metaphyseal area if required for reduction. Careful dissection through the subcutaneous tissue reveals a thin layer of fibrous tissue. It is just under this layer, and above the periosteum, that a scissor should be inserted and slid proximally. A drill guide is attached to the most distal hole of the plate to act as a handle for plate insertion.
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Fig. 9 (a–e) MIPO with an anatomically-contoured plate and angle stable screws (locking screws) of a type 43-A fracture. The successive steps are described in the text
The plate is placed into the layer created by the scissor and slid proximally on top of the periosteum (Fig. 9b). The position of the plate along the subcutaneous border of the tibia is determined by palpation. One must resist the strong tendency for the plate to slide posteriorly. The first step is to accurately determine the position of the distal end of the plate, which should extend approximately half-way along the medial malleolus but not as far as the tip. Once this is correctly determined with the help of the C-arm, a temporary Kirschner wire (K-wire) is introduced into the drill guide that is already in place. The goal is to secure the plate in the distal metaphysis. The next step is to assess the sagittal position of the plate proximally. This is easiest done by making a small incision at the proximal end of the plate which can be easily palpated or seen with the C-arm. At this point one must be sure that the fracture is reduced, specifically with regards to length and rotation, and then temporarily fix the plate proximally with another provisional K-wire. Once the plate is secured to the bone at both ends one must control for any flexion or extension deformity occurring at the fracture. If there is an extension deformity one helpful manoeuvre is to place a rolled sheet beneath the leg just proximal to the fracture. Conversely, if there is a flexion deformity the rolled sheet is placed posteriorly just distal to the fracture site. At this point one needs to use the C-arm to evaluate frontal plane alignment. If the alignment is satisfactory then one must be careful in using non-locked screws in situations where the plate is not firmly against the bone. Otherwise, the standard screw will pull the bone to the plate and may create a varus or valgus deformity. On the other hand, if there is mild frontal plane mal-alignment, a standard non-locked screw should be inserted first as a “reduction screw” to correct the alignment via indirect reduction (Fig. 9c). At this point locked screws are inserted proximal and distal to the fracture in an alternating fashion. The plate-holes that are at the level of the fracture, for its
entire length, are left empty (Fig. 9d). In those cases where a reduction screw was used it should be removed so as not to have any screws too close to the fracture. Again, this is to support the concept of relative stability. In those cases where the reduction cannot be achieved in this minimallyinvasive fashion, one can extend the proximal limb of the oblique incision and perform a limited open reduction. The wound is closed in standard fashion (Fig. 9e).
Intra-Articular Fractures, AO 43-B These fractures are always intra-articular and have at least one fracture line separating the horizontal articular surface of the distal tibia. They are distinguished from the 43-C in that one or two of the three columns of the distal tibia (the medial column including the medial malleolus, the lateral column including the tubercle of Tillaux-Chaput, or the posterior column including the posterior malleolus) remains in contact with the diaphysis of the tibia (Figs. 10 and 11). Therefore, these are partial-articular fractures. There is a broad spectrum of fracture configurations from the simple undisplaced split to the tibio-talar dislocation with articular impaction. Although they have varying prognoses they all require ORIF. Only by this technique can one expect to achieve anatomic restoration of the articular surface. The anterior (and less frequently, posterior) marginal impaction injuries have a particularly poor prognosis due to the development of early post-traumatic osteoarthritis secondary to cartilage damage, and these fractures require excellent intra-operative visualisation to achieve an accurate reduction and place an autologous cancellous graft. For fractures involving the medial column one can opt for an antero-medial approach as described by the AO [61], exposing the antero-medial articular surface.
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Antero-Medial (AO) Approach for Osteosynthesis of the Medial Column [61]
Fig. 10 Anterior-posterior radiographic views of a type 43-B fracture. There is a fracture of the lateral column at the level of the tubercle of Tillaux-Chaput and the medial column at the level of the medial malleolus
Fig. 11 Lateral radiographic views of a type 43-B partial pilon fracture with marked impaction and comminution of the articular surface anteriorly and anterior subluxation of the talus
Evaluation of the nature of the fracture should be carried out with a CT scan, which will additionally help with preoperative planning. In addition, the application of a provisional external fixator and delay between injury and definitive surgery should be considered for these higher energy injuries, as previously mentioned.
The indication for the antero-medial approach is typically for the fracture of the medial column of the distal tibia. It provides access to the medial malleolus and to the medial and middle thirds of the anterior tibio-talar joint. The anterior marginal fractures are also addressed through this approach. It does not provide an easy access to the lateral column, and therefore it is not an approach of choice for those fractures. The patient is placed supine on a radio-lucent operating table. Prophylactic antibiotics and anticoagulation are administered 1 h prior to surgery. The surgical incision begins 15 mm distal to the tip of the medial malleolus and gently curves antero-medially crossing the tibio-talar joint in its middle third and extends proximally along the subcutaneous border of the tibia (Fig. 12). The branches of the sapheneous nerve as well as the saphenous vein are found in the subcutaneous tissue and spared if possible. The developed fascio-cutaneous flap is mobilized en bloc. The extensor retinaculum is visualised and incised vertically medial to the tibialis anterior tendon, and care should be taken not to open the sheath of this tendon. The ankle joint is opened anteriorly. The fracture fragments are identified and reduced in standard fashion. Those characterized by a simple split should be treated with compression lag screws perpendicular to the fracture line(s) and application of a neutralization plate. This can frequently be a small anti-glide plate, such as a one-third tubular plate, which will prevent the proximal gliding of the articular fragment. In cases of articular impaction the subchondral bone and articular fragments are dis-impacted, anatomically reduced, and temporarily stabilised with K-wires. The reduced articular surface is supported by autologous graft taken from the proximal tibia or iliac crest. Intra-operative C-arm control is mandatory to ensure anatomic reduction of the articular surface. The implants which are generally used are independent lag screws to rigidly fix articular fragments, the anatomic medial metaphyseal plate with locking screws (3.5 mm, 4.0 mm, 5.0 mm) either in stainless steel or titanium, and as well as a small anterior buttress plate, either 2.7 mm or 3.5 mm. The retinaculum and subcutaneous tissue are closed with 2–0 resorbable sutures, and the skin is carefully closed with interrupted nylon sutures after the method of Allgöwer [55]. When the partial articular fractures affect the lateral column, an antero-lateral approach is preferable in order to have good access to the Tillaux-Chaput tubercle, as described below.
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Fig. 12 (a–c) Antero-medial approach of AO. The successive steps are described in the text
Antero-Lateral Approach for Osteosynthesis of the Lateral Column This approach, also known as the lateral approach [26] is indicated for pilon fractures that involve the lateral column (Fig. 13). This does not exclusively occur in 43-B fractures and therefore this approach may well be indicated for the more complex 43-C injuries. When the lateral column fracture is associated with a fibular fracture ORIF of both fractures is done through a single incision. It provides the access to the lateral and middle thirds of the anterior tibiotalar joint, but does not provide access to the medial column. If there is a fracture of the medial malleolus or medial column, an additional medial approach is advised. There are two contra-indications to the antero-lateral approach [26]. First is in the case where there is an oblique fracture
Fig. 13 Anterior-posterior and lateral radiographic views preoperative and post-operative of a Type 43-B pilon fracture. ORIF was performed with an anatomically-contoured antero-
line running from posterior-lateral to anterior-medial. For such injuries an antero-medial incision (AO) would be preferable. And secondly when there is a traumatic wound or other soft tissue injury preventing a safe approach. The patient is placed supine on a radio-lucent operating table. Prophylactic antibiotics and anticoagulation are administered 1 h prior to surgery. At the time of definitive surgery any previously placed external fixator can be left in place with removal of the lateral bar to facilitate the surgical approach. A thigh tourniquet is generally used. An incision is begun 4 cm distal to the ankle joint and extended proximally along the anterior border of the fibula to a point above the most proximal extent of the tibia fracture (Fig. 14a). The incision is carried down to the anterior border of the fibula, taking care to protect the superficial peroneal nerve. It is preferable not to fix the fibula first. The advantage in
lateral plate with angle stable screws and ORIF of the fibula via the same antero-lateral (lateral) surgical approach
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Fig. 14 (a–b) The antero-lateral incision permits a simultaneous approach to both the lateral column of the tibia and the fibula. The successive steps are described in the text
addressing the tibia first is that the fibula fracture can be displaced and used as an interval to improve visualisation of the tibia. Next, careful blunt dissection over the anterior border of the fibula is carried out to the interosseous membrane, and the plane between the interosseous membrane and the overlying contents of the anterior compartment developed with a large elevator or finger. At the joint level, the anterior syndesmotic ligament is identified on the fibula and followed medially to the antero-lateral Tillaux-Chaput fragment (Fig. 14b). This (usually large) fragment is hinged laterally to allow visualisation and reduction of the posterior articular surface and posterior column. The articular surface is dis-impacted and anatomically reduced, often progressing from posterior to anterior and lateral to medial. Temporary K-wires are placed to maintain the reduction, and cancellous autologous bone is used to support the reduced articular surface. Posterior or lateral column reduction requires further visualisation proximal to the joint which can be achieved by elevating the contents of the anterior compartment. An anatomic antero-lateral metaphyseal plate with locking screws (3.5 mm, 4.0 mm, 5.0 mm) either in stainless steel or titanium, is carefully positioned just proximal to the distal tibial articular margin and passed submuscularly up the lateral surface of the tibia. Finally, the fibula is reduced and stabilised with a one-third tubular plate (Fig. 14c). The soft tissues are carefully closed in routine fashion (Fig. 14d).
Intra-Articular Fractures, AO 43-C These fractures are almost always the result of high energy trauma and are well-known as a real challenge in orthopaedic traumatology, not only because of the bony injury
but because of the potential for severe soft tissue damage. This group of fractures involves a complete separation of the three columns of the tibia from the metaphysis or diaphysis. Thus no portion of the articular surface remains in contact with the shaft, the definition of a Type C articular fracture. The joint surface is often comminuted with articular fragments that are impacted into the metaphysis (Fig. 15). Therefore three factors must be considered: the soft tissues, the degree of intra-articular comminution, and any metaphyseal-diaphyseal extension. Stabilisation of the soft tissues by application of a joint-spanning external fixator is always a necessity. These principles have been previously described. As with the other less complicated fractures, careful pre-operative planning is essential in order to determine the surgical approaches for ORIF. Clearly, visualisation of the entire articular surface is required in order to restore joint congruency and local anatomy. The status of the soft tissues will play a role in the choice of surgical approach, and therefore one requires knowledge of the possible options. Up until recently there was no single incision described that permitted simultaneous exposure of the medial and lateral columns. The AO antero-medial approach in its original description offers excellent visualisation of the medial column, but does not provide for good access to the lateral column and fracture of Tillaux-Chaput. The antero-lateral approach, while offering very good exposure to the lateral column, does not allow for excellent visualisation of the medial column. The extensile approach has been recently described [2] and provides complete access to both medial and lateral columns through a single incision, and offers the advantage of plate placement medial, lateral, and/or anterior. For those fractures with proximal extension the plates can be passed subcutaneously from
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Fig. 15 Anterior-posterior and lateral radiographic views pre-operative and post-operative of a Type 43-C pilon fracture with proximal extension. ORIF was performed with anatomically contoured antero-lateral and medial plates with angle stable screws, and ORIF of a segmental fracture of the fibula
distal to proximal through the skin incision. It is a useful surgical approach in those fractures involving more than one column, however, it is not necessary for fractures of one column (Type 43-B) or those that are extra-articular (Type 43-A).
Extensile Approach for Osteosynthesis of the Medial and Lateral Columns A tourniquet is applied. If an external fixator has been previously placed, it is usually left in place and the lower limb is draped in the sterile field from the level of the tourniquet to the toes. Exsanguination of the limb is accomplished only by elevating the lower extremity and not with use of any compressive bandages. The incision is begun 10 mm below the tip of the medial malleolus and proceeds transversely across the ankle to a point just lateral to the midline and then turns at a 105–110° angle, proceeding proximally 10 mm lateral to the tibial crest (Fig. 16a). Thus, the incision lies lateral to the
tibialis anterior tendon. It is important to make the turn in the incision at the 105–110° angle and not more acutely approaching 90°. Generally, the vertical limb of the incision measures 15 cm but can be extended more proximally as desired. In situations with more extensive injury to the lateral column of the distal tibia, the point of the turn can be moved a bit more laterally. The transverse and vertical limbs of the incision are made using a No. 24 scalpel blade, but the 105–110° turn is made with a No. 15 blade, which permits the incision to be perfectly perpendicular to the plane of the skin, and skiving of the tissues is thus avoided. The incision is carried down through the subcutaneous tissue and a full-thickness flap is elevated. The incision continues onto the extensor retinaculum (Fig. 16b) exposing the underlying tibialis anterior tendon. The retinaculum is incised, with an attempt to leave the tibialis anterior tendon undisturbed in its sheath. This is not always possible because it is intimately connected to the retinaculum, and thus frequently the sheath is opened. The inferior extensor retinaculum is opened following the line of the incision. The
Fig. 16 (a–f) The extensile approach permits access to the medial and antero-lateral tibial pilon fracture. The successive steps are described in the text
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full-thickness flap is retracted medially while the tendon of the tibialis anterior is retracted laterally (Fig. 16c). The flap is handled atraumatically without strong retraction or use of forceps, frequently using nylon sutures in the skin to apply traction. At the level of the ankle joint, the articular capsule is opened longitudinally, exposing the talus. Sub-periosteal dissection exposes the ankle joint and fracture site, and retraction of the tissues laterally exposes the entire lateral articular fragment of Tillaux-Chaput (Fig. 16d). The articular surface is reduced progressively, frequently beginning with any displaced lateral column fragments (Tillaux-Chaput). The reduction proceeds from posterior to anterior and lateral to medial, and the articular fragments are provisionally stabilised with K-wires, first the TillauxChaput fragment and then the antero-medial articular fragment. Once the articular block has been reconstituted it is joined to the proximal fragment. It is not necessary to anatomically reduce metaphyseal or diaphyseal fragments, but length and alignment are restored. Specific plate placement is determined by the nature of the fracture, but frequently two plates are used, one antero-lateral and the other medial. For proximal extension of the fracture, the plates are introduced through the open incision and slid proximally in a subcutaneous fashion (Fig. 16e). If the surgeon elects to use only one plate it should be placed on the compression(concave) side of the fracture to act as a buttress. In other words, a fracture with displacement into varus needs a medial plate as a buttress, and a fracture in valgus, an antero-lateral plate. Failure to recognize this may lead to collapse of the construct on the compression side. The holes in the plate can be easily palpated and screws inserted through small incisions. To fill the metaphyseal defect and support the reconstructed articular surface, autologous bone graft is added. As we previously explained, we no longer fix the fibula prior to ORIF of the pilon fracture. After fixation of the pilon we always perform ORIF of the fibula provided it is a distal-third fracture, with the objective to make the construct more stable. Closure of the wound begins with the extensor retinaculum with interrupted 2–0 resorbable sutures. The subcutaneous tissue is then closed with the same size sutures, and the skin with interrupted 3–0 nylon suture using the technique of Allgöwer (Fig. 16f). Post-operatively, patients are maintained at bed rest for 48–72 h with the limb elevated. If the wound appears satisfactory after that time, the patient begins ambulation allowing only 10 kg of weight-bearing for 10–12 weeks. Range-of-motion and muscle-strengthening exercises are prescribed. The patient is discharged with a removable splint to prevent equinus deformity.
M. Assal and R. Stern
Dual Incision Approach for Osteosynthesis of the Medial and Lateral Columns Recently a dual incision technique has been described [15]. It is in reality a combination of the previous surgical approaches we have presented, the antero-lateral (lateral) and the distal portion of antero-medial (AO). It provides for excellent visualisation of both medial and lateral columns. However, it does require working with an intact soft tissue flap over the anterior aspect of the ankle joint causing a more limited view of this area for judging articular reduction. The choice of using this dual approach or the extensile approach should be based upon the condition of the soft tissues.
Conclusion Fractures of the distal tibia in the adult result from a combination of axial compression and rotation forces. One must first distinguish between the extra-articular and intraarticular fractures, the latter being partial or complete articular. The former can be treated by true minimally-invasive techniques (IM nailing or MIPO), or even hybrid external fixation (tibio-tibial) if desired. The intra-articular fractures require a formal ORIF. Clinical judgment of the condition of the soft tissues is a critical point in the management of these fractures. Delay between injury and definitive ORIF with use of a bridging external fixator is the standard of care for these high energy injuries. The surgical approach depends upon fracture pattern and any associated soft tissue injury, and we have presented a number of surgical approaches which offer different options to the surgeon. The recent development of more distal locking options with IM nails and anatomically-contoured angle-stable plates have improved our ability to stabilise these fractures. Unfortunately, an excellent pre-operative plan, careful attention to the soft tissues, and well-performed surgery may still result in a poor outcome due to primary articular cartilage damage at the time of the injury.
References 1. Anglen JO, Aleto T. Temporary transarticular external fixation of the knee and ankle. J Orthop Trauma 1998; 12: 431–4.
Surgical Management of Distal Tibial Fractures in Adults 2. Assal M, Ray A, Stern R. The extensile approach for the operative treatment of high-energy pilon fractures: surgical technique and soft-tissue healing. J Orthop Trauma 2007; 21: 198–206. 3. Babis GC, Vayanos ED, Papaioannou N, Pantazopoulos T. Results of surgical treatment of tibial plafond fractures. Clin Orthop Relat Res 1997; 341: 99–105. 4. Barbieri R, Schenk R, Koval K, Aurori K, Aurori B. Hybrid external fixation in the treatment of tibial plafond fractures. Clin Orthop Relat Res 1996; 332: 16–22. 5. Bartlett C, Weiner L. Fractures of the tibial pilon. In: Browner B, Jupiter J, Levine A, Trafton P, eds. Skeletal Trauma (3rd ed.), WB Saunders; Philadelphia, PA 2003: 2257–306. 6. Biga N, Laurent M, Thomine J. Fractures récentes du pilon tibial de l’adulte. Ostéosynthèse à foyer fermé. Le fixateur externe avec ostéosynthèse a minima du tibia. Rev Chir Orthop 1992; 78 (suppl l): 57–8. 7. Blauth M, Bastian L, Krettek C, Knop C, Evans S. Surgical options for the treatment of severe tibial pilon fractures: a study of three techniques. J Orthop Trauma 2001; 15: 153–60. 8. Böhler L. Technique du traitement des fractures. Editions Médicales de France, Paris, 1944. 9. Bonar SK, Marsh JL. Unilateral external fixation for severe pilon fractures. Foot Ankle 1993; 14: 57–64. 10. Bone L, Stegemann P, McNamara K, Seibel R. External fixation of severely comminuted and open tibial pilon fractures. Clin Orthop Relat Res 1993; 292: 101–7. 11. Borens O, Kloen P, Richmond J, Roederer G, Levine DS, Helfet DL. Minimally invasive treatment of pilon fractures with a low profile plate: preliminary results in 17 cases. Arch Orthop Trauma Surg 2009; 129: 649–59. 12. Borrelli J, Jr., Catalano L. Open reduction and internal fixation of pilon fractures. J Orthop Trauma 1999; 13: 573–82. 13. Brumback RJ, McGarvey WC. Fractures of the tibial plafond. Evolving treatment concepts for the pilon fracture. Orthop Clin North Am 1995; 26: 273–85. 14. Burgess AR, Dischinger PC, O’Quinn TD, Schmidhauser CB. Lower extremity injuries in drivers of airbag-equipped automobiles: clinical and crash reconstruction correlations. J Trauma 1995; 38: 509–16. 15. Chen L, O’Shea K, Early JS. The use of medial and lateral surgical approaches for the treatment of tibial plafond fractures. J Orthop Trauma 2007; 21: 207–11. 16. Collinge C, Kuper M, Larson K, Protzman R. Minimally invasive plating of high-energy metaphyseal distal tibia fractures. J Orthop Trauma 2007; 21: 355–61. 17. Colmar M, Langlais F. Complications précoces des fractures du pilon tibial avec rupture métaphysaire totale. Rev Chir Orthop 1992; 78 (suppl I): 71–3. 18. Copin G, Nerot C. Les fractures du pilon tibial de l’adulte. Symposium SOFCOT. Paris, Nov 1991. Rev Chir Orthop 1992; 78 (suppl I): 33–83. 19. Court-Brown CM, Walker C, Garg A, McQueen MM. Halfring external fixation in the management of tibial plafond fractures. J Orthop Trauma 1999; 13: 200–6.
111 20. DeLestang M, Hourlier H. Ostéosynthèse à foyer ouvert des fractures du pilon tibial. Traitement opératoire par voie antéro-exteme. Rev Chir Orthop 1992; 78 (suppl I): 54–6. 21. Dickson KF, Montgomery S, Field J. High energy plafond fractures treated by a spanning external fixator initially and followed by a second stage open reduction internal fixation of the articular surface-preliminary report. Injury 2001; 32 Suppl 4: SD92–8. 22. Fitzpatrick DC, Marsh JL, Brown TD. Articulated external fixation of pilon fractures: the effects on ankle joint kinematics. J Orthop Trauma 1995; 9: 76–82. 23. French B, Tornetta P, 3rd. Hybrid external fixation of tibial pilon fractures. Foot Ankle Clin 2000; 5: 853–71. 24. Giordano CP, Koval KJ. Treatment of fracture blisters: a prospective study of 53 cases. J Orthop Trauma 1995; 9: 171–6. 25. Griffiths GP, Thordarson DB. Tibial plafond fractures: limited internal fixation and a hybrid external fixator. Foot Ankle Int 1996; 17: 444–8. 26. Grose A, Gardner MJ, Hettrich C, Fishman F, Lorich DG, Asprinio DE, Helfet DL. Open reduction and internal fixation of tibial pilon fractures using a lateral approach. J Orthop Trauma 2007; 21: 530–7. 27. Gustilo RB, Anderson JT. Prevention of infection in the treatment of one thousand and twenty-five open fractures of long bones: retrospective and prospective analyses. J Bone Joint Surg Am 1976; 58: 453–8. 28. Hahn MP, Thies JW. Pilon tibiale fractures. Chirurg 2004; 75: 211–30. 29. Hasenboehler E, Rikli D, Babst R. Locking compression plate with minimally invasive plate osteosynthesis in diaphyseal and distal tibial fracture: a retrospective study of 32 patients. Injury 2007; 38: 365–70. 30. Heim V. Die pilon tibial fractur. Springer; Berlin, 1990. 31. Helfet DL, Shonnard PY, Levine D, Borrelli J, Jr. Minimally invasive plate osteosynthesis of distal fractures of the tibia. Injury 1997; 28 Suppl 1: A42–7. 32. Hontzsch D, Karnatz N, Jansen T. One- or two-step management (with external fixator) of severe pilon-tibial fractures. Aktuelle Traumatol 1990; 20: 199–204. 33. Hutson JJ Jr, Zych GA. Infections in periarticular fractures of the lower extremity treated with tensioned wire hybrid fixators. J Orthop Trauma 1998; 12: 214–8. 34. Kim HS, Jahng JS, Kim SS, Chun CH, Han HJ. Treatment of tibial pilon fractures using ring fixators and arthroscopy. Clin Orthop Relat Res 1997; 334: 244–50. 35. Lau TW, Leung F, Chan CF, Chow SP. Wound complication of minimally invasive plate osteosynthesis in distal tibia fractures. Int Orthop2008; 32: 697–703. 36. Lecestre P, Lortat-Jacob A, Ramadier J. Les fractures du pilon tibial. Analyse de 40 cas et discussion. Ann Chir 1977; 31: 665–71. 37. Lechevallier J, Biga N. Fixateur externe tibio-calcanéen dans le traitement des fractures du pilon tibial. Rev Chir Orthop 1988; 74: 52–60. 38. Lee PT, Clarke MT, Bearcroft PW, Robinson AH. The proximal extent of the ankle capsule and safety for the insertion of
112 percutaneous fine wires. J Bone Joint Surg Br 2005; 87: 668–71. 39. Marsh JL, Bonar S, Nepola JV, Decoster TA, Hurwitz SR. Use of an articulated external fixator for fractures of the tibial plafond. J Bone Joint Surg Am 1995; 77: 1498–509. 40. Marsh JL, Buckwalter J, Gelberman R, Dirschl D, Olson S, Brown T, Llinias A. Articular fractures: does an anatomic reduction really change the result? J Bone Joint Surg Am 2002; 84-A: 1259–71. 41. Marsh JL, Weigel DP, Dirschl DR. Tibial plafond fractures. How do these ankles function over time? J Bone Joint Surg Am 2003; 85-A: 287–95. 42. McDonald MG, Burgess RC, Bolano LE, Nicholls PJ. Ilizarov treatment of pilon fractures. Clin Orthop Relat Res 1996; 325: 232–8. 43. Müller M, Nazarian S, Koch P, Schatzker J. The Comprehensive Classification of Fractures of Long Bones. Edited, Springer; Berlin, 1990. 44. Nordin J-Y, Barna L, Pages C, PlanteBordeneuve P. Ostéosynthèse par fixateur externe de 35 fractures ouvertes et/ou comminutives de la cheville. Rev Chir Orthop 1988; 74 (suppl II): 230–3. 45. Nork SE, Schwartz AK, Agel J, Holt SK, Schrick JL, Winquist RA. Intramedullary nailing of distal metaphyseal tibial fractures. J Bone Joint Surg Am 2005; 87: 1213–21. 46. Pai V, Coulter G. Minimally invasive plate fixation of the tibia. Int Orthop 2007; 31: 491–6. 47. Paiement G, Gosselin R, Contreras D. Traitement par fixation interne minimale et fixation externe des fractures complexes du pilon tibial. 38e Congrès de l’AOLF, Québec. Rev Chir Orthop 1992; 79: 145–71. 48. Papadokostakis G, Kontakis G, Giannoudis P, Hadjipavlou A. External fixation devices in the treatment of fractures of the tibial plafond: a systematic review of the literature. J Bone Joint Surg Br 2008; 90: 1–6. 49. Parameswaran AD, Roberts CS, Seligson D, Voor M. Pin tract infection with contemporary external fixation: how much of a problem? J Orthop Trauma 2003; 17: 503–7. 50. Patterson MJ, Cole JD. Two-staged delayed open reduction and internal fixation of severe pilon fractures. J Orthop Trauma 1999; 13: 85–91. 51. Plaweski S, Abu M, Butel J, Faure C. Ostéosynthèse à foyer ouvert des fractures du pilon tibial: Techniques classiques. Rev Chir Orthop 1992; 78(suppl I): 51–4. 52. Pollak AN, McCarthy ML, Bess RS, Agel J, Swiontkowski MF. Outcomes after treatment of high-energy tibial plafond fractures. J Bone Joint Surg Am 2003; 85-A: 1893–900. 53. Pugh KJ, Wolinsky PR, McAndrew MP, Johnson KD. Tibial pilon fractures: a comparison of treatment methods. J Trauma 1999; 47: 937–41.
M. Assal and R. Stern 54. Redfern DJ, Syed SU, Davies SJ. Fractures of the distal tibia: minimally invasive plate osteosynthesis. Injury 2004; 35: 615–20. 55. Rüedi T, Allgöwer M. Fractures of the lower end of the tibia into the ankle joint: results 9 years after open reduction and internal fixation. Injury 1973; 5: 130–4. 56. Rüedi T, Matter P, Allgöwer M. Die intraartikularen fracturen des distalen unterschentekendes. Helv Chir Acta 1968; 35: 556–82. 57. Samaran P, Bonnevialle P, Copin G, Murga R. Fractures récentes du pilon tibial de l’adulte. Ostéosynthèse à foyer fermé. Fixateur externe d’Ilizarov et fracture du pilon tibial. Rev Chir Orthop 1992; 78 (suppl I): 59–60. 58. Siguier M, Pacault J-Y, Judet T, Brumpt B: Fractures du pilon tibial. In: Actualités de chirurgie orthopédique de l’hôpital Raymond-Poincaré. Masson, Paris, 1978, 34–47. 59. Sirkin M, Sanders R, DiPasquale T, Herscovici D, Jr. A staged protocol for soft tissue management in the treatment of complex pilon fractures. J Orthop Trauma 1999; 13: 78–84. 60. Strauss EJ, Alfonso D, Kummer FJ, Egol KA, Tejwani NC. The effect of concurrent fibular fracture on the fixation of distal tibia fractures: a laboratory comparison of intramedullary nails with locked plates. J Orthop Trauma 2007; 21: 172–7. 61. Summer C, Rüedi T. Tibia: distal (pilon). In: Rüedi T, Murphy W, eds. AO Principles of Fracture Management. Thieme; Stuttgart, 2000: 539–56. 62. Tornetta P, 3rd, Gorup J. Axial computed tomography of pilon fractures. Clin Orthop Relat Res 1996; 323: 273–6. 63. Tornetta P, 3rd, Weiner L, Bergman M, Watnik N, Steuer J, Kelley M, Yang E. Pilon fractures: treatment with combined internal and external fixation. J Orthop Trauma 1993; 7: 489–96. 64. Tscherne H, Gotzen L. Fraktur und Weichteilschaden. Springer; Heidelberg, 1983. 65. Tscherne H, Oestern H: Pathophysiology and classification of soft tissue injuries associated with fractures. In: Tscherne H, Gotzen L, eds. Fractures with Soft Tissue Injuries: Springer; Berlin, 1984: 1–9. 66. Varela CD, Vaughan TK, Carr JB, Slemmons BK. Fracture blisters: clinical and pathological aspects. J Orthop Trauma 1993; 7: 417–27. 67. Vidal J, Terschiphorst P, Molhy A, Maury P, Boisard J, Martin B. Ligamentotaxis. Méthode de réduction et de contention des fractures articulaires complexes. Rev Chir Orthop 1990; 76: 90–9. 68. Vives P, Hourlier H, DeLestang M, Dorde T, Letot P, Senlecq F. Etude de 84 fractures du pilon tibial de l’adulte. Essai de classification. Rev Chir Orthop 1984; 70: 129–39. 69. Vrabl M. Primary closed, stabilisation of type C 3 pilon fractures with external fixator without bridging the ankle joint. Unfallchirurg 1997; 100: 406–8.
The Distal Radio-Ulnar Joint: Functional Anatomy, Biomechanics, Instability and Management Panayotis N. Soucacos and Nickolaos A. Darlis
Functional Anatomy For most surgeons, the distal end of the radius is viewed as the anatomic foundation of the wrist joint. The distal end of radius, about 2 cm proximal to the radiocarpal joint at the metaphyseal flare, is uniquely designed to transmit axial load and provide mobility [1]. The distal articular surface of the radius is biconcave and triangular. The apex of the triangle points towards the radial styloid process, and the base forms the sigmoid notch that articulates with distal end of the ulna. Two distinct concave facets are found on the articular surface (Fig. 1). These facets articulate with the scaphoid and the lunate of the carpus. The articular surface slopes in an ulnar and palmar direction. Although the carpus tends to slide in this direction, this is resisted by the intracapsular and interosseous carpal ligaments. The DRUJ is a di-athrodial joint, comprised of the triangular fibrocartilage complex (TFCC), ligament complex and oblique fibres of the distal interosseous membrane. It is classified as a uni-axial synovial pivot joint between the convex head of the ulna and concave ulnar notch of the radius. The convex distal ulna is covered with articular cartilage and articulates with the sigmoid or ulnar notch of the distal end of the radius. The sigmoid notch is semicylindrical (concave) and oriented parallel to the ulnar head. It presents with three distinct margins (dorsal, palmar and distal) and angles distally and ulnarly about 20°. The shape of the sigmoid notch varies considerably, ranging from relatively flat to a shallow hemicylinder. Stability of the joint is partially (about 20%) provided by articular contact [2]. However, the dorsal and palmar rims work with the radio-ulnar ligaments to provide the main constraining mechanisms. The dorsal rim is usually
Panayotis N. Soucacos () Department of Orthopaedic Surgery, University of Athens, School of Medicine, Athens, Greece e-mail:
[email protected]
angled acutely, while the palmar rim has a prominent osteocartilaginous lip. Injury to the sigmoid notch, such as rim fracture, or even developmently flat notches are significantly more prone to produce instability [3].
Fig. 1 As the radio-ulnar ligaments pass ulnarwards from the distal rim of the sigmoid notch, each divides in the coronal plane into two limbs or branches. The superficial or distal limb attaches to the base or mid-portion of the ulnar styloid, while the deep or proximal limb attaches at the fovea. Note the distal articular surface of the radius is biconcave and triangular. Two distinct concave facets are found on the articular surface. These facets articulate with the scaphoid and the lunate of the carpus
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Distally, the flat ulnar head is beneath the triangular fibrocartilage complex (TFCC) and is covered partially with articular cartilage from the ulnar styloid. The ulnar styloid is a continuation of the subcutaneous ridge of the ulna and projects from 2 to 6 mm distally, providing attachments for the components of the TFCC. The styloid provides increased area for soft-tissue attachments and is frequently fractures, resulting in ligament destabilization. At the base of the styloid is a shallow concavity called the fovea. This is the site of attachment for the ulnocapitate ligament and majority of fibers of the distal radio-ulnar ligaments. The TFCC inserts into the distal ulna around the fovea. During surgery, the fovea is an important landmark critical for accurate ligament repair [4]. The triangular fibrocartilage complex (TFCC) was originally described by Palmer and Werner in 1981 [5] as a complex of several structures. Although these components are anatomically confluent, they are structurally and functionally distinct, providing multiple functions to the DRUJ [2]. Among the structures included in the TFCC are the dorsal and volar radio-ulnar ligaments, the ulnar collateral ligament, the meniscus homologue, the articular disk and the extensor carpi ulnaris (ECU) sheath. The ECU subsheath is a strong structure that extends from the groove in the ulnar head to the dorsal carpus and contributes to DRUJ stability. The meniscal homologue is believed to be derived from synovium and varies in size and shape. The TFCC is a ligamentous and cartilaginous structure that suspends the distal radius and the ulnar carpus from the distal ulna. It arises from the ulnar aspect of the lunate fossa of the radius and courses toward the ulna. At the ulna, it inserts in the fovea at the base of the ulnar styloid. As it courses distally, it receives fibers from the ulnar collateral ligament and thickens to become the meniscus homologue before it inserts distally into the lunate, triquetrum, hamate and base of the fifth metacarpal. The distal insertions of the meniscal homologue vary. Dorsolaterally, the TFCC incorporates the floor of the sheath of the extensor carpi ulnars. The TFCC forms a weak attachment with the carpus dorsally. In about 5–10% of the cases it forms a broad, sturdy attachment to the luno-triquetral interosseous ligament and the triquetrum with the ulnotriquetral ligament volarly [2, 5, 6]. This insertion partially or completely covers the triquetrum’s articular surface; a variation that may obscure the arthroscopic visualization of the luno-triquetral ligament, as is discussed later in this chapter. Its attachment to the lunate, hamate and base of the fifth metacarpal are weak and inconsistent. The insertions of the TFCC on the triquetral and lunate do not directly stabilize the DRUJ. Both of these ligaments, the ulno-triquetral and ulno-lunate ligaments originate from the palmar radio-ulnar
P. N. Soucacos and N. A. Darlis
ligament. They are commonly implicated in rheumatoid arthritis, and contribute to the caput ulna syndrome. The palmar and dorsal radio-ulnar ligaments are the primary components of the TFCC that stabilize the DRUJ. These appear as thickenings at the junctures of the triangular fibrocartilage articular disk, DRUJ capsule and ulno-carpal capsule. As the radio-ulnar ligaments pass ulnarly from the distal rim of the sigmoid notch, each divides in the coronal plane into two limbs or branches. The superficial or distal limb attaches to the base or mid-portion of the ulnar styloid, while the deep or proximal limb attaches at the fovea (Fig. 1). The clinical significance for DRUJ stability of this anatomical arrangement is noteworthy following ulnar styloid fractures. A basilar styloid fracture results in mechanical discontinuity to the superficial limbs, with potential disruption of the deep limbs because of the injury proximity. The deep limbs may remain intact preserving DRUJ stability [2, 6]. The dorsal radio-ulnar ligament merges with the ECU subsheath and both radio-ulnar ligaments merge with the central fibrocartilaginous disk. The central disk is a triangular, biconcave, fibrocartilaginous disk that extends from the distal rim of the sigmoid notch and blends with the radio-ulnar ligaments. Its thickness varies inversely with ulnar variance.
Biomechanics The unique structure of the joint permits rotation, while preserving stability and transmitting the load transmitted by the radiocarpal joint to both forearm bones. The bony anatomy of the DRUJ contributes very little to stability. Rather, stability is supported by the triangular fibrocartilage complex, the tendon sheath of the extensor carpi ulnaris, the pronator quadratus muscle and other tendons on the ulnar side of the wrist. In addition to stabilization of the joint, the TFCC plays an important role in load-bearing across the wrist, as well. The DRUJ is a complex joint involved in pronosupination and ulno-carpal motion and support. During this motion, the ulnar head glides from the dorsal to the volar rim of the sigmoid notch as the joint moves from pronation to supination. In this process, the TFCC is taut dorsally at first, and then volarly. Under dynamic loading, the DRUJ has a piston-like movement that is not resisted by the TFCC [7].
Kinematics The distal end of the radius articulates with the convex surface of the distal end of the ulna at the sigmoid notch. This
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articulation plays an integral role in the functional anatomy and biomechanics of the hand and wrist, as the radius and hand rotate about the fixed ulna. The radius rotates about the distal ulna during forearm rotation. As the forearm axis moves laterally in space, the distal radius and hand rotate about the ulnar head (up to 150°). This takes place at the distal radioulnar joint. During pronation and supination, the ulnar head is not immobile, rather it moves slightly in the opposite direction (laterally) of the distal radius. Specifically, the ulnar head moves distally in relation to the distal radius in pronation and proximally in supination [8]. During forearm rotation, the ulnar head glides in the sigmoid notch of the radius from a dorsal distal position to a volar proximal position, resulting in an area of articular contact as little as 2 mm. Rotation of the radius and hand around the fixed ulna is accompanied by a relative volar translation of the ulna with forearm supination and a relative dorsal translation with forearm pronation. The axis of motion is near the centre of the ulnar head, and passes through or near the fovea. Translation of the DRUJ occurs as a consequence of the anatomical features of the sigmoid notch: it is shallow and its radius of curvature is about 50% more than that of the ulnar head. In neutral position and under load, translation can be up to 1 cm [9].
Kinetics In addition to providing the distal link between the radius and ulna and a pivot for pronation-supination, the DRUJ also supports the ulnar carpus and transmits wrist loads. The latter is accomplished in combination with the TFCC and other soft-tissues. The radius appears to carry about 80% of the axial load of the forearm through its articulation with the lateral carpus, while the ulna carries only about 20% of the total force transmitted across the wrist. The main function of the central fibrocartilagenous disk is bear the compressive load across the ulnocarpal joint. This disk has been reported to attenuate 53% of the normal compressive loading. It is believed that chronic and excessive loading may likely contribute to disk degeneration, a component of ulnar impaction syndrome [10]. About 20% of DRUJ stability is attributed to articular contact alone. The TFCC plays an important role in load-bearing across the wrist, as well as in DRUJ stabilization. The TFCC performs several important functions in the wrist. In addition to its role as cushion for the ulnar carpus, (where it carries about 20% of the axial load across the wrist) it is an important stabilizer of the DRUJ. The palmar and dorsal radio-ulnar ligaments are the primary components of the TFCC that stabilize the DRUJ [11], although the role of these two ligaments have been debated by various authors [12, 13].
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Because the skeletal architecture of the DRUJ provides minimal stability, it predisposes the restraining soft-tissues to injury. As a consequence of the functional inter-relationship of the DRUJ and proximal radio-ulnar joint, any injury to either of these joints ultimately impinges on the function of both joints. The soft-tissue structures that contribute to DRUJ stability include the pronator quadratus, extensor carpi ulnaris, the interosseous membrane, the capsule of the DRUJ, as well as the structures of the TFCC [14]. Although the relative contributions of these structures to stability of the DRUJ is still debated, it is generally agreed that severe instability requires disruption of multiple structures [11, 14]. Although multiple structures contribute to DRUJ stability, the TFCC is believed to be the major soft-tissue stabilizer. Its anatomic configuration is mechanically suited to stabilize the joint, while allowing for a wide arc of forearm rotation.
Injuries of the DRUJ: Pathophysiology Traumatic injury to the DRUJ can be associated with complex pathology of the wrist, resulting in chronic instability. Injury to the DRUJ can occur isolated, but more frequently in association with almost any fracture of the forearm (distal radius fractures, Galeazzi fractures, Essex-Lopresti injuries and both-bone forearm fractures). DRUJ injuries can be stable, partially unstable (subluxation) and unstable (dislocation). Dislocation of the joint can be isolated or combined with fractures. DRUJ injuries in addition to being simple or complex (irreducible or severe instability, can be acute or chronic. In addition to injury, the DRUJ is frequently plagued with rheumatoid arthritis. Rheumatoid arthritis involves the wrist in about 80% of the cases, of which 30–75% of these patients have DRUJ involvement. The mobile unit of the DRUJ is comprised of the radius along with the carpus. Nonetheless, by convention DRUJ dislocation or instability is described by the position of the ulnar head relative to the distal radius [6]. The majority of isolated DRUJ dislocations are dorsal and are caused by hyperpronation and wrist extension, usually resulting from a fall on an outstretched hand. Volar dislocations are related to a direct blow to the ulnar aspect of the forearm or in a supinated forearm. The most common skeletal injuries involve fractures of the distal radius, which account for about 20% of all fractures. About half of these involve the articular surface of the distal radius. The vast majority of these fractures result from falls on an outstretched hand, and these are particularly prevalent in two patient groups: young patients (6–10 years) and older patient (60–70 years). Both in regards to the frequency of these injuries and the difficulties related to
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diagnosis and treatment, it has been referred to as the “low back pain” of upper extremity afflictions [5, 8]. The most common cause for DRUJ instability is a distal radius fracture. Dorsal angulation of the radius induces palmar instability of the ulna. Angulation of more than 20°, creates marked incongruity of the DRUJ, distorts the TFCC and alters kinematics of the joint [6, 15]. With excessive radial shortening the TFCC typically tears at its ulnar attachments. With increased severity of the injury, the secondary stabilizers of the DRUJ, as well as the structures on the ulnar side of the wrist also sustain injury. These include the interosseous membrane, the extensor carpi ulnaris sheath, ulnocarpal ligaments and the luno-triquetral interosseous ligament. The ulnar styloid provides attachments for the ulnocarpal ligaments, extensor carpi ulnaris tendon sheath and superficial portion of the radio-ulnar ligaments. There are no softtissue attachments on the tip of the styloid process. For the most part, fractures of the ulnar styloid do not result in DRUJ instability. Fractures through the styloid base is more frequently associated with a TFCC tear, compared to the more frequent styloid tip fracture. Following distal radius fractures, the outcome of injuries to the DRUJ depends primarily on residual joint stability and the development of post-traumatic arthrosis [1]. Important parameters of DRUJ injuries include: (1) presence of DRUJ subluxation or dislocation of the ulnar head from concomitant rupture of the TFCC and capsular ligaments; and (2) the amount of joint surface involved.
Diagnosis of DRUJ Instability Pain, reduced motion, weakness and mechanical symptoms may persist after wrist injuries, particularly after distal radial fractures. These are frequently related to residual dysfunction of the DRUJ and often go misdiagnosed. DRUJ instability may be present with other pathologies, such as DRUJ arthritis, ulnar impaction syndrome, tendonitis of the extensor carpi ulnaris tendonitis, among other causes of wrist pain [6]. These need to be considered in the differential diagnosis before treatment of instability is addressed. In most cases, post-traumatic DRUJ instability is associated with falling on an outstretched hand or forced wrist rotation. In children late DRUJ instability is frequently associated with a previous fracture of the distal radius or forearm. In adults, on the other hand, DRUJ instability after distal radius or forearm mal-union usually presents with loss of forearm motion, ulnar head prominence and ulnar-sided wrist pain [1, 2, 6]. In the evaluation DRUJ instability, other lesions associated with ulnar-sided wrist pain should also be considered. Ulnar-sided wrist pain can be attributed to bone,
P. N. Soucacos and N. A. Darlis Table 1 Differential diagnosis of ulnar side pain: associated lesions Luno-triquetral instability Midcarpal instability Foveal disruption of distal radio-ulnar ligaments Ulno-triquetral ligament injuries Extensor carpi ulnaris subluxation DRUJ pathology TFCC tears Tendonitis Flexor carpi ulnaris Extensor carpi ulnaris Fracture Hamate (hook) Pisiform Hypothenar hammer syndrome Arthrtis DRUJ Piso-triquetral joint Essex-Lopresti lesion Ulnar impaction syndrome Ulnar wrist mass Ganglion cysts (may be ulnar artery aneurysms)
soft-tissue, as well as neurovascular causes (some causes associated with ulnar-sided pain are shown in Table 1). An obvious deformity is usually apparent upon physical examination of an acute dislocation, with the ulnar head locked over a rim of the sigmoid notch. This is associated with swelling, tenderness and limited motion. In chronic dislocation, there are usually visible and palpable clunks as the ulnar head dislocates and reduces in the sigmoid notch during active or passive forearm rotation. Palmar subluxation of the DRUJ will present with a slight prominence of the ulnar head on the palmar aspect of the wrist and a depression on the dorsal surface. These features are subtle and frequently difficult to detect. Tenderness may be acute over the fovea of the ulnar head. Imaging of the DRUJ is an essential component of diagnosis. Plain radiographs provide information regarding bony deformities from acute or old fractures, joint degeneration, etc. Limb positioning is critical for accuracy of radiographs. The position of the extensor carpi ulnaris groove can be used for postero-anterior views [16]. When the cortical outline of the groove’s concavity is radial to the ulnar styloid’ long axis, the view is appropriate for measuring ulnar variance. When ulnar impaction syndrome is suspected, the pronated grip view can demonstrate dynamic positive ulnar variance. CT has become the gold standard for imaging DRUJ instability. In order to make comparisons between the normal and affected sides, CT imaging requires that both wrists
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A solid knowledge of the stabilizers of the DRUJ is essential in understanding treatment options. Conservative treatment can be used to manage DRUJ dislocation when recognized acutely and reduction is uncomplicated. However, non-operative management of severe, chronic DRUJ instability is usually not effective in relieving symptoms. Surgical repair of post-traumatic DRUJ instability is aimed at restoring stability and a full painless arc of motion. The DRUJ can be approached from three sides with a refined dorsal approach retaining a robust retinacular-dorsal capsular layer, preferred by most [19]. This approach allows inspection of the luno-triquetral ligament, the triquetrum, the dorsal part of the TFCC from proximally and distally, the major portion of the ulnar articular surface and the dorsal aspect of the sigmoid notch. Recently, surgeons have described a safe and extensive volar approach with broad indications. A subcutaneous ulnar approach remains an option, particularly when dealing with additional distal ulnar pathology.
and include minimally-displaced avulsion of the tip of the ulnar styloid or a stable fracture of the neck of the ulna. Type II are unstable DRUJ lesions with either an avulsion fracture of the base of the ulnar styloid or massive tear of the TFCC and/or secondary distal radio-ulnar joint stabilizers (Extensor Carpi Ulnaris subsheath, distal part of the interosseous membrane). With the introduction of wrist arthroscopy, ligamentous injuries are increasingly recognized in distal radius fractures. Type III are potentially unstable lesions caused by fractures through the sigmoid notch (4-part fracture of the distal radius) or the ulnar head. Anatomic reduction and stabilization of these fractures will usually restore the DRUJ stability. Regardless of this classification, rupture of the DRUJ restraints must be considered highly possible in distal radius fractures when there is (a) shortening of the radius more than 5–7 mm, (b) a displaced fracture of the base of the ulnar styloid, (c) distal radius angulation of more than 25–30° in any plane and (d) DRUJ diastasis in the PA radiographic projection. Although TFCC tears can occur with any distal radius fracture configuration, they have been shown to occur more frequently in conjunction with Frykman type VI and VIII fractures [21]. A high index of suspicion for this injury must be maintained. In Galeazzi fracture-dislocations, reduction of the distal radius metaphyseal fracture will usually restore DRUJ stability. If DRUJ instability persists it should be treated using the same principals as for more complex distal radius fracture configurations described below. Fractures of the base of the ulnar styloid must be fixed especially when they are accompanied by clinical DRUJ instability. Kirschner wires, tension band wire, interfragmental lag screw compression, or suture anchors may be used to stabilize the ulnar styloid fragment. The interval between the extensor digit quinti and the extensor carpi ulnaris is used to expose the styloid fragment. However, it must be noted that ulnar styloid fixation may not necessarily restore DRUJ stability since there may be a concomitant TFCC tear in 16–46% of the patients [22, 23]. Wrist arthroscopy is extremely helpful in such cases in order to diagnose and treat these lesions. Another option is to immobilize the wrist for 4–6 weeks in neutral rotation expecting the TFCC lesion to heal.
Management of Acute DRUJ Instability
TFCC Repair
Acute DRUJ instability usually accompanies displaced distal radius fractures. Geissler et al. [20] classified the resultant DRUJ instability in three types. Their classification is applicable after the distal radius fracture is adequately reduced and stabilized and the anatomic relations of the DRUJ restored. Type I are clinically stable DRUJ lesions
TFCC lesions are categorized according to the Palmer [24] classification into traumatic (class 1) and degenerative (class 2) tears. Traumatic tears are increasingly recognized early after trauma with the introduction of wrist arthroscopy. Their incidence in distal radius fractures is reported to be between 39 and 78% [20, 23, 25], however only a small
are evaluated on the same images and in identical positions, including neutral, supination and pronation. Several measurements have been used to identify instability. The use of MRI to diagnosis TFCC injuries remains controversial, with its sensitivity, specificity and accuracy varying among reports [17]. Other modalities such as arthrography and scintigraphy have been used to assess DRUJ instability, although their roles are limited. They have been found useful when other concurrent problems are suspected, such as ulnar impaction syndrome, non-destabilizing TFCC tears, etc. Wrist arthrography has a low sensitivity compared to arthroscopy, and is consequently used less commonly to evaluate wrist pain. While arthroscopy is sensitive for identifying TFCC tears in the central portion of the disk, it is difficult to detect peripheral tears. In addition, arthroscopy can be used to identify co-existing lesions that may contribute to symptoms, and equally important can be used for concomitant therapeutic debridement or repair [18].
Treatment Options
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percentage will be accompanied by clinically detectable DRUJ instability. Wrist arthroscopy should be considered in DRUJ instability following distal radial fractures especially in young active patients. Degenerative tears are often caused by ulno-carpal impaction syndrome. Patients typically present with ulnar-sided wrist pain and a positive ulno-carpal stress test [26] (pain with axial compression, ulnar deviation and passive pronation and supination). Pronated grip view radiographs should be used to access ulnar variance and MRI can be helpful in revealing «kissing lesions» on the ulnar side of the lunate [27]. In cases with ulno-carpal impaction TFCC management must be supplemented by an ulnar recession procedure. Ulnar shortening can be performed either arthroscopically (arthroscopic wafer procedure [28–30] Fig. 2d) or open. Several techniques of open extra-articular ulnar shortening have been described [31–35]. The goal is to restore ulnar variance to neutral or 1 mm of negative [36]. Shortening of more than 2 mm of negative may lead in DRUJ incongruence. The treatment of TFCC lesions depends mainly on their location. TFCC tears can be central, peripheral (mainly ulnar) and radial (Fig. 3). Central tears are often degenerative. They
Fig. 2 Treatment of a central TFCC tear accompanied by ulno-arpal impaction syndrome. (a) A tear of the central membranous part of the TFCC is identified and probed. Degeneration of the luno-triquetral ligament is also identified. (b) The tear is debrided to a stable rim using a radio-frequency probe. (c) At the end of the debridement the ulnar head is visible through the defect and a chondral lesion (“kissing lesion”) is identified. (d) An arthroscopic wafer procedure is initiated trough the TFCC defect using a mechanized burr. r radius; u ulna; lt luno-triquetral ligament; p radio-frequency probe
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present in the thin and relatively avascular central part of the TFCC. Their healing potential is considered minimal and they are treated with arthroscopic debridement. As much as two thirds of the diameter of the TFCC can be safely debrided without destabilizing the DRUJ (Fig. 2a, b). After the debridement the head of the ulna should be visible through
Fig. 3 Classification of TFCC tears based on their location (central, peripheral, radial)
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the defect thus confirming that the full thickness of the TFCC has been debrided (Fig. 2c). Care should be also taken to remove all residual tissue attaching to the radius. Both mechanized resectors (shavers) and small radio-requency probes can be used for the debridement [35, 36]. Peripheral (ulnar) tears involve well-vascularized tissue and are considered repairable. The pre-styloid recess is a normal anatomic finding that can be confused by an inexperienced arthroscopist for an ulnar tear. The retention of the tramboline effect on probing of the TFCC can confirm its integrity in doubtful cases. Peripheral tears should be repaired especially when accompanied by clinical DRUJ instability. The repair can be either arthroscopic or open. Several techniques of arthroscopic repair have been described [18, 38–43]: outside-in, inside-out and all-inside as well as the use of specialized repair kits. They all aim at attaching the torn tissue to the capsule. In outside-in and inside-out techniques most surgeons prefer to enlarge the skin incision of one of the ulnar portals in order to confirm that the suture loop or the knot will not catch one of the terminal branches of the sensory branch of the ulnar nerve. Open techniques of capsular re-attachment have been also described. Recently, the clinical importance of the deep bundle of the normal TFCC attaching to the ulnar fovea (Fig. 3) has been highlighted. This deep attachment can be re-created by repairing an ulnar tear with the use of a small suture anchor inserted to the ulnar fovea through a mini-open incision [44]. Radial TFCC tears can include either the attachment of the membranous part of the TFCC to the radius or the attachments of the volar and dorsal radio-ulnar ligaments (Figs. 3 and 4). When the radio-ulnar ligaments are involved there is usually resultant DRUJ instability. Treatment of radial TFCC lesions remains controversial. It seems that arthroscopic debridement alone is adequate if there is no clinical DRUJ instability. In cases with instability, re-attachment of the TFCC should be performed. Arthroscopic repair is performed using trans-osseous sutures through the distal radius with an insideout technique [18, 45–47]. If there is bony avulsion of the
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volar or dorsal radio-ulnar ligaments from the radius, osteosynthesis of the small avulsed fragment may also be attempted [48]. In the acute trauma setting some surgeons elect not to repair radial TFCC tears and keep the wrist immobilized in neutral rotation for 4–6 weeks possibly with the use of a K-wire transfixing the DRUJ. Results of early arthroscopic detection and treatment of TFCC lesions following trauma are promising. Arthroscopically-assisted distal radius fracture management has been shown to yield better results than both ORIF and fluoroscopically-assisted fixation in the mid-term (2–3 years) followup [42, 49–51]. It is unclear, however if these differences can be attributed to the early detection and treatment of ligamentous and TFCC lesions or to the more accurate osseous reduction. The long-term effect of arthroscopically assisted management of distal radius fractures on post-traumatic arthritis is still unknown. This approach may be advantageous especially in young active patients. Results of arthroscopic treatment of chronic TFCC lesions depend mainly on the recognition and treatment of the concomitant ulno-carpal impaction syndrome. TFCC debridement supplemented by an ulnar recession procedure when indicated, yielded above 80% good and excellent results in most series [52–55].
Reconstruction of Radio-Ulnar Ligaments In cases of DRUJ instability with an irreparable TFCC (because of retraction or primary tissue damage, usually more than 6 weeks post trauma), reconstruction of the volar and dorsal radio-ulnar ligaments using autologous tendon graft (palmaris longus or plantaris tendons) can be attempted [56] (Fig. 5). The graft is routed through drill holes in the distal ulnar border of the radius, and the ulnar fovea and around the distal ulna. The procedure is contra-indicated in the presence of DRUJ arthritis. If instability occurs, secondary to a previous mal-union, ligament reconstruction may be performed in conjunction with a corrective osteotomy of the radius or ulna or sigmoid notch osteoplasty. The initial results of this procedure are promising.
DRUJ Hemi-Arthroplasty Fig. 4 Tear of the radial attachment of the TFCC (radial tear). R radius
Interest in ulnar head endoprostheses has been recently renewed with the introduction of metallic modular ulnar head designs. They can be introduced press-fit or cemented into the intra-medullary canal of the distal ulna. Their primary indications are a failed previous distal ulnar resection
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have DRUJ involvement. Arthritis can be caused by osteoarthritis, long-standing instability, intra-articular factures or inflammatory disease [2, 6]. In its early stages, arthritis of the DRUJ can be managed by procedures that retain the ulnar head, such as ulnar shortening shaft osteotomy which alters the contact surfaces of the DRUJ. When this fails, distal ulna resection or radio-ulnar fusion can be used; among possible options are the Darrach resection, hemi-resection arthroplasty, Sauve-Kapandji procedure, one-bone forearm, wide distal ulna resection and implant arthoplasty [58]. These procedures however, do not restore normal anatomy, thus in addition to frequently compromising function, they often do not lead to complete pain relief [1, 2, 6].
References
Fig. 5 Radio-ulnar ligaments reconstruction. An autologous tendon graft is routed through drill holes in the distal ulnar border of the radius, and the ulnar fovea and around the distal ulna
arthroplasty (Darrach, Sauve-Kapandji or Bower’s procedures) and painful DRUJ arthrosis. The initial mid-term (2-year follow-up) results are promising [57], but its longterm value is still unknown.
Ulnar Impaction Wear of the ulnar head, lunate, triquetrum and TFCC resulting in ulnar impaction syndrome can be caused by repetitive ulno-carpal joint overloading. Ulnar variance is usually present in ulnar impaction syndrome which can be caused by distal radius fractures, Essex-Lopresti injury, and traumatic physeal arrest. Arthroscopic debridement of the articular disk and chondral surface can be effective in managing patients with neutral ulnar variance. However, when ulnar variance is positive, ulnar shortening with shaft osteotomy or distal ulna resection is indicated [29].
Arthritis In addition to injury, the DRUJ is frequently plagued with rheumatoid arthritis. Rheumatoid arthritis involves the wrist in about 80% of the cases, of which 30–75% of these patients
1. Jafarnia K, Jupiter J. Distal radius fractures: anatomy, biomechanics and classification. In: Trumble TE, ed. Hand Surgery Update 3. Hand, Elbow, & Shoulder. Rosemont, American Society for Surgery of the Hand, 2003, pp. 83–95 2. Adams BD. Distal radioulnar joint. In: Trumble TE, ed. Hand Surgery Update 3. Hand, Elbow, & Shoulder. Rosemont: American Society for Surgery of the Hand, 2003, pp. 147–157 3. Deshmukh SC, Shanahan D, et al. Distal radioulnar joint incongruity after shortening of the ulna. J Hand Surg [Br] 2000;25(5):434–8 4. af Ekenstam F, Hagert CG. Anatomical studies on the geometry and stability of the distal radioulnar joint. Scand J Plast Reconstr Surg 1985;19:17–25. 5. Palmer AK, Werner FW. The triangular fibrocartilage complex of the wrist – anatomy and function. J Hand Surg [Am] 1981; 6:153–62 6. Adam BD. Distal radioulnar joint instability. In: Berger RA, Weiss AP, eds. Hand Surgery. Vol 1. Philadelphia: Lippincott Williams & Wilkins, 2004, pp. 337–54 7. Ward LD, Abrose CG, et al. The role of the distal radioulnar ligaments, interosseous membrane and joint capsule in distal radioulnar joint stability. J Hand Surg [Am] 2000;25(2): 341–51 8. Palmar AK, Gilsson RR, Serner FW. Ulnar variance determination. J Hand Surg 1982;7:376 9. Gupta R, Allaire RB, et al. Kinematic analysis of the distal radioulnar joint after a simulated progressive ulnar-sided wrist injury. J Hand Surg [Am] 2002;27(5):854–62. 10. Schuurman AH, Kauer JM. Impact load on the triangular fibrocartilage of the wrist: A cadaver study. J Surg Res 2002; 103(2):129–33 11. Stuart PR, Berger RA. The dorsopalmar stability of the disrtal radioulnr joint. J Hand Surg [Am] 2000;25(4):689–99 12. Schuind F, An KN, Berglund L, et al. The distal radioulnar ligaments: a biomechanical study. J Hand Surg [Am] 1991; 16:1106–14
The Distal Radio-Ulnar Joint 13. af Ekenstam F. Anatomy of the distal radioulnar joint. Clin Orthop Relat Res. 1992;275:14–8. 14. Kihara H, Short WH, Werner FW, et al. The stabilizing mechanism of the distal radioulnar joint during pronation and supination. J Hand Surg [Am] 1995;20:930–36 15. Kihara H, Palmer AK, SWerner FW, et al. The effect of dorsally angulated distal radius fractures on distal radioulnar joint congruency and forearm rotation. J Hand Surg [Am] 1996;21:40–7 16. Levis CM, Yang Z, et al. Validation of the extensor carpi ulnaris groove as a predictor for the recognition of standard posteroanterior radiographs of the wrist. J Hand Surg [Am] 2002;27(2):252–7 17. Haims AH, Sachweitzer ME, et al. Limitations of MR imaging in the diagnosis of peripheral tears of the triangular fibrocartilage of the wrist. Am J Roentgenol 2002;178(2):419–22 18. Shih JT, Lee HM, Tan CM. Early isolated triangular fibrocartilage complex tears: management by arthroscopic repair. J Trauma 2002;53:922–7. 19. Bain GI, Pourgiezis N, Roth JH. Surgical approaches to the distal radioulnar joint. Tech Han Up Extrem Surg 2007;11:51–6 20. Geissler WB, Fernandez DL, Lamey DM. Distal radioulnar joint injuries associated with fractures of the distal radius. Clin Orthop Relat Res 1996;327:135–46. 21. Bombaci H, Polat A, Deniz G, Akinci O. The value of plain X-rays in predicting TFCC injury after distal radial fractures. J Hand Surg Eur Vol 2008;33:322–6. 22. Geissler WB. Arthroscopically assisted reduction of intraarticular fractures of the distal radius. Hand Clin 1995;11: 19–29. 23. Richards RS, Bennett JD, Roth JH, Milne K Jr. Arthroscopic diagnosis of intra-articular soft tissue injuries associated with distal radial fractures. J Hand Surg [Am] 1997;22-A:772–6. 24. Palmer AK. Triangular fibrocartilage complex lesions: a classification. J Hand Surg [Am] 1989;14-A:594–606. 25. Lindau T, Arner M, Hagberg L. Intraarticular lesions in distal fractures of the radius in young adults. A descriptive arthroscopic study in 50 patients. J Hand Surg [Br] 1997;22-B:638–43. 26. Nakamura R, Horii E, Imaeda T, Nakao E, Kato H, Watanabe K. The ulnocarpal stress test in the diagnosis of ulnar-sided wrist pain. J Hand Surg [Br] 1997;22-B:719–23. 27. Tomaino MM. The importance of the pronated grip x-ray view in evaluating ulnar variance. J Hand Surg [Am] 2000; 25-A:352–7. 28. Bernstein MA, Nagle DJ, Martinez A, Stogin JM Jr, Wiedrich TA. A comparison of combined arthroscopic triangular fibrocartilage complex debridement and arthroscopic wafer distal ulna resection versus arthroscopic triangular fibrocartilage complex debridement and ulnar shortening osteotomy for ulnocarpal abutment syndrome. Arthroscopy 2004;20:392–401. 29. Tomaino MM, Weiser RW. Combined arthroscopic TFCC debridement and wafer resection of the distal ulna in wrists with triangular fibrocartilage complex tears and positive ulnar variance. J Hand Surg [Am] 2001;26-A:1047–52. 30. Constantine KJ, Tomaino MM, Herndon JH, Sotereanos DG. Comparison of ulnar shortening osteotomy and the wafer resection procedure as treatment for ulnar impaction syndrome. J Hand Surg [Am] 2000;25-A:55–60.
123 31. Wehbe MA, Cautilli DA. Ulnar shortening using the AO small distractor. J Hand Surg [Am] 1995;20-A:959–64. 32. Minami A, Kato H. Ulnar shortening for triangular fibrocartilage complex tears associated with ulnar positive variance. J Hand Surg [Am] 1998;23-A:904–8. 33. Rayhack JM, Gasser SI, Latta LL, Ouellette EA, Milne EL. Precision oblique osteotomy for shortening of the ulna. J Hand Surg [Am] 1993;18-A:908–18. 34. Mizuseki T, Tsuge K, Ikuta Y. Precise ulna-shortening osteotomy with a new device. J Hand Surg [Am] 2001;26-A: 931–9. 35. Darlis NA, Ferraz IC, Kaufmann RW, Sotereanos DG. Stepcut distal ulnar-shortening osteotomy. J Hand Surg [Am] 2005;30-A:943–8. 36. Darlis NA, Weiser RW, Sotereanos DG. Arthroscopic triangular fibrocartilage complex debridement using radiofrequency probes. J Hand Surg [Br] 2005;30-B:638–42. 36. Friedman SL, Palmer AK. The ulnar impaction syndrome. Hand Clin 1991;7:295–310. 38. Trumble TE, Gilbert M, Vedder N. Arthroscopic repair of the triangular fibrocartilage complex. Arthroscopy 1996;12:588–97. 39. Corso SJ, Savoie FH, Geissler WB, Whipple TL, Jiminez W, Jenkins N. Arthroscopic repair of peripheral avulsions of the triangular fibrocartilage complex of the wrist: a multicenter study. Arthroscopy 1997;13:78–84. 40. Cober SR, Trumble TE. Arthroscopic repair of triangular fibrocartilage complex injuries. Orthop Clin North Am 2001; 32:279–94. 41. Bohringer G, Schadel-Hopfner M, Petermann J, Gotzen L. A method for all-inside arthroscopic repair of Palmer 1B triangular fibrocartilage complex tears. Arthroscopy 2002;18:211–3. 42. Ruch DS, Yang CC, Smith BP. Results of acute arthroscopically repaired triangular fibrocartilage complex injuries associated with intra-articular distal radius fractures. Arthroscopy 2003;19:511–6. 43. Estrella EP, Hung LK, Ho PC, Tse WL. Arthroscopic repair of triangular fibrocartilage complex tears. Arthroscopy 2007; 23:729–37. 44. Chou KH, Sarris IK, Sotereanos DG. Suture anchor repair of ulnar-sided triangular fibrocartilage complex tears. J Hand Surg [Br] 2003;28-B:546–50. 45. Cooney WP, Linscheid RL, Dobyns JH. Triangular fibrocartilage tears. J Hand Surg [Am] 1994;19-A:143–54. 46. Jantea CL, Baltzer A, Ruther W. Arthroscopic repair of radialsided lesions of the triangular fibrocartilage complex. Hand Clin 1995;11:31–6. 47. Sagerman SD, Short W. Arthroscopic repair of radial-sided triangular fibrocartilage complex tears. Arthroscopy 1996;12: 339–42. 48. Henry MH. Review article. Management of acute triangular fibrocartilage complex injury of the wrist. J Am Acad Orthop Surg 2008;16:320–9. 49. Ruch DS, Vallee J, Poehling GG, Smith BP, Kuzma GR. Arthroscopic reduction versus fluoroscopic reduction in the management of intra-articular distal radius fractures. Arthroscopy 2004;20:225–30. 50. Doi K, Hattori Y, Otsuka K, Abe Y, Yamamoto H. Intra-articular fractures of the distal aspect of the radius: arthroscopically
124 assisted reduction compared with open reduction and internal fixation. J Bone Joint Surg [Am] 1999;81-A:1093–110. 51. Varitimidis SE, Basdekis GK, Dailiana ZH, Hantes ME, Bargiotas K, Malizos K. Treatment of intra-articular fractures of the distal radius: fluoroscopic or arthroscopic reduction? J Bone Joint Surg [Br] 2008;90-B:778–85. 52. Husby T, Haugstvedt JR. Long-term results after arthroscopic resection of lesions of the triangular fibrocartilage complex. Scand J Plast Reconstr Surg Hand Surg 2001;35:79–83. 53. Minami A, Ishikawa J, Suenaga N, Kasashima T. Clinical results of treatment of triangular fibrocartilage complex tears by arthroscopic debridement. J Hand Surg [Am] 1996;21-A:406–11.
P. N. Soucacos and N. A. Darlis 54. Osterman AL. Arthroscopic debridement of triangular fibrocartilage complex tears. Arthroscopy 1990;6:120–4. 55. Westkaemper JG, Mitsionis G, Giannakopoulos PN, Sotereanos DG. Wrist arthroscopy for the treatment of ligament and triangular fibrocartilage complex injuries. Arthroscopy 1998;14:479–83. 56. Adams BD, Lawler E. Chronic instability of the distal radioulnar joint. J Am Acad Orthop Surg 2007;15:571–5. 58. Watson HK, Manzo RL. Modified arthroplasty of the distal radio-ulnar joint. J Hand Surg [Br] 2002;27:322–5 57. Willis AA, Berger RA, Cooney WP 3rd. Arthroplasty of the distal radioulnar joint using a new ulnar head endoprosthesis: preliminary report. J Hand Surg [Am] 2007;32-A:177–89.
Distal Radius Fractures: Evolution in the Treatment Standard of Care 2009 Antonio Abramo and Philippe Kopylov
Introduction The recent developments of many osteosynthesis and fixation devices are the reason for the rapid changes in the treatment of distal radial fractures (DRFs). From a relative conservative policy of treatment according to the expected good results of these injuries, as reported by Colles and many authors, we are facing now a very aggressive treatment with open reduction and internal fixation. There is very often confusion between the different fractures types, the character of the injury and not least the patient groups, their age and activity level or expected activity level. We have to be careful not to treat all patients in the same way using the latest implant presented on the market. DRFs are unique in that emergence of technology has generated renewed interest in the treatment of these fractures and an increase in production of a variety of specific fixation devices. We cannot deny the economical factor and accept that this abundance of implants is driven by the manufacturers who envisage a huge new market. However we are still lacking evidence-based research which argues definitively for the new approach. The treatment of distal radial fracture remains a matter of debate and we aim in this paper to present where we are today in 2009. We are conscious that the actual solution to the problem is not definitive and the standard of care of today is not definitive either.
Epidemiology DRFs are common fractures accounting for about one-sixth of the fractures treated at emergency rooms [1] or one-tenth of the total number of fractures in adults over 35 years of
Philippe Kopylov (*) Hand and Upper Extremity Unit, Department of Orthopaedics, Lund University Hospital, Lund Sweden e-mail:
[email protected]
age [2]. The incidence of DRF is approximately 19–43 per 10,000 inhabitants annually with females out-numbering males in an overall distribution of 4:1. Several epidemiologic studies have been performed and incidences vary according to Country and Region. In Sweden, the incidence in the city of Malmö has almost doubled from the 1950s to the 1980s. This change over time can not be explained by an increase in diagnosed DRF as the incidence of shaft fractures of the forearm remained the same [3]. The overall ageing of the population and an increased incidence of osteoporosis may offer an explanation. This trend can be reversed with community interventions which promote health-education programmes that address dietary intake, physical activity, smoking habits and environmental risk factors for Osteoporosis and falls. An intervention program as described has reduced the forearm fracture incidence in women over 40 years from 83 per 10,000 to 46 per 10,000 and in men over 40 years from 17 per 10,000 to 7 per 10,000 [4]. With increasing age DRF, as well as fractures in general, tend to be more common. The DRF is most common among older women with an incidence of 60–120 per 10,000 inhabitants annually [3, 5, 6] (Fig. 1). Over the last decades there has been an increase in incidence especially in the age group greater than 60 years. The higher incidence among older women could be explained by the increasing incidence of Osteoporosis. Bone mineral density (BMD) is measured by DEXA scans and expressed as “T-score standard deviation” (SD) compared to a reference group of young sex-matched adults. By definition a T-score of −2.5 SD represents Osteoporosis and a T-score between −2.5 and −1 represents Osteopenia. A T-score > −1 is considered normal (WHO 2000). A screening of patients with wrist fractures between the ages of 50 and 75 years revealed that only 19% had normal BMD in the hip and vertebrae [7]. In another study 85% of the women between the ages 55 and 79 years had a low BMD with a T-score of less than −1 [8]. The occurrence of a DRF can be used as a predictor for a later hip fracture. In a Swedish study an overall relative
G. Bentley (ed.), European Instructional Lectures. European Instructional Course Lectures 9, DOI: 10.1007/978-3-642-00966-2_14, © 2009 EFORT
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A. Abramo and P. Kopylov Incidence per 10,000 person/year – men
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200 1953–1957 1980–1981 2001 150
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Fig. 1 Age-specific incidence of DRF per 10,000 persons/year in the southern Sweden in 10-year age-groups in Malmö 1953–1957 [5], in Malmö 1980–1981 [3], in Hässleholm/Kristianstad 2001 [6]
risk to sustain a hip fracture after a previous DRF was 1.54 for women and 2.27 for men [9] and in an American study the relative risk for a hip fracture was 1.4 for women and 2.7 for men. Although the fracture is most common in older women, also men have DRF with increasing incidence in the ages over 60 years. DEXA-screening reveals that also men have Osteoporosis to a large extent with increasing incidence with increasing age [7, 10]. For DRF in younger patients the proportions of men and women are equal. These fractures are often the result of a high energy trauma and should therefore be treated differently from the osteoporotic fractures [11]. The fractures in younger patients are more often intra-articular and associated with a high incidence of ligamentous injuries [12] with the scapho-lunate ligament being the most commonly injured [13]. As the fracture is so common, it imposes large costs to society. In the UK in 1997, each fracture was estimated at £325 (425€) in direct costs prior to discharge [14]. In France in 2005, the cost for in-patient treatment for a DRF was calculated in the range between 2,363 and 2,574€ [15]. In Rochester, USA the calculated cost for the year following a DRF due to a moderate trauma was $1,628 (1,050€) [16]. In Sweden, the costs in the year following the fracture were 2,147€, including both direct and indirect costs [17] resulting in an annual cost to the country of about 50 million Euro for the adult (7.26 million persons) population (November 2007). However, costs for fractures after the first year, such as costs for surgery of mal-unions, are not
taken to account. With an increasing proportion of elderly people, not only in the Western communities but also in the Developing Countries, the DRF remains an important and increasing economic problem that has to be assessed. However, not only the costs of the fracture are of importance, but also the outcome and disability from the patients’ perspective and therefore reliable objective measurements are of importance.
Results and How to Measure Them The final result of a fracture can be difficult to define and measure. The type of the injury, the expectation of the patient and/or the medical team may have an impact on the complete appreciation of the quality of the result. Various modalities have to be considered, such as the subjective, objective and economical outcome; a broad view which incorporates pain, range of motion and cosmetic appearance was suggested by Colles as “One consolation only remains, that the limb will at some remote period again enjoy perfect freedom in all of its motions and be completely exempt from pain: the deformity, however, will remain undiminished through life”. This description of the outcome following a DRF is still valid today as found and described by Kopylov et al. [18] in a 30-year follow-up of 76 patients with most patients experiencing a good long-term outcome.
Distal Radius Fractures: Evolution in the Treatment Standard of Care 2009
In a shorter perspective it is somewhat different. Most fractures do heal and function is restored almost completely after 1 year but 16% of patients have been shown to suffer from residual symptoms such as nerve symptoms, pain and disability [19]. The outcome thus can be described differently and restitution is more or less complete. To fully evaluate any diagnosis or treatment option, we believe both subjective parameters from the patient’s perspective as well as objective clinical assessment and radiographic examination are important and should be used (Fig. 2). In our practice and for research purposes we use the following tools in assessment of the results: Objective parameters: The range of motion is measured in the three axes of rotation around the wrist joint. Extension and flexion as well as radial and ulnar deviation take place in the radio-carpal joint and are measured and expressed as one parameter as these could be regarded as one motion around the radio-ulnar and dorso-volar axis. Forearm rotation takes place in the distal and proximal radio-ulnar joints around the longitudinal axis. Grip strength, the next objective clinical parameter of interest, is measured with the Jamar dynamometer, expressed in kg and related to the strength of the contra-lateral hand. Grip strength in an older population has been shown to correlate well to the health-related quality of life measured by the SF-36 [20]. Normative values for the grip strength exist for both the younger population under 65 years [21] and for the older population over 60 years [22]. A decrease in grip strength has been shown with increasing age [21]. Radiographs: Radiographs were first used for examination of DRF at the end of the nineteenth century. Since then, radiographic examination has improved technically and forms a basis of classification and outcome. However, they have in some studies been shown to correlate poorly with final clinical outcome [23–26] and the inter-observer
Radiographic evaluation
Fig. 2 Three ways to define outcome in DRF. In the middle we might be able to get a more comprehensive picture of the outcome
Subjective patient reported
Objective clincal assessment
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reliability and intra-observer reproducibility of different radiographic classifications is low [27]. In some studies, however, an association has been shown between the initial radiographs and the final radiographic outcome. Lafontaine et al. [28] created an instability index incorporating an increased number of instability factors on the initial radiograph, i.e., dorsal angulation more than 20°, dorsal comminution, intra-articular radio-carpal fracture and associated ulnar fracture and an age over 60 years were all correlated to worse radiographic outcome. Mackenney et al. [29] demonstrated that ulnar variance, metaphyseal comminution and patient age were predictors for the radiographic outcome, as was the dorsal angulation as a predictor in primary displaced fractures. In a recent study, the radiographic appearance in the initial radiograph, radial shortening >2 mm, dorsal angulation >15°, and radial angulation >10° were each significantly associated with a poorer DASH score [30]. This brings us to the third cornerstone in assessing outcome in DRF, the patient’s perspective. Subjective parameters: Colles considered that apart from range of motion, relief of pain which can be regarded as a subjective parameter, is an important outcome measure. In recent years there has been interest in the development of patient-related outcome scores – generic, region-specific and organ- or joint-specific. In the early years of health measurement, generic tools measuring the general health or health-related quality of life were dominating and one of the first was the sickness-impact profile [31]. Other generic outcome scores which became widely used in the Orthopaedic literature are the Nottingham Health Profile [32] and the SF-36 [33]. The latter is today the most frequently used and measure health in eight domains; physical functioning, role physical, bodily pain, general health, vitality, social functioning, role emotional and mental health. EQ-5D [34] and other generic and short-form tools are designed to measure general health. They calculate a utility score using population-assigned weights and can be expressed as a utility value ranging from −0.59 to 1. These generic instruments all measure general health and are valuable in covering general health issues such as diabetes, heart disease or other combined conditions but are less sensitive to small changes in various disorders such as Orthopaedic conditions [35]. In order to try to catch smaller but clinically important changes in a particular disorder such as distal radius fractures, we have used a region-specific outcome scoring system, the DASH which is one of the most commonly used region-specific scoring systems for the upper extremity. DASH is an abbreviation for Disabilities of the Arm Shoulder and Hand, initially published, and later corrected, as the Disabilities of the Arm, Shoulder and Head [36]. DASH is a self-administered questionnaire developed
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by the AAOS and the Institute for Work & Health in Canada (http://www.dash.iwh.on.ca/). DASH has been translated and validated in many languages for general use in upper extremity disorders but not specifically for DRF. The questionnaire consists of 30 items pertaining to difficulties to perform physical activities (21 questions), symptom severity (5 questions) and the effect of the injury on social activities, self-image, work and sleep (4 questions). Each question has 5 response options. A score is calculated and the disability of the patient is expressed on a scale from 0 to 100, with 100 being the worst result. A minimum of 27 items must be answered for the result to be valid and in order to calculate the DASH score. A change in mean DASH score of 10 points after an intervention such as surgery is considered as a minimally-important change [37]. As the original DASH is sometime perceived as difficult to work with and time-consuming, a shorter form, QuickDASH has been developed. It consists of 11 questions from the original DASH [38] and correlates excellently with the standard DASH [39]. Even more specific are the disease- or sitespecific outcome instruments. For the wrist, a joint-specific outcome instrument for wrist injuries and disorders exists – the patient rated wrist evaluation (PRWE) which has a somewhat higher specificity than the DASH [40].
Treatment Alternatives Non-Invasive Techniques Conservative Treatment Colles described a method for closed reduction and also suggested a tin splint for stabilizing the fracture. Other surgeons such as Dupuytren (1847) described their methods for reducing the fracture and the method of immobilization: “I apply the usual apparatus for fractures of the forearm – that is to say a bandage for the hand, two graduated compresses on the anterior surface of the forearm and two on the posterior and over these two broad splints” (Fernandez and Jupiter 1996). Closed reduction and splinting is still today the most commonly-used method of treatment in the DRF. The type of splinting is of importance as is the position of immobilization. In supination there is less likelihood of re-dislocation [41]. In the Cochrane database report on closed reduction methods, only three randomized or quasi-randomized studies were found including 404 patients [42]. Many methods of closed reduction have been developed during the years but there is no evidence-based on randomized studies to support the choice of a closed
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reduction method. Handoll and Madok found more studies (33), when also systematically evaluating non-randomized reports of methods of closed reduction. Even in this study, there is no robust evidence to support any treatment in favour of another and the authors simply recommend the use of a method with which the practitioner is familiar [43]. However, in many cases conservative treatment is not enough, and especially for primarily or secondarily unstable fractures, surgical options are needed.
External Fixation External fixation of DRF has been in use for more than three decades [44]. In Sweden, it is considered to be the standard method for operative treatment of the fracture- and for this reason it can be chosen as the method of reference with which newer methods can be compared. External fixation uses ligamentotaxis to both reduce as well as to hold the fracture in position during healing [45]. Better results have been reported with external fixation than with a belowelbow cast evaluated at 2.5 years post-fracture, but the external fixation was noted as having more complications [46]. The external fixator can be used also for complex and intra-articular fractures [47]. The recommended time for immobilization varies, ranging from 4 [48] to 6 weeks [49] and even up to at least 8 weeks [50]. In general, long immobilization time increases the risk for reflex sympathetic dystrophy (RSD) [49]. At the Department of Orthopaedics in Lund we aim at a 5-weeks immobilization period. The traction of the wrist ligaments may cause stiffness and therefore dynamic fixation with an articulated device [51, 52] or nonbridging fixation has been proposed with better results reported than for traditional bridging technique [53]. A recent randomized study was unable to find any difference between the bridging and the non-bridging external fixator in regard to clinical results in elderly patients [54].
Pinning Other closed reduction techniques includes fixation of the fracture by pinning. Various techniques have been described such as intra-focal pinning [55], intra-focal intra-medullary pinning [56] or pinning in combination with external fixation [57]. In some studies pinning resulted in a large number of mal-unions [58], whereas other authors report satisfying results with the technique [59]. In the Cochrane report on percutaneuos pinning of DRF it is stated that the high rate of complications casts some doubt on its general use [60]. The volar-locking plate technique is the dominating trend
Distal Radius Fractures: Evolution in the Treatment Standard of Care 2009
for fixation of distal radius fracture in recent years (see below). Compared to this, intra-focal pinning was in one comparative study shown to be inferior [61]. In another study of extra-articular fractures in patients over 60 years pinning was found to provide only a marginal improvement in the radiological parameters compared with immobilisation in a cast alone [62].
129 Fig. 3 The fragment-specific wrist-fixation system
Open Surgery Plates For volarly-dislocated fractures especially of the Barton or Smith type, a volar plate is preferably used [63]. For other types of DRF, other techniques have been considered. Standard AO-plates and screws can be used with good results, however, to get good stability, usually two or more columns of the radial cortex have to be fixed to achieve good results [64, 65]. With the introduction of implants designed specifically for the distal radius, the open technique has become increasingly popular. The Pi plate, named after its shape like the Greek symbol π, is designed to fit on the dorsal side of the radial metaphysis. Good results have been reported [66, 67] but interference with the extensor tendons and high complication rates have been noted [66, 68]. This has made a change in design of the plate necessary.
Fragment-Specific Fixation A fragment-specific system addresses the radial and ulnar columns separately as well as single fracture fragments both dorsally and at the volar rim by a combination of plates, pins and screws. It is primarily based on pinning of the fracture but since additional stability is needed to prevent the pins from bending or the fragments from sliding on the pins, a stabilizing plate to secure the pins has been added. In addition, wire forms to support the subchondral bone or small fragments can be used. The system is low profile and offers good stability [69–71] (Fig. 3). The fracture is approached through a radial incision through the first extensor compartment for placement of the pins and fixation with a radial pin-plate and secondly through a second incision through the fourth compartment for fixation with wire forms, buttress pins and an ulnar pinplate. A volar approach can also be performed to secure the fracture with a volar buttress pin (Fig. 4). The surgical approach is determined by the type of fracture and the type of fixation needed to address the fragments.
Volar-Locking Plates (Fig. 5) The newest concept, the volar-locking plates with anglestable screws or pegs is becoming widely used as it offers stability and a safe approach to the fracture. The fracture is approached from the volar side using the Henry approach just radially to the flexor carpi radials, ulnarly to the radial artery. This offers an easy access to the volar part of the radius. The volar-locking plate has, in biomechanical testing, been shown to be sufficiently stable for fixation of the dorsally-comminuted fracture [72–74] and has been shown to offer equivalent stability when compared to the fragment-specific fixation [75]. The best stability is provided by a combination of a volar-locking plate with the fragment-specific system [76]. Good clinical results have reported in a few series [77, 78]. Complications such as tendon ruptures have been reported [79, 80]. No randomized study has been published yet comparing this concept to conventional DRF fixation.
Bone Grafts and Bone Cements After open reduction a void is commonly seen in the metaphysis and the fixation needs to be combined with a bone graft or bone substitute to fill the gap caused by the crushed osteoporotic bone. Bone grafts: The most common bone graft is an autograft, often from the iliac crest. An autograft has the advantage of
130 Fig. 4 Volar buttress pin for fixation of a small volar fragment. Patient with a severely dislocated fracture of the volar rim
A. Abramo and P. Kopylov
Distal Radius Fractures: Evolution in the Treatment Standard of Care 2009 Fig. 5 Volarlocking plates have become increasingly popular in recent years
being both osteo-conductive (allows bone to grow into it) as well as osteo-inductive (induces formation of new bone). The major disadvantage is the limited amount of bone available and post-operative morbidity from the donor site. Complications can occur such as minor infections or seromas in 10% and even major complications requiring hospitalization in 6% of patients [81]. At discharge nearly all patients, not surprisingly, complain of pain at the harvest site [82]. More troublesome is the persisting pain over 6 months in 26–41% of patients [82–84]. Therefore there is a need for an alternative to autograft. The risk of transmitting viral or, today, unknown diseases has made the use of human and even animal grafts less attractive [85]. The need for alternatives to bone grafts has therefore arisen and various substitutes have been developed. Bone substitutes: Synthetic bone substitutes have the advantage of comparable mechanical properties while diminishing the risk for transmission of diseases. Calcium sulphate (plaster-of-Paris) was commonly used since the late nineteenth century but has the disadvantage of having poor mechanical resistance and fast resorption rate. It resorbs by dissolution during a period of approximately 4–6 weeks [86] and complete resorption has been noted in dogs after 13 weeks [87]. An advantage of a material resorbing by dissolution is its ability to act as a drug carrier. However, in a clinical setting with fracture treatment or
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healing of an osteotomy a short resorption time could be a drawback when in-growth of bone and bony healing might not be completed before the material has lost its strength. Therefore slowly-resorbing and stronger substitutes have been developed. To mimic bone various bone substitutes using calcium phosphate, the major mineral component of bone, have been developed. It is used as hydroxyapatite Ca10(PO4)6 (OH)2, which is poorly soluble and as tricalcium phosphate Ca3(PO4)2, which is relatively soluble, or a combination of both. These substitutes can be obtained in granules or monoblocks but to facilitate minimally-invasive surgery injectable substitutes have been developed. An injectable calcium phosphate consisting of a powder of tricalcium sulphate, calcium carbonate and monocalcium phosphate monohydrate is mixed with a sodium phosphate solution and forms a hydroxyapatite (dahlite) in vivo [88, 89], and also a mixture of hydroxyapatite and calcium sulphate [90] has been developed. All the above mentioned types of bone substitutes are highly biocompatible but have no osteoinductive properties in contrast to bone graft. This can, however, be dealt with when designing composite grafts, combining bone substitute either with substances increasing ingrowth such as osteogenic proteins (BMP) or bone marrow aspirate or substances reducing resorption such as bisphosphonates.
The Future For many it seems that the volar-locking plates have given the final solution to the treatment of DRF. From the existing literature it is clear that volar-locking plates can be used successfully in both intra- and extra-articular DRF. However this treatment is not without complications [80, 91]. The evolution of treating DRF according to the reports at conferences and the published results is to treat all fractures depending on types, injury mechanism or age by the same method: open reposition and internal fixation with, in most cases, volar- locking plates. Using this approach we certainly overtreat an undefined number of patients with an increased morbidity and potential complication rates and without control of the potential benefits in term of increased quality of the results for each patient. We also increase the cost of the treatment of these common fractures. As mentioned by Downing and Karantana [92], the questions remains: do we with these plates offer any definite advantage over traditional methods in term of the long-term outcome, what is the cost of the procedure and can we still make it simpler? This leads to the necessity of more studies.
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Although considered as the highest level of evidence-based medicine, the randomized study has shortcomings. In the clinical surgical setting, the studies are difficult to perform and are rarely supported by the Industry in contrast to drug testing. Therefore, studies of sufficient quality are lacking particularly in important broad diagnoses such as the DRF. The randomized studies most often are limited in size and large differences are necessary to show statistically-significant differences. Small but important differences like reoperation rate or mal-union rate will easily be missed and parameters which are less important but easier to measure exactly are wrongly focussed on. Studies in larger non-randomized cohorts of distal radius fractures therefore are needed to complement the more specified randomized studies. It is important for us clinicians to learn how a consensus treatment protocol or guidelines work in the everyday clinical setting away from the artificial conditions of a randomized study. We no longer look upon the DRF as a homogenous entity but instead as a rather heterogeneous group.
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In our Department in Lund (Sweden) we have an ongoing registration with a prospective follow-up of the DRF with the DASH. This will allow us to pick out smaller groups, analyze the results and perhaps change the treatment for that specific group. Ideally, the Registry works as a hypothesis-generating tool for selection of randomized studies as the next step. To this date more than 2,000 patients have been sent the questionnaire. Collection of data is done to correlate the DASH with ability to cope with pain. A sub-group analysis of all patients operated with one or another technique will be done as well as a specific analysis of the patients with poor DASH results. A tendency of the secondarily-unstable fractures to have a worse subjective outcome also warrants a further analysis. More predictors for future instability and final outcome of DRF are needed and would be an invaluable asset in designing future treatment programmes. Another randomized study has been initiated comparing external fixation with the currently-dominating volar-locking plate.
Distal Radius Fractures: Evolution in the Treatment Standard of Care 2009
A Treatment Protocol A standardized treatment programme, based on the radiographic appearance but taking into account the age and the demands of the patients when selecting the proper treatment, was developed by “The consensus group for distal radius fracture in southern Sweden” in 2004. This group consisting of dedicated Surgeons from the Orthopaedic and Hand Surgery departments in south of Sweden and with special interests in the treatment of DRF analysed the literature at that time and defined according to it the following protocol (Fig. 6). The treatment protocol is meant to be used as a guideline for treatment but a strict compliance to it is not expected. A prospective follow-up of a large number of patients collected from the previously- mentioned DASH – Registry have shown that a treatment protocol is of value and might help us to select the optimal treatment for each patient [93].
Conclusions The use of a standardized treatment protocol may make it possible to select the patients with DRF for appropriate treatment. The chosen treatment should guarantee in each case the expected results with an almost, but not fully, normalized function at 1 year. All fracture types independent of their severity Should reach the same good results. There is no evidence-based reason, with the actual knowledge in 2009, to apply a standardized treatment with volar-locking plates to all patients and/or type of DRF. Further studies on this subject are needed and might change the actual standard of care in the future. We always have to be aware of the morbidity of the applied treatment.
References 1. Fernandez DL, Jupiter J. Epidemiology, mechanism, classification. In: Fractures of the distal radius. A practical approach to management., 2nd ed. New York: Springer, 1996, pp. 24–6. 2. Melton LJ, 3rd, Crowson CS, O’Fallon WM. Fracture incidence in Olmsted County, Minnesota: comparison of urban with rural rates and changes in urban rates over time. Osteoporos Int 1999;9(1):29–37.
133 3. Bengner U, Johnell O. Increasing incidence of forearm fractures. A comparison of epidemiologic patterns 25 years apart. Acta Orthop Scand 1985;56(2):158–60. 4. Grahn Kronhed AC, Blomberg C, Karlsson N, Löfman O, Timpka T, Möller M. Impact of a community-based osteoporosis and fall prevention program on fracture incidence. Osteoporos Int 2005;16(6):700–6. 5. Alffram PA, Bauer GC. Epidemiology of fractures of the forearm. A biomechanical investigation of bone strength. J Bone Joint Surg Am 1962;44-A:105–14. 6. Brogren E, Petranek M, Atroshi I. Incidence and characteristics of distal radius fractures in a southern Swedish region. BMC Musculoskelet Disord 2007;8:48. 7. Åstrand J, Thorngren KG, Tägil M. One fracture is enough! Experience with a prospective and consecutive osteoporosis screening program with 239 fracture patients. Acta Orthop 2006;77(1):3–8. 8. Hegeman JH, Oskam J, van der Palen J, Ten Duis HJ, Vierhout PA. The distal radial fracture in elderly women and the bone mineral density of the lumbar spine and hip. J Hand Surg [Br] 2004;29(5):473–6. 9. Mallmin H, Ljunghall S, Persson I, Naessen T, Krusemo UB, Bergstrom R. Fracture of the distal forearm as a forecaster of subsequent hip fracture: a population-based cohort study with 24 years of follow-up. Calcif Tissue Int 1993;52(4): 269–72. 10. Tuck SP, Raj N, Summers GD. Is distal forearm fracture in men due to osteoporosis? Osteoporos Int 2002;13(8):630–6. 11. Lindau T, Aspenberg P, Arner M, Redlundh-Johnell I, Hagberg L. Fractures of the distal forearm in young adults. An epidemiologic description of 341 patients. Acta Orthop Scand 1999;70(2):124–8. 12. Lindau T, Arner M, Hagberg L. Intraarticular lesions in distal fractures of the radius in young adults. A descriptive arthroscopic study in 50 patients. J Hand Surg [Br] 1997; 22(5):638–43. 13. Forward DP, Lindau TR, Melsom DS. Intercarpal ligament injuries associated with fractures of the distal part of the radius. J Bone Joint Surg Am 2007;89(11):2334–40. 14. Kakarlapudi TK, Santini A, Shahane SA, Douglas D. The cost of treatment of distal radial fractures. Injury 2000;31(4): 229–32. 15. Maravic M, Le Bihan C, Landais P, Fardellone P. Incidence and cost of osteoporotic fractures in France during 2001. A methodological approach by the national hospital database. Osteoporos Int 2005;16(12):1475–80. 16. Melton LJ, 3rd, Gabriel SE, Crowson CS, Tosteson AN, Johnell O, Kanis JA. Cost-equivalence of different osteoporotic fractures. Osteoporos Int 2003;14(5):383–8. 17. Borgström F, Zethraeus N, Johnell O, Lidgren L, Ponzer S, Svensson O, Abdon P, Ornstein E, Lunsjö K, Thorngren KG, Sernbo I, Rehnberg C, Jonsson B. Costs and quality of life associated with osteoporosis-related fractures in Sweden. Osteoporos Int 2006;17(5):637–50. 18. Kopylov P, Johnell O, Redlund-Johnell I, Bengner U. Fractures of the distal end of the radius in young adults: a 30-year follow-up. J Hand Surg [Br] 1993;18(1):45–9.
134 19. MacDermid JC, Roth JH, Richards RS. Pain and disability reported in the year following a distal radius fracture: a cohort study. BMC Musculoskelet Disord 2003;4(1):24. 20. Sayer AA, Syddall HE, Martin HJ, Dennison EM, Roberts HC, Cooper C. Is grip strength associated with health-related quality of life? Findings from the Hertfordshire Cohort Study. Age Ageing 2006;35(4):409–15. 21. Hanten WP, Chen WY, Austin AA, Brooks RE, Carter HC, Law CA, Morgan MK, Sanders DJ, Swan CA, Vanderslice AL. Maximum grip strength in normal subjects from 20 to 64 years of age. J Hand Ther 1999;12(3):193–200. 22. Desrosiers J, Bravo G, Hebert R, Dutil E. Normative data for grip strength of elderly men and women. Am J Occup Ther 1995;49(7):637–44. 23. Altissimi M, Antenucci R, Fiacca C, Mancini GB. Longterm results of conservative treatment of fractures of the distal radius. Clin Orthop Relat Res 1986;206:202–10. 24. Tsukazaki T, Takagi K, Iwasaki K. Poor correlation between functional results and radiographic findings in Colles’ fracture. J Hand Surg [Br] 1993;18(5):588–91. 25. Flinkkilä T, Raatikainen T, Hämäläinen M. AO and Frykman’s classifications of Colles’ fracture. No prognostic value in 652 patients evaluated after 5 years. Acta Orthop Scand 1998;69(1):77–81. 26. Anzarut A, Johnson JA, Rowe BH, Lambert RG, Blitz S, Majumdar SR. Radiologic and patient-reported functional outcomes in an elderly cohort with conservatively treated distal radius fractures. J Hand Surg [Am] 2004; 29(6):1121–7. 27. Andersen DJ, Blair WF, Steyers CM, Jr., Adams BD, elKhouri GY, Brandser EA. Classification of distal radius fractures: an analysis of interobserver reliability and intraobserver reproducibility. J Hand Surg [Am] 1996;21(4):574–82. 28. Lafontaine M, Hardy D, Delince P. Stability assessment of distal radius fractures. Injury 1989;20(4):208–10. 29. Mackenney PJ, McQueen MM, Elton R. Prediction of instability in distal radial fractures. J Bone Joint Surg Am 2006; 88(9):1944–51. 30. Wilcke MK, Abbaszadegan H, Adolphson PY. Patientperceived outcome after displaced distal radius fractures a comparison between radiological parameters, objective physical variables, and the DASH score. J Hand Ther 2007; 20(4):290–9. 31. Gilson BS, Gilson JS, Bergner M, Bobbit RA, Kressel S, Pollard WE, Vesselago M. The sickness impact profile. Development of an outcome measure of health care. Am J Public Health 1975;65(12):1304–10. 32. Hunt SM, McKenna SP, McEwen J, Williams J, Papp E. The Nottingham Health Profile: subjective health status and medical consultations. Soc Sci Med [A] 1981;15(3 Pt 1): 221–9. 33. Ware JE, Jr., Sherbourne CD. The MOS 36-item short-form health survey (SF-36). I. Conceptual framework and item selection. Med Care 1992;30(6):473–83. 34. Burström K, Johannesson M, Diderichsen F. Swedish population health-related quality of life results using the EQ-5D. Qual Life Res 2001;10(7):621–35.
A. Abramo and P. Kopylov 35. Hawker G, Melfi C, Paul J, Green R, Bombardier C. Comparison of a generic (SF-36) and a disease specific (WOMAC) (Western Ontario and McMaster Universities Osteoarthritis Index) instrument in the measurement of outcomes after knee replacement surgery. J Rheumatol 1995; 22(6):1193–6. 36. Hudak PL, Amadio PC, Bombardier C. Development of an upper extremity outcome measure: the DASH (disabilities of the arm, shoulder and hand) [corrected]. The Upper Extremity Collaborative Group (UECG). Am J Ind Med 1996;29(6):602–8. 37. Gummesson C, Atroshi I, Ekdahl C. The disabilities of the arm, shoulder and hand (DASH) outcome questionnaire: longitudinal construct validity and measuring self-rated health change after surgery. BMC Musculoskelet Disord 2003;4(1):11. 38. Beaton DE, Wright JG, Katz JN. Development of the QuickDASH: comparison of three item-reduction approaches. J Bone Joint Surg Am 2005;87(5):1038–46. 39. Gummesson C, Ward MM, Atroshi I. The shortened disabilities of the arm, shoulder and hand questionnaire (QuickDASH): validity and reliability based on responses within the fulllength DASH. BMC Musculoskelet Disord 2006;7:44. 40. MacDermid JC, Tottenham V. Responsiveness of the disability of the arm, shoulder, and hand (DASH) and patientrated wrist/hand evaluation (PRWHE) in evaluating change after hand therapy. J Hand Ther 2004;17(1):18–23. 41. Wahlström O. Treatment of Colles’ fracture. A prospective comparison of three different positions of immobilization. Acta Orthop Scand 1982;53(2):225–8. 42. Handoll HH, Madhok R. Closed reduction methods for treating distal radial fractures in adults. Cochrane Database Syst Rev 2003;1:CD003763. 43. Handoll HH, Madhok R. Conservative interventions for treating distal radial fractures in adults. Cochrane Database Syst Rev 2003;2:CD000314. 44. Jakob RP. Development of the small AO fixator to the current set. Injury 1994;25(Suppl 4):S-D26–7. 45. Cooney WP, 3rd, Linscheid RL, Dobyns JH. External pin fixation for unstable Colles’ fractures. J Bone Joint Surg Am 1979;61(6A):840–5. 46. Solgaard S. External fixation or a cast for Colles’ fracture. Acta Orthop Scand 1989;60(4):387–91. 47. McKenna J, Harte M, Lunn J, O’Bierne J. External fixation of distal radial fractures. Injury 2000;31(8):613–6. 48. Svensson O, Ahrengart L, Ekholm C, Andersson GL, Höglund M, Jonsson U, Juhlin L, Kopylov P, Lagerström C, Lundborg G, Made C, Mallmin H, Raf L, Törnkvist H. [Malpractice in connection with radius fractures must be reduced. Clear guidelines for treatment and follow-up are required]. Läkartidningen 2000;97(15):1800–4, 1807–9. 49. Gausepohl T, Pennig D, Mader K. Principles of external fixation and supplementary techniques in distal radius fractures. Injury 2000;31(Suppl 1):56–70. 50. Prince H, Worlock P. The small AO external fixator in the treatment of unstable distal forearm fractures. J Hand Surg [Br] 1988;13(3):294–7.
Distal Radius Fractures: Evolution in the Treatment Standard of Care 2009 51. Agee JM. External fixation. Technical advances based upon multiplanar ligamentotaxis. Orthop Clin North Am 1993; 24(2):265–74. 52. Pennig DW. Dynamic external fixation of distal radius fractures. Hand Clin 1993;9(4):587–602. 53. McQueen MM. Redisplaced unstable fractures of the distal radius. A randomised, prospective study of bridging versus non-bridging external fixation. J Bone Joint Surg Br 1998; 80(4):665–9. 54. Atroshi I, Brogren E, Larsson GU, Kloow J, Hofer M, Berggren AM. Wrist-bridging versus non-bridging external fixation for displaced distal radius fractures: a randomized assessor-blind clinical trial of 38 patients followed for 1 year. Acta Orthop 2006;77(3):445–53. 55. Kapandji A. [Intra-focal pinning of fractures of the distal end of the radius 10 years later]. Ann Chir Main 1987;6(1):57–63. 56. Walton NP, Brammar TJ, Hutchinson J, Raj D, Coleman NP. Treatment of unstable distal radial fractures by intrafocal, intramedullary K-wires. Injury 2001;32(5):383–9. 57. Trumble TE, Wagner W, Hanel DP, Vedder NB, Gilbert M. Intrafocal (Kapandji) pinning of distal radius fractures with and without external fixation. J Hand Surg [Am] 1998;23–3: 381–94. 58. Oskam J, Kingma J, Bart J, Klasen HJ. K-wire fixation for redislocated Colles’ fractures. Malunion in 8/21 cases. Acta Orthop Scand 1997;68(3):259–61. 59. Harley BJ, Scharfenberger A, Beaupre LA, Jomha N, Weber DW. Augmented external fixation versus percutaneous pinning and casting for unstable fractures of the distal radius–a prospective randomized trial. J Hand Surg [Am] 2004;29(5): 815–24. 60. Handoll HH, Vaghela MV, Madhok R. Percutaneous pinning for treating distal radial fractures in adults. Cochrane Database Syst Rev 2007;3:CD006080. 61. Oshige T, Sakai A, Zenke Y, Moritani S, Nakamura T. A comparative study of clinical and radiological outcomes of dorsally angulated, unstable distal radius fractures in elderly patients: intrafocal pinning versus volar locking plating. J Hand Surg [Am] 2007;32(9):1385–92. 62. Azzopardi T, Ehrendorfer S, Coulton T, Abela M. Unstable extra-articular fractures of the distal radius: a prospective, randomised study of immobilisation in a cast versus supplementary percutaneous pinning. J Bone Joint Surg Br 2005; 87(6):837–40. 63. Keating JF, Court-Brown CM, McQueen MM. Internal fixation of volar-displaced distal radial fractures. J Bone Joint Surg Br 1994;76(3):401–5. 64. Jakob M, Rikli DA, Regazzoni P. Fractures of the distal radius treated by internal fixation and early function. A prospective study of 73 consecutive patients. J Bone Joint Surg Br 2000;82(3):340–4. 65. Rikli DA, Regazzoni P. The double plating technique for distal radius fractures. Tech Hand Up Extrem Surg 2000; 4(2):107–14. 66. Rozental TD, Beredjiklian PK, Bozentka DJ. Functional outcome and complications following two types of dorsal plating for unstable fractures of the distal part of the radius. J Bone Joint Surg Am 2003;85-A-10:1956–60.
135 67. Krukhaug Y, Hove L. Experience with the AO Pi-plate for displaced intra-articular fractures of the distal radius. Scand J Plast Reconstr Surg Hand Surg 2004;38(5):293–6. 68. Grewal R, Perey B, Wilmink M, Stothers K. A randomized prospective study on the treatment of intra-articular distal radius fractures: open reduction and internal fixation with dorsal plating versus mini open reduction, percutaneous fixation, and external fixation. J Hand Surg [Am] 2005; 30(4):764–72. 69. Konrath GA, Bahler S. Open reduction and internal fixation of unstable distal radius fractures: results using the trimed fixation system. J Orthop Trauma 2002;16(8):578–85. 70. Schnall SB, Kim BJ, Abramo A, Kopylov P. Fixation of distal radius fractures using a fragment-specific system. Clin Orthop Relat Res 2006;445:51–7. 71. Benson LS, Minihane KP, Stern LD, Eller E, Seshadri R. The outcome of intra-articular distal radius fractures treated with fragment-specific fixation. J Hand Surg [Am] 2006; 31(8):1333–9. 72. Osada D, Fujita S, Tamai K, Iwamoto A, Tomizawa K, Saotome K. Biomechanics in uniaxial compression of three distal radius volar plates. J Hand Surg [Am] 2004;29(3): 446–51. 73. Koh S, Morris RP, Patterson RM, Kearney JP, Buford WL, Jr., Viegas SF. Volar fixation for dorsally angulated extraarticular fractures of the distal radius: a biomechanical study. J Hand Surg [Am] 2006;31(5):771–9. 74. Willis AA, Kutsumi K, Zobitz ME, Cooney WP, 3rd. Internal fixation of dorsally displaced fractures of the distal part of the radius. A biomechanical analysis of volar plate fracture stability. J Bone Joint Surg Am 2006;88(11):2411–7. 75. Taylor KF, Parks BG, Segalman KA. Biomechanical stability of a fixed-angle volar plate versus fragment-specific fixation system: cyclic testing in a c2-type distal radius cadaver fracture model. J Hand Surg [Am] 2006;31(3):373–81. 76. Grindel SI, Wang M, Gerlach M, McGrady LM, Brown S. Biomechanical comparison of fixed-angle volar plate versus fixed-angle volar plate plus fragment-specific fixation in a cadaveric distal radius fracture model. J Hand Surg [Am] 2007;32(2):194–9. 77. Musgrave DS, Idler RS. Volar fixation of dorsally displaced distal radius fractures using the 2.4-mm locking compression plates. J Hand Surg [Am] 2005;30(4):743–9. 78. Gruber G, Bernhardt GA, Kohler G, Gruber K. Surgical treatment of distal radius fractures with an angle fixed bar palmar plating system: a single center study of 102 patients over a 2-year period. Arch Orthop Trauma Surg 2006; 126(10):680–5. 79. Benson EC, DeCarvalho A, Mikola EA, Veitch JM, Moneim MS. Two potential causes of EPL rupture after distal radius volar plate fixation. Clin Orthop Relat Res 2006;451:218–22. 80. Arora R, Lutz M, Hennerbichler A, Krappinger D, Espen D, Gabl M. Complications following internal fixation of unstable distal radius fracture with a palmar locking-plate. J Orthop Trauma 2007;21(5):316–22. 81. Arrington ED, Smith WJ, Chambers HG, Bucknell AL, Davino NA. Complications of iliac crest bone graft harvesting. Clin Orthop Relat Res 1996;329:300–9.
136 82. Sasso RC, LeHuec JC, Shaffrey C. Iliac crest bone graft donor site pain after anterior lumbar interbody fusion: a prospective patient satisfaction outcome assessment. J Spinal Disord Tech 2005;18(Suppl):S77–81. 83. Heary RF, Schlenk RP, Sacchieri TA, Barone D, Brotea C. Persistent iliac crest donor site pain: independent outcome assessment. Neurosurgery 2002;50(3):510–6; discussion 516–7. 84. Silber JS, Anderson DG, Daffner SD, Brislin BT, Leland JM, Hilibrand AS, Vaccaro AR, Albert TJ. Donor site morbidity after anterior iliac crest bone harvest for single-level anterior cervical discectomy and fusion. Spine 2003;289(2):134–9. 85. Damien CJ, Parsons JR. Bone graft and bone graft substitutes: a review of current technology and applications. J Appl Biomater 1991;2(3):187–208. 86. Stubbs D, Deakin M, Chapman-Sheath P, Bruce W, Debes J, Gillies RM, Walsh WR. In vivo evaluation of resorbable bone graft substitutes in a rabbit tibial defect model. Biomaterials 2004;25(20):5037–44. 87. Turner TM, Urban RM, Gitelis S, Haggard WO, Richelsoph K. Resorption evaluation of a large bolus of calcium sulfate in a canine medullary defect. Orthopedics 2003;26(5 Suppl):s577–9.
A. Abramo and P. Kopylov 88. Kopylov P, Jonsson K, Thorngren KG, Aspenberg P. Injectable calcium phosphate in the treatment of distal radial fractures. J Hand Surg [Br] 1996;21(6):768–71. 89. Abramo A, Tagil M, Geijer M, Kopylov P. Osteotomy of dorsally displaced malunited fractures of the distal radius: no loss of radiographic correction during healing with a minimally invasive fixation technique and an injectable bone substitute. Acta Orthop 2008;79(2):262–8. 90. Nilsson M, Wang JS, Wielanek L, Tanner KE, Lidgren L. Biodegradation and biocompatability of a calcium sulphatehydroxyapatite bone substitute. J Bone Joint Surg Br 2004; 86(1):120–5. 91. Rampoldi M, Marsico S. Complications of volar plating of distal radius fractures. Acta Orthop Belg 2007;73(6):714–9. 92. Downing ND, Karantana A. A revolution in the management of fractures of the distal radius? J Bone Joint Surg Br 2008;90(10):1271–5. 93. Abramo A, Kopylov P, Tagil M. Evaluation of a treatment protocol in distal radius fractures: a prospective study in 581 patients using DASH as outcome. Acta Orthop 2008;79(3): 376–85.
Dupuytren’s Contracture Hanno Millesi
Introduction Dupuytren’s contracture (DC) is a unique disease. It does not cause intolerable pain, it does not endanger life. It is located superficially and its course can be followed and documented easily. It is understandable that this disease attracts researchers and as far as I know about 30 publications appear every year about DC. Still we do not have a universal idea about the aetiology or the pathogenesis. The therapy is mainly surgical but the optimal approach is still controversial. The recurrence rate of the most often-applied techniques is still unacceptably high. DC was mentioned as early as 1614 by the Professor of Anatomy in Basel, Felix Platter [1]. Until the early nineteen century it was regarded as a contracture of the flexor tendon. Baron Guillaume Dupuytren, surgeon of the Hotel Dieu in Paris, described cases suffering from finger contractures in his lectures, which were published in 1831 [2]. He recognized the palmar aponeurosis as the location of the disease. This knowledge made a rational surgical therapy with preservation of the flexor tendons possible. It became known worldwide and consequently his name was attached to the disease, in spite of the fact, that others had already published the same idea before Dupuytren. In 1834 Goyrand [3] came to the conclusion that the disease starts in the skin. This idea was re-vitalized by Hueston [4], who attributed to the skin a certain influence on the occurrence of recurrences and recommended skin excision to avoid them. If the palmar aponeurosis as described in the anatomical textbooks is recognized as the site of the disease other problems arise. From which structures do the manifestations outside of the palmar aponeurosis originate? Is the palmar aponeurosis a part of a larger system at the palmar
Hanno Millesi Wiener Privatklinik, Pelikangasse 15 1090 Wien, Austria, e-mail:
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side of the hand and fingers with the capacity to develop the disease? Or are the manifestations of the disease outside of the palmar aponeurosis expressions of a tumour-like growth? This aspect would support the classification of Dupuytren’s disease as a fibromatosis. Knowledge of all details of descriptive anatomy, functional anatomy, history of development, natural course of the disease is necessary to get a vague idea of the problem. In my lecture I intend to discuss the following subjects: 1. Structures, properties and function of the palmar aponeurosis and related tissues. 2. The clinical features and natural course of DC. 3. Facts to understand the pathogenesis of the disease. 4. Considerations concerning the treatment.
Structures, Properties and Function of the Palmar Aponeurosis and Related Tissues The palmar side of the hand is especially designed for gripping. The skin (glabrous skin) has a thick Keratin layer. The cutis is thicker than in other regions. There are many sweat glands and sensory end-organs. The skin is fixed to the underlying fascia by a network of dense connective-tissue fibres with fat lobules inbetween forming a three-dimensional body. The system is designed to accept and distribute pressure. Such a system was studied many years ago by Nauck [5] of the skin and subcutaneous tissue over the tuber of the calcaneum bone. The fat is not compressible like a liquid. The pressure from outside is transmitted not directly to the bone but to the thin connective tissue layer, which surrounds each fat lobule and distribute it to a large area. The actual pressure per unit area is in this way minimized. In addition the skin is fixed and does not allow lateral deviation. In similar way the palmar skin acts as a pressureaccepting device and prevents too much deviation. Both conditions contribute to a firm grip. The skin of the palmar
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side of the hand has to be able to adapt to flexion of the finger joints, opposition of the thumb and changes of the arch of the metacarpus. Adaptation to flexion and extension of the fingers is provided by the flexion creases at the distal interphalangeal joint, the proximal interphalangeal and the flexion crease in the middle of the proximal phalanx. At the level of these flexion creases there are in the cutis and the subcutis only transverse fibres which allow a certain elongation in the longitudinal direction. Transmission of tension across the creases is prevented. The system breaks down if longitudinal collagen fibres cross the creases e.g., after a longitudinal incision a flexion contracture will develop. The skin between the flexion creases becomes relaxed with flexion but it remains fixed. No fold can be elevated. At the mid-lateral line between the palmar and the dorsal space of the phalanges the skin is fixed to the bone. These ligaments are rarely involved. At the lateral surface of the phalanges located dorsally and laterally to the neuro-vascular bundle of the digit a regular fibre bundle is met which extends from the interdigital fold to the palmar side of the distal phalanx. The greatest amount of relaxation is required in the palm. Without fixation a large skin fold would be elevated with flexion and the skin would have a large amount of mobility in the longitudinal and lateral direction. A firm grip would be impossible. The skin of the palm has a similar fat layer as the skin of the fingers but less stiff. The skin is fixed by ascending connective tissue fibre bundles which are a part of the threedimensional arrangement of the palmar aponeurosis “sensu strictori” ascending to the skin and inserting into the dermis (cutis) on both sides of the flexion creases. These fibres keep the skin in place and, as far as they originate from the palmaris longus muscle are pulling the skin into proximal direction if the fingers are flexed. The palmaris longus muscle contracts simultaneously with the finger flexors. The skin distal to the flexion creases in the palm covers another important structure. It consists of a network of tiny fibre bundles with a lot of fat lobules in between. The fibres are arranged mainly in a transverse direction (superficial transverse fibres). They also support the interdigital folds (Natatory ligament of Gerdy [6]). Four elevations are formed, the monticule at the base of each finger forming soft cushion to contact an object to be kept in the palm. The skin can be elevated with flexion in a very limited way. This network is in continuation with the network underneath the skin over the distal half of the proximal phalanx, but there is no longitudinal passing across. At the proximal side the network is in contact with the main bulk of longitudinal fibres of the
H. Millesi
palmar aponeurosis “sensu strictori” and the whole network is pulled in the proximal direction if the fingers are flexed. A third group of longitudinal fibres of the palmar aponeurosis descend between the flexor tendon sheaths into the depth of the palm (fibreuses intertendineuses de Legueu and Juvara 1892) [7] which forms a kind of channel for the flexor tendons, the neuro-vascular bundles and the lumbrical muscles. They fix the palmar aponeurosis “sensu strictori” to the deep fascia of the palm. Apart from the distinct longitudinal fibres bundles of secondary or tertiary order branch off forming a network. From the superficial and the deep transverse fibres further fibre bundles bridge the space between index finger and thumb in two distinct layers. Between the radial border of the palmar aponeurosis and the fascia of the thenar eminence large fat lobules are located corresponding roughly with the territory of the palmar branch of the median nerve in the skin. The skin of the thenar eminence is fixed to the fascia in the same way as the skin of the phalanges. Towards the hypothenar eminence there is a fixation of the palmar aponeurosis to the fifth metacarpal bone. There is also a collection of fat lobules between the hypothenar eminence and the palmar aponeurosis. Between the fascia of the hypothenar eminence and the skin a fibro-fatty layer fixes the skin. Corresponding to the proximal third one finds a thicker layer of a connective tissue network with transverse orientation containing the muscle bundles of the palmaris brevis muscle irradiating into the lateral border of the palmar aponeurosis. The dorso-lateral bundle on the ulnar side of the little finger originates from the tissue on top of the distal end of the hypothenar fascia and may have connections to the fascia over the tendons over the hypothenar muscles. The palmar aponeurosis “sensu strictori” originate proximally from the flexor retinaculum and the fascial tissue superficial to it being a continuation of the forearm fascia. In a somewhat more superficial layer the tendon of the palmaris longus tendon divides fan-like and merges into the palmar aponeurosis forming mainly the longitudinal ascending fibres to the skin in the area of the transverse palmar creases. The deep descending fibres proceed between the tendon sheaths, the neuro-vascular bundles and the lumbrical muscles to the deep fascia of the palm. The fibres of the middle layer enter the superficial transverse fibre system. The macroscopic appearance of the palmar aponeurosis has different aspects. It may look like a true aponeurosis covering the palm from the radial side of the second metacarpal bone to the radial side of the fifth metacarpal bone. This aspect is most frequently met with in children.
Dupuytren’s Contracture
In adults the aponeurosis-like aspect is limited to the area above the index and part of the middle finger ray. The more ulnar part shows a varying arrangement of longitudinal bundles. Kalberg [8] in 1935 studied the individual arrangement of the fibre bundles in a vast number of cadaver dissections and differentiated six distinct types. All neonatal cadavers showed what he called type II. In adults all six types were represented. This is an extremely important observation, which has been forgotten. It proves that the anatomical arrangement of the palmar aponeurosis is not fixed once and for ever. It is exposed to changes according to functional requirements during life. There are two ways to perform an anatomical dissection of the palm of the hand: 1. One can excise the skin, remove carefully the subcutaneous tissue and isolate the thicker collagen fibre bundle. This way provides a survey of the connective tissue framework. One has to have in mind that all the bundles dissected in this way are not necessarily permanent structures but show a large amount of variation from individual to individual but also within one individual during life. 2. The more functional approach is to remove the skin like a full-hickness skin graft and leave the subcutaneous tissue in contact with the fasciae. The next step is to pick out all the fat lobules leaving the connective tissue framework intact. By such a dissection only, one will understand the functional importance of the threedimensional connective tissue body and one will realize that the palmar aponeurosis “sensu strictori” is only one part of the system.
How Does the Palmar Aponeurosis Function in Non-Human Primates? Doing experiments with baboons in South Africa I had the opportunity to study the palmar aponeurosis in 18 individuals. The basic design of the palm corresponds to the human hand. The skin has the characteristics of glabrous skin, is fixed and can be elevated in a limited way only. The palmar aponeurosis consists of a superficial layer which originates from the tendon of the palmaris longus muscle with connective tissue fibres ascending and fixed to the skin at the level of the flexion creases in the palm. The palmaris longus muscle is very strong and contributes significantly to the flexion of the metacarpo-phalangeal joints. This function helps to increase the longitudinal arch of
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metacarpus and basal phalanges without or before flexing the interphalangeal joints. Like the monticuli in humans the hand of the baboon has cushions of fat tissue at the distal half of the palm above the proximal half of the fingers which provides the first contact when grasping a bar. Between the centre of the palm and the thenar eminence a large fat cushion is located and in a similar way two fat cushions fill the space between the centre of the palm and the hypothenar eminence. In the centre of the palm the palmar aponeurosis is covered by a rather thin fibro-fatty layer only. There is no fat cushion at this level. The skin is here better fixed to the palmar aponeurosis and less mobile. Extensions of the palmar aponeurosis fix the fat cushions and are able to pull the fat cushions towards the centre of the palm. Baboons use their hand to grasp objects, mainly pieces of food and bring them to the mouth. The second important function is grasping bars when jumping in a cage or branches when doing so on a tree. The gripping act is performed in two ways: 1. If the baboon intends to get hold of a bar, which runs in transverse direction to its movement, it grasps the bar by flexing the fingers on the bar from above and using the thumb in opposition to get hold from below like a human individual. The thumb is smaller than in humans but is anatomically structured like a human thumb. The fat cushions nestle against the bar to get a firm contact but also allow loose grip if movement is required. The longitudinal arch of the hand has to be adjusted to the different stages of the function. 2. If the baboon intends to get hold of a bar, which runs parallel to the direction of its movement, it puts the middle finger ray on the bar. The palmar aponeurosis gets in close contact with the bar. Index finger and thumb are moved around one side and ring and little finger around the other side of the bar to keep the contact. In this situation the transverse arch of the carpus is increased. This function is provided by thenar and hypothenar muscles. It is supported by the “Musculi contrahentes” in the depth of the palm, which pull the metacarpal bones 2, 4 and 5 towards a rhaphe along the metacarpal bone 3 like the adductor pollicis in humans. The “Musculi contrahens” except the adductor pollicis muscle have disappeared in the human hand. The palmaris longus muscle is absent in about 12% of human hands. All this are expressions of new functional requirements to the human hand. Especially catching bars and swinging around them does not belong to frequent functional tasks except doing exercises on the high bar. Over the years I have done
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several hundred complete fasciectomies. During follow-up studies all patients were asked which function they could not perform after surgery. The only patients who had problems with certain functions were patient doing exercises with the high bar. After surgery they have to use a leather sheath in the palm to provide necessary quick change between firm grip and loose gliding.
Considerations Concerning the Plantar Aponeurosis The skin of the plantar side of the foot and toes is glabrous skin. It is fixed to the plantar aponeurosis and to the plantar fascia of the toes by a fibro-fatty layer to absorb pressure. The plantar aponeurosis consists of longitudinal collagen fibre bundles which originate from the tuberosity of the calcaneum and reach the area plantar to the heads of the metatarsal bones were they are interwoven with superficial transverse fibres. Here the fibre system comprises fibrofatty cushions above the big toes and the toes which absorb the pressure when standing along with the fibro-fatty tissue on top of the tuberosity of the calcaneum and a narrow zone along the lateral border of the sole. The plantar aponeurosis is the hypotenuse of a triangle along with the tarsus and metatarsus and the calcaneus. If the patient sets the foot on the floor with full weight, the angle between tarsus and metatarsus on one side and calcaneus widens and the plantar aponeurosis is under tension. Since it has certain ability for elongation, it elongates and stores energy. This energy is freed when the patient lifts the foot again and lifting is enhanced. A similar function occurs with the palmar aponeurosis if the patient puts his weight on palm and fingers. The medial border of the plantar aponeurosis is the area most exposed to tension. There is no connection between longitudinal fibres of the plantar aponeurosis and the fibrofatty tissue at the plantar side of the toes which at the proximal and middle phalanx is poorly-developed.
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In the position of rest the collagen fibres are relaxed and adept a wavy, undulated course. This can be made visible by a cross-striated appearance seen when light is coming in a low angle in a longitudinal direction. The height of the wave is in light, the depth in shadow. With pull in a longitudinal direction the fibre bundle is extended and the “cross striation disappears. Very little stress is necessary to achieve this. This is the toe part of a stress–strain curve. If the fibre bundles are fully extended, they resist further stress and the stress–strain curve rises steeply. If one compares the stress–strain curve of a tendon and the one of palmar aponeurosis it becomes evident that the stress-strain curve of a tendon is much stiffer than the one of palmar aponeurosis. In other words the palmar aponeurosis is more elastic than tendon (Fig. 1). If a fibre bundle is elongated to a certain value and kept at this level, the stress to maintain the strain decreases (mechanical relaxation). If a fibre bundle is elongated to a certain value and the stress is kept constant the fibre bundle continues to elongate (mechanical retardation). If the stress is brought to zero, the strain is reduced and the fibre bundle returns nearly to its original length. If the fibre bundle consisted of an ideal elastic material the return to the original length would happen fully and immediately (instantaneous elasticity) along the same curve as the extension. Biologic tissue is not an ideal elastic material. Therefore the return of the stress-strain curve somewhat below the LOAD (Newton)
NORMAL PALMAR APONEUROSIS
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TENDON
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The Mechanical Properties of the Palmar Aponeurosis Like a tendon the palmar aponeurosis consists of collagen fibres surrounded and separated by loose connective tissue. The fibres consist of collagen type I the surrounding peritenon tissue of collagen type III. The fibres have an optimal size. Several fibres are collected to a fibre bundle surrounded by epitenonal loose connective tissue. The collagen fibres consist of collagen micro-fibrils lying in ground substance. Between the collagen fibres there are tiny elastic fibres.
STRAIN (%) E(u) 5
Fig. 1
E(o)
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Dupuytren’s Contracture
original curve and the starting point is not reached (viscous elasticity). There remains a residual elongation. This is for normal palmar aponeurosis 0.1 or 0.2%. The difference between the two curves represents the histeresis and is, with normal palmar aponeurosis, small. If the stress–strain experiment is immediately repeated the new stress–strain curve differs significantly from the original one. If there is a certain time interval between original and second stress-strain experiment the stress-strain curve becomes like the original one. The time necessary to achieve this is called the mechanical recovery time. For palmar aponeurosis the time is 10 min.
The Clinical and Natural Course of Dupuytren’s Disease Onset of the Disease Dupuytren’s disease starts with a funnel or dimple just proximal or distal to the distal palmar flexion crease exactly where the ascending longitudinal fibre bundles of the palmar aponeurosis merge into the skin. No “nodule” has formed so far. A thickening of the involved collagen fibre bundle develops and a band is formed. This happens most frequently along the ring finger ray but little and middle finger may also show the first appearance of the disease. With time middle, ring and little finger can be involved. The bands lose the ability for elongation and shrink. This leads to moderate loss of extension of the metacarpo-phalangeal joints of the involved fingers (lateral extension of the early disease). Other longitudinal fibre bundles of the palmar aponeurosis being in contact with the network of the superficial transverse fibres in the distal segment of the palm undergo the same changes. Instead of causing a dimple of the skin as the ascending fibre bundles do, they cause a thickening of segments of the network. The tension distribution of this system gets changed and tension is transmitted to the connective tissue system under the skin of the first phalanx. The important point is that a band can develop from longitudinal fibre bundles of the palmar aponeurosis to the fibre systems of the first and second phalanx in spite of the fact the such structures normally do not exist. On the contrary it is a general rule of functional anatomy that a tensiondistributing system on the flexion side proximal to a joint may not be connected to a similar system distal to the joint. If such a connection is established e.g., by a longitudinal scar after an incision crossing the flexion crease of a joint a flexion contracture will develop.
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If such a longitudinal extension has developed to the connective tissue system of the second phalanx and this band starts to shrink the contracture will mainly involve the proximal interphalangeal joint. Since the connective tissue body of the second phalanx has connections to the extensor apparatus along the retinacular ligament further progression will be transmitted to the extensor aponeurosis and cause an extension contracture of the distal interphalangeal joint. Sometimes the first manifestation of the disease may be just proximal to the flexion crease of the proximal interphalangeal joint and cause a small dimple there. In rare cases the dorso-lateral fibre bundle may be involved as the first sign of Dupuytren’s disease producing a hard longitudinal band at the lateral surface of the finger. External pressure causes pain and paresthesias due to transmission of the pressure to the digital nerve. In some of these cases the diagnosis neuroma-incontinuity of the digital nerve was established and the finger nerve resected. Contracture of the dorso-lateral band causes flexion contracture of the distal interphalangeal joint [9]. At the little finger’s ulnar side a band may develop, which originates from the hypothenar eminence. Bands irradiates into the skin especially at the proximal segment of the hypothenar eminence. At the first interdigital fold two different bands occur corresponding to the two layers of the connective tissue system, causing adduction contracture of the thumb. Contracture bands at the thumb originate from the palm causing contracture in opposition position or from the thenar eminence. Collagenisation and shrinkage of the network of the superficial transverse fibres causes not only the creation of a connection between palm and first phalanx but also an adduction contracture of the fingers. In contrast the deep transverse fibre bundles are usually not involved. If one accepts the concept of the connective tissue body of the palmar side of the hand with its distinct fibre bundle and the net-like connections with tiny, non-collagenized fibre bundles which, however, have the potential to become collagenized, if the tension pattern changes and that the formation of bands in the sense of a fibrosis is limited to the structures of the pre-existing systems, there is no real neoformation of tissue. The irregularity which extends between the collagenization of parts of the network and the irregular connections e.g., between the palmar and the dorso-lateral band explain easily the irregular involvement of the neurovascular bundles in the contracture bands which causes many problems for the Surgeons.
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Plantar Duypuytren’s Disease Twelve percent of patients with Dupuytren’s disease of the hands suffer from a similar disease at the foot. The disease involves at first the free border of the plantar aponeurosis which extends between the calcaneum and the head of the first metatarsal bone. Since the thickening is located in the cavity of the tarsus the patient is aware of its existence, if it touches the floor when walking. There is no comparable network of superficial transverse fibre bundles distal to the pressure-accepting cushions on the plantar side of the metacarpo-phalangeal joints and consequently the development of connections to the fibre systems of the toes is not formed and flexion contractures of the toes are extremely rare. There is no anatomical substrate for a contracture of the metatarso-phalangeal joints due to the different development of the pressure-accepting cushions on the plantar side of the metacarpo-phalangeal joints in relation to the monticule of the palm and the lack of ascendant fibre bundles of the plantar aponeurosis to the skin.
The Patient The typical patient is a man in its fifties who becomes aware of a thickening in the palm of one of his hands. He may have problems with shaking hands and fully extending his digits. He does not really know when the disease started because it does not cause pain or other problems and the early changes are usually neglected. This means that the disease exists already for years before the patient consults a doctor. Men are involved five times more frequently than woman. If a study of a population is performed registering not only patients who asked for treatment but also minor manifestations which are not recognized by the patient the relationship is 2.5–1. This means there is a sex disposition but it is less important as far as overall occurrence and more important as far as progression is concerned. There is an age disposition. The frequency increases with age and in the seventies every fourth man of a northern European population has manifestations of Dupuytren’s disease. The disease occurs much less frequently in Mediterranean and near-East countries and it is rare in Negroes, Chinese and Japanese. The theory of a racial disposition is however, weakened by studies in homes for old age people in Japan revealing a frequency of about 14%. Studies with patients suffering from Diabetes Mellitus, liver diseases, rheumatoid diseases or epilepsy revealed a
H. Millesi
higher frequency of Dupuytren’ disease in these groups. Studies with patients being operated on because of Dupuytren’ disease do not show significant connections. Consumption of alcohol may be contributing factor as far as the global distribution of the disease is concerned. The most significant factor is certainly heredity. On-third of the patients operated upon because of Dupuytren’s disease remember one case with Dupuytren’s in their ancestry. This is a high percentage if one takes into account that not every individual remembers the hand of the grandfather and father or grandfather may have died before developing the disease. An enormous amount of work has been invested to prove a mechanical origin of Dupuytren’s disease and to declare it a professional disease for certain workers with the right of compensation. All these attempts failed.
The Natural Course of Dupuytren’s Disease The natural course of the disease for a particular individual is unpredictable. There is no continuous progression which might be interrupted as the result of a certain therapy. A minor nodule or band may remain unchanged for years and is therefore no indication for treatment if it does not cause pain because of compression of a digital nerve. Even regression has been observed. After a quiet period for years for an unknown reason progression may occur. Periods of progression and standstill alternate. In advanced stages the progression is more rapid. We have followed cases in stage 0(A) for years without treatment and registered the time and percentage of progression of the disease. After 3–5 years only 37% of 70 cases showed progression and after 6–12 years the percentage was 46.5 of 54 cases (Figs. 2, 3).
[%] 50
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54 Hände 46,5
40 37 30 20 19 Progression ohne Therapie 37,5% von 150 Händen im Stadium 0
10 0
Fig. 2
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Dupuytren’s Contracture [%] 50
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Neuerkrankungen während der Beobachtungszeit 36,3 % von 113 Händen
the world. This theory does not explain the occurrence of the disease in Japanese collectives [13], without contact of Japan with Celts or Vikings. The fact that Dupuytren’s disease goes along with an increase of the formation of collagen type III was the reason for Bailey [14] to regard the disease as a hereditary disturbance of the collagen metabolism. The increase of collagen type III is a typical event in wound healing and scar formation and it may be rather a consequence than a cause of the disease.
0 ≥6 1 3 5 [Jahre] 9 Hände (6 % von 150) zeigen spontane Regression
Fig. 3
We have also studied hands without disease in Patients having been operated upon because of Dupuytren’s disease of the contra-lateral hand. After 5 years the originally free hand became involved in 39% and after 6–12 years in 49%. These figures indicate that the disease is a bilateral one. It is only a question of time until the second hand develops the disease. If the flexion contracture proceeds as well as the contracture of the superficial transverse fibres the skin of the palmar side of the digits and of the interdigital folds cannot be cared for in a proper way and suffers degenerative changes. Being for a long time in flexion the flexor tendons and the tendon sheaths shrink and limit the range of motion not because of involvement in the disease but just because of inactivity. The same is true for the collateral ligaments of the metacarpo-phalageal joints and the joint capsules in general leading to increasing stiffness of the joints.
Circulatory Deficiency Vascular occlusions were regarded as a causative factor [15]. A local hypoxia of the tissue may cause the proliferation of peri-vascular satellite cells and cause the production of free radicals [16].
Irritation of the Ulnar Nerve The more frequent involvement of the ring and little finger tempted authors to regard an irritation of the ulnar nerve as a causative factor [17]. As a matter of fact electrophysiological changes of intrinsic, ulnar nerve-innervated muscles were described [18, 19]. Personal studies confirmed these findings. However, the changes disappeared with increasing contracture. The explanation is that the contracture bands to the little and ring finger irritate the deep branch of the ulnar nerve in the palm with each finger extension as long as the there is a low grade contracture only. With increasing flexion contracture the bands are elevated and do not influence the nerve.
Inflammation
To what Chapter of Pathology does Dupuytren’s Disease belong? Hereditary Disease It was already mentioned that a hereditary component is the only proven factor of possible causes. Families with a high number of patients with Dupuytren’s disease have been published [10], identical occurrence in twins [11] also supports this aetiology. The racial disposition has been already mentioned. Murrell and Hueston [12] held the view, that Dupuytren’s disease is a hereditary disease of the Celts or the Vikings and was distributed by them over
Meyerding et al. [20] regarded Dupuytren’s disease as an inflammatory disease based on histological evidence. Wick et al. [21] described inflammatory-immunologic processes during the monocyte infiltration at the “early” stages of Dupuytren’s disease. This is an inflammatory, immunological and predominantly T-cell dependent immune response. The problem with this and similar papers is the fact that early stages with cell proliferation are studied which in reality are not early stages but a response to proceeding processes as I shall outline later and not the pathogenesis of the initial phase of the disease.
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Specific Infection In the late nineteenth century a specific bacterium was identified in Dupuytren’s tissue, in the 1950’s a virus was cultured and now it is related to AIDS.
Trauma The traumatic aetiology is the oldest theory. It was already mentioned by Baron von Dupuytren. It was put forward by Tord Skoog [22], who believed that small, repetitive traumata cause the disease. He described small ruptures of fibre bundles and established the term “micro-trauma”. The fascinating aspect is that location of changes in Dupuytren’s disease follows the tension pattern of the aponeurosis and consequently tension certainly plays a role in the pathogenesis. The question is how micro a trauma must be to finish being a trauma but being rather an effect of normal tension in pathological tissue as [23]. Flint [24, 25] and McGrouther [26] considered micro-ruptures and micro-dehiscence in the centre of the fibre bundles as a cause. The authors admit that such ruptures are preceded by some type of fibrosis which reduces the resistance against normal tension.
Tumour At the peak of the cellular proliferation the impression of a malignant sarcoma may be induced. Consequently, Herzog [27] classified the disease as a malignant tumour and amputations of the hand have been performed. Today Dupuytren’s disease is classified as a fibromatosis, a term which is rather descriptive than informative. Fibromatoses are a group of locally aggressive but nonmetastasizing conditions. Highly differentiated fibrous proliferations characterized by infiltrative growth and a tendency to local recurrence after surgery occur [28]. Based on 140 cases Allan [29] differentiated juvenile and adult fibromatosis, Dupuytren’s disease consequently belonging to the adult type. Enzinger and Weiss [30] regard it as a superficial fibromatosis. Azzarone et al. [31] studied the growth characteristics of “normal fibroblasts”, fibroblasts cultured from Dupuytren’s tissue and from Sarcomas. Eleven characteristics were studied. In five the fibroblasts from Dupuytren’s tissue corresponded to “normal fibroblasts” and in six to sarcoma fibroblasts indicating that the cells derive from a rapid cell proliferation which as we shall see is a short phase of the morphologic development of the disease.
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Fletcher et al. [32] differentiated superficial fibromatoses (Palmar fibromatosis, plantar fibromatosis and Peyronie’s disease from deep fibromatosis (desmoid tumours). Desmoid tumours occur in the abdominal wall in young women, within the abdominal cavity and in limbs or limb girdles. They are usually simple sporadic lesions, only occasionally multiple tumours occur in the same anatomical region. Some showed a familial context together with colonic polyps [33]. Juvenile fibromatosis occur in children. De Wever et al. [28] described clone chromosome aberrations in 51% out of 41 cases of deep extra-abdominal desmoid tumours. Among 28 cases of superficial fibromatosis only three showed aberrations: trisomy (and additional loss of X-chromosome in one case of plantar fibromatosis. This means that the “superficial” fibromatoses form a distinct group, different from the others.
Micro-Morphology and Course of the Pathology Review of the Literature The surgeon sees early cases with a nodule in the palm and an initial contracture of the metacarpo-phalangeal joint. If the nodule and the band proximal to it is excised the nodule shows a cellular proliferation with immature mononuclear cells which may resemble a tumour. Proximally there is a fibrotic band as a part of the palmar aponeurosis. It has to be remembered that at this “early” stage the disease is present already for years. If more advanced cases were operated upon in the histologic specimen still areas of cellular proliferation could be seen but also areas with less numerous and more mature cells. Between them are collagen deposits now containing much more type III collagen than normal palmar aponeurosis. There were other areas with masses of collagen arranged like in a hypertrophic scar containing very few mature cells. It seemed logical to establish a sequence of patterns: ● Initial cellular proliferation ● Peak of cellular proliferation ● Maturing of the cells and collagen production ● Scar-like final stage Luck [34] interpreted the nodule as the site of the disease and site of the contracting process. The band proximal to it was regarded as a reaction to the increasing tension. The nodule with the cell proliferation is a tumour-like condition, which can occur everywhere. The excision of the nodule (noduleectomy) and the band, if it causes contracture, is the
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treatment. It does not make sense to excise neighbouring normal-looking tissue of the palmar aponeurosis. Millesi in 1965 [23] realized the surgical specimens of excised contracture bands and nodules are not typical and performed a cadaver study in the anatomical institute of Vienna investing all palmar aponeurosis during the courses of one semester and expecting due to the average age of the cadavers to find a certain percentage of clear Dupuytren’s disease but also all early stages of the initial disease. The result was the following: The disease starts with a thickening of normal-looking fibre bundles: Fibre thickening. The adjacent thickening fibre bundles fuse. The peritenon tissue disappears: Fibre fusion. At this stage there is already some shrinking e.g., to form the dimple of the skin in cases of the ascending longitudinal fibre bundles. The basic structure of the fibre bundles can still be identified. Within such thickened fibre bundles the cellular proliferation starts around the vessels. Fig. 4
Initial Cellular Proliferation ● The proliferating cells cover the whole cross-section: Peak of cellular proliferation ● The cells mature and produce collagen: Cell maturation and collagen production ● The cells are reduced to a minimum in collagen masses: Scar-like final stage How can we differentiate between the stage of fibre fusion and the final scar-like stage? In the stage of fibre fusion the original pattern can still be detected. The pattern of the final scar-like stage is completely irregular. If the surgeon performs a more extended fasciectomy one can frequently see all these stages in the same patient. Figure 4 shows photographs of a 56-years-old patient suffering for 5 years from Dupuytren’s disease of the left hand. He shows a contracture band along the ring finger ray to the middle phalanx causing a flexion contracture of the metacarpo-phalangeal joint and the proximal interphalangeal joint. Another contracture band had caused a skin dimple at the level of the distal flexion crease in the palm but reaches beyond this to the palmar side of the basal and the middle phalanx of the little finger causing an initial contracture of the joints. In the tissue of both fingers we might expect stages of cell proliferation and collagen production. The skin over the index finger ray in the palm looks normal. Along the middle finger ray one sees the skin tight and pulled in proximal direction (Fig. 4).
Fig. 5
In Fig. 5 the palmar aponeurosis is exposed by a Y-shaped Incision. Over the index finger ray one sees normal-looking palmar aponeurosis from a patient with Dupuytren’s disease. Is this really normal? We use to speak of such specimens as apparently normal. On top of the middle finger ray one sees one sees thickened fibre bundles of the palmar aponeurosis with some
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fusion. This corresponds to the stage of fibre fusion. There is no nodule to be seen. Figure. 6 shows a longitudinal section of this tissue with a Van Gieson stain. One sees the thickened band consisting of collagen again without a nodule or cellular proliferation. Note that the transverse fibres on the left look normal. By this time we would expect that in the thickened fibre bundles a cellular proliferation would occur producing a contracture of the middle finger as in the ring and little finger. Figure 7 shows the surgical specimen with the palmar aponeurosis completely removed. You see the extension to the ulnar side of the little finger. You see the extension to the radial side of the little finger and you see diseased transverse fibres coming from the ring finger underneath the interdigital fold which causes the narrowing of the fold.
Fig. 6
Fig. 7
H. Millesi
One can clearly appreciate the irregular extensions on the palmar side of the ring finger. This is not aggressive growth of a fibromatosis but collagenisation of the pre-existing network in the subcutaneous space of the ring finger developed at random and enveloping the neuro-vascular bundle.
Epicritic Discussion of the Basic Problems Nature and Origin of the Disease There are two alternatives. (a) Dupuytren’s disease is a fibromatosis, in other words a tumour-like condition which can originate from any point within the connective tissue and shows local aggressive growth and tendency to recurrences. In this case the original site should be excised in a local radical way including neighbouring tissue of other type as in a tumour. To excise still normal-looking parts of the palmar aponeurosis does not make sense. The disease starts with the nodule with cellular proliferation. This hypothesis cannot answer the question why the disease occurs in specially designed tissue with a high extensibility and elasticity. Why does it spread in this type of tissue only and the local aggressive growth does never spread to other dense connective tissue like the flexor tendons which are located in the direct vicinity. (b) Dupuytren’s disease is a systemic disease of tissues which need a high degree of extensibility and elasticity to meet their functional demands like the palmar aponeurosis and the plantar aponeurosis with all their extensions in the sense of the palmar and plantar connective tissue body or the tunica albuginea of the penis. Ectopic sites like knuckle pads fulfil the above-mentioned criteria. The disease spreads and recurs within these tissues and dos not grow aggressively into tissues beyond the system. It is therefore not necessary to perform a radical excision including neighbouring tissues outside the system. If possible not yet involved segments of the system should be included to reduce the frequency of extensions and recurrences. According to all our knowledge Dupuytren’s disease is a systemic disease in the sense of (b). This opinion is based on mechanical studies: We have compared the residual elongation after a stress strain test with 2.5, 5 and 10% elongation between: Normal palmar aponeurosis of patients without Dupuytren’s disease Apparently normal palmar aponeurosis of patients with Dupuytren’s disease
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Bands with fibre thickening and fusion Bands with cellular proliferation Bands with scar-like final stage.
What is the Reason for the Mechanical Deficiency?
The residual elongation is minimal in normal palmar aponeurosis in normal patients (Fig. 8). It is significantly elevated in apparently normal palmar aponeurosis of Dupuytren patients after elongation by 10%. It is much elongated in specimens with fibre thickening and fusion and it is very much elevated in more advanced stages. What is the reason for these changes? The reduced return close to original values after a stress–strain test is the result of the deficiency of the elastic fibres. In fact one sees in the micro-morphology changes of the elastic fibres. Even in early cases one sees spots with fragmented and clumsy elastic fibres. Treatment of the specimens of normal palmar aponeurosis with elastase produces a similar increase of the residual elongation as in the stage of fibre thickening and fusion. Any collagen fibre exposed to longitudinal traction shows a “transverse contraction” in mechanical sense, in other words the diameter towards the middle of the fibre decreases. This transverse contraction can be neglected in thin fibres but it is significant if the diameter of the fibre increases. These mechanical observations support the hypothesis that changes of the collagen fibre proceed the cellular proliferation which represents a reaction to get rid of the thickened band and start a regeneration which is however not successful. Any theory of Dupuytren’s disease must be able to explain the mechanical phenomena. Residual strain
Residual Strain (o/oo)
35 30 25 20 15 10 5 0
Fig. 8
1
2
3 Classes
4
5
An explanation of these phenomena can be only provided by speculation so far. The elastic fibre system may have a life span and a deficiency may manifest itself at first in tissues with special elastic properties. This would explain the age factor. The genetic background of the elastic fibre system may be deficient for hereditary reasons. Any of the metabolic changes may have a negative input on the system. So, a spectrum of causes may coincide.
What is the Reason for the Contracture? We know about contracture of a granulating wound (wound contracture), which is a problem for the Plastic Surgeon because it causes deformities but is a life-saving procedure in an animal which had suffered a large wound on its back. There are good reasons to believe that myofibroblasts are responsible for wound contracture. We know about scar contracture. A scar which is constantly exposed to repetitive elongation In addition to the transverse tension to keep the edges of the wound together becomes hypertrophic and develops a contracture. We have more problems to explain the contracture in Dupuytren’s disease. It was therefore a happy moment, when Gabbiani et al. [35, 36] described fibroblasts in Dupuytren’s tissue which contained myosin and actin as in smooth muscle cells considered myofibroblasts as responsible for the contracture in Dupuytren. However, it turned out that myofibroblasts are not pathognomic for Dupuytren’s disease. They occur in wound healing, in scars, especially in burn scars with an enormous capacity to shrink but also in scars after congelation which usually do not shrink. Action of myofibroblasts could be effective only in the phase of cell maturation and collagen production. Otherwise we must see a folding in the deposited collagen but we do not. The phenomenon of contracture is still not fully understood. Certainly there is a constant rebuilding of the collagen structures. In these phases the mechanical properties are changed. We know e.g., that the mechanical recovery, which is in the normal palmar aponeurosis 10 min, is increased in contracture bands up to seven hours. In other words new functional stress starts much before the tissue has recovered.
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Treatment and Results Pre-Operative Status For the evaluation of the final result the original functional status is of significant importance. For each joint the active range of motion and the amount of flexion contracture has to be registered. Based on the actual figures any evaluation scheme can be applied. A widely used scheme was published by Tubiana et al. [37] It has five stages: Stage 0 No flexion contracture Stage 1 Flexion contracture up to 45° Stage 2 Flexion contracture 46–90° Stage 3 Flexion contracture 91–135° Stage 4 Flexion contracture more than 135° The flexion contracture is understood as the sum contracture of all joints of the most affected digit. I have used a similar scheme: Stage A: No contracture Stage B: Flexion contracture up to 30° Stage C: Flexion contracture up to 90° Stage D: Flexion contracture more than 90° The most involved joint of the most involved digit is registered. The motivation for this scheme is the following: Stage B: A flexion contracture of up to 30° of the most involved joint does not need lengthening of the skin. Of course the election of the type of incision is essential to avoid a scar contracture. Stage C: Flexion contractures of this degree need a Z-plasty or a similar procedure for skin lengthening. Stage D: Flexion contractures of this amount need skin grafting and eventually local flaps.
Functional Results The basis for evaluation of the result is the post-operative status. We differentiated four degrees according to the remaining contracture of the worst finger. Degree 1 No remaining contracture Degree 2 Remaining contracture up to 30° Degree 3 Remaining contracture more than 30° but clear improvement Degree 4 No improvement to the pre-operative status or deterioration The remaining contracture may be due to an inadequate removal of diseased tissue (RM = remaining disease), to an
H. Millesi
arthrogen or tendogen contracture due to long-lasting state in the contracted position, scar contracture as a consequence of inadequate skin release or skin necrosis as a consequence of a post-operative complication. The functional result is impaired due to a loss of sensibility, par- and dysesthesias or pain in consequence of a nerve lesion during surgery. A new contracture may develop as a result of the appearance of new diseased tissue. A recurrence (R) is defined as the occurrence of new diseased tissue at the site of a previous surgery. It means that at the pervious surgery the diseased tissue was not completely removed. An extension (E) is defined as the occurrence of new disease at a site which had not been touched during a previous surgery. It means that previously normal-looking tissue had been involved in the progressing activity of the systemic disease.
Rate of Activity It was already mentioned that we cannot predict how the disease will develop in a given individual. We can however calculate the percentage of cases of a given collective who show activity. For cases of stage O of Tubiana and Michon or A of Millesi a percentage of 37% showing activity after an observation of 3–5 years. For post-operative studies the rate of activity is the sum of the percentages of recurrences and extensions. Studies on more advanced cases demonstrated that the rate of activity increases against stage with a progressing disease. It is higher in stage B, higher in C and again higher in D.
Aims of Treatment Three different aims may be distinguished: 1. To achieve a standstill of the progression. 2. To relieve the contracture. 3. To remove the diseased tissue.
Standstill of the Disease This is the aim of all conservative treatments e.g., Vitamin E, cortisone, DMSO, ultrasound, X-ray and many more. Spontaneous regression was noticed in very few cases at a very early stage and such an event may coincide with a conservative treatment by random chance. An effect of any conservative treatment can be proven if the rate of activity of the treated collective differs significantly from rate of activity of non-treated patients.
Dupuytren’s Contracture
Release of the Contracture Elongation by a fixateur externe was recommended by Messina and Messina [38] with surprising temporary effect. It may be applied to release a severe contracture in order to have a better access for surgery.
Interruption of the Contracture Band If the Dupuytren’s disease has involved a well-defined fibre bundle in the palm and this band is the main reason of the contracture an interruption of the band achieves a release of the contracture. Since tension is an activating factor the interruption causes an overall beneficial effect on the palmar tissue. The diseased tissue remains in situ and tension recurs if continuity is restored. The interruption can be produced by: Manipulating the band transcutaneously with an injection needle to weaken it and finally to rupture it (Needle fasciotomy). It is a question of time until the continuity is re-established and the contracture recurs. Within 2.5 years this is the case in 50%. The interruption can be achieved by surgical transection (Open or closed fasciotomy). A recurrence of the contracture occurs within some years. This may be retarded by open fasciotomy and covering the defect with a full thickness skin graft. We recommend this technique for very old patients with a limited life expectancy. Injection of collagenase followed by rupture of the contracture band was recommended by Badalamante and Hurst [39]. Long-term follow-ups of this method are still wanted.
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there were a high number of haematomas and skin problems as compared to local excision using a longitudinal incision with multiple Z-plasties.
Limited Fasciectomy [41, 42] Along with others Hueston [41, 42] argued against the radical operation and claimed to have similar results as far as recurrences are concerned with less complications. Supported by the theory of a tumour-like disease he recommended the excision of the diseased tissue only and called this approach limited fasciectomy which in fact is a local excision. He believed the all recurrences occur within 2 years. With 2 years follow-up his percentage of recurrences did not differ from the more radically-operated cases which had a much longer follow-up. Today we know that recurrences occur even after many years and a follow-up of 6–12 years is necessary to get realistic figures. After such time the recurrence rate of limited fasciectomy is 70% and more.
Open Palm Technique [43] To minimize complications, especially haematoma McCash [43] suggested leaving the transverse incision in the palm open. The wound healed by secondary intention. Active exercises are necessary to avoid a scar contracture. If this therapy is done consequently by the patient healing proceeds very well ending with a nice transverse scar.
Complete and Partial Fasciectomy (Millesi [23])
Removal of the Diseased Tissue Local Excision The simple excision of the diseased tissue is followed by a high rate of recurrences. Therefore the surgical approach became more radical.
Radical Fasciectomy [22, 40] A “radical” excision of the palmar aponeurosis is performed with additional incisions and Z-plastics at the basal phalanges of the involved digits in order to reduce the percentage of recurrences. In fact Skoog [22] reported a very low rate of recurrences after 2 years follow-up. The application of this technique in all cases is very doubtful. In fact
The problems with the so-called radical fasciectomy and the knowledge about the high recurrence rate of the limited procedure stimulated me to think about a better solution. I developed the concept to remove the palmar aponeurosis as an anatomical entity and called this procedure “Complete fasciectomy”. Complete because based on the concept of a systemic disease the palmar aponeurosis “sensu strictori” should be removed as an anatomical specimen involving diseased and still normal but potentially-diseased parts. In order to have a better access the Y-shaped incision was developed based on the vessel distribution within the palmar skin. Skin necrosis was avoided and bleeding could be much better controlled due to the wide exposure. Rational application of this technique is limited to cases of moderate contractures (up to 60°), because only then we have a proper access to the finger bases and can establish a good connection to the isolated incision on the palmar side of the
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basal phalanges. If the contracture exceeds this amount we need a better access to the finger basis and therefore we have to use a longitudinal incision. With this incision and its closure by multiple Z-plasty we can also much better achieve a lengthening of the skin. However in this case we cannot perform a complete fasciectomy with its wide undermining and the Y-shaped incision. We perform a partial excision of the palmar aponeurosis over the involved and the two neighbouring finger rays. (Usually the ring, middle and little finger.) This is a Partial Fasciectomy but still a fasciectomy because diseased and normal-looking tissue is removed. If necessary we can remove the radial part (Index finger and thumb) in a second stage.
H. Millesi
A tendon contracture can be improved by a lateral incision of the fibrous tendon sheath. In severe cases a lengthening of the flexor tendons could be performed by a Z incision of the tendon far proximal or by tenotomy of both flexor tendons and suturing the proximal stump of the superficial tendon to the distal stump of the profundus tendon. A stiffness of the metacarpo-phalangeal joint is treated by capsulotomy, a stiffness of the proximal interphalangeal joint by arthrolysis or in severe cases by arthrodesis in functional position.
Complications Skin Grafting and Local Flaps It was already mentioned that the ascending fibres of the palmar aponeurosis merge into the skin. Contracture bands can be in close contact to the skin. The thickening and fusing fibre bundles cause an atrophy of the subcutaneous fat tissue and the connective tissue network between the fading fat lobules becoming involved in the formation of contracture band. Such skin segments adherent to contracture bands can be raised with difficulties, have a poor blood supply and may have diseased tissue on their under-surface. It is obvious that such skin segments represent a potential for complications and should be removed and the defect covered by a full thickness skin graft. In this sense the surgery is more “radical” and was applied since ever. Hueston [44] made the observation that under such skin grafts no recurrences occurred and attributed an influence to promote recurrences to the skin. Based on this observation he published the technique of Dermato-fasciectomy [42] which became popular in AngloAmerican centres. Skin flaps are necessary if during the dissection the tendon sheath has to be removed partially or a joint is exposed. Local flaps or cross-finger flaps may be applied followed by secondary skin grafting.
Secondary Contractures It was already mentioned that by a long-standing positioning in flexion caused by the Dupuytren’s disease secondary shrinking occurs not related directly to the disease, Even after complete removal of the diseased tissue full extension of the involved digits is not achieved.
Haematoma: The occurrence of a haematoma is a severe complication which influences the post-operative course in a negative way. This can be avoided if the patient is brought to the theatre again, the palm opened and the haematoma evacuated. Skin necrosis: The skin of certain areas, especially over a contracture band may develop circulatory problems. If this happens the surgeon should not hesitate to excise the involved segment and use a free skin graft to cover the defect. Use of skin grafts to achieve tensionless wound closure avoids such skin problems. Vascular lesion: During dissection a digital artery may be damaged. Under normal conditions this is not a problem. If the surgery is performed because of a recurrence one does not know whether and which vessels had been cut during the pervious operation. In such cases a pre-operative angiogram is helpful. The problem of an eventual amputation has to be discussed with the patient before surgery. Nerve lesion: The common and especially the digital nerves are very much involved in irregular running contracture bands. A very patient and careful dissection is necessary to liberate the nerve. A lesion of such a nerve may happen even to a very experienced surgeon. Loss of sensibility, paresthesia and eventual the formation of a painful neuroma may be the consequence. It is mandatory to recognize the lesion and to perform an immediate repair. Chronic regional pain syndrome type I: The only really awful complication is a chronic regional pain syndrome type I (former Sudeck dystrophy) which causes a lot of problems and a long post-operative recovery period. Fortunately it occurs rarely if immediate exercises are started. Its occurrence is not related to the extent of the surgery and it may happen even after a simple fasciotomy.
Dupuytren’s Contracture
Indications for Surgery and Election of Techniques A patient without contracture (Stage 0 or A) should not be operated upon because nobody could predict when and to what extend the disease will proceed. If a flexion contracture starts to develop surgery should be considered and discussed with the patient. There is no hurry but the intention is to perform the surgery before the contracture has advanced to a degree making surgery difficult. In this case I recommend a complete fasciectomy. The prospect of a recurrence or an extension is significantly reduced and the continuous activity of the disease manifests itself mainly as extension at digits causing a rather small secondary surgery. If the contracture has already advanced a partial fasciectomy is indicated which reduces also recurrences but have a higher percentage of extensions to primarily non-involved areas. If the patient does not accept a real fasciectomy and prefers a local excision (limited fasciectomy) because of a shorter time for post-operative recovery it is justified but the patient should know that the prospect of a recurrence is about 70%. If the patient accepts only minor surgery a fasciotomy is indicated but again the patient has to be informed about the high percentage of recurrences and extension.
References 1. Platter F. Observationum in hominis affectibus. Basileae, L. König. Platter first described flexion contracture deformity of the fingers (Dupuytren’s contracture) in Liber I, page 140. This work also contains the first known report of death from hypertrophy of the thymus in an infant 1614;172. 2. Dupuytren G. De la rétraction des doigts par suite d’une affection de l’aponévrose palmaire, opération chirurgicale qui convient dans ce cas. Journal universel et hebdomadaire de médecine et de chirurgie pratiques et des institutions médicales, Paris, 1831, 2nd series; 5: 352–365. Reprinted, in Medical Classics, 1939, 4: 127–150. Translated into English and published in 1833 by Alexandre Louis Michel Paillard (1803–1835) and Edmond Marx (1797–1865). Permanent retraction of the fingers, produced by affection of the palmar fascia. Lancet, London, 1833–1834, 2: 222–225. 3. Goyrand C. Nouvelles recherches sur la rétraction permanente des doigts. Mem R Méd Belg 1833;3: 489. 4. Hueston J T. Dupuytren’s contracture and specific injury. Med J Aust 1968;1(25): 1084–1085. 5. Nauck E.TH. Die Wellung der Sehnenfasern, ihre Ursache und ihre funktionelle Bedeutung. Morph. Jb. 1931;68: 79. 6. Gerdy M. Retractions des tissus albugines. BullAcadroyMed (Paris) 1844;9 G. II: 766.
151 7. Legueu F, Juvara G. Des aponevroses de la paume de la main. Bull Socanat Paris 1892;6: 383. 8. Kalberg W. Zur Anatomie der Palmaraponeurose. Anat Anz 1935;81: 149. 9. Millesi H. On the flexion contracture of the distal interphalangeal joint within the scope of Dupuytren’s contracture. Bruns Beiträge zur klinischen Chirurgie 1967;214: 400–405. 10. Ling R S M. The genetic factor in Dupuytren’s disease. J Bone Joint Surg 1963;45B: 709–718. 11. Jentsch F R. Zur Erblichkeit der Dupuytrenschen Kontraktur. Der Erbarzt 1937;4: 85. 12. Murrell G A, Hueston J T. Aetiology of Dupuytren’s contracture. Aust N Z J Surg 1990;60(4): 247–52. 13. Egawa T et al. The incidence of Dupuytren’s contracture in Japan: Survey in old people’s homes. Cent Jpn J Orthop Trauma Surg (in Japanese) 1976;19: 984–986. 14. Bailey A J. Collagen. In: McFarlane R M, McGrowther D A, Flint M H (eds). Dupuytren’s disease, vol.6. Churchill Livingstone, Edinburgh, 1990; pp. 58–71. 15. Comtet J, Bourne-Branchu B. La maladie de Dupuytren estelle d’origine vasculaire? In: Tubiana R, Hueston J T (Hrsg.). La maladie de Dupuytren, Expansion Scientifique Francaise Paris, 1986; pp. S. 79–83. 16. Kischer C W, Speer D P. Mikrovascular changes in Dupuytren’s contracture. J Hand Surg 1984;9A: 58–62. 17. Mumenthaler M. Die neurogene Ätiologie der Dupuy tren’schen Kontraktur. Handchirurgie 1970;(Suppl): 7–10. 18. Cotta H. Dupuytrensche Kontraktur. In: Cotta H (ed). Orthopädie. Thieme, Stuttgart, 1984; pp. S. 242–243. 19. Salzberg C A, Weinberg H. Dupuytren’s disease as a cause of ulnar tunnel syndrome. J Hand Surg 1987;12 A: 91–92. 20. Meyerding H W, Black J R, Broders A C. The etiology and pathology of Dupuytren’s contracture. Surg Gynecol Obstretric 1941;72: 582–590. 21. Wick G, Mayerl C, DelFrari B, Piza H. Entzündlichimmunologische Vorgänge bei der Dupuytrenschen Kontraktur. 49.österreichischer Chirurgen Kongress Innsbruck, 2008; 21–23. 22. Skoog T. Dupuytren’s contraction with special reference to aetiology and improved surgical treatment, its occurrence in epileptics. Note on knuckle pads. Acta Chir Scand 1948;96 (Suppl 139): 1–190. 23. Millesi H. Zur Pathogenese und Therapie der Dupuytrenschen Kontraktur (eine Studie an Hand von mehr als 500 Fällen). Ergebnisse der Chirurgie und Orthopädie 1965;47: 51–101. 24. Flint M H. Connective tissue biology. In: McFarlane R M, McGrouther D A, Flint M H (Hrsg.). Dupuytren’s disease. Biology and treatment. Churchill Livingstone, Edinburgh, 1990; pp. S. 13–24. 25. Flint M H. The genesis of the palmar lesion. In: McFarlane R M, McGrowther D A, Flint M H (eds). Dupuytren’s disease, vol.13. Churchill Livingstone, Edinburgh, 1990; pp. 136–154. 26. McGrouther D A. The extensor mechanism and knuckle pads. In: McFarlane R M, McGrouther D A, Flint M H (Hrsg.). Dupuytren’s disease. Biology and treatment. Churchill Livingstone, Edinburgh, 1990; pp. 168–171. 27. Herzog E G. The aetiology of Dupuytren’s contracture. Lancet 1951;I: 1305.
152 28. De Wever I, Dal Cin P, Fletcher C D, Mandahl N, Mertens F, Mitelman F, Rosai J, Rydholm A, Sciot R, Tallini G, Van Den Berghe H, Vanni R, Willén H. Cytogenetic, clinical, and morphologic correlations in 78 cases of fibromatosis: A report from the CHAMP Study Group. Chromosomes And Morphology. Mod Pathol 2000;13(10): 1080–1085. 29. Allan P W. The fibromatoses: A clinicopathologic classification based on 140 cases. Am J Pathol 1977;1: 255. 30. Enzinger F M, Weiss S W. Soft tissue tumors. C V Mosby, St Louis, 1983; pp. 45–70. 31. Azzarone B, Failly-Crepin C, Daya-Grosjean L, Chaponnier C, Gabbiani G. Abnormal behaviour of cultured fibroblasts from nodule and nonaffected aponeurosis of Dupuytren’s disease. J Cell Physiol 1983;117: 353–361. 32. Fletcher J A, Naeem R, Xiao S, Corson J M. Chromosome aberrations in desmoid tumors: Trisomy 8 may be a predictor of recurrence. Cancer Genet Cytogenet 1995;79(2): 139–143. 33. Kadmon M, Möslein G, Buhr H J, Herfarth C. Desmoid tumors in patients with familial adenomatous polyposis (FAP). Clinical and therapeutic observations from the Heidelberg polyposis register [Desmoide bei Patienten mit familiärer adenomatöser Polyposis (FAP). Klinische und therapeutische Beobachtungen des Heidelberger Polyposis-Registers]. Der Chirurg; Zeitschrift für alle Gebiete der operativen Medizen 1995;66(10): 997–1005. 34. Luck J V. Dupuytren’s contracture: A new concept of the pathogenesis correlated with surgical management. J Bone Joint Surg Am 1959;41-A(4): 635–664.
H. Millesi 35. Gabbiani G, Ryan G B, Majno G. Presence of modified fibroblasts in granulation tissue and their possible role in wound contraction. Experimentia 1971;27: 549–550. 36. Gabbiani G, Hirschel B J, Ryan G B, Statkov P R, Majno G. Granulation tissue as a contractile organ. A study of structure and function. J Exp Med 1972;135: 719. 37. Tubiana R, Michon J, Thomine J M. Scheme for the assessment of deformities in Dupuytren’s disease. Surg Clin North Am 1968;48(5): 979–984. 38. Messina A, Messina J. The TEC treatment (continuous extension technique) for severe Dupuytren’s contracture of the fingers. Ann Chir Main Memb Super 1991;10(3): 247–250. 39. Badalamente M A, Hurst L C. Enzyme injection as nonsurgical treatment of Dupuytren’s disease. J Hand Surg 2000;25A: 629–636. 40. McIndoe (1942), zitiert nach Skoog T: Dupuytren’s contraction with special reference to aetiology and improved surgical treatment, its occurrence in epileptics. Note on knuckle pads. Acta Chir Scand 1948;96 (Suppl 139): 1–190. 41. Hueston J T. Limited fasciectomy for Dupuytren’s contracture. Plast Reconstr Surg 1961;27: 569–585. 42. Hueston J T. Dermofasciectomy: Skin replacement in Dupuytren’s disease. In: Hueston J T, Tubiana R (eds). Dupuytren’s disease, 2nd edn. Churchill Livingstone, Edinburgh, 1985; pp. 149–153. 43. McCash C R. The open palm technique in Dupuytren’s Contracture. Br J Plast Surg 1964;17: 271. 44. Hueston J T. The role of the skin in Dupuytren’s disease. Ann R Coll Surg Engl 1985;167: 372–375.
Low Back Pain R. Eyb and G. Grabmeier
Strategies and Management Unspecific low back pain is second to upper respiratory problems as a reason to visit general practitioners and first to visit an Orthopaedic Surgeon’s office. The reported prevalence is as high as 73% [1]. For active adults not seeking medical attention, the annual incidence of significant low back pain (visual analogue scale VAS 4 on a ten point scale) with functional impairment ranges between 10 and 15% [2]. These numbers are for low back pain without sciatica, spinal stenosis, instability or deformity. If low back pain occurs acutely (3–6 weeks), it usually resolves after several weeks [3], the problem is the persistent or chronic disabling back pain.
Diagnostic Strategies History With these questions the medical history can be briefly elicited: Systemic diseases include the history of cancer, chronic infection or chronic polyarthritis. Neurological involvement includes usually sciatica or spinal claudication combined with paraesthesia and numbness of one or both legs. Disc herniation with neurological impairment usually increases with sneezing, coughing or abdominal pressure. A massive mid-line herniation can lead to a cauda syndrome with bladder or bowel dysfunction and sensory loss in a “saddle” distribution and bilateral gait weakness.
R. Eyb () Orthopaedic department, Danube Hospital Vienna, Austria e-mail:
[email protected]
Psychosocial reasons may be found in depression, job or family problems, somatisation, litigation involvement and/ or disability compensation issues. If dealing with low back pain in adolescence the following risk factors have been implicated [5]: high growth, smoking, tight quadriceps femoris, tight hamstrings, intensive working during the school year, poor mental health (but no correlation to Schober sign). If dealing with older adults the diagnosis probabilities change: cancer, compression fractures, spinal stenosis, aortic aneurysma become more common. Osteoporotic fractures may even occur in the absence of a recognised trauma. An overview of differential diagnosis of low back pain is shown in Table 1. Before starting an exhaustive diagnostic procedure it is useful to address three questions 1. Is a systemic disease causing the pain? 2. Are there social or psychological disorders? 3. Is there neurological compromise [4]?
Physical Examination 1. Muscle tenderness is almost always found but without specificity and not reproducibly. 2. Spinal stiffness is not strongly associated with any diagnosis, but may help in monitoring physical therapy [6]. 3. Lasegue’s test can indicate nerve root irritation (straight leg raising with symptoms of sciatica if elevation is less than 60°). Crossed Lasegue’s test is rare but highly specific [7]. 4. Further examinations should include hip range of motion and tests of the sacro-iliac joint (Menell and Patrick’s test), to exclude possible L3 symptoms. 5. Motor weakness of L5 and S1 nerve root (great toe dorsiflexion and plantar flexion).
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Table 1 Differential diagnosis of low back pain [4] Mechanical (97%)
Non-mechanical (1%)
Visceral disease (2%)
Unspecific LBP 80% Deg. discs and facets 10% Disc herniation 4% Spinal stenosis 3% Osteoporotic fracture 4% Olisthesis 2% Traumatic fracture < 1% Congenital deformity < 1% Kyphosis, scoliosis
Neoplasia 0.7% Mult.myeloma
Disease of pelvic organ Prostatitis
Metastasis
Endometriosis
Retroperiton. tumours Primary vertebral tumours Infection 0.01% Osteomyelitis
Renal diseases
Discitis Epidural abscess Rheumatoid arthritis 0.3% Ankylosing spondylitis Psoriatric arthritis Reiter’s syndrome Scheuermann disease Paget disease
Table 2 “Red flags” [8] “Red flags” indicate possible underlying spinal pathology Onset age <20 or >55 Non-mechanical pain Previous history of carcinoma, steroids, HIV Thoracic pain Feeling unwell Weight loss Neural symptoms Structural spinal deformity
Nephrolithisasis Pyelonephritis Aortic aneurysma Gastroint. Diseases Pancreatitis Cholecystitis Gastric ulcer
CT and MRI should be reserved for patients with strong clinical suggestion of infection, cancer and neurological pathology. Both CT and MRI are equivalent for detecting spinal stenosis and disc herniation, but MRI is more sensitive for cancer, infection, neural tumours and fracture (bone marrow edema) [10]. On the other hand these techniques show often “falsepositive” results: herniated discs are frequently seen especially in older patients who are asymptomatic [11]. In symptomatic individuals with low back pain this may lead to overdiagnosis, dependence on medical care and unnecessary treatment, and even to surgery. Only in cases of “red flags” these imaging tests are indicated, but the prevalence of these specific pathologies is low.
Natural History 6. Dermatomal sensory loss are indicative of L5 or S1 nerve root lesions, which are present in approximately 95% of lumbar disc herniations [4]. 7. Reduction of the patellar tendon (L4) and Achilles tendon (S1)reflexes conclude the neurologic “overview” to exclude serious neurologic pathology (Table 2).
Imaging Plain radiography should be limited to patients with: 1. Suggestion of systemic disease or 2. History of trauma 3. Weight loss 4. Fever 5. History of cancer 6. Age over 50 7. Alcohol, drug abuse, HIV 8. Neural deficit 9. Pain duration >6 weeks [9]
The prognosis of unspecific low back pain is that about a third of patients substantially recover within 1 week, twothirds at 7 weeks [12] and 40% suffer recurrences within 6 months. Most of these recurrences are not disabling, the result is frequently that of a chronic problem with intermittent acute phases, but low back pain is rarely permanently disabling [13]. Nevertheless there is a certain risk of chronicity and ongoing research is looking for the identification of patients with acute low back pain who are individuals with a high likelihood to become chronic low back pain patients. Certain risk factors can be identified (Table 3).
Therapy Non-steroidal anti-inflammatory drugs are effective for symptom relief, the evidence compared to placebo is strong, the same is true for muscle relaxants but with side-effects
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Table 3 Risk factors for LBP (Van Tulder 1997) [29] Risk factors
Occurrence
Chronicity
Individual
Age, physical fitness Smoking
Obesity
Psychosocial Negative emotions Poor cognitive function Pain behaviour Occupational
Manual material handling Bending and twisting Whole body vibration Job dissatisfaction Monotonous tasks Poor work relationship
Low educational level High level of pain and disability Distress Depressive mood Somatisation
Job dissatisfaction Unavailability of light duty on return to work Heavy lifting work
which are drowsiness and sedation. Medication should be taken regularly rather than on an “as-needed”basis [14]. Spinal manipulation and physical therapy have limited effect [15], strong evidence shows that bed rest and specific back exercises (strengthening, flexibility, stretching, flexion and extension exercises) are not effective in the acute phase. For most patients the best recommendation is rapid return to their daily activities with neither exercises nor bed rest in the acute phase, but heavy lifting, trunk twisting and vibrating work should be avoided. Back exercises are useful for later preventing recurrences and for treating chronic low back pain [16] (Table 4). If low back pain becomes chronic, exercise and intensive multidisciplinary pain treatment are highly effective. Table 4 Recommendations for acute LBP [8] Clinical guidelines for acute LBP Re-assure patients Advise patients to stay active Prescribe medication (preferably) at fixed time intervals Paracetamol NSAIDs Muscle relaxants or weak opioids Discourage bed rest Consider spinal manipulation Do not advise back specific exercises
Some evidence supports the effectiveness of behavioural therapy, analgesics, anti-depressive medication, NSAIDs, back school and manipulations. No evidence was found for steroid injections, traction and lumbar support and many commonly-used therapies lack sufficient evidence for clinically relevant long-term effects [17]. Acupuncture, spinal manipulation and massage are popular alternative therapies. Systemic reviews have found little effect for acupuncture [18], but some support for massage and spinal manipulation [15]. Available data suggest that a combination of medical care with physical therapy may be moderately more effective in reducing pain and disability than is a single method of treatment. For patients with chronic low back pain intensive exercises improve function and reduce pain [19, 20]. It is however difficult to maintain these exercise regimes for a longer period of time. Anti-depressant drug therapy is useful for one third of patients with low back pain and depression. Conflicting evidence is found for patients without depression [21]. Opioids are also proposed and may have a greater effect on pain and mood than NSAIDs, but they seem not to raise the activity level and cause side-effects such as headache, nausea and constipation. Referral to a multidisciplinary pain centre may be appropriate for patients with chronic low back pain. These centres combine cognitive behaviour therapy, patient education, supervised exercise, selective nerve blocks and other strategies to relieve pain and improve function. Complete relief is unrealistic and therapeutic goals are necessary to be re-focussed to keep the level of function obtained in these centres [4]. Even for effective treatment, the effects are usually small and short-time, many commonly-used therapies lack sufficient evidence for clinically relevant long- term effects [17] (Table 5). Invasive treatment for chronic low back pain involves a wide variety of techniques such as facet joint, epidural, trigger point and sclerosant injections. In randomized trials however they have not clearly improved outcomes, if the patient had no radiculopathy. Radiofrequency ablation of the small nerves of the facet joints showed at best a moderate effect which lasted only for 4 weeks [22]. It may have possible benefit in patients with low back pain who respond to placebo-controlled anaesthetic blocks [23]. Other techniques advocated include percutaneous heat or radiofrequency application directly at the disc altering the internal mechanics or innervation. Data supporting their use are lacking, and a randomized trial showed no
158 Table 5 Recommendations for chronic LBP [8] Recommendations of the European clinical guidelines for chronic LBP Recommended: Cognitive behaviour treatment Supervised exercise therapy Brief educational interventions Multidisciplinary (biopsychosocial) treatment Short term use of NSAID and weak opioids Consider: Short courses of manipulation and mobilisation Anti-depressants Muscle relaxants Not recommended: Passive treatment (ultrasound, short wave) Gabapentin Invasive treatment
effect [24] or a benefit in only a small proportion of highlyselected patients [25].
Surgical Treatment The role of surgery for chronic low back pain is under debate. The most common surgical treatment for persistent low back pain with degenerative changes is spinal fusion. One randomized trial comparing spinal fusion vs. a rehabilitation programme showed no difference at 1 year in back pain, function, use of medication, working status and general satisfaction [26]. Another randomized study revealed better results in the level of back pain and improvement of function after 2 years in the group of patients who had been managed with spinal fusion [27]. The study showed no clear benefit of fusion surgery 5 years post-operatively. The outcome of spinal fusion surgery is improved for patients with isolated one or two level dgenerative disc diseases, if they are carefully selected and only individuals without co-existing psychosocial disorders, distress or other chronic pain are identified [27]. The expectation of the patient about the benefits of surgery should be discussed in advance. In a study of patients scheduled for fusion surgery due to degenerative disc diseases, 90% indicated as an acceptable outcome: return to some gainful work, no more use of analgesics and a high level of physical function [28]. These expectations are not realistic and patients should be informed that pain reduction will be at about 50%, recurrent back pain will be common
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and further activity will be necessary to keep their function level acceptable.
Conclusion and Future Perspectives Treatment should mainly be differentiated between acute and chronic back pain patients. For both natural history is favourable and patients need this re-assurance. In the case of acute low back pain pharmacologic treatment should be recommended. The patient should know that there is no danger of serious neurologic injury, bed rest will not help and return to daily activity as soon as possible will be the best course. In cases of chronicity again pharmacological treatment in combination with intensive multidisciplinary exercise and cognitive behaviour therapy is the best choice. The patient should understand that the primary goal of treatment is to maximize function and that some on-going or recurrent back pain is likely but not dangerous. Imaging like plain radiography should only be performed when there is suspicion of an underlying systemic disease and advanced imaging can be reserved for potential candidates for surgery. Generally imaging is of little help due to the poor association between symptoms and morphologic findings. In the absence of severe spinal disease or radiculopathy, surgery should generally be avoided. On-going research focuses mainly on possible prevention of chronicity of low back pain and identifying sub-groups of patients, for whom specific treatment modalities are helpful. There are numbers of randomized trials, systemic reviews and epidemiologic studies regarding the value of specific therapeutic interventions for low back pain treatment.
Reference 1. Cassidy JD, Carroll LJ, Côté P. The Saskatchewan health and back pain survey. The prevalence of low back pain and related disability in Saskatchewan adults. Spine. 1998;23(17):1860–6. 2. Carragee E, Cohen S. Reliability of LBP history in asymptomatic subjects? The prevalence and incidence of reported back pain correlates with surveillance frequency. Proceedings of the 14th Annual Meeting of the North American Spine Society, Chicago, October 26–30, 2004, pp. 216, abstract. 3. Pengel LH, Herbert RD, Maher CG, Refshauge KM. Acute low back pain: Systematic review of its prognosis. BMJ. 2003;327(7410):323. 4. Deyo RA, Weinstein JN. Low back pain. N Engl J Med. 2001;344(5):363–70. 5. Feldman DE, Shrier I, Rossignol M, Abenhaim L. Risk factors for the development of low back pain in adolescence. Am J Epidemiol. 2001;154(1):30–6.
Low Back Pain 6. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268(6):760–5. 7. Vroomen PC, de Krom MC, Knottnerus JA. Diagnostic value of history and physical examination in patients suspected of sciatica due to disc herniation: A systematic review. J Neurol. 1999;246(10):899–906. 8. Koes BW, van Tulder MW, Thomas S. Diagnosis and treatment of low back pain. BMJ. 2006;332(7555):1430–4. 9. Bigos S, bowyer O, Braen G, et al. Acute low back pain problems in adults. Clinical practice guidelines no.14 Rockville, Md.: Agency for Health Care Policy and Research. December 1994; CPR publication no. 95–0642. 10. Thornbury JR, Fryback DG, Turski PA, Javid MJ, McDonald JV, et al. Disk-caused nerve compression in patients with acute low-back pain: Diagnosis with MR, CT myelography, and plain CT. Radiology. 1993;186(3):731–8. 11. Bochen SD, Davos DO, Dina TS, Patronas NJ, Wiesel SW. Abnormal magnetic resonance scans of the lumbar spine in asymptomatic subjects: A prospective investigation. J Bone Joint Surg Am. 1990;72:403–8. 12. Cherkin DC, Deyo RA, Street JH, Barlow W. Predicting poor outcomes for back pain seen in primary care using patients’ own criteria. Spine. 1996;21(24):2900–7. 13. Carey TS, Garrett JM, Jackman A, Hadler N. Recurrence and care seeking after acute back pain: Results of a longterm follow-up study. North Carolina Back Pain Project. Med Care. 1999;37(2):157–64. 14. Fordyce WE, Brockway JA, Bergman JA, Spengler D. Acute back pain: A control-group comparison of behavioral vs traditional management methods. J Behav Med. 1986;9(2):127–40. 15. Andersson GB, Lucente T, Davis AM, Kappler RE, Lipton JA, Leurgans S. A comparison of osteopathic spinal manipulation with standard care for patients with low back pain. N Engl J Med. 1999;341(19):1426–31. 16. Lahad A, Malter AD, Berg AO, Deyo RA. The effectiveness of four interventions for the prevention of low back pain. JAMA. 1994;272(16):1286–91. 17. Van Tulder MW, Koes BW. Low back pain: Chronic, clinical evidence. London: BMJ Publishing Group, 2006. 18. Van Tulder MW, Ostelo R, Vlaeyen JW, et al. Behavioral treatment for chronic low back pain: A systematic review within the framework of the Cochrane Back Review Group. Spine. 2001;26:270–81.
159 19. Manniche C, Hesselsøe G, Bentzen L, Christensen I, Lundberg E. Clinical trial of intensive muscle training for chronic low back pain. Lancet. 1988;2(8626–8627):1473–6. 20. Frost H, Lamb SE, Klaber Moffett JA, Fairbank JC, Moser JS. A fitness programme for patients with chronic low back pain: 2-year follow-up of a randomised controlled trial. Pain. 1998;75(2–3):273–9. 21. Turner JA, Denny MC. Do antidepressant medication relieve chronic low back pain? J Fam Pract. 1993;37:545–50. 22. Van Kleef M, Barendse GA, Kessels A, Voets HM, et al. Randomized trial of radiofrequency lumbar facet denervation for chronic low back pain. Spine. 1999;24: 1937–42. 23. Dreyfuss P, Halbrook B, Pauza K, Joshi A, et al. Efficacy and validity of radiofrequency neurotomy for chronic lumbar zygapophysial joint pain. Spine. 2000;25:1270–7. 24. Barendse GA, van Den Berg SG, Kessels AH, Weber WE, van Kleef M. Randomized controlled trial of percutaneous intradiscal radiofrequency thermocoagulation for chronic discogenic back pain: Lack of effect from a 90 second 70° lesion. Spine. 2001;26:287–92. 25. Pauza KJ, Howell S, Dreyfuss P, Peloza JH, Dawson K, Bogduk N. A randomized, placebo-controlled trial of intradiscal electrothermal therapy for the treatment of discogenic low back pain. Spine J. 2004;4(1):27–35. 26. Ivar Brok J, Sorenson R, Friis A, et al. Randomized clinical trial for lumbar instrumented fusion and cognitive intervention and exercises in patients with chronic low back pain and dics degeneration. Spine. 2003;28:1913–21. 27. Fritzell P, Hägg O, Wessberg P, Nordwall A; Swedish Lumbar Spine Study Group. Volvo Award Winner in Clinical Studies: Lumbar fusion versus nonsurgical treatment for chronic low back pain: A multicenter randomized controlled trial from the Swedish Lumbar Spine Study Group. Spine. 2001;26:2521–32. 28. Carragee E, Alamin T. A prospective assessment of patient expectations and statisfaction in spinal fusion surgery. Proceedings of the 30th Annual meeting of the International Society for the study of the lumbar spine, Vancouver, B.C., Canada, May 13–17, 2003, abstract. 29. Van Tulder MW, Koes BW, Bouter LM. Conservative treatment of acute and chronic nonspecific low back pain. A systematic review of randomized controlled trials of the most common interventions, Spine 1997 Sep 15; 22(18): 2728–56.
Total Hip Arthroplasty: A Comparison of Current Approaches Martin Krismer
Introduction Several approaches to the hip joint have been described. Five of them are regularly used for total hip arthroplasty (THA), others are seldom used for primary THA (e.g., Ganz trochanteric flip, medial Ludloff approach) or are only used for minimally-invasive surgery (2-incision approach) [1]. The five approaches (Table 1) can be executed either minimally-invasively or conventionally, either supine or in lateral decubitus position. The names for approaches are sometimes confusing. E.g. is the so called antero-lateral abductor split approach of Frndak et al. [8] or Mallory et al. [9] in the terminology used above a lateral approach? The considerable variability of approaches stands in contrast to a few comparative studies on approaches. Only minimally-invasive approaches have got more attention in comparative studies. The outcome of different approaches may be different with regard to peri-operative complications, pain, muscle trauma, cut-suture time, post-operative rehabilitation time, complications, outcome parameters and survival. The variation of all these parameters is caused not only by the approach, but by the implant, the technique of implantation, the experience and training level of the surgeon and by often not explicitly mentioned modification of approaches in different departments. An analysis of the Cochrane collaboration [10] compared the lateral and posterior approach in 2006. Only four publications fulfilled the criteria for a Cochrane review. Comparisons were made between 77 (posterior) and 72 (lateral) patients regarding dislocation, 43 vs. 49 concerning nerve palsy, 21
vs. 29 dealing with pain. With respect to some parameters significant differences could be demonstrated, however, the included studies showed remarkable deviations between their results and those of other studies with much higher numbers. They demonstrated e.g., for the lateral approach a dislocation rate of 6%, a result which will perhaps not occur in the hands of other surgeons. A health technology assessment on minimal-incision total hip replacement approaches showed [11] came to the conclusion that single mini-incision THA may have peri-operative advantages with regard to blood loss. Mini-incision THA was less costly under the assumption of a 1-month earlier return to usual activities and a decreased hospital length of stay. However, this assumption has to be proven. The method of this article is a literature review, supplemented by systematic considerations. This article will list also some non-comparative studies, in order to give an estimate on differences between the approaches based on higher numbers than the Cochrane report [10]. The patient samples, however, are not defined, so comparability between the studies is worse. Navigation is another parameter increasing variability. Articles focussing mainly on navigation are therefore not mentioned in the following. The intention of this article is to ask systematically for differences between the five main approaches mentioned above, bearing in mind the considerable lack of conclusive comparative studies.
Differences Muscle Trauma
Martin Krismer Department of Orthopaedics, Innsbruck Medical University, Anichstrasse 35, A-6020 Innsbruck, Austria e-mail:
[email protected]
The gluteal muscles form the most superficial layer. The five approaches overcome them either at their anterior border without cutting one of them (anterior), between the tensor
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Table 1 Approaches often used for THA Approach
Eponyms
MIS
Supine
Lateral decubitus
Direct anterior/anterior Antero-lateral Lateral/transgluteal/direct lateral Trans-trochanteric/lateral with trochanteric osteotomy Posterior/posterolateral
Hueter or Smith-Peterson [2] Watson-Jones [3] Hardinge [4]/Bauer et al. [5] Charnley [6]
Yes Yes Yes No
Yes Yes Yes Yes
Yes Yes Yes Yesa
Kocher-Langenbeck [7]
Yes
No
Yes
The terms used in the article are quoted in the table in italic a The author does not know a surgeon performing the transtrochanteric approach in a lateral decubitus position, but there is no important anatomic reason not to do so Table 2 Superficial muscle trauma (gluteal muscles) Approach/muscle
Glut. max.
Glut. med. + min.
Author
Anterior
None
None
MIS Antero-lateral MIS Lateral MIS Posterior MIS
None None None None None Split Split
None None None Glut. med and glut min split Glut. med and glut min split None None
Hoppenfeld and deBoer [12], Light and Keggi [13], Kennon et al. [14], Judet and Judet [15] Krismer et al. [16], Matta et al. [17], Rachbauer [18] Hoppenfeld and deBoer [12] Bertin and Röttinger [19] Hoppenfeld and deBoer [12], Austin and Rothman [20] De Beer et al. [21] Hoppenfeld and deBoer [12], Moore [7] Lafosse et al. [22]
and the gluteus medius with the need to cut the minimus (antero-lateral), by splitting the gluteus medius and minimus fibres (transgluteal), by mobilizing the gluteus medius and minimus by a trochanteric osteotomy (trans-trochanteric) or by splitting the gluteus maximus (posterior) (Table 2, Fig. 1). It is not well-established whether the different lesions to the gluteal muscles cause differences in outcome. Minimally-invasive surgery may reduce the size of the approach-related muscle lesion to some extent by the use of special retractors, by a more careful technique and by the shorter extent of a muscle split. The deep layer of external rotators is cut for two different reasons. In the anterior, antero-lateral, trans-trochanteric and lateral approach, the main purpose is to mobilize the femur sufficiently for external rotation. In most publications dealing with these approaches, the extent of detachment or dissection of these tendons is kept as a secret. The reason is perhaps that these tendons, especially the conjoined tendon of gemelli and obturator externus muscles are not considered as important, or are considered mainly as an obstacle to enter the femoral canal. The impact of external rotator preservation on outcome and dislocation rate is not established.
In the posterior approach, it is necessary to cut the external rotators to get access to the hip joint. This fact explains the more extensive dissection of external rotators in the posterior approach (Table 3).
Fig. 1
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Minimally-invasive surgery may reduce the dissection of external rotators in the anterior, antero-lateral and lateral approach to some extent, if no full external rotation is intended. In the posterior approach, the piriformis tendon and gemelli can be re-inserted by bone anchors or sutures. Muscle damage can be measured by parameters like CRP (C-reactive protein) or myoglobin. We have to bear in mind that these parameters express a global damage to muscle cells. A dissected tendon or a lesion of branches of a motor nerve may deteriorate muscle function, but are not represented in these muscle damage parameters (Table 4). Meneghini [29] tried to determine the degree of muscle damage in cadavers. The author of this article believes that the methods mentioned above are more adequate for this purpose.
Non-Union This problem is typical for the trans-trochanteric approach. In Horwitz et al. [30] 4/51 (8%) of trans-trochanteric approaches had a non-union at 1 year post-operatively. Non-union is the main reason that the trans-trochanteric approach was used increasingly less frequently.
Nerve Palsy and Neuralgia In a literature review, Weale et al. [31] showed the incidence of nerve injury being 48/3,870 in transgluteal and 31/2,654 in posterior approaches, with the same rate of 1.2% in both groups. They also performed an electrophysological examination and detected 2/20 (10%) sciatic nerve palsies in the lateral and 0/22 (0%) in the posterior approach. Farrell et al.
Table 3 Dissection of external rotators Approach/muscle
Piriformis
Gemelli + obt. int.
Obt. ext.
Quadr. fem.
Author
Anterior MIS
No No Rarely ? ? ? ?
Ev. Sometimes Rarely ? ? ? ?
No No No ? ? ? ?
No No No ? ? ? ?
Cut Cut
Resutured Cut
Cut Cut
Cut Cut
Resutured Unchanged
Resutured Cut
Resutured Unchanged
Resutured Unchanged
Hoppenfeld and deBoer [12] Krismer et al. [16] Matta et al. [17] Hoppenfeld and deBoer [12] Bertin and Röttinger [19] Hoppenfeld and deBoer [12] De Beer et al. [21], O’Brian and Rorabeck [23] Lafosse et al. [22] Moed and McMichaelm [24], Goldstein et al. [25] Rommens [26], Pellicci et al. [27] Lafosse et al. [22]
Antero-lateral MIS Lateral MIS Posterior
MIS
Table 4 Muscle damage parameters MIS
Author
Normal approach
N MIS/normal
Outcome parameter
FU time
MIS
Normal
Anterior
Pilot et al. [28]
Posterior
10/10
H-FABP IL-6 myoglobin
1 day
14 ± 14
9±5
1 day 1 day 1 day 2 days
90 ± 90 363 ± 119 800 ± 500 700 ± 300
90 ± 40 365 ± 53 1,100 ± 700 600 ± 400
Antero-lateral
Wohlrab et al. [29]
Lateral
20/20
myoglobin
All parameters were taken from graphs H-FABP (µg/l) heart type fatty acid-binding protein; parameter of muscle damage; IL-6 interleuleukin-6 (pg/ml)
p
<0.05
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[32] found a rate of 47/27,004 (0.17%) nerve palsies in a single institution series. The odds ratio was 2 (p = 0.03) for a posterior, and 0.6 for a trans-trochanteric approach in comparison with an antero-lateral approach. The anterior approach uses the superficial internervous planes between the sartorius (femoral nerve) and the tensor fasciae latae (superior gluteal nerve) and the deep internervous plane between the rectus femoris (femoral nerve) and the gluteus medius (superior gluteal nerve) [12]. It is the only true internervous approach to the hip. Neuralgia of the lateral femoral cutaneous nerve was described in several articles dealing with the anterior approach. The nerve shows huge variation and is located in 2–5 branches in the tensor fascia. Far lateral incision of the fascia and subfascial preparation to access the intermuscular plane between sartorius and tensor may reduce considerably the risk [33]. The antero-lateral approach is performed between the gluteus medius and the tensor fasciae latae, which have a common nerve supply (superior gluteal nerve). The nerve branch enters the tensor fasciae latae close to the muscle origin. According to Hoppenfeld and deBoer [12] it remains intact as long as the plane is not developed to the muscle origins. Ince et al. [34], however, have shown that there is a distal intermuscular branch between gluteal medius and tensor fasciae latae muscle in half of the cases, with a mean of 27 mm caudal and 38 mm ventral to the tip of the greater trochanter. This distal branch is considered to create a loop with upper branches of the superior gluteal nerve within the tensor fasciae muscle. This branch may be compromised by an antero-lateral approach. The lateral approach uses no internervous plane. The gluteus medius is split. The supplying branch of the superior gluteal nerve enters the anterior part of the muscle 3–5 cm proximal to the tip of the greater trochanter. The vastus lateralis is split as well. The supplying branch of the femoral nerve enters the medial part of the vastus lateralis in the proximal third of the femur together with the descending branch of the lateral femoral circumflex artery. Both branches can be damaged if the approach is extended [12]. In nine cadavers, the inferior branch of the superior gluteal nerve could be found posteriorly 6–8 cm cranial of the tip of the greater trochanter, and anteriorly only 3–5 cm [35]. In dysplastic hips, this safe distance is reduced to 25–45 mm in the anterior third, according to a study on intra-operative nerve stimulation [36]. In a cadaver study, Eksioglu et al. [37] found the branches of the superior gluteal gluteus to be safe in 80% of lateral approaches. In the posterior approach the gluteus maximus is split [12]. The inferior gluteal nerve enters the gluteus maximus less than 5 cm medial from the tip of the greater trochanter. The nerve branches are situated deep in the muscle and therefore cannot
M. Krismer
be easily identified during splitting of the gluteus maximus. If the gluteus maximus fibres are split more than 5 cm from the tip of the greater trochanter in a classical posterior approach, damage to the inferior gluteal nerve may occur [38]. Thus, denervation of an entire muscle or part of a muscle can occur in some of the approaches. In an electromyography study, 10/29 in the lateral approach group and 3/21 in the posterior approach group showed signs of denervation after 2 weeks and 5/29 vs. 1/21 three months after operation [35]. Picardo et al. [39] studied 40 patients undergoing THA using the Hardinge direct lateral approach. Seventeen patients (42%) had damage to the superior gluteal nerve 4 weeks post-operatively, but only one after 1 year. Weale et al. [31] found 2 injuries to the obturator nerve, 1 to the femoral nerve, 1 to the posterior tibial nerve, 1 to the common peroneal nerve and 1 to both the obturator and femoral nerve in 22 patients undergoing the lateral approach and no injury in 20 patients undergoing the posterior approach. Although clinical tests underestimate the incidence of nerve injuries, a 10% rate of femoral nerve lesions is much higher than most other authors have found. Generally speaking there are several factors which can cause nerve palsy: (a) Lesion of branches of the gluteal or the femoral nerves caused by splitting of the gluteal muscles or of the vastus lateralis (b) Distraction of major nerves (sciatic or femoral nerve) during dislocation, or reposition (c) Blunt injury to major nerves by retractors (d) Direct sharp injury Only (a) is related to the approach itself, all the other reasons depend on operative technique and skills. Case (b) can be considerably reduced by removing a small wafer of the femoral neck before dislocation, as proposed in minimally-invasive approaches [1, 16, 18, 19]. A partial removal instead of complete removal of the capsule may also help to avoid distraction. Severely dysplastic hips require lengthening, increasing the risk of distraction trauma to nerves. The use of Hohmann retractors close to nerves may increase the risk of a nerve lesion (c). Other retractors (Richardson, Langenbeck, Aufranc, Müller, etc.) or selfretaining retractors with blunt blades may reduce the risk. The anatomical differences between approaches, the techniques for detection (clinical, electrophysiological) and perhaps other factors like case mix (dysplasia, severity of osteoarthritis) may explain the large variation in the rate of nerve lesions. Only lesions of abductor muscle branches are really related to anatomic reasons. Depending on anatomic variations and the degree of dysplasia, denervation of parts of a gluteal muscle will occur as a consequence of
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the normal technique of the approach. In this respect, the lateral approach is associated with the highest risk and the anterior approach with no risk at all. The other causes are technique-related. Modifications of the operative technique can perhaps considerably reduce the lesion rate due to nerve distraction, retractor-related trauma and direct sharp nerve injury in all approaches. The main consequence of gluteus medius lesions is Trendelenburg sign and limb. Stähelin [40] has also described clinical signs: ● “Drop-in” sign – fingers palpating the greater trochanter drop into a hole when proceeding anteriorly. ● Superior bulge – cranial to this hole occurs sometimes a bulge due to contracted muscle. ● External rotation during abduction in lateral decubitus position, due to loss of internal rotation force as a function of anterior abductors.
Trendelenburg Sign and Gait In the Hardinge lateral approach, Picardo et al. [39] found a positive Trendelenburg in 20/40 cases pre-operatively (50%) and in 10 patients (25%) 1 year post-operatively. In
Table 5 Frequency of Trendelenburg sign
Gait and Limp Masonis and Bourne [43] conducted a literature review in 2004 and identified eight studies on limp involving 2,455 THA. The incidence of limb was 4–20% for patients who had had the lateral approach, and 0–16% for patients who had had the posterior approach (Table 6). A few gait lab analyses were dedicated to this topic. Madsen et al. [46] examined 10 subjects 6 months after THA with an antero-lateral approach, 10 after posterior approach and 9 controls. The antero-lateral group showed trunk inclination and the smallest hip range of motion. Menighini et al. [29] performed a gait analysis 6 weeks post-operatively on patients minimally-invasive operated
Approach
Articles
FU period
Frequency of Trendelenburg sign
Antero-lateral Lateral
Picardo et al. [39] Baker and Bitounis [35] (Cochrane) Barber et al. [42] (Cochrane) Downing et al. [60] (Cochrane) Moskal and Mann [44] Baker and Bitounis [35] (Cochrane) Barber et al. [42] (Cochrane) Downing et al. [60] (Cochrane)
1 year 3 months 12 months 12 months ? 3 months 12 months 12 months
10/40 (25%) 9/24 (36%) 2/21 (10%) 2/33 (6%) 86/319? (27%) 2/20 (10%) 3/28 (10%) 2/40 (5%)
Posterior
Table 6 Frequency of limb in selected articles
Baker’s study [35] 7/29 hips operated with a lateral Hardinge approach, 1/29 operated with a modified Dall lateral approach [41] (a sliver of the greater trochanter is taken with the gluteal flap, leading to non-union in 11 cases) and 0/21 hips operated with the posterior approach showed grade II Trendelenburg sign (unsupported pelvis dropped below the horizontal line) 3 months after operation (Table 5).
Approach
Articles
FU period
Frequency of limb in percent
Trans-trochanteric
Horwitz et al. [30]
Lateral
Horwitz et al. [30] Moskal and Mann [44] Ritter et al. [45]
Posterior
Ritter et al. [45]
6 months 1 year 6 months 1 year ? 9–29 months 9–29 months
14/51 (27%) 8/51 (15%) 14/49 (29%) 10/49 (20%) 57?/319? (18%) 35/81 (authors: 29%) 31/132 (authors: 17%)
It is not clear how the percentages were calculated in the article of Ritter et al. Therefore they are quoted with the remark (authors). The numbers given in their publication are quoted in the table. Ritter et al., refer to an antero-lateral approach, but give the citation of a description of a modified lateral approach
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M. Krismer
with a posterior, a mini-antero-lateral and a 2-incision approach (N = 8, 7, 8 respectively). The posterior and the 2-incision approach were equal, whereas the vertical ground reaction force of the mini-antero-lateral approach was decreased indicating abductor muscle trauma. We do not know how long these changes will persist.
Trochanteric Pain Greater trochanteric pain syndrome (GTPS) is the clinical representation of gluteus medius pathology, which occurs in patients with and without osteoarthritis of the hip [47]. Therefore, it may be present pre-operatively, but its symptoms are perhaps more prevalent post-operatively after pain relief in the hip joint. It is not known how many postoperative GTPS are caused by a pre-operative GTPS, and how many by a lesion to the gluteus medius caused by the approach. The rate of GTPS 3 months after operation was 7/29 hips in a lateral group, 2/29 in a modified lateral group (Dall) [35]. Ioria et al. [48] identified 23/461 (5%) GTPS in the lateral, and 1/82 (1%) in the posterior approach (p = 0.01). A higher rate of GTPS in the lateral approach is likely.
Possibility of Enlargement of Approaches Possibilities of enlargement are listed in Table 7. The main restriction is the nerve supply of muscles.
Dislocation In the Swedish hip arthroplasty register the 2-year dislocation rate calculated on re-operations between 2003 and 2006 was 326/53,962 (0.6%) [51]. Phillips et al. [52] reported on a dislocation rate of 2,276/58,521 (3.9%) in primary THA of varying aetiology, fracture excluded, observation time 6 months. There is no explanation for the striking difference between Sweden and the USA. Masonis and Bourne [43] studied dislocation with regard to approaches in a literature review. They identified four prospective studies with insufficient statistical power. Fourteen studies involving 13,203 THA met inclusion criteria. The combined dislocation rate was 2.2% for the anterolateral approach, 0.5% for the lateral approach, 1.3% for the trans-trochanteric approach and 3.9% for the posterior approach without repair, as well as 2.0% for the posterior approach with repair. The observation time was different for different studies. Berry et al. [53] showed that the cumulative risk of dislocation in Charnley prosthesis was 1% at 1 month, 2% at 1 year and 7% at 20 years. The trans-trochanteric approach was used in 90% of the cases (N = 5,972). No difference was found to the cases operated with another approach (N = 651). Non-union or fracture of the greater trochanter increased the relative risk of dislocation by 1.8. In a former study of the same institution, 19,680 THA were studied. It was also found that the risk of late dislocations was under-estimated in former studies [54] (Table 8). In a study of the Norwegian arthroplasty register [55] the posterior approach showed a higher risk of dislocation (Relative revision risk for dislocation posterior approach
Table 7 Possibility of enlargement of approaches Approach
Superficial
Deep
Author
Anterior
Detachment of origins of sartorius and tensor fasciae latae
Weber and Ganz [49], Reinert et al. [50]
Trans-trochanteric Antero-lateral
Not possible Incision into the posterior flap of the fascia lata
Lateral Posterior
Not possible Extend skin and fascial incision
Detachment of the origins of gluteus medius and minimus Interval between rectus and vastus lateralis (branch of femoral nerve to vastus lateralis has to be identified!) Lateral approach to the femur Split vastus lateralis Interval between rectus and vastus lateralis (branch of femoral nerve to vastus lateralis has to be identified!) Lateral approach to the femur Detach upper half of quadratus femoris. Detach insertion of the gluteus maximus tendon from the femur
Hoppenfeld and deBoer [12] Hoppenfeld and deBoer [12]
Hoppenfeld and deBoer [12] Hoppenfeld and deBoer [12]
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RR = 1.9, lateral 1.0, lateral with trochanteric osteotomy 0.2) (Table 9). An overview of different studies on the dislocation rate of approaches shows a huge variation between different
Table 8 Early (<5 years) and late (>5 years) dislocations in three different approaches performed in a single institution (van Knoch et al. [54]) Early dislocation
N Antero-lateral 8,479 Trans-trochanteric 8,402 Posterior 2,799 Total 19,680
37 113 15 165
0.44% 1.34% 0.54%
Late dislocation 125 126 97 348
Table 9 Dislocation rates according toa study of the Norwegian Arthroplasty Register Arthursson 07
1.47% 1.50% 3.47%
studies. A reason may be the different degree of dissection of external rotators. Pellicci et al. [27] have used a posterior technique without repair, and later with repair, causing a significant decrease of dislocations (Table 10). A further difference may be caused by techniques to determine implant position. Archbold et al. [56] for example has used the transverse acetabular ligament as a landmark, and has achieved a 0.6% dislocation rate during a minimum follow-up of 8 months using the posterior approach. Overall, there is a high variance of dislocation rates. Studies published before 1990 show higher dislocation rates. The two studies with sufficient power from van Knoch et al. [54] and Arthursson et al. [55] demonstrate a higher dislocation rate with the posterior approach.
Estimated revision (%)
Lateral Trans-trochanteric Posterior
p
N total
7 years
15 years
Risk ratio
99/30,800 5/4,642 21/3,166
0.8 0.1 1.1
1.2 0.4 2.1
1 0.2 1.9
<0.01 0.02
Table 10 Dislocation rates with regard to the approach in selected studies Approach
Articles
FU-time
Frequency of disclocation in percent
Anterior Antero-lateral
Siguier et al. [57] Vicar and Coleman [58] Woo and Morrey [59] Vicar and Coleman [58] Woo and Morrey [59] Barber et al. [42] (Cochrane) Downing et al. [60] (Cochrane) Demos et al. [61] Mallory et al. [9] Biedermann et al. [62] Peak et al. [63] Moskal and Mann [44] Barber et al. [42] (Cochrane) Downing et al. [60] (Cochrane) Archbold et al. [56], special technique Jolles et al. [64], special technique Vicar and Coleman [58] Pellicci et al. [27], first author, no repair Pellicci et al. [27], first author, with repair Pellicci et al. [27], second author, no repair Pellicci et al. [27], second author, with repair
? >2 years >1 year >2 years >1 year >2 years >1 year >1 year ? >2 years ? >2 years >2 years >1 year ? ? >2 years 1 year 1 year 1 year 1 year
10/1,037 (1%) 2/91 (2.2%) 18/770 (2.3%) 3/136 (2.2%) 59/1,898 (3.1%) 0/21 (0%) 3/51 (6%) 6/1,515 (0.4%) 12/1,518 (0.8%) 90/3,781 (2.4%) 1/630 (0.2%) 2/306 (0.7%) 0/28 (0%) 1/49 (2%) 6/1,000 (0.6%) 2/2,023 (1%) 4/42 (9.5%) 16/395 (4%) 0/395 (0%) 10/160 (6%) 1/124 (1%)
Trans-trochanteric Lateral
Posterior
The two comparative studies used in the Cochrane assessment are quoted with (Cochrane)
170
Infection In the Swedish hip arthroplasty register [51], the 2-year infection rate calculated on re-operations between 2003 and 2006 was 297/53,962 (0.6%). Phillips et al. [52] reported on an infection rate of 537/58,521 (0.9%) in primary THA of varying aetiology, fracture excluded, observation time 6 months. Concerning different infection rates in different approaches, Arthurson et al. [55] found no differences between approaches in their Norwegian register study. The number of revisions due to infection for Charnley prosthesis was 91/30,800 (0.6% in a 7-year observation period) with the lateral approach, 6/3,166 (0.2%) with the posterior approach and 10/4,642 (0.3%) for the trans-trochanteric approach, without statistical significance.
M. Krismer
usually refer to this position. Usually, the up, treated leg will appear slightly shorter than the down leg because it is in an adducted position. Using the posterior approach and lateral decubitus position, pre-operative templating and referencing the well leg intra-operatively, 20/410 hips showed a lengthening of 15 mm or more and 4/410 of 20 mm or more (1%) [65]. Malouny and Keeney [66] recommends several techniques. Before prepping and draping the leg the patient’s feet with symmetric knee flexion can be assessed. During the surgical procedure, one can measure the height of the osteotomy from the top of the lesser trochanter and perform the osteotomy at the level determined by pre-operative templating. After the trial reduction is performed, the surgeon can re-assess the relationship of the feet with the knees bent equally. As an additional crossreference, one can use the relationship of the tip of the greater trochanter with respect to the centre of the femoral head, both before and after femoral neck osteotomy, to assess restoration of leg length.
Outcome Studies related to minimally-invasive approaches are dealt with later in the text. Ritter et al. [45] compared the 81 patients operated with the lateral approach and 132 operated with the posterior approach. The HHS (Harris hip score) after 9–29 months was 93 ± 12 in the lateral group and 92 ± 10 in the posterior.
Leg Length Leg-length discrepancy is one of the most common complaints of patients after THA, and one of the most common reasons for litigation. It is relatively easy to determine leg length in a patient in supine position, palpating both medial malleoli and the superior border of both patellae. A technique leaving a part of the capsule in place helps also to avoid unintentional lengthening. The author is not aware of any comparative studies between different approaches on leg length discrepancies with sufficient statistical power. Horwitz et al. [30] found no differences in leg length between the trans-trochanteric and the lateral approach, based on a total of only 100 patients. The main reason may be that the difference between lateral decubitus and supine position is much more important than the difference between different approaches using the same position. In a lateral decubitus position lengthening is more likely. Descriptions for special techniques to avoid lengthening
Heterotopic Ossification Horwitz et al. [30] found 2/49 Brooker class IV ossifications in the lateral approach and 0/51 in the trans-trochanteric approach at 12 months. Moskal and Mann [44] found 0% Brooker class IV and 6% Brooker class III ossification in a modified lateral approach. Differences between approaches of minor Brooker degrees may occur, differences in class IV can only be detected using high numbers. No study with sufficient statistical power on this topic is known to the author of this article.
Implant Survival The influence of approaches on survival was studied in a study from the Norwegian arthroplasty registry [55]. The survival was the same for the lateral and the posterior approach. For the Charnley prosthesis, the lateral approach with trochanteric osteotomy was associated with a better survival than the lateral approach without trochanteric osteotomy.
Patient Preference Pagnano et al. [67] asked 26 patients who had received a bilateral THA using a 2-incision approach on the one side and a mini-posterior on the other side. 16/26 preferred the mini-posterior approach.
Total Hip Arthroplasty: A Comparison of Current Approaches
171
Such comparative studies are interesting, but encounter considerably difficulties. The technical skills of the surgeons should be the same for both approaches. A comparison between an approach performed by a surgeon being in the learning curve for a new approach vs. the approach the surgeon used almost always during his professional life may reflect rather differences in skills than differences of the approach. Bilateral cases are much less frequent, so the number of observed cases does not allow decisive conclusions.
In a health technology assessment analysis, 9 randomised controlled trials and 17 non-randomised comparative studies were identified, comparing minimally-invasive with normal approaches [11], most of them on posterior approaches. Small peri-operative advantages concerning blood loss and operation time were found, and it may offer a shorter hospital stay and quicker recovery. Evidence on differences in longer-term performance is very limited.
Comparison Between Normal and Minimally-Invasive Technique in the Same Approach Minimally-Invasive Modifications Surgeons have not agreed on what “minimally-invasive” means. Perhaps the intention is meant to cause not more trauma than absolutely necessary to conduct an operation safely and in an acceptable time. Scar length is no criterion, although often advertised. A mobile window technique is typical for some procedures. As long as only the skin incision is reduced in length, and the underlying structures are treated as in a standard approach through a mobile skin window, a better outcome in comparison to a standard approach is not likely.
Outcome of various studies is quoted in Table 11. Several authors [70, 72, 76, 78] have used the posterior approach with a mobile window, dissecting the deep levels as in a standard approach. They could not demonstrate important differences between the MIS and the normal technique, with the exception of reduced blood loss. Laffosse et al. [22] used a modified posterior approach, where only the common tendon of gemelli and obturator internus was cut, and the prirformis tendon was cut and re-sutured, found that a better outcome of MIS could be achieved in the WOMAC total score: at 3 months with 89
Table 11 Comparison of WOMAC or HHS (Harris hip score) between MIS and conventional technique of the same approach
Lateral
Author
Difference of MIS vs. normal
N MIS / normal
Outcome parameter
FU time
MIS
Normal
p
Charles et al. [68] Asayama et al. [69]
Skin incision Skin incision, gluteus max. Skin incision, deep “identical” Incision of skin and fascia lata Skin incision Skin incision Skin incision Skin incision Skin incision, navigation Skin incision Skin incision Skin incision Skin incision, external rotators
16/19 52/50
WOMAC HHS
12 weeks >2 years
92 96
90 96
0.7 ns
30/30
HHS
6 weeks
71 ± 10
67 ± 12
0.2
107/108
WOMAC
6 weeks
74 ± 14
74 ± 13
0.5
27/29 60/60 ? 70/70 60/60 33/33
HHS HHS HHS HHS HHS
2 years ~1 years 2–3 years 6 weeks 1 year
94 95 93 91 96
94 93 91 95 94
ns ns 0.7 ns 0.08
109/56 20/14 37/39 58/58
SF-36 phys HHS HHS WOMAC HHS
>6 months >17 months 5 year 3 months
54 ± 4 99 87 ± 4 89 ± 11
56 ± 4 97 84 ± 6 84 ± 12
Sign 0.4 0.04 0.02
6 months 3 months 6 months
91 ± 12 87 ± 14 79 ± 21
84 ± 14 90 ± 12 83 ± 16
0.01 ns 0.06
De Beer et al. [21] Posterior
Ogonda et al. [70] Chimento et al. [71] Chung et al. [72] Kim [73] Ciminello et al. [74] Di Gioia et al. [75] Dorr et al. [77] Mow et al. [76] Wright et al. [78] Laffosse et al. [22]
172
M. Krismer
Table 12 Comparisons MIS vs. normal of different approaches MIS
Author
Normal approach
N MIS/normal
Outcome parameter
FU time
MIS
Normal
p
Anterior Antero-lateral
Zhang et al. [79] Wohlrab et al. [29]
Posterior Lateral
60/60? 20/20
HHS HHS
3 months 12 weeks
91 96
79 92
<0.05 0.02
FU time
MIS 1
MIS 2
84 94 67 8 94 ± 5 91 96
84 88 88 16 95 ± 4 79 92
Table 13 Comparisons MIS of different approaches MIS 1
Author
MIS 2
N MIS/normal
Outcome parameter
2 Incision
Duwelius et al. [80]
Posterior
43/43?
HHS WOMAC pain 6 weeks 1 year 6 weeks Preferred side 6 months HHS >1 year HHS 3 months HHS 12 weeks
Anterior Antero-lateral
Pagnano et al. [67] Tanavalee et al. [81] Zhang et al. [79] Wohlrab et al. [29]
Posterior Posterior Posterior Lateral
26/26 35/35 60/60? 20/20
p
0.003 0.02 0.9 <0.05 0.02
Duwelius’ values were taken from graph, WOMAC was changed to 100 is best
MIS vs. 84 normal, and at 6 months with 91 vs. 84 in 58 patients each.
Comparison Between Normal and Minimally-Invasive Technique in Different Approaches Anterior and antero-lateral approaches were compared with the more common conventional lateral and posterior approaches (Table 12).
Comparison of Different Minimally-Invasive Approaches Different minimally-invasive approaches were compared as well (Table 13).
Discussion Many studies have demonstrated considerable differences of surgery rates when comparing geographic areas. Much less is known about technical differences between departments. Wennberg [82] created the term “practice-style factor” meaning that “the type of medical service provided is often found to be as strongly influenced by subjective factors related to the attitudes of individual physicians as by science”. Wennberg’s main focus was on cost-containment and indication for expensive or less expensive treatment methods.
The current study deals with the practice-style factor in a broader definition, focussed on differences in techniques. Nevertheless, this practice-style factor may affect outcome. In the Norwegian Arthroplasty Register 2006 [83] the approaches for primary total hip arthroplasties are listed. The changes are minimal, and the data support the strong effect of the practice-style factor (Table 14). Surgical techniques, and especially the use of a favourite approach, are usually learned during a residency training program. After residency, knowledge from colleagues, from the literature and other sources may be assimilated into this pre-conceived knowledge base. Each change is associated with effort and often with a temporary increase of adverse events euphemistically called “learning curve”. Comparative studies between different surgical approaches for the same indication encounter the difficulty that surgeons rarely use two approaches with the same frequency and develop the same skills in both approaches. A welltrained skier starting with the snowboard will demonstrate the superiority of skiing, a well-trained snow-boarder starting with skiing will show the opposite. Table 14 Approaches used in Norway at three different times, according to the Norwegian Arthroplasty Register 2006 [83] Approach/year
1987–1990
1996–2000
2005
Anterior (%) Antero-lateral (%) Lateral (%) Posterior (%) N
0.1 7.1 63.5 28.4 15,295
0.2 7.6 67.8 24.0 26,638
0.1 7.9 67.7 23.2 6.56%
Total Hip Arthroplasty: A Comparison of Current Approaches
The four studies used for the Cochrane review [31, 35, 42, 60] did not randomize but compared patients referred to different surgeons who used the different approaches which were compared. A sample-size calculation came to the conclusion that about 1,500 participants in each arm will be necessary to compare the risk of dislocation between surgical approaches. More patients would be required to detect differences in infection.
Conclusions The anterior approach uses the only safe internervous plane. Neuralgia of the cutaneous femoris lateralis nerve may occur. More studies are required to get an impression of the entire risk pattern. The antero-lateral approach may cause denervation of the tensor fasciae latae muscle. More studies are required to assess the risk pattern. The trans-trochanteric approach has the advantages of slightly better prosthesis survival and a low dislocation rate, and a significant and clinically-relevant risk of nonunion of the greater trochanter of about 10%. In the lateral approach a branch of the gluteus medius will be cut in about 20%, causing limp. It is perhaps also associated with a higher rate of greater trochanter pain syndrome. In the posterior approach the inferior gluteal nerve may be compromised. The consequences are not well documented. The conventional approach, where the external rotators are cut, is associated with a well-documented higher dislocation rate. Repair of the external rotators can help to avoid this consequence. Leg-length discrepancy may occur more frequently in a lateral decubitus position than in a supine position. Techniques to reduce this risk are available. All but the trans-trochanteric approaches can be performed minimally-invasively. A smaller skin incision in a mobile window technique combined with the usual preparation technique in the depth does not change outcome. Approaches which allow preservation of gluteal muscles and external rotators or reconstruction of external rotators may have a better outcome. Currently, there is not enough data available to support this hypothesis.
References 1. Berger RA. Total hip arthroplasty using the minimally invasive two-incision approach. Clin Orthop 2003;417:232–241.
173 2. Smith-Petersen, MN. A new supra-articular subperiosteal approach to the hip joint. Am J Orthop Surg 1917;15:592–595. 3. Watson-Jones R. Fracture of the neck of the femur. Br J Surg 1935;23:787–808. 4. Hardinge K. The direct lateral approach to the hip. J Bone Joint Surg Br 1982;64-B:17–19. 5. Bauer R, Kerschbaumer F, Poisel S, Oberthaler W. The transgluteal approach to the hip joint. Arch Orthop Traumatol 1979;95:47–49. 6. Charnley J. Low friction arthroplasty of the hip. Theory and practice. Berlin: Springer, 1979. 7. Moore AT. The self-locking metal hip prosthesis. J Bone Joint Surg Am 1957;39-A:811–827. 8. Frndak PA, Mallory TH, Lombardi AV. Translateral surgical approach to the hip. The abductor muscle “split.” Clin Orthop Relat Res 1993;295:135–141. 9. Mallory TH, Lombardi Jr AV, Fada RA, Herrington SM, Eberle RW. Dislocation after total hip arthroplasty using the anterolateral abductor split approach. Clin Orthop Relat Res 1999;358:166–172. 10. Jolles BM, Bogoch ER. Posterior versus lateral surgical approach for total hip arthroplasty in adults with osteoarthritis. Cochrane Database Syst Rev 2006;3:CD003828. 11. De Verteuil R, Imamura M, Zhu S, Glazener C, Frazer C, Munro N, Hutchinson J Grant A, Coyle D, Coyle K, Vale L. A systematic review of the clinical effectiveness and costeffectiveness and economic modelling of minimal incision total hip replacement approaches in the management of arthritic disease of the hip. NIHR Health Technol Assess 2008;12:iii–iv, ix-223. DOI 10.3310/hta12260. 12. Hoppenfeld St, deBoer P. Surgical exposures in orthopaedics. The anatomic approach. Philadelphia: Lippincott, 1984. 13. Light TR, Keggi KJ. Anterior approach to hip arthroplasty. Clin Orthop Relat Res 1980;152:255–260. 14. Kennon R, Keggi J, Zatorski LE, Keggi KJ. Anterior approach for total hip arthroplasty: Beyond the minimally invasive technique. J Bone Joint Surg Am 2004;86:91–97. 15. Judet J, Judet H. Anterior approach in total hip arthroplasty. Presse Med 1985;14:1031–1033. 16. Krismer M, Nogler M, Rachbauer F. Direct anterior single incision approach. In: Hozak WJ, Krismer M, Nogler M, Bonutti PM, Rachbauer F, Schaffer JL, Donnelly (eds.) Minimally invasive total joint arthroplasty. Heidelberg: Springer, 2004, pp 47–53. 17. Matta JM, Shahrdar C, Ferguson T. Single-incision anterior approach for total hip arthroplasty on an orthopaedic table. Clin Orthop Relat Res 2005;441:115–124. 18. Rachbauer F. Minimal-invasive Hüftendoprothetik. Der vordere Zugang. Orthopäde 2006;35:723–724, 726–729. 19. Bertin KC, Röttinger H. Anterolateral mini-incision hip replacement surgery. A modified Watson-Jones approach. Clin Orthop Relat Res 2004;428:248–255. 20. Austin MS, Rothman RH. Acetabular orientation: Anterolateral approach in the supine position. Clin Orthop Relat Res 2009;467:112–118. 21. De Beer J, Petruccelli D, Zalzal P, Winemaker MJ. Singleincision, minimally invasive total hip arthroplasty. Length doesn’t matter. J Arthroplasty 2004;18:945–950.
174 22. Laffosse JM, Chiron P, Tricoire JL, Giordano G, Molinier F, Puget J. Prospective and comparative study on minimally invasive posterior approach versus standard posterior approach in total hip replacement. Rev Chir Orthop 2007;93: 228–237. 23. O’Brien DAL, Rorabeck, CH. The mini-incision direct lateral approach in primary total hip arthroplasty. Clin Orthop Relat Res 2005;441:99–103. 24. Moed BR, McMichael JC. Outcomes of posterior wall fractures of the acetabulum. Surgical technique. J Bone Joint Surg Am 2008;90-A(suppl 2):87–107. 25. Goldstein WM, Branson JJ, Berland KA, Gordon AC. Minimal-incision total hip arthroplasty. J Bone Joint Surg Am 2003;85–A(suppl):33–38. 26. Rommens PM. The Kocher-Langenbeck approach for the treatment of acetabular fractures. Operat Orthop Traumatol 2004;16:59–74. 27. Pellicci PM, Bostrom M, Poss R. Posterior approach to total hip replacement using enhanced posterior soft tissue repair. Clin Orthop Relat Res 1998;355:224–228. 28. Pilot P, Kerens B, Draijter WF, Kort NP, ten Kate J, Buurman WA, Kuipers H. Is minimally invasive surgery less invasive in total hip replacement? A pilot study. Injury 2006; 37S:S17–S23. 29. Wohlrab D, Droege JW, Mendel T, Brehme K, Riedl K, Leuchte S. Minimal-invasiver vs. transglutealer Hüftgelenkersatz. Orthopäde 2008;37:1121–1126. DOI 10.1007/ s00132-008-1343-0 E-publication. 30. Horwitz BR, Rockowitz NL, Goll SR, Booth Jr RE, Balderston RA, Rothman RH, Cohn JC. A prospective randomized comparison of two surgical approaches to total hip arthroplasty. Clin Orthop Relat Res 1993;291:154–163. 31. Weale AE, Newman P, Ferguson IT, Bannister GC. Nerve injury after posterior and direct lateral approaches for hip replacement. A clinical and electrophysiological study. J Bone Joint Surg Br 1996;78-B:899–902. 32. Farrell CM, Springer BD, Haidukewych GJ, Morrey BF. Motor nerve palsy following primary total hip arthroplasty. J Bone Joint Surg Am 2005;87-A:2619–2625. 33. Dellon AL, Mont M, Ducic I. Involvement of the lateral femoral cutaneous nerve as source of persistent pain after total hip arthroplasty. J Arthroplasty 2008;23:480–485. 34. Ince A, Kemper M, Waschke J, Hendrich Christian. Minimally invasive anterolateral approach to the hip. Risk to the superior gluteal nerve. Acta Orthop 2007;78:86–89. 35. Baker AS, Bitounis VC. Abductor function after total hip replacement. An electromyographic and clinical review. J Bone Joint Surg 1989;71-B:47–50. 36. Ikeuchi M, Kawakami T, Yamanaka N, Okanoue Y, Tani T. Safe zone for the superior gluteal nerve in the transgluteal approach to the dysplastic hip. Intraoperative evaluation using a nerve stimulator. Acta Orthop 2006;77:603–606. 37. Eksioglu F, Uslu M, Gudemez E, Sahap Atik O, Tekdemir I. Reliability of the safe area for the superior gluteal nerve. Clin Orthop Relat Res 2003;412:111–116. 38. Ling ZX, Kumar VP. The course of the inferior gluteal nerve in the posterior approach to the hip. J Bone Joint Surg Br 2006;88-B:1580–1583.
M. Krismer 39. Picado CHF, Garcia FL, Marques W. Damage to the superior gluteal nerve after direct lateral approach to the hip. Clin Orthop Relat Res 2006;455:209–211. 40. Stähelin T. Abduktorennahtversagen und Nervenschädigung beim transglutealen Zugang zur Hüfte. Gründe und Lösungsansätze für einen weniger invasiven Gelenksersatz. Orthopade 2006;35:1215–1224. 41. Dall D. Exposure of the hip by anterior osteotomy of the greater trochanter. A modified anterolateral approach. J Bone Joint Surg Am 1962;44-A:1047–1460. 42. Barber TC, Roger DJ, Goodman SB, Schurman DJ. Early outcome of total hip arthroplasty using the direct lateral vs. the posterior surgical approach. Orthopedics 1996;19:873–875. 43. Masonis JL, Bourne RB. Surgical approach, abductor function, and total hip arthroplasty dislocation. Clin Orthop Relat Res 2002;405:46–53. 44. Moskal JT, Mann III JW. A modified direct lateral approach for primary and revision total hip arthroplasty. A prospective analysis of 453 cases. J Arthroplasty 1996;11:255–266. 45. Ritter MA, Harty LD, Keating ME, Faris PM, Meding JB. A clinical comparison of the anterolateral and posterolateral approaches to the hip. Clin Orthop Relat Res 2001;385: 95–99. 46. Madsen MS, Ritter MA, Morris HH, Meding JB, Berend ME, Faris PM, Vardaxis VG. The effect of total hip arthroplasty surgical approach on gait. J Orthop Res 2004;22:44–50. 47. Bird PA, Oakley SP, Shnier R, Kirkham BW. Prospective evaluation of magnetic resonance imaging and physical examination findings in patients with greater trochanteric pain syndrome. Arthritis Rheum 2001;44:2138–2145. 48. Iorio R, Healy WL, Warren PD, Appleby D. Lateral trochanteric pain following primary total hip arthroplasty. J Arthroplasty 2006;21:233–236. 49. Weber M, Ganz R. Der vordere Zugang zu Becken und Hüftgelenk. Operat Orthop Traumotol 2002;10:245–257. 50. Reinert CM, Bosse MJ, Poka A, Schacherer T, Brumback MJ, Burgess AR. A modified extensile exposure for the treatment of complex or malunited acetabular fractures J. Bone Joint Surg Am 1988;70-A:329–337. 51. Swedish Hip Arthroplasty Register. Annual Report 2006. http://www.jru.orthop.gu.se. 52. Phillips CB, Barrett JA, Losina E, Mahomed NN, Lingard EA, Guadagnoli E, Baron JA, Harris WH, Poss R, Katz JN. Incidence rates of dislocation, pulmonary embolism, and deep infection during the first six months after elective total hip replacement. J Bone Joint Surg Am 2003;85-A:20–26. 53. Berry DJ, von Knoch M, Schleck CD, Harmsen WC. The cumulative long-term risk of dislocation after primary Charnley total hip arthroplasty. J Bone Joint Surg Am 2004; 86-A:9–14. 54. Von Knoch M, Berry DJ, Harmsen WS, Morrey BF. Late dislocation after total hip arthroplasty. J Bone Joint Surg Am 2002;84-A:1949–1953. 55. Arthursson AJ, Furnes O, Espehaug B, Havelin LI, Söreide JA. Prosthesis survival after total hip arthroplasty – does surgical approach matter? Analysis of 19,304 Charnley and 6,002 Exeter primary total hip arthroplasties reported to
Total Hip Arthroplasty: A Comparison of Current Approaches the Norwegian Arthroplasty Register. Acta Orthop 2007;78: 719–729. 56. Archbold HA, Mockford B, Molloy D, McConway J, Ogonda L, Beverland D. The transverse acetabular ligament. An aid to orientation of the acetabular component during primary total hip replacement. A preliminary study of 1000 cases investigating postoperative stability. J Bone Joint Surg Br 2006;88-B:883–886. 57. Siguier T, Siguier M, Brumpt B. Mini-incision anterior approach does not increase dislocation rate. A study of 1037 total hip replacements. Clin Orthop Relat Res 2004;426: 164–173. 58. Vicar AJ, Coleman CR. A comparison of the anterolateral, transtrochanteric, and posterior surgical approaches in primary total hip arthroplasty. Clin Orthop Relat Res 1984;188: 152–159. 59. Woo RYG, Morrey BF. Dislocations after total hip arthroplasty. J Bone Joint Surg Am 1982;64-A:1295–1306. 60. Downing ND, Clark DI, Hutchinson JW, Colclough K, Howard PW. Hip abductor strength following total hip arthroplasty – A prospective comparison of the posterior and lateral approach in 100 patients. Acta Orthop Scand 2001;72: 215–220. 61. Demos HA, Rorabeck CH, Bourne RB, MacDonald SJ, McCalden RW. Instability in primary total hip arthroplasty with the direct lateral approach. Clin Orthop Relat Res 2001; 393:168–180. 62. Biedermann R, Tonin A, Krismer M, Rachbauer F, Eibl G, Stöckl B. Reducing the risk of dislocation after total hip arthroplasty. The effect of orientation of the acetabular component. J Bone Joint Surg Br 2005;87-B:762–769. 63. Peak EL, Parvizi J, Ciminiello M, Purtill JJ, Sharkey PF, Hozack WJ, Rothman RH. The role of patient restrictions in reducing the prevalence of early dislocation following total hip arthroplasty. J Bone Joint Surg Am 2005;87-A:247–253. 64. Jolles BM, Zangger P, Leyvraz PF. Factors predisposing to dislocation after primary total hip arthroplasty: A multivariate analysis. J Arthroplasty 2002;17:282–288. 65. Iagulli ND, Mallory TH, Berend KR, Lombardi AV Jr, Russell JH, Adams JB, Groseth KL. A simple and accurate method for determining leg length in primary total hip arthroplasty. Am J Orthop 2006;35:455–457. 66. Maloney WJ, Keeney JA. Leg length discrepancy after total hip arthroplasty. J Arthroplasty 2004;19:108–110. 67. Pagnano MW, Trousdale RT, Meneghini RM, Hanssen AD. Patients preferred a mini-posterior THA to a contralateral twoincision THA. Clin Orthop Relat Res 2006;453:156–159. 68. Charles MN, Fejbel RJ, Kim P. Minimally invasive surgery of the hip – a randomized pilot study. Annual Meeting of the Canadian Orthopaedic Association, Toronto, June 2006. Poster 88. (Citation and data from De Verteuil R et al. NIHR Health Technol Assess 2008).
175 69. Asayama I, Kinsey TL, Mahoney OM. Two-year experience using a limited-incision direct lateral approach in total hip arthroplasty. J Arthroplasty 2006;429:232–238. 70. Ogonda L, Wilson R, Archbold P, Lawlor M, Humphreys P, O’Brien S, Beverland D. A minimal-incision technique in total hip arthroplasty does not improve early postoperative outcomes. A prospective, randomized, controlled trial. J Bone Joint Surg Am 2005;87-A:701–710. 71. Chimento GF, Pavone V, Sharrock N, Kahn B, Cahill J, Sculco TP. Minimally invasive total hip arthroplasty: A prospective randomized study. J Arthroplasty 2005;20: 139–144. 72. Chung WK, Liu D, Foo LS. Mini-incision total hip replacement – surgical technique and early results. J Orthop Surgery 2004;12:19–24. 73. Kim YH. Comparison of primary total hip arthroplasties performed with a minimally invasive technique or a standard technique. A prospective and randomized study. J Arthroplasty 2006;21:1092–1098. 74. Ciminello M, Parvizi J, Sharkey PF, Eslampour A, Rothman RH. Total hip arthroplasty: Is small incision better? J Arthroplasty 2006;21:484–488. 75. Di Gioia AM III, Plakseychuk AY, Levison TJ, Jaramaz B. Mini-incision technique for total hip arthroplasty with navigation. J Arthroplasty 2003;18:945–950. 76. Mow CS, Woolson ST, Ngarmukos SG, Park EH, Lorenz HP. Comparison of scars from total hip replacements done with a standard or a mini-incision. Clin Orthop Relat Res 2005;441:80–85. 77. Dorr LD, Maheshwari AV, Long WT, Wan Z, Sirianni LE. Early pain relief and function after posterior minimally invasive and conventional total hip arthroplasty. A prospective, randomized, blinded study. J Bone Joint Surg Am 2007;89A:1153–1160. 78. Wright JM, Crockett HC, Delgado S, Lyman S, Madsen M, Sculco TP. Mini-incision for total hip arthroplasty: A prospective controlled investigation with 5-year follow-up evaluation. J Arthroplasty 2004;19:538–545. 79. Zhang XL, Wang Q, Jiang Y, Zeng BF. Minimally invasive total hip arthroplasty with anterior incision. Chung Hua Ko Tsa Chih 2006;44:512–515. 80. Duwelius PJ, Burkhart RL, Hayhurst JO, Moller H, Butler JB. Comparison of the 2-incision and mini-posterior total hip arthroplasty technique. J Arthroplasty 2007:22:48–56. 81. Tanavalee A, Jaruwannapong S, Yuktanandana P, Itiravivong P. Early outcomes following minimally invasive total hip arthroplasty using a two-incision approach versus miniposterior approach. Hip Int 2006;16:S17–S22. 82. Wennberg JE. Dealing with medical practise variations: A proposal for action. Health Aff 1984;3:6–32. 83. Norwegian Arthroplasty Register 2006. http://info.haukeland.no/nrl/
Chapter How to Do a Cemented Total Hip Arthroplasty Chapter author Eduardo Garcia-Cimbrelo
Introduction Polymethylmethacrylate (PMMA) bone cement is still widely used to anchor artificial joints. Charnley introduced the use of bone cement in 1962 to fix both prosthetic components to the bone [1]. Principles of the Charnley prosthesis are well-known: a 22.25 mm diameter for the femoral head, cemented fixation, and an all-polyethylene cemented cup. He introduced the prosthesis in the early nineteen sixties and, despite the somewhat obsolete cementing techniques, 30-year good results are common [2–6]. With the so-called contemporary cementing techniques, the long-term results will probably be even better [7–11]. Scandinavian hip registers have demonstrated the benefits of modern cementing techniques [12–15]. The objectives of total hip arthroplasty (THA) are to relieve pain and increase mobility and function for as long as possible, and a well-cemented THA remains the gold standard. In the nineteen seventies, early complications following cemented THA’s were infection and stem loosening. Nowadays, osteolysis, bone defects and loosening, which are produced by polyethylene wear, are the main problems in cemented THA.
The Femoral Stem Different series report excellent long-term results using wellknown designs, such as Charnley (Thackray, Leeds, UK) and Exeter (Howmedica, Rutheford, NJ). A femoral stem functions as either a composite beam or a loaded taper [16, 17]. In the composite beam model, the stem is considered a
Eduardo Garcia-Cimbrelo Hospital La Paz, Universidad Autónoma de Madrid, Paseo de la Castellana 261, Madrid 28046, Madrid, Spain e-mail:
[email protected]
rod within two tubes; an inner cement tube and an outer bone tube. The composite beam depends on strong bonding at both the prosthesis-cement interface and the bone-cement interface to form a stable construct from three materials with different mechanical properties: metal, cement and bone. The load is transmitted from the prosthetic femoral head via the stem to its tip, by-passing the proximal femur. From the stem tip, the load is transferred to the distal bone cement and subsequently to the host bone [16]. A loaded, polished, tapered stem transfers load by a different mechanism [18]. A tapered stem must be able to move within its cement mantle to function as a loaded taper. The load is transmitted from the prosthetic femoral head and forces the taper to subside within the cement mantle. This subsidence creates radial compressive forces within the cement and subsequent hoop stresses within the bone. Proximal stress- shielding is minimized because these forces are generated throughout the length of the femoral stem. A good cement technique requires a distal void, usually within the centraliser, to allow subsidence without cement fracture. Roentgen stereophotogrammetric analysis (RSA) of the polished tapered Exeter stem has demonstrated distal migration at the cement implant interface. Not only did the nonpolished design migrate at the cement-implant interface, but it also migrated at the cement-bone interface, where migration can impair fixation [19]. RSA techniques have also demonstrated significant differences in early posterior head migration with a polished Exeter stem as compared to migration with the a non-polished design [20]. Subsidence of the polished, collarless, tapered stem within the cement mantle compresses the interfaces enabling them to better resist shear forces generated by the posteriorly-directed loads on the femoral head. Polished, collarless, tapered stems are more forgiving than conventional designs [21]. Based on RSA data all cemented femoral stems exhibit subsidence and retroversion in the first 6 months after implantation. All stem designs migrate, so they must de-bond at the stemcement interface. Stems that subside more than 0.1 mm within 2 years of implantation show a significantly higher
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revision rate than stems with less subsidence. Thus, these two biomechanical systems require a different prosthesiscement interface: a perfect stem-cement bond for the composite beam system but no bond between the stem and the cement in a loaded taper system [17]. The first generation of Charnley stems, the flat-back design, was introduced in 1962. These stems were polished implants with a single straight taper in coronal plane. However, the Exeter stem is tapered along both the coronal and sagittal planes. While slight subsidence of the Charnley stem produced excellent functional results despite an occasional distal cement fracture in patients, Ling reported that with the Exeter stem subsidence produced no damage to the bone-cement interface as long as no fracture occurred [22]. The most recent tapered design is the cone. Because the femoral head is medially offset with regard to the longitudinal axis of the femur, loading of the femoral head results in torsional forces on the femoral stem. A cone does not resist these torsional forces, and will allow premature loosening. This anterior and posterior twisting of the prosthesis within the cement mantle and femur is suspected to be one of the most important aspects of femoral component loading with respect to loosening [23]. Friedman et al. recommended that a cemented femoral stem have a smooth surface with no sharp edges so as to eliminate sites of stress concentration between the prosthesis and the cement [24]. They also recommended that the stem be broader laterally than medially so as to diffuse the compressive stress medially and increase torsional and bending rigidity. However, the Exeter stem, which does not incorporate these features, has shown excellent results [23, 24]. The C-stem implant design (DePuy, Warsaw, IN) reflects these principles; it has two longitudinal tapers to transfer compressive load to the femur and a third taper, as the stem narrows from lateral to medial, that supposedly improves torsional and axial stability. However, longterm data from use of this stem are not yet available [25]. The French Paradox. It has become generally accepted that the cement surrounding a proximal femoral implant should be not less than 2 mm thick and that it should be complete without any “windows” in the mantle. In 1971, Marcel Kerboull, using the original Charnley stem, noted a high rate (24%) of de-bonding associated with a supero-medial crack in the cement mantle that appeared to be associated with stem subsidence. However, this problem was not observed in dysplastic femurs, where a tightly-fitted stem left room for only a thin cement layer [26]. Changes were made resulting in the different size ranges of the Charnley-Kerboull prosthesis. The proper component alignment was thought to maintain cement compression. Although the stem showed a thin cement mantle on the antero-posterior radiograph, the mantle might be thicker on the lateral view. This philosophy has
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resulted in excellent long-term results except when fashion determined changes in surface roughness [27]. The MK mark I had an aseptic loosening rate of 1–2% at 20 years. Excellent results have also been reported in young patients [28]. It seems that the success of the Kerboull prosthesis lies in the considerable compression of the cement generated by hammering a tightly fitting implant into the dough-like material; thus even in the event that de-bonding occurs, particulate debris will not be produced, and the tapered geometry will continue to exert compressive forces on the cement bone interface under load as a result of the interlocking between the femur and polished surface finish. However, poor results have been reported using a matt surface finish after short- to mid-term follow-ups [29]. Surface finish. Different series report that a highly polished surface is essential for the longevity of a doubletapered cemented design, and they also report that the surface finish of a femoral stem seems to influence loosening and osteolysis [22, 23, 30, 31]. When the Exeter design was modified in 1976, the essential geometry remained unchanged but the surface finish was modified from polished to a matt finish that, nevertheless, was associated with early loosening despite an improved cementing technique [23]. In addition, the matt stem was associated with extensive localised osteolysis. As a result of this study, the highly polished surface was re-instated in 1986 [23].
The Acetabular Cup Uncemented cups have became increasingly popular. Their use has been particularly recommended for younger patients, since the long-term results of cemented implants in such patients has been relatively poor and the short-term results of the uncemented cup have been good [15]. Havelin et al. reported that only one of 1,61,672 Charnley cups had been revised because of wear based on information recorded in the Norwegian Arthroplasty Register [15]. They stated that the good results of the Charnley cup inserted with high-viscosity Palacos cement may not apply to all cemented cups, and could vary depending on operative techniques, as well as, probably, the diameter, material and surface roughness of the head. According to the Norwegian Arthroplasty register, the 0–12-year results were generally good for all brands of cemented cup, and the Charnley cup did not perform better than other cemented all-polyethylene cups. Finite element analysis shows that THA changes the load pattern in the acetabular region as compared with a normal hip joint. A cemented cup increases the stresses in the cancellous bone immediately superior to the cup. With a noncemented press-fit component the load is transferred to the
How to Do a Cemented Total Hip Arthroplasty
acetabular rim, resulting in a loss of trabecular bone in the central part of the ilium at the medial part of the acetabulum. Using a longitudinal densitometry study, Shetty et al. report that the bone loss after the insertion of a cemented Charnley cup was small, transient and occurred mainly at the medial wall of the acetabulum [32]. After 2 years bone mass had returned to baseline values, with a pattern suggesting a uniform transmission of load to the acetabulum. A loose femoral component is associated with clinical symptoms more often than is a loose cup, even when the cup has migrated [33, 34]. Although a loose cup rarely causes marked early clinical symptoms, with time movement at the bone-cement interface will cause considerable bone resorption as well as clinical signs and symptoms of failure. Acetabular cup loosening is determined by the quality of the cementing technique [34]. Any demarcation of the bonecement interface around the acetabular component on the immediate post-operative radiograph must be considered as an important factor affecting the long-term result. Demarcation may be due to poor operative technique [35, 36], the result of a failure to remove all of the articular cartilage, particularly at the periphery of the acetabulum, or the result of poor bone-cement apposition during polymerisation of the cement [36]. We have found that the extent of the radiolucent line is more important than its thickness [34], and a progression of the line within the first year after the operation is a useful prognostic indicator of late failure of the acetabular cup. In order to establish the very best cement-bone interface at the time of surgery, flanged sockets have been recommended [36–38]. A pressure-injection flanged socket was introduced in Wrightington in 1976. The continuous flange restricts the size of the region through which cement can escape during cup insertion, thus increasing pressure on the cement. Shelley and Wroblewski found that flanged cups produced higher peak pressures as well as higher intruded cement volumes compared to unflanged cups [36]. However, Parsch et al. did not find a significant difference in cement penetration using either a flanged or an unflanged cup [38]. They stated that pressurisation of the cement should be completed before cup insertion using a pressuriser and that the use of flanged cups as the sole means of cement pressurisation in the acetabulum was not recommended [38]. However, different series have reported excellent long-term results using flanged cups [12, 35, 37].
Bone Cement At first sight, cold-curing PMMA bone cement seems to be a rather simple material consisting of a powder and a liquid. But, in fact, it is a complex material that performs various
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functions at its application site after placement. Its properties vary according to the composition of its basic elements, which are decisive in the behaviour during mixing. These differences considerably affect the cementing technique and the accurate in vivo application thus influencing the mechanical performance of the cured mantle cement and the longterm results of the implantation. What is more, PMMA bone cements can even act as a drug delivery system for local antibiotics [39]. The mechanical properties of acrylic bone cement, used in Orthopedic surgery, are very influential in determining the successful long-term stability of a prosthesis [40]. A large number of commercial formulations are available, offering different chemical compositions and physical properties of both the powder and monomer constituents. Harper et al. [40]. have investigated a number of the most commonlyused bone cements along with some of the newer formulations, and found significant differences in both static and fatigue properties between the various bone cements. Tensile tests revealed that Palacos R, Sulfix-60 and Simplex P had the highest values of ultimate tensile strength, closely followed by CMW 3, while Zimmer Dough cement had the lowest strength. The correlation between improved cementing techniques and improved long-term results after THA is well known. Both pressurisation and rapid cement application reduce the risk of interface bleeding and blood lamination. However, only a few institutions use modern cemented THA techniques employing pulsed lavage. Breusch et al. have determined that pulsatile jet lavage significantly improves interdigitation between cancellous bone and cement – both in vitro and in vivo – and should be regarded as mandatory in cemented THA [41]. They stated that high pressurising technique is an effective means to improve cement penetration, but should only be administered with jet lavage to reduce the risk of fat embolism [41]. Fractures and cracks in the cement mantle of a THA may facilitate mechanical loosening of the prosthesis. Especially large voids and flaws within the cement can cause fatigue fractures. Porosity weakens the cement, increasing the formation of the microfractures that contribute to crack propagation. Retrograde cement application and reduction of cement porosity attempt to improve the quality and durability of the bone cement. The vacuum mixing method for cement preparation can remove nearly all the porosity and enhance cement strength by about 17%. Acrylic bone cement is a visco-elastic material and several aspects of the cement mantle have been shown to be important in regard to prostheses with a polished tapered design. These include the ability of the prosthesis to subside within the mantle or into a void in the centraliser [22],
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good cementation in the proximal femur [23], and the absence of defects in the cement mantle or the ability of the stem to subside and occlude the space for debris transportation [42]. With the tapered Exeter system, the quality of the cement mantle in Gruen’s zone 7 ensures that most of the load is transmitted to the proximal third of the femur [43]. This load transmission has been achieved with the use of a removable plastic calcar cement-retainer, or so-called “horse-collar”, held against the cut surface of the femoral neck while the cement polymerises under pressure [23]. Anthony et al. pointed out the importance of a complete cement mantle without any defects [42]. They stated that localised endosteal osteolysis occurred with femoral stems that were not radiographically loose although localised defects in the cement mantle were found in the area of osteolysis. They postulated that the stem-cement interface was sufficient for the passage of debris and, as the space became larger, for direct transmission of pressure changes, fluid and rapidly increasing amounts of debris to the endosteal surface of the femur through a cement mantle defect [42]. Fig. 1 Thirty-year follow-up antero-posterior radiograph showing a Charnley cemented prosthesis with an excellent result
Clinical Outcome There is considerable evidence from register studies [12–15] that cemented implants in both femur and acetabulum give satisfactory long-term results. These findings apply for both young and old patients, and for all diagnostic groups. The Charnley and Exeter total hip implants (cup and stem) have been widely used all over the world. The Charnley low-friction arthroplasty still produces good results after 30 years (Fig. 1). Pain relief is reported by over 96% of patients [6]. The Exeter stem was the first double-tapered, polished, collarless, straight femoral stem for cemented total hip replacement to be used and it is still the most commonly-implanted cemented stem in the world (Fig. 2).
Cemented Femoral Component The cemented stem with the most published long-term follow-up data is the original flatback Charnley prosthesis. The Charnley low-friction arthroplasty has reached more than 40 years of clinical application. Wroblewski et al. have reported that at 31 years, when 40 hips were still attending follow-up, survival with revision for a loose stem was 72.5% and for a loose acetabular component 53.7% [6].
Fig. 2 Five-year follow-up antero-posterior radiograph showing a well-fixed Exeter Universal hip
How to Do a Cemented Total Hip Arthroplasty
Wear and cup loosening were the main long-term problems (Fig. 3). Older [44] in a worldwide retrospective survivorship analysis review at 15–20 years of 5,089 Charnley prostheses performed as a primary procedure at eight hospitals, reported a survival of 83% for the whole series, 67% for patients aged under 40 years at surgery and 92% for patients aged 70–80 years at surgery. The results at a minimum 20-year follow-up of the prevalence of revision for aseptic loosening of the femoral stem, reported by Schulte et al. [4] was only 2%. With radiographic evidence of definite or probable loosening and revision for aseptic loosening included as end-points, the mean survivorship at 22 years in that study was 83% for the femoral component [4]. In a series of 680 Charnley prostheses implanted in our institution between 1971 and 1979, 11% of the cups and 14% of the stems had been revised after 18 years. Cup loosening was found in 40% of the hips and stem loosening in 26% at 15 years in the under-40-year-old patients, whose average age was 32.4 years [33]. Munuera and Garcia-Cimbrelo [45] in a series of 623 Charnley low-friction arthroplasties ten years after implantation, found that 70 hips showed loosening of the femoral component (18% after 16 years). Loosening had appeared in 84% within 10 years of surgery. Fracture of the stem occurred in 4.3% of cases. Stem loosening was related to poor surgical technique, such as varus or valgus
Fig. 3 Seventeen-year follow-up antero-posterior radiograph showing a loosened acetabular and stem Charnley components with osteolysis and polyethylene wear
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alignment of the stem and defects in the cementing technique [45]. Garcia-Cimbrelo et al. in the same 680 hips reported 63 cases of femoral osteolytic cavities with a mean follow-up of 15 years and 9 months (11% according to survivorship analysis) [46]. The mean time of appearance of the osteolytic lesion was 9 years after the operation. Most of the cavities were seen in Gruen zones 3, 5 and 7 in decreasing order. Loosening of the stem and acetabular wear were the more influential factors in the progression of cavities [46]. Stem fracture was initially the most common complication, but it has been totally eliminated because of stronger stems with a better geometry and an improved method of stem fixation. Stem fracture, proximal endosteal cavitation and aseptic stem loosening have been identified as a consequence of having a lack or loss of proximal stem support and consequently good distal fixation. By closing off the medullary canal distally with an intra-medullary cement restrictor, the success rate was attained in 99% at 10 years in patients with a mean age of 41 years [47]. Improvements and modifications in surgical technique, design and even materials, have formed an integral part of the evolutionary progress. The introduction of the tripletapered polished stem – the C-Stem – (DePuy, Leeds, UK) has improved the femoral changes in most of the cases [25, 48]. Series using a polished double-tapered Exeter stem show even better results than those using a Charnley prosthesis. Fowler et al. report [23], in a series with the first 426 polished Exeter stem with an average follow-up of 13.4 years, 1.64% of aseptic stem loosening and 1.87% of stem fractures. Ling reported a revision rate for aseptic loosening of 2.15% at an average follow-up of 17 years [22]. The early series also showed a 93.1% survival of the stem in the 33rd year of follow up [49]. In 1988, a modular version of the original doubletapered polished collarless Exeter stem was introduced. It retained a similar geometry to the original Exeter stem and was tapered throughout its length, with a morse taper at the end of the neck. This allowed a range of head sizes and offsets to be used with the stem. Using third-generation cementing techniques and with a mean follow-up of 9 years, the modular universal Exeter stem revealed a mean subsidence of 1.32 mm without migration at the cement-bone interface. Localised endosteal lysis was only seen in one hip (0.5%). At a followup of 12 years, survivorship, with revision of the femoral component for aseptic loosening as an end-point, was 100% [50]. Scandinavian hip registers present large numbers of implants used in a variety of Institutions by a variety of Surgeons. The Norwegian Arthroplasty Register showed that, of 4,776 hips reviewed, the polished Exeter stem had a 12-year survival rate for aseptic stem loosening of approximately 98% [13]. The Swedish National Total Hip Arthroplasty register showed the polished Exeter stem to
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have a 9-year survival rate for aseptic loosening of 96% for 3,380 hips implanted after 1987 [14]. Scandinavian hip registers and RSA studies have clearly demonstrated the benefits of different designs such as the Lubinus SP II, Spectron EF, Bi-Metric, or Müller (straight) stems, and of the modern cementing technique [12–15, 51].
Cemented Acetabular Component Loosening of the acetabular cup, although uncommon in the first years after implantation, became apparent after 10 years. Garcia-Cimbrelo and Munuera reported that, in their study, early loosening of the cup, which was defined as occurring within the first 10 years after the operation, was related to mild deficiency of acetabular coverage in congenital dysplasia, a previous acetabular fracture and acetabular protrusion [33]. The authors recommended preservation or reconstruction of a solid acetabular covering with use of autogenous graft or allografts, if necessary (Fig. 4) [52, 53]. However, the only apparent risk factor for late cup loosening, occurring more than 10 years after the operation, was depth of acetabular wear. In vitro studies demonstrating excessive wear in polyethylene cups sterilised using gamma irradiation and stored in air led to the abandonment of this sterilization technique. Williams et al. measured penetration in 33 Charnley Ogee cups implanted for more than 20 years and sterilised using the gamma irradiation in air technique [54]. The authors stated that if degradation occurred in vivo over time, it was not reflected by an increased penetration rate; even 20 years after implantation, the degree of wear remained low. Williams et al. report an average penetration rate of 0.11 mm/ year [54]. Gamma irradiation has been used for a long time and most of the clinical data compiled so far have been on material gamma-irradiated in air. These data indicate that although this sterilisation method may be detrimental to overall wear performance, the problem is not catastrophic. Furthermore, if the degradation of polyethylene does continue in vivo, this has had no measurable effect on the penetration rate over the 20-year implantation period [54].
The Cemented Prosthesis in Young Patients Since cemented total hip arthroplasties (THA) have commonly been reported to give poor results in young patients, cementless THAs are widely used in these patients. The poor results of the cemented prosthesis have been attributed to the greater level of activity in young patients. Most of the
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series with poor results followed young patients for only a short time and used different implant designs. We assessed 67 Charnley low-friction arthroplasties in patients under 40 years [55]. The mean age was 32.4 years, and the mean follow-up until revision or the most recent evaluation was 21.7 years. Although primary osteoarthrosis is the most frequent diagnosis leading to THA in general series, these younger patients did not present this diagnosis. Pre-operative diagnoses reflected some bone deficiency in the acetabular structure, such as congenital dysplasia of the hip, acetabular fracture, acetabular protrusio, or rheumatoid arthritis. We used an old surgical technique employing a lateral approach with a trochanteric osteotomy and the insertion of the then-standard Charnley components. No grafts or metallic re-inforcement devices were used to reconstruct the acetabulum, and only cement was used to fill the acetabular defects. Cement was packed in both components with thumb pressure. There were 19 revisions: 18 cups and 12 stems; in only one hip was the stem alone revised. At 24 years, the total cumulative probability of not having cup loosening was 60% according to the Kaplan-Meier data. Early cup loosening appearing before 10 years post-op was related with diagnoses in which there was an acetabular bone defect (congenital hip dysplasia, acetabular fracture, or acetabular protrusio), while late cup loosening appearing after 10 years post-op was only related with polyethylene wear. The mean annual rate of cup wear was 0.12 mm/year for the entire series, 0.16 mm/year for the revised cups and 0.11 mm/year for the other cups. Increased wear was associated with increased rates of cup loosening and cup revision (p = 0.0044). The cumulative probability of not having stem loosening was 74%. Stem loosening was related with varus position, cement defect, femoral osteolysis and cement fracture. The two major factors limiting the longevity of the cemented LFA (low-friction arthroplasty) cup in this series were acetabular bone quality and polyethylene wear. These findings indicate that the acetabulum must be reconstructed with grafts or metallic devices when necessary, before the cup is implanted in order to ensure sufficient fixation. Polyethylene wear is the other major factor in low-friction arthroplasty failure, so new biomaterials and designs, which seek to limit wear, such as alumina-on-alumina, metal-onmetal and cross-linked polyethylene, could theoretically be used in young patients. These results were obtained using older surgical techniques. Using contemporary cementing techniques, the results at 10–15 years are comparable to the 15-year results obtained in patients over 50-years old using a cementless prosthesis. In a series containing 130 Exeter Universal stems in patients 50 years or younger with a minimum follow-up of 10 years, 12 hips have been revised, nine of which had
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a
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c
d b
Fig. 4 Antero-posterior radiographs of a hip with acetabular protrusion in a 66-year-old woman with a Charnley arthroplasty without cancellous autograft (a). Cup loosening was found 4 years after operation (b). Antero-posterior radiographs of a pelvis with bilateral acetabular protrusion in a 62-year-old woman
before operation (c). Post-operative radiograph of the same woman treated with two Charnley arthroplasties using cancellous autograft from the femoral head showing a normal structure of cancellous bone without resorption (d)
aseptic cup loosening. Radiographs show that 12.8% of the remaining acetabular prostheses were loose but no femoral loosening was found in this series. The sockets revised for aseptic loosening were associated with higher linear wear rates than the group as a whole. High rates of socket wear result in large volumes of particulate polyethylene debris, which stimulates osteolysis at cement-bone interface. Survivorship of the stem from any cause was 99% and no stem was revised for aseptic loosening [56]. The best midterm results with the modern cementless designs, particularly
those using hydroxyapatite-coated stems, are no better than those obtained with contemporary cemented techniques [57]. There is no study of these designs with a 25-year follow-up yet available, so we cannot compare the long-term results [58, 59]. The existing studies, all with patients under 50-years old report worse survival than with the cemented Exeter stem. It is expected, when a cemented Exeter stem is coupled with acetabular components that are less prone to wear, that there will be further improvement in overall performance [56].
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Table 1 Evolution of cementing techniques
First generation
Second generation
Third generation
Bone-bed preparation Cement restrictor Cement Cement introduction Pressurisation Cement mixing
Limited No High viscosity By hand Digital Hand
Pulsatile lavage Yes Low viscosity By cement gun Pressuriser Vacuum-mixing
Stem centraliser
No
Irrigation Yes Low viscosity By cement gun Pressuriser Open atmosphere, mixing by hand No
Contemporary cementing techniques aim to improve the mechanical interlock between bone and cement in order to obtain a durable interface [60]. Evolution of cementing techniques is detailed in Table 1. Improved outcome has been proven with meticulous bone preparation and preservation, use of a cement restrictor, pulsatile lavage, cement application via gun, and sustained cement pressurisation using a pressuriser. Evidence has also been reported for a better outcome using vacuum-mixing of bone cement and a distal femoral stem centraliser [60].
The Current Cementing Technique Pre-Operative Planning Pre-operative planning is a mandatory step before surgery; it determines optimal offset and leg- length by using templates. This planning is especially indicated in situations such as congenital dysplasia, acetabular protrusion, achondroplasia, etc. In these cases, the need for custom implants or bone transplants must be checked. We also must formulate the surgical approach and determine the size and placement of the femoral neck osteotomy, intr-medullary plug and stem centraliser.
Positioning of the Patient and Surgical Approach Patient position should always be checked by the surgeon to ensure the pelvis is fixed as rigidly as possible. Any displacement of the hip during manipulation leads to a high risk of incorrect placement of the acetabular component. Although different approaches can be made, we prefer the postero-lateral approach. Common sense indicates that the surgeon ought to use the smallest incision possible in order to produce minimal trauma in soft tissues; this is obtained by careful splitting of muscles and partial incision of capsular soft tissue, but an adequate exposure of the acetabulum
Yes
and the proximal femur must always exist so as to avoid complications. Minimally-invasive surgery does not compromise the result of the THA, but if there is any doubt, it is better to make a more extensive incision.
Acetabular Cup Preparation The acetabular component must be completely contained under the roof of the acetabulum. This usually requires deepening the acetabulum by a variable amount to ensure medial component placement. It is important to remove central osteophytes, but be sure to respect the transversal ligament in order to obtain optimal pressurisation when the cup is cemented. The acetabulum must be reamed at the anatomical site to the size determined during pre-operative planning, and part of the subcondral bone must be preserved. The reaming should be over-sized so as to allow a 2–3 mm cement mantle. If the acetabular roof is deficient or dysplastic, an acetabular roof graft could be necessary. It is important to understand the biomechanical consequences of reaming the acetabulum. The most common mistake is made by reaming the acetabulum on its natural 45° axis, which can put the centre of the cup higher than the anatomical level, especially when there is any lateral femoral subluxation is present. So, the first reamer must be directed transversely to reach into the inner floor. The next reamers are directed superiorly to enlarge the cavity (Fig. 5), but no attempt should be made to remove the eburnated roof sclerosis. In order to remove as little bone as possible, it is necessary to drill and/or impact five to eight holes, 6 mm deep, in the cranial and central aspect of the acetabulum. These anchorage holes increase the contact area between bone and cement, providing better fixation. After that, soft tissue and loose cancellous bone are removed with a brush and then pulsed-lavage in order to obtain a micro-interlock, using repeated high-pressure lavages. Always use a nozzle with front-facing orifices and a splash-shield. Irrigation not only renders white strands of any soft tissue remnants visible, but also effectively removes blood and bone marrow
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Fig. 5 The first reamer is directed transversely to reach the inner floor (a) before upward reaming is done. The reamer is kept inferior in close contact to the transverse ligament (b)
from the bone interstices, thus aiding cement penetration. A sponge impregnated with adrenaline or liquid hydrogen peroxide is adequate to secure haemostasis. In contrast to the femur, a higher viscosity cement is preferred for cup implantation in order to reduce the risk of blood laminations at the interface. In the acetabulum the cement is applied en bloc, so immediate pressurisation can be implemented [61]. In order to minimise blood lamination, the cement is normally applied 3–4 min after beginning the mixing procedure (depending on the type of cement). Pressure is applied with an acetabular pressuriser and maintained until the cement is sufficiently doughy. The time will vary (average 2–3 min) with the type of cement used. Collected data has shown that high pressurisation is needed to achieve micro-interlock. This reaffirms the necessity of working in a contained cavity and not removing the transverse ligament. The introduction and alignment of the cup is the most difficult part of the operation. An acetabular cup diameter of at least 4 mm smaller in diameter than the largest reamer used is choosen to ensure a 2–3 mm cement mantle around the cup. The acetabular component is inserted using the cup holder. Applying the same principle as when preparing the socket, the cup is inserted horizontally and pushed fully medially first, before gradually angulating it to the desired inclination of 45° [61]. Then a cup pressuriser with a ball is inserted to maintain pressure on the cement. Reduction of so-called third body wear is of the greatest importance to protect the cup.
Femur: Bone Bed Preparation A straight reamer is used to open the femoral canal. Be sure to open both the posterior and lateral walls sufficiently. The cortical bone of the piriformis fossa is breached using an
initial trochar awl. A “T” –handle canal finder with a blunt section is rotated and inserted while maintaining the posterior calcar bone contact. Insufficient reaming will make it impossible to align the femoral stem properly in both planes. Start with the smallest available rasp impactor and increase until the size determined at pre-operative planning has been achieved. Be prepared to use a flexible reamer to enlarge the isthmus if necessary. Before introducing the cement, the medullary canal is cleaned with copious pulsatile lavage [41]. Ideally this should even be done before templating for the cement restrictor to reduce the risk of fat embolism. We determine plug size using the special instrument or a flexible reamer. Insert the appropriate distal femoral plug. Place the plug 1.5–2 cm distal to the intended level of the tip of the stem and remove soft tissue and loose cancellous bone with a femoral brush. It is necessary to rotate the brush counterclockwise to remove debris from the femur. The cleaning sequence is continued with repeated high-pressure pulse lavages in order to facilitate micro-interlock between bone and cement. This will also prevent micro-embolisation of the marrow contents and significantly minimise circulatory changes. Use a nozzle with side orifices, so the pulse lavage can act perpendicular to the bone surface. Secure haemostasis with an adrenaline or liquid hydrogen peroxideimpregnated sponge. Eighty grams of cement is normally sufficient for stem fixation. The cement is mixed and collected in the cartridge under vacuum. The cartridge is then positioned in the cement gun. Make a final pulse lavage before injecting the cement. Cement delivery uses a long nozzle in order to reach the distal femoral plug. Inject the cement in retrograde fashion, letting the cement gun work its own way out of the femur. The cement should never be delivered in low viscosity stage [62]. Normally, wait approximately 3 min (depending
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on type of cement used) after starting mixing. Apply the proximal seal and pressurise the cement. A positive sign of pressurisation is marrow extrusion in the greater trochanter (the so-called sweating trochanter sign). As with the acetabulum, maintain pressure until the cement is sufficiently doughy to withstand bleeding. The time varies with the of cement used. The distal centraliser should be used to avoid malposition of the stem in both planes. If pressurisation is adequate and timing (depending on viscosity) is correct, full cement penetration has been achieved at this point. The femoral stem is inserted slowly in line with the longitudinal axis of the femur using sustained manual pressure. During the insertion process, a slight posterior pressure is applied to direct the stem tip anteriorly and achieve good component alignment [61]. When centralisers are used, the stem should not be inserted too late, as the centraliser will disrupt the cement causing voids and laminations.
Conclusions THA with use of cement continues to be the treatment of choice for severe degeneration of the hip in older and relatively inactive patients. Various versions of the cemented prosthesis design have been used for 40 years with excellent results. Cemented, polished, tapered femoral stems offer a wellestablished option for satisfactory long-term clinical results in THA. The stems maintain proximal bone through hoop stresses and subside to positions of stability. They have been shown to be associated with extremely low rates of aseptic loosening. Modern cementing techniques are also now wellunderstood. A good cement technique requires a distal void, usually within the centraliser, to allow subsidence without cement fracture. Cement mantle defects must be avoided because they provide a passage for debris to reach the endosteal surface of the femur [42]. The recommended optimal cement mantle thickness is not universally agreed, and varies with different prostheses.
References 1. Charnley J. The long-term results of low-friction arthroplasty of the hip performed as a primary intervention. J Bone Joint Surg [Br] 1972;54-B:61–6.
E. Garcia-Cimbrelo 2. Wroblewski BM. 15–21-year results of Charnley low-friction arthroplasty. Clin Orthop 1986;211:30–5. 3. Joshi AB, Porter ML, Trail IA, Hunt LP, Murphy JCM, Hardinge K. Long-term results of Charnley low-friction arthroplasty in young patients. J Bone Joint Surg [Br] 1993; 75-B:616–23. 4. Schulte KR, Callaghan JJ, Kelley SS, Johnston RC. The outcome of Charnley total hip arthroplasty with cement after a minimum twenty-year follow-up: The results of one surgeon. J Bone Joint Surg [Am] 1993;75-A:961–75. 5. Garellick G, Herberts P, Strömberg C, Malchau H. long-term results of Charnley arthroplasty. A 12–16-year followupstudy. J Arthroplasty 1994;9:333–40. 6. Wroblewski BM, Siney PD, Fleming PA. Charnley low friction arthroplasty. Survival patterns to 38 years. J Bone Joint Surg [Br] 2007;89-B:1015–8. 7. Harris WH, McCarthy JC Jr, O’Neill DA. Femoral component loosening using contemporary techniques of femoral cement fixation. J Bone Joint Surg [Am] 1982;64-A:1063–7. 8. Mulroy RD Jr, Harris WH. The effect of improving cementing techniques on component loosening in total hip replacement. An 11-year radiographic review. J Bone Joint Surg [Br] 1990;72-B:757–60. 9. Oishi CS, Walker RH, Colwell CW Jr. The femoral component in total hip arthroplasty. Six to eight-year follow-up on one hundred consecutive patients after use of a third-generation cementing technique. J Bone Joint Surg [Am] 1994;76-A: 1130–6. 10. Ballard WT, Callaghan JJ, Sullivan PM, Johnston RC. The results of improved cementing techniques or total hip arthroplasty in patients less than fifty years old. A ten-year followup study. J Bone Joint Surg [Am] 1994;76-A:959–64. 11. Klapach AS, Callaghan JJ, Gotees DD, Olejmiczak JP, Johnston RC. Charnley total hip arthroplasty with use of improved cementing techniques. A minimum twenty-year follow-up study. J Bone Joint Surg [Am] 2001;83-A:1840–47. 12. Garellick G, Malchau H, Herberts P. Survival of hip replacements. A comparison of a randomized trial and registry. Clin Orthop 2000;375:157–67. 13. Furnes O, Lie SA, Espehaug B, Vollset SE, Engesaeter LB, Havelin LI. Hip disease and the prognosis of total hip replacements. A review of 53698 primary total hip replacements reported to the Norwegian arthroplasty register 1987–1999. J Bone Joint Surg [Br] 2001;83-B:579–86. 14. Malchau H, Herberts P, Eisler T, Garellick G, Soderman P. The Swedish total hip replacement register. J Bone Joint Surg [Am] 2002;84(Suppl 2):2–20. 15. Havelin LI, Espehaug B, Engesaeter LB. The performance of two hydroxyapatite-coated acetabular cups compared with Charnley cups. From the Norwegian arthroplasty register. J Bone Joint Surg [Br] 2002;84-B:839–45. 16. Shen G. Femoral stem fixation: An engineering interpretation of the long-term outcome of Charnley and Exeter stems. J Bone Joint Surg [Br] 1998;80-B:754–6. 17. Dunlop DJ, Masri BA, Greidanus NV, Garbuz DS, Duncan CP. Tapered stems in cemented primary total hip replacement. In: Beaty JH (ed), Instructional course lectures. Rosemont,
How to Do a Cemented Total Hip Arthroplasty American Academy of Orthopaedic Surgeons, 2002, vol. 51, ch. 10, pp. 81–91. 18. Bell CGR, Weinrauch P, Pearcy M, Crawford R. In vitro analysis of Exeter stem torsional stability. J Arthroplasty 2007;22:1024–30. 19. Alfaro-Adrian J, Gill HS, Murray DW. Cement migration after THR. A comparison of Charnley Elite and Exeter femoral stems using RSA. J Bone Joint Surg [Br] 1999;81-B:130–4. 20. Hauptfleisch J, Glyn-Jones S, Beard DJ, Gill HS, Murray DW. The premature failure of the Charnley Elite-Plus stem. A confirmation of RSA predictions. J Bone Joint Surg [Br] 2006;88-B:179–83. 21. Alfaro-Adrian J, Gill HS, Murray DW. Should total hip arthroplasty femoral components be designed to subside? A radiosterometric analysis study of the Charnley Elite and Exeter stems. J Arthroplasty 2001;16:598–606. 22. Ling RS. The use of a collar and precoating on cemented femoral stems is unnecessary and detrimental. Clin Orthop 1992;285:73–83. 23. Fowler JL, Gie GA, Lee AJ, Ling RS. Experience with the Exeter total hip replacement since 1970. Orthop Clin North Am 1988;19:477–89. 24. Friedman RJ, Black J, Galante JO, Jacobs JJ, Skinner HB. Current concepts in orthopaedic biomaterials and implant fixation. J Bone Joint Surg [Am] 1993;75-A:1086–109. 25. Ek ET, Choong PFM. Comparison between triple-tapered and double tapered cemented femoral stems in total hip arthroplasty. A prospective study comparing the C.Stem versus the Exeter Universal early results after 5 years of clinical experience. J Arthroplasty 2005;20:94–100. 26. Scott G, Freeman M, Kerboull M. Femoral components: The French paradox. In: Breush SJ and Malchau H (eds), The wellcemented total hip arthroplasty. Theory and practice. Springer, Berlin; 2005, pp. 249–53. 27. Langlais F, Kerboull M, Sedel L, Ling RSM. The French paradox. J Bone Joint Surg [Br] 2003;85-B:17–20. 28. Kerboull L, Hamadouche M, Courpied JP, Kerboull M. Longterm results of Charnley-Kerboull hip arthroplasty in patients younger than 50 years. Clin Orthop 2004;418:112–18. 29. Hamadouche M, Baqué F, Lefevre N, Kerboull M. Minimum 10-year survival of Kerboull cemented stems according to surface finish. Clin Orthop 2008;466:332–9. 30. Howie DW, Middleton RG, Costi K. Loosening of matt and polished cemented femoral stems. J Bone Joint Surg [Br] 1998;80-B:573–6. 31. Collis DK, Mohler CG. Comparison of clinical outcomes in total hip arthroplasty using rough and polished cemented stems with essentially the same geometry. J Bone Joint Surg [Am] 2002;84-A:586–92. 32. Shetty NR,Hamer AJ, Kerry RM, Stockley I, Eastell R, Wilkinson JM. Bone remodelling around a cemented polyethylene cup. A longitudinal densitometry study. J Bone Joint Surg [Br] 2006;88-B:455–9. 33. Garcia-Cimbrelo E, Munuera L. Early and late acetabular loosening in low friction arthroplasty. J Bone Joint Surg [Am] 1992;74-A:1119–29. 34. Garcia-Cimbrelo E, Diez-Vázquez V, Madero R, Munuera L. Progression of radiolucent lines adjacent to the acetabular
187 component and factors influencing migration after Charnley low-friction total hip arthroplasty. J Bone Joint Surg [Am] 1997;79-A:1373–80. 35. Hodgkinson JP, Maskell AP, Paul A, Wroblewski BM. Flanged acetabular components in cemented Charnley hip arthroplasty. Ten-year follow-up of 350 patients. J Bone Joint Surg [Br] 1993;75-B:464–7. 36. Shelley P, Wroblewski BM. Socket design and cement pressurization in the Charnley low-friction arthroplasty. J Bone Joint Surg [Br] 1988;70-B:358–63. 37. Della Valle CJ, Kaplan K, Jazrawi A, Ahmed S, Jaffe WL. Primary total hip arthroplasty with a flanged, cemented allpolyethylene acetabular component: Evaluation at a minimum of 20 years. J Arthroplasty 2004;19:23–6. 38. Parsch D, Diehm C, Schneider S, New A, Breusch SJ. Acetabular cementing technique in THA – Flanged versus unflanged cups, cadaver experiments. Acta Orthop Scand 2004;75: 269–75. 39. Breusch SJ, Kühn KD. Bone cements based on polymethylmethacrylate. Ortopaede 2003;32:41–50. 40. Harper EJ, Bonfield W. Tensile characteristics of ten commercial acrylic bone cements. J Biomed Mat Res 2000;53: 605–16. 41. Breusch SJ, Norman TL, Schneider U, Reitzel T, Blaha D, Lukoschek M. Lavage technique in total hip arthroplasty: Jet lavage produce better cement penetration than syringe lavage in the proximal femur. J Arthroplasty 2000;15:921–7. 42. Anthony PP, Gie GA, Howie CR, Ling RS. Localised endosteal bone lysis in relation to the femoral components of cemented total hip arthroplasties. J Bone Joint Surg [Br] 1990;72-B:971–9. 43. Gruen TA, McNeice GM, Amstutz HC. “Modes of failure” of cemented stem-type femoral components. Clin Orthop 1979; 171:17–27. 44. Older J. Charnley low-friction arthroplasty. A worldwide retrospective review at 15 to 20 years. J Arthroplasty 2002;17: 675–80. 45. Munuera L, Garcia-Cimbrelo E. Femoral component after ten years in low friction arthroplasty. Clin Orthop 1992; 279:163–75. 46. Garcia-Cimbrelo E, Madero R, Blasco-Alberdi A, Munuera L. Femoral osteolysis after low-friction arthroplasty. A planimetric study and volumetric estimate. J Arthroplasty 1997;12: 624–34. 47. Wroblewski BM, Fleming PA, Siney PD, Hall RM. Stem fixation in the Charnley low friction arthroplasty in young patients using an intramedullary bone block. J Bone Joint Surg [Br] 1998;80-B:273–8. 48. Wroblewski BM, Siney PD, Fleming PA. Triple taper polished cemented stem in total hip arthroplasty. J Arthroplasty 2001;16(8):37–41. 49. Hubble MJW, Timperley J, Ling RSM. Femoral components: Long-term success with a double tapered polished straight stem. In: Breush SJ and Malchau H (eds), The well-cemented total hip arthroplasty. Theory and practice. Springer, Berlin, 2005, pp. 228–34. 50. Williams HD, Browne G, Gie GA, Ling RS, Timperley AJ, Wendover NA. The Exeter cemented femoral component at
188 8–12 years-a clinical, radiological and survivorship study of the first 325 cases. J Bone Joint Surg [Br] 2002;84-B:324–34. 51. Kärrholm J, Borssen B, Lowenhielm G, Snorrason F. Does early micromotion of femoral stem prostheses matter? 4–7 year stereoradiographic follow-up of 84 cemented prosthesis. J Bone Joint Surg [Br] 1994;76-B:912–7. 52. Garcia-Cimbrelo E, Munuera L. Low friction arthroplasty in severe acetabular dysplasia. J Arthroplasty 1993;8:459–69. 53. Garcia-Cimbrelo E, Díaz-Martín A, Madero R, Munuera L. Loosening of the cup after low-friction arthroplasty in patients with acetabular protrusion. The importance of the position of the cup. J Bone Joint Surg [Br] 2000;82-B:108–15. 54. Williams S, Isaac G, Porter N, Fisher J, Older J. Long-term radiographic assessment of cemented polyethylene acetabular cups. Clin Orthop 2008;466:366–72. 55. Garcia-Cimbrelo E, Cruz-Pardos A, Cordero J, SanchezSotelo J. Low-friction arthroplasty in patients younger than 40 years. 20- to 25-year results. J Arthroplasty 2000;15:825–32. 56. Lewthwaite SC, Squires B, Gie GA, Timperley AJ, Ling RSM. The Exeter™ Universal hip in patients 50 years or younger at 10–17 years’ follow-up. Clin Orthop 2008;466: 324–31.
E. Garcia-Cimbrelo 57. Kim Y-H, Oh S-H, Kim J-S, Koo K-H. Comtemporary total hip arthroplasty with and without cement in patients with osteonecrosis of the femoral head. J Bone Joint Surg [Am] 2003;85-A:675–81. 58. Duffy GP, Prpa B, Rowland CM, Berry DJ. Primary uncemented Harris-Galante acetabular components in patients 50 years old or younger. Results a 10 to 12 years. Clin Orthop 2004;427:157–61. 59. McAuley JP, Szuszczewicz ES, Young A, Engh CA Sr. Total hip arthroplasty in patients 50 years and younger. Clin Orthop 2004;418:119–25. 60. Breusch SJ, Malchau H. Optimal cementing technique – The evidence: What is modern cementing technique? In: Breush SJ and Malchau H (eds), The well-cemented total hip arthropalsty. Theory and practice. Springer, Berlin, 2005, pp. 146–9. 61. Breusch SJ, Malchau H, Older J. Operative steps: Acetabulum and Femur. In: Breush SJ and Malchau H (eds). The wellcemented total hip arthropalsty. Theory and practice. Springer, Berlin, 2005, pp. 16–36. 62. Dayton MR, Incavo SJ, Churchill DL,Uroskie JA, Beynnon BD. Effects of early and late stage cement intrusion into cancellous bone. Clin Orthop 2002;405:39–45.
How to Do a Cementless Hip Arthroplasty Klaus-Peter Günther, Firas Al-Dabouby, and Peter Bernstein
Introduction Since the early 1960s, when Sir John Charnley was performing cemented total hip replacement (THR) regularly with good results, techniques and component designs have been improved substantially. At that time THR was mainly an operation for elderly patients crippled with arthritis. Today, however, young patients with hip disease increasingly hope to restore their quality of life, which typically includes physically-demanding activities. As cement fixation can break down over time, there has been considerable effort and research especially in trying to enhance the methods of fixation. The goal was to create a living type of bond between implant and bone, which would be longer-lasting and stronger than the cement-bone-interface. Advances in bioengineering technology have driven the development of cementless hip implants with textured surfaces, which allow bone ingrowth. Recent studies suggest, that uncemented hips can provide durable fixation as well as cemented implants. In addition, better materials and designs have allowed the use of large-diameter bearings which provide an increased range of motion with enhanced stability and very low wear. Less invasive surgery can limit soft-tissue damage and might facilitate accelerated discharge and rehabilitation. Currently, studies are being performed to evaluate whether computerassisted surgery can contribute to reproducible and accurate placement of implants, which is still a crucial factor for long-term survival especially in uncemented THR. We will briefly describe the different anchorage concepts of the most popular uncemented implants and available
Klaus-Peter Günther () Department of Orthopaedic Surgery, University Hospital Carl Gustav Carus Dresden, Fetscherstr. 74, D-01307 Dresden, Germany e-mail:
[email protected]
bearing materials. Then – after an overview on widely-used surgical approaches – a very basic description of implantation technique, potential complications and rehabilitation principles is provided. In order to compare different implant and approach philosophies, a short summary of available long-term studies will be presented. As this lecture is focussing on conventional hip replacement, recent alternatives (surface replacement and shortstemmed implants such as “bone-preserving” prosthesis) are not discussed in depth.
Implant Selection Cementless Acetabular Cups The rationale for cementless fixation lies in the surface structure of implant components that should allow bone ongrowth. To secure a long-term fixation of uncemented implants, two important factors must be provided: primary stability and secondary long-term osseointegration. Primary acetabular stability is obtained by either inserting pressfit cups (with or without additional screws) or inserting threaded cups (Fig. 1). To support osseointegration, most current implants are made of pure titanium or a titaniumaluminum alloy. A rough surface area – produced by corundum blasting, titanium-plasma spray, titanium balls, nets or other grid designs – is essential for osseointegration. To allow for any osseous ongrowth, a 20 µm minimum porosity is required. To actually achieve osseointegration and vascularization, porosity can be between 100 and 1,500 µm. During the recent years, hydroxyapatite (HA) coating has been advocated to improve and secure osseointegration. HA-coating achieves the closing of micro-defects in the implant-bone interface, thus preventing clefts for wear debris entry.
G. Bentley (ed.), European Instructional Lectures. European Instructional Course Lectures 9, DOI: 10.1007/978-3-642-00966-2_19, © 2009 EFORT
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Fig. 1 Cementless press-fit cup and stem with proximal fixation (left side); threaded cup and stem with meta-diaphyseal fixation (right side)
Press-fit Cups
Threaded Cups
Most press-fit cups have a hemispherical design. The principle of implant press-fit is based on force transmission over the equator of the cup (mainly in the ilioischial direction) which requires: ● A 1–2 mm oversize of the implant diameter compared to the reamed bone bed. When this difference is missed (exact fit technique), additional screwing might be necessary to secure primary implant fixation. If the acetabular under-reaming exceeds 3–4 mm, the risk of acetabular fracture rises. ● A flat-bottom pole to avoid the rim bulging over the bony circumference. This design allows for a more tilt-secure position and is responsible for polar bone atrophy, which itself demonstrates the new force transmission balance. A circumferential closed bone rim avoids PE-distribution to the bone bed. ● A certain surface porosity that ensures additional primary stability through friction.
The main advantage of threaded cups is an arbitrary selection of implant position, which can be helpful especially in acetabular protrusion or hip dysplasia with poor bone quality. Additionally hemispherical threaded cups require less bone resection than press-fit designs. Cup design and thread geometry are decisive for the implant performance during the screw-in process and positioning. A conical-shaped threaded cup guarantees high tilting stability and requires a less exact preparation of the bone bed [1]. However, threaded cup implantation requires good sensing of insertion torque slope and the final seating point to achieve optimal stability and avoid overturning. In addition a correction of cup position after the first threads – which can be still applied in press-fit cups – is not anymore possible.
Some Surgeons prefer cups with additional stabilization through screws, pegs, rings, fins, spikes or hollow cylinders. These modifications, however, can alter the mechanical responses of the acetabular host bone significantly.
Several stem designs are available on the market. The stem, is responsible for the fixation of the prosthesis and for transmitting forces to the bone. Therefore in nearly all stem types adaptive bone changes of the proximal femur can
Cementless Stems
How to Do a Cementless Hip Arthroplasty
be observed after several years and they vary according to design geometry, biomaterials and surface texture. The types of fixation are epiphyseal (the femoral head is covered by a cup prosthesis), metaphyseal and meta-diaphyseal (with straight or anatomically-shaped monoblock-prostheses of different lengths, modular and custom-made prostheses) and diaphyseal (using predominantly modular systems). In primary cementless THR most stems are either straight or anatomically-shaped monoblock-prostheses, which rely on metaphyseal or meta-diaphyseal anchorage concepts (Fig. 1): ● Proximal (metaphyseal) fixation: The concept is based on the preservation of proximal bone and fixation without an attempt to fill the canal distally. Although many implants have been developed, one of the most popular representatives of this philosophy in Europe is the “Spotorno stem” [2]. It’s high initial stability depends on a series of flutes or ribs on the proximal anterior and posterior aspects of the tapered, straight, grit-blasted titanium stem which, with its rectangular cross-section, provides an interference fit in the femur. A slim diaphyseal part of the stem, without distal canal fill, leads to mainly metaphyseal load transfer without distal cortical hypertrophy as a result of stress-shielding. ● In contrast to the straight design of the Spotorno stem, several other prosthesis are anatomically-shaped. Although these stems with a mild curvature do not show a generally better survival, they are easier to implant with the antero-lateral and anterior approach. ● In recent years, short-stemmed prostheses have been developed, which claim neck-sparing and thus bonepreserving implantation. As this concept – as well as the resurfacing technique – is still under observation, we will not specifically address it within this article. ● Meta-diaphyseal fixation: The classic representative of this philosophy is the “Zweymüller” stem. This cementless, tapered, rectangular titanium stem was introduced in the early eighties and the concept is still very popular in Europe [3]. The rectangular geometry avoids the need to ream the femoral canal and advocators of this concept argue, that the conservative bone preparation reduces damage to the endosteal circulation. Cortical thickening, however, could be observed in severeal series and seems to be probably due to the concentration of focal stress in the transitional zone between the stiff area around the stem and the elastic area distal to the implant [4]. In spite of the frequency of this radiographic phenomenon, it is not related to stem loosening or inferior clinical outcome.
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Stems with diaphyseal fixation are mostly modular and mainly used in revision surgery. For primary THR they offer an advantage of independent adjustment of anteversion, which can be important in deformed femora after a history of dysplasia or femoral osteotomy. Conical stems can also be implanted independent from the underlying femoral anteversion and might therefore be indicated in special situations. All implants should provide a possibility to reconstruct adequately the femoral offset. This can be obtained through stem designs with different neck-stem angles, different offset versions (regular and increased offset) or modular neck concepts. Although different implant materials are available, most cementless stems are made of titanium or titanium alloys. The flexibility of titanium stems seems to prevent severe stress-shielding, as the Young’s modulus of elasticity of titanium is near to human bone. More rigid implants made of other materials (e.g., cobalt-chromiumalloys) tend to produce higher rates of proximal stressshielding and distal cortical thickening especially with diaphyseal fixation. Most cementless stems have some kind of surface modification to enhance osseointegration. As in cementless cups a rough surface area – produced by corundum blasting, titanium-plasma spray, titanium balls, nets or other grid designs – can stimulate osteoblast activity. Additionally, some implants are also coated with Hydroxyapatite. As proximal bone stress-transfer has been thought to be less in association with proximally-coated stems as compared with extensively-coated stems, the latter have nearly disappeared from the market.
Bearing Materials Survivorship of total joint arthroplasty depends on the durability of fixation and durability of articulation. Therefore not only the appropriate choice of cup and stem implants is important, but also the bearing material. In cemented THR, metal-on-polyethylene articular couple has been the most widely-used. Polyethylene wear, however, has been identified as a major factor adversely influencing the durability of joint replacement. Therefore alternative bearings with lower wear rates have been developed and they offer improved survival especially for young and active patients with higher life expectancy, where cementless THR might be indicated. All “hard-on-hard bearings” have been shown to be associated with reduced wear [5].
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Metal-on-metal bearings have wear rates that are 20–100 times lower than metal on conventional polyethylene. However, metal-on-metal articulations may lead to local adverse responses (metallosis) and increased systemic levels of cobalt and chromium. Therefore patients with kidney dysfunction, child-bearing age or known metal sensitivities should not receive these couplings. Ceramic-on-ceramic bearings have been in clinical use for nearly 40 years. The wear rates are also very low, but potential disadvantages are the risk of component fracture (especially rim fractures due to impingement in cup malpositioning) and audible squeaking in a small number of patients. Recently ceramic-on-metal bearings have been introduced, which address these risks. Finally “Highly Cross-Linked” Polyethylene bearings have evolved into the most frequently used bearing material for total hip arthroplasty. The liners can be combined with metal as well as ceramic heads and show significantly less wear than conventional polyethylene. Due to a still limited observation time, we do not know enough at the moment about potential long-term risks (i.e., ageing of the material). Although the combination of cups, heads and stems from different manufacturers is theoretically possible, it should be avoided! In case of material problems (i.e., early component fracture) medical device directives acknowledge the responsibility of a manufacturer only if his certified implants had been combined. If surgeons combine products from different manufacturers, they become liable for the “new product”.
Surgical Technique Indication for Cementless Implants The first step of cementless THR is always to check the indication for this technique. Quantity as well as quality of host bone must be good enough to guarantee primary stability of the implant as well as susequent osseointegration. In patients with certain bone disorders or impaired bone metabolism (e.g., osteoporosis, osteomalacia) or a history of radiation exposure, initial bone strength and consecutive biological response might not be sufficient. With regard to the cup it must be considered if primary stability and circumferential bone contact can be achieved: ● Is the bone bed strong enough to resist the impaction force of a 1–2 mm oversized implant? ● Is there enough structural support to relay forces through the ischio-ilio-pubic columns of the acetabulum?
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● Is there any defect (e.g., in a dysplastic acetabulum) which might impair primary stability through insufficient contact area? In order to achieve a proper stem position and long-term fixation, the following questions must be addressed: ● Is the cortical bone strong enough to resist proper broaching and impaction of a cementless stem? ● Is the shape of the medullary canal appropriate for the selected stem type? ● Can previous osteotomies prevent proper broaching and cortical stem contact? ● Does the design of the selected stem allow for adequate reconstruction of offset and leg-length? Generally, the implantation of cementless THR is more appropriate in younger than in elderly patients, although there are no evidence-based age limits. A definite indication can be the documented allergy against components of bone cement.
Pre-Operative Planning Proper pre-operative planning and templating is one of the most important issues in THR. The choice of implants with adequate design and size depends on correct radiographs. For several reasons, an antero-posterior (a-p) view of the pelvis together with an axial view of the involved hip is mandatory. A weight-bearing a-p view of the pelvis allows grading of osteoarthritis, evaluation of acetabular as well as proximal femoral anatomy and proper measurement of leg-length discrepancies (together with the clinical investigation, which determines the presence of contractures). Modern computer programmes are offered for electronic templating (Fig. 2), but the elementary planning steps can also be performed very easily with appropriate drawing on template films (Fig. 3). Basic steps of planning are: ● Determination of correct hip centre: If possible, by projection from normal contra-lateral side. Alternatively, (in dysplastic hips with high dislocation), through determination of “true acetabular region” according to Ranawat (1980): A perpendicular line with a length of 20% of the pelvic height is plotted on the vertical of the Köhler line connecting the bottom of the teardrops. A parallel line of the same length is then drawn laterally, starting from the most proximal point of the first segment. Finally, the end-points of these two segments are connected with a line. The triangular area enclosed by these lines defines the anatomically correct acetabular region (Fig. 4).
How to Do a Cementless Hip Arthroplasty
Fig. 2 Pre-operative planning: example of electronic templating in a patient with hip osteoarthritis after failed pelvic osteotomy
Fig. 3 Conventional pre-operative planning in a patient with secondary hip osteoarthritis due to developmental dysplasia
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Fig. 4 (a) Estimation of correct hip centre and “true acetabular region” (see pre-operative planning) in a patient with hip dislocation due to acetabular dysplasia. (b) Post-operative radiograph
with reconstruction of correct hip centre via implantation of bone- and screw-augmented press-fit cup and conical stem
● Selection of appropriate cup size and position. ● Definition of femoral shaft axis and appropriate neckshaft angle (off-set). ● Determination of neck resection level and leg-length adjustment.
exposure of the acetabulum, facilitating cup positioning which may decrease rates of dislocation and the decreased risk of sciatic nerve injury which is not close to the operative field. Critics of the direct lateral approach suggest that the violation of the hip abductors may lead to delay in recovery of abductor strength and late Trendelenburg gait. The antero-lateral approach addresses the intermuscular plane between the gluteus medius and tensor fascia lata. The vastus lateralis muscle is left undisturbed. This approach provides sufficient anatomic orientation and exposure with minimal dissection and without excessive retraction. There is no danger of injury to the superior gluteal nerve or its branches. Due to the intact attachment of the gluteus medius, however, the insertion of straight stems (and reamers) can be difficult and might put the muscle under pressure. With this approach the implantation of so-called “anatomic” (curved) stems is preferred. The anterior approach between sartorius and tensor fascia latae muscles is avoiding any tension on the abductors at all. The acetabular exposure is very good and even the femur can easily be accessed with the hip in extension and/ or traction. Care must be taken to avoid damage of cutaneous femoral nerve branches. It is claimed that minimally-invasive surgical approaches for THR reduce soft-tissue trauma, decrease post-operative pain and blood loss, speed-up recovery and reduce the length of the hospital stay. These new procedures either use one small 6–10 cm incision through a posterior, lateral,
Choice of Surgical Approach Many different surgical approaches to the hip joint have been described. Currently, THR is most commonly performed via a posterior, an antero-lateral or a direct lateral (transgluteal) approach. Anterior as well as medial approaches are possible, but not as popular. The posterior approach is considered to be associated with less problems regarding gait, since the abductor muscles are not dissected and damage to the superior gluteal nerve is very unlikely. Disadvantages are a less reliable cup positioning and increased rates of dislocation. Adequate soft tissue repair by re-attachment of posterior capsule and external rotators, however, greatly reduces the relative risk of dislocation using the posterior approach. In the lateral approach a longitudinal incision of the fibres of the gluteus medius and minimus and the vastus lateralis muscles takes advantage of the tendinous junction of these muscles over the greater trochanter. The incision should not be extended too far cranially in order to protect the superior gluteal nerve. Proposed advantages are the good
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Fig. 5 Simultaneous bilateral hip replacement through a minimally-invasive (anterior) approach. (a) Pre-operative and (b) postoperative radiographs
antero-lateral or anterior approach. The “two-incisionapproach” (a short posterior incision for placement of the femoral component and an anterior incision for placement of the acetabular component) is more popular in the U.S.A. than in Europe. Controversy exists on whether these small incision THRs are actually minimally-invasive. It is debated whether a small skin incision that requires the application of high forces on the soft tissues for exposure of the joint but less muscle dissection will produce less overall trauma to the patient than a larger incision with wider muscle dissection but with lower retraction forces. Another question is whether decreased visualization provided by these techniques can ensure proper implant position and prevent neurovascular complications. A review of the literature to date provides no convincing evidence of any significant advantages of small incision THR compared with standard incision THR other than a shorter surgical scar [5]. There is also little evidence of the benefit of one minimallyinvasive approach over another in the literature. We have recently performed a prospective randomized trial to compare the functional outcome of two different less-invasive approaches (anterior and antero-lateral) with the conventional lateral approach and could only observe minor functional differences [6]. We therefore offer surgery through a minimally-invasive approach mainly for patients who demand this technique as well as in patients with bilateral simultaneous hip replacement (Fig. 5).
Basic Surgical Steps in Cementless THR As the sequence of surgical steps depends at least partially on the selected approach, we describe more general aspects of cup and stem implantation and give some additional remarks referring to different approaches when indicated.
Cup First or Stem First? Most surgeons tend to perform a stepwise approach with preparing and implanting the acetabular cup first followed by broaching and implanting the femoral stem. While the acetabular component inclination is relatively independent from femoral geometry and should be targeted between 30 and 50° (“safe zone” according to Lewinnek et al. [7]), proper anteversion of the cup depends at least partially on the amount of femoral version. In cementless THR the positioning of the stem with regard to anteversion or retroversion is more limited than in cemented implantation techniques, as uncemented stems must follow the natural geometry of the medullary canal to a certain degree. Therefore some surgeons prefer to broach the proximal femur after neck osteotomy first and to estimate the stem anteversion before implanting the acetabular cup. This offers the opportunity to adjust an appropriate cup anteversion in cases with abnormal femoral version and to avoid impingement and/or dislocation.
Femoral Neck Osteotomy After the capsule of the hip joint has been exposed, a capsulotomy is performed with an electrical knife. In anterior, antero-lateral and lateral approaches the anterior portion of the capsule can be excised. In the posterior approach the incision should leave an intact capsular flap – together with the released tendons of the short external rotators – which can be repaired at completion of arthroplasty. The femoral head is then dislocated (depending on the approach anteriorly or posteriorly), and the neck of the femur is osteotomized at the pre-determined level. In cases where the femoral head is deformed or enlarged, it can be broken into fragments to facilitate removal, removing the
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head piece by piece. Another alternative is to perform two parallel cuts through the neck and remove the fragment inbetween the cuts first. This can reduce tension and allows removal of the head easily. Then the distance between the lesser trochanter and the performed cut is controlled by palpation in order to check whether the pre-operatively planned level of neck osteotomy has been realized. This is also a good moment to perform an additional release of tight capsular remnants or contracted short external rotators in anterior, antero-lateral or lateral approaches if necessary. The femoral head should be kept for potential grafting purposes during the following procedure.
Preparation of the Acetabulum and Cup Implantation Long, curved, narrow, sharp Hohmann retractors are applied to the anterior wall and the inferior acetabular notch, and the femur is retracted posteriorly (in anterior, antero-lateral and lateral approaches) or anteriorly (in the posterior approach). Most surgeons now excise the capsule entirely from the antero-superior rim and remove the labrum. It is essential to get full exposure of the acetabular rim and the transverse ligament in order to reach an optimal position of the cup. To get an estimation of the adequate reaming depth, the acetabular fossa can be considered as reference point and therefore should also be cleared of soft tissues. Sometimes a chisel has to be used to remove osteophytes. The acetabulum is prepared using spherical reamers of increasing diameter. In routine cases we use reamers with outside diameters measuring from 44 to 68 mm, incrementing 2-mm at each step. We start always with a 44 mm reamer, which is pointing centrally to the bottom of the acetabulum. Once central exposure of cancellous bone is achieved, we continue with progressively larger reamers to remove the subchondral plate until enough cancellous bone with adequate blood supply is exposed. This ensures necessary activity of inflammatory mediators and bone-forming cells in contact with the implant surface as a pre-requisite for sufficient bone ongrowth. In average cases a penetration of the rim/circular wall as well as the acetabular floor should be avoided. The better the remaining bone stock, the better will be cup stability and secondary osseointegration. In acetabular dysplasia, however, a mild medialisation of the cup even with a perforation of the medial wall is proposed by some surgeons. In order to avoid cranialization of the implant, the inferior margin of the last reamer should be level with the transverse ligament. After a horizontal direction of the first 1–2 reamers (to ensure distal positioning) the remaining
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reamers are angulated at an inclination angle (abduction) of about 45°. Prior to acetabular reaming the corresponding diameter of the last reamer to the planned cup size must be checked (depending on implants and bone quality some manufacturers propose over- or even under-reaming by 1 or 2 mm in order to achieve stable cup seating). When the desired reaming depth has been reached and inspection confirms appropriate bone quality, a trial cup can be inserted to check adequate positioning. The trial cup – as well as the definitive implant – should be positioned according to the “safe zone” [7]. ● Inclination of 30–50° with reference to the transverse teardrop line (higher inclination can lead to excessive loading at the superior edge with liner wear and/or instability) ● Anteversion of 10–30° depending on the anticipated antetorsion of the femoral components (less anteversion can lead to ventral impingement in flexion and/or dorsal instability, higher anteversion can lead to ventral dislocation) Once an acetabular trial component – which should fit snugly – is placed to assess the coverage and optimum position, image intensifier control can be performed. This is especially helpful in obese patients where the position on the operating table is difficult to determine. In a dysplastic acetabulum the lateral coverage can be insufficient. If less than 70% of the trial component is in contact with bone, the stability can be improved by performing bony augmentation. For that purpose an appropriate cortico-cancellous fragment is cut out of the femoral head and fixed to the cranial wall with two screws (Fig. 6). It might also be necessary to remove inflamed synovial tissue from arthritic cysts. If the cysts are large enough, grafting by cancellous bone chips out of the preserved femoral head can be performed. After removal of debris the definitive implant can be seated. Press-fit cups are impacted with a heavy hammer. During impaction, one should be aware of the correct position and angulation. If in doubt, the position of the patient on the table is checked again and even fluoroscopy can be performed. Confirmation of stable seating is achieved by a combination of acoustic (sound change during impaction) and tactile indicators (increasing resistance of the impactor against manual movements). Some cup designs allow checking the approximation towards the central bone bed through the impactor’s screw-hole. One should not try to maximize stability by overhammering as this will eventually result in loosening or acetabular fracture. Adaption of pelvic bone to raising mechanic stress can be supported by waiting intervals between repeated hammerings.
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a
f
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Fig. 6 Bony augmentation of the acetabulum in a patient with unilateral osteoarthritis due to hip dysplasia (a) primary reaming in the true acetabular region (b) would lead to insufficient cranial acetabular coverage of the cup (c). Screw fixation of a cancello-cortical fragment retrieved from the deformed femoral head (d) results in circular bony augmentation and adequate stability of the cup (e, f)
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If no stable implant fixation can be achieved, the following potential reasons should be checked: ● Is there still enough stable bony support on the anterior, posterior and cranial rim? ● Has an acetabular fracture appeared? ● Has the right implant size been chosen? ● Was the impact position (angulation) of the implant identical with the desired position? ● Does soft tissue prevent bony contact?
ment of the liner against the neck of the stem, which is especially critical for hard bearings. Prior to impaction of the liner, the shell must be thoroughly cleaned and soft tissue remnants at the circumference removed. After impaction check carefully circumferential seating of the liner and stable fixation.
If no distinct reason for insufficient stability can be identified and the bone stock is good enough, repeated reaming to a deeper position with the finally-used size can be tried. A larger cup size or mild reduction of anteversion (to get better dorsal support) can also be tried, if no fracture has occurred. Some surgeons propose the application of additional screws to enhance stability and many implants provide screw holes for that purpose. Those screws should be placed in the direction of the main force vector and not override the medial wall nor the ischial foramen to avoid injury of major vessels and nerves. We should be aware of the fact, however, that additional screws change the pelvic strain distribution (thereby potentially influencing secondary osseointegration) and can lead to backside wear (particle transport through screw holes). Finally a grossly unstable cup will never be sufficiently fixed by augmenting screws. Threaded cups require basically the same acetabular preparation as press-fit cups. The definitive implantation process is somewhat different, however. Because of thread geometry it is not possible to correct implant angulation during turning the cup. As the threads support good stability very early during impaction, sensing of the correct seating point is the most critical part of cup implantation. In hemispherical designs it is more demanding to maintain the correct angulation during turning than in conical cups. Achievement of correct seating point and angulation, however, will always require a certain learning curve in threaded as well as in press-it cups.
Exposure of the femur depends on positioning of the patient and surgical approach. In anterior and lateral approaches, the leg is externally rotated, in the postero-lateral approach (lateral position) the leg is turned inwards (up to 90°) together with bending and adduction of the hip. It is generally recommended to bend the knee joint 90° in order to use the lower leg as a reference line for appropriate anteversion. A short, narrow Hohmann retractor is applied to the posterior aspect of the femur to protect the soft tissues and the skin from damage during rasping. The femoral canal is mostly prepared using a canal finder and a series of chipped tooth broaches which increase in size. The canal finder (sometimes an awl) has to be inserted laterally and slightly dorsal in order to avoid varus positioning of the stem. A good estimate for the entry point is the piriformis fossa as it is normally in line with the medullary canal. To prepare the entry point, most manufacturers provide a chisel, which removes a corticocancellous bone block from the neck. While pushing the canal finder (awl) into the medullary cavity, it must be pressed in the direction of the greater trochanter. In straight stems it is sometimes even necessary to remove a small piece of the trochanter base from the femoral neck, as the medullary cavity has to be opened more from dorsally than in anatomic (curved) stems. In hips with a deformation of the trochanteric region (i.e., after proximal femoral osteotomy) anatomic stems can be easier to implant than straight stems (Fig. 7). Then the bed for the stem is prepared, using rasps of increasing size, until the highest possible degree of stability is obtained. Mostly this process is started with the smallest rasp available. Curved handles or even off-set handles help to avoid contact with soft tissues. With the first rasp, care must be taken, to ensure a correct anteversion (usually 10–15°). This is necessary, as the sum of femoral and acetabular anteversion should aim at 20–30° (in posterolateral approaches even a little bit more). Constant bending of the lower leg (90° flexion in the knee joint) helps to determine the desired anteversion very precisely. In patients with pathological anteversion or retroversion, a second osteotomy more distal towards the lesser trochanter or
Liner Choice Most cup implants offer several liner options (conventional Polyethylene as well as hard bearings). The choice depends on patient’s age and activity as well as Surgeon’s preference. Modern liners offer the advantage of optional elevated lips and compatibility with different head ball sizes (mostly 28–36 mm) in order to improve the range of motion and reduce wear. It must be re-emphasized, however, that wrong cup position can lead to edge loading and impinge-
Preparation of the Femur and Stem Implantation
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Fig. 7 Choice of femoral stem type: in hips with a deformity of the trochanteric region after femoral osteotomy (a), anatomic stems might be easier to implant than straight stems (b)
removal of some cortical bone may be necessary. Another option in these cases is, to change the prosthesis system and implant a conical stem, which allows free rotation (Figs. 4b and 6f). Progressive and step-wise rasping with increasing dimensions now compresses the cancellous bone. The rasps are inserted with small hammer blows and care is taken not to fracture the cortex. If it is necessary, the cortex can even be reamed. The desired stability of cementless stems is based on a press-fit-concept in cortical and cancellous bone. It is therefore very important to get the best press-fit possible. Undersizing of the stem must be avoided, as this
can lead to subsidence and loosening over time. On the other hand, oversizing bears the risk of damaging cortex stability, which can lead to an intra-operative or early postoperative fracture. If a stable position of the final rasp has been reached, it must be checked to ensure that the distance between the proximal shoulder of the prosthesis and the greater trochanter is equal to the pre-operatively templated position. If the actual distance is shorter, the neck osteotomy can be repeated in a lower position and a smaller rasp introduced. If the distance is higher than pre-operatively determined either a larger rasp with a less deeper position or a long neck can be tried.
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This is the opportunity to check alignment with a trial reduction. For that purpose most systems offer trial necks of different length and/or off-set, which can be inserted into rasp holes after removing the handles. Once the trial neck which corresponds to the pre-operatively planned offset is selected, a trial head can be positioned. After reduction of the trial prostheses, three main issues should be checked: ● Range of motion ● Leg-length ● Stability Although this can be performed clinically, we also control the reconstruction under fluoroscopy. The radiographic evaluation allows us to document, if the pre-operatively planned off-set and leg-length reconstruction have been achieved. If the alignment has to be changed, a repeat trial with heads of different length (or even a different neck) is possible. The range of motion is checked to avoid bony impingement and instability. Depending on the surgical approach, especially external rotation in extension (anterior and lateral approaches) or internal rotation in hip flexion (posterolateral approach) should be performed in order to simulate anterior or posterior dislocation mechanisms. After removal of the rasp, a prosthesis of the appropriate size is inserted and driven into the medullary canal, until it is completely stable. This manoeuvre has to be performed with the necessary light touch, as most implants have a slightly larger dimension than the corresponding rasp. Because of the wedge mechanism an excessive load might be exerted in addition. This load on the neck cortex – or the greater trochanter when a straight stem is implanted – can lead to a fracture. It is therefore very important to adjust the force of the hammer blows according to the bone quality. The hammer blows should be stopped immediately, if a change in the sound of the blows from dull (cancellous bone) to sharp (cortical bone) is perceived. This is one of the most critical steps in cementless THR and can only be learned by experience. Rarely the stem needs to be removed intra-operatively (i.e., when the position after insertion is different from the previous rasp position). For this situation a specific extraction instrument should be available, which protects the neck and cone of the stem. Then the prosthesis can be used again after necessary changes (as for example repeated rasping) have been performed. After insertion of the stem, another trial reduction can be performed with a test head as before (especially if the final level of the imlant shoulder is different from the level of the rasp – indicating a different depth of insertion). Finally the taper must be cleaned and dried thoroughly,
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before the definitive femoral head is mounted and tapped into position. Before wound closure we perform another range-of-motion as well as final stability testing. A final fluoroscopic control serves as post-operative radiographic documentation of correct alignment and bone integrity.
Computer Navigation Navigation is sometimes used in an effort to increase the accuracy and consistency of hip arthroplasty component position. Most recent studies have demonstrated equal or superior accuracy in association with the use of navigation systems as compared with manual techniques. It still has to be evaluated, however, if patients have any clinical benefit from that improvement and under which circumstances navigation is cost-effective. Therefore currently, navigated THR cannot be recommended as a routine procedure [5].
Peri- and Post-Operative Management Prophylaxis of Heterotopic Ossification To avoid heterotopic ossification it is crucial to protect the soft tissues throughout the whole procedure and to prevent the apposition of bone fragments around the joint. We therefore remove meticulously any debris from acetabular reaming and femoral rasping prior to insertion of the implants, trial reduction and final reduction. Additionally patients receive NSAIDs for 2 weeks post-operatively, if no contraindication exists.
Peri-Operative Antibiotics As one of the major risks in THR is the development of peri-prosthetic infection, we deliver a single-dose prophylaxis with cephalosporine intravenously.
Post-Operative Rehabilitation Our post-operative management in routine cases involves protected full weight-bearing (with crutches) for 3–4 weeks. After that time full weight-bearing without crutches is encouraged. Physical therapy is performed to strengthen the thigh and hip muscles. Depending on the surgical approach, certain muscles might need protection (i.e., re-attached external rotators in the postero-lateral approach or abductors in the lateral approach). In minimally-invasive anterior
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or antero-lateral approaches there is no specific limitation of range of motion.
Complications Generally, the complications of cementless THR are very similar to the comlications of cemented implantation tecniques. Therefore patients should be informed about specific risks of artificial joints (i.e., venous thromboembolic disease, damage of neurovascular structures, dislocation, peri-prosthetic infection, leg-length discrepancy, component loosening and heterotopic ossification). One specific issue is the prevalence of peri-prosthetic fractures, which seems to be higher in cementless THR: In a recent large cohort study risk factors associated with femoral fractures and their effect on femoral stem survivorship were determined. The incidence of proximal femoral fracture was 2.3%. Risk factors associated with fractures included an antero-lateral approach, uncemented femoral fixation and female sex. In case of intra-operative fracture most often cerclage wiring is sufficient. If the fracture occurs post-operatively, treatment depends on the type of fracture and stability of the implant. While mal-positioning of the acetabular cup can lead to edge load (increased wear), impingement and dislocation, the sequelae of stem mal-positioning are less clear. Some surgeons have observed that stem mal-positioning, particularly varus, has been associated with higher failure rates. Min et al., however, reviewed a consecutive series of THR’s performed with a cementless tapered-wedge stem and a mean duration of follow-up of 7.7 years, where the stem position was neutral in only 63% of the hips, valgus in 21% and varus in 16%. No revision was necessary, there was no difference in the three groups in clinical outcome (HHS or thigh pain) and similar bone re-modeling changes were observed in all patients, regardless of stem position [8].
Implant Survival The short- and medium-term results of modern cementless THR are normally good and similar to those reported after cemented THR, with respect to relief from pain and function. Mallory et al. reported on 2,000 consecutive arthroplasties with a tapered stem that were performed between 1984 and 2001. The rate of femoral stem survival was 98.6% at 5 years, 98.6% at 10 years and 96.6% at 15 years.
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This success was attributed to the stem geometry and surface texture [9]. Long-term results with a follow-up of more than 10 years are only available for a limited number of uncemented implants. Aldinger et al. reviewed a series of cementless, double-tapered straight femoral stems (CLS) in 326 patients at a mean follow-up of 12 years (10–15 years). The mean age of the patients was 57 years (13–81). The overall survival was 92% and survival with femoral revision for aseptic loosening as an end-point was 95% [2]. The survival of cementless cups is still somewhat lower than the stem survival. Considering the mode of primary fixation, results between press-fit and threaded cups are still controversial [1, 10]. Using revision for any reason as an end point, 10–12 year survivorship rates from 93 to 99% and 15–18 year survivorship rates from 83 to 88% seem to be possible, especially in younger patients for both implant types [11–14]. In patient cohorts with uncemented implants many factors can influence survivorship, such as geometry, materials, surface finishes and bearings. Other factors including patient age and activity, surgical approach, expertise of the Surgeon and study design may also add to baseline differences between studies. Due to these limitations, National hip replacement Registries seem to be a valid instrument to compare the performance of different implants. In the most popular Swedish Registry the number of documented cementless THR is still significantly lower than the number of cemented arthroplasties. While the 10-year survival of all cementless prostheses in this registry is still somewhat lower than that of cemented prostheses, certain cementless implants show equal performance (i.e., CLS stems and Trilogy cups). In the Finnish registry a recent analysis at a mean follow-up of 12 years was performed [15]. The authors found that cementless THRs, as well as the stems and cups when analyzed separately, had a lower risk of revision for aseptic loosening than did the cemented THRs in patients with osteoarthritis who were 50–74 years-old. In patients who were 75 years of age or older, there were no significant differences in the results, other than the reduced risk of revision for aseptic loosening of hydroxyapatite-coated cementless cups compared with cemented all-polyethylene cups. Excessive wear of the polyethylene liner, however, resulted in numerous revisions of the modular cementless cups in patients who were 55–74 years-old. Thus, the long-term survival of the cementless THRs, with revision for any reason as the end-point, did not differ from that of the cemented THRs in any of the age groups. In conclusion, modern-design threaded and press-fit cups as well as cementless stems show promising survival
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rates. With the increasing use of hard bearings especially in younger patients we can expect even further improvement.
References 1. Effenberger H, Imhof M, Richolt J, Rehart S. Cement-free hip cups. Current status. Orthopäde 2004;33(6):733–50. 2. Aldinger PR, Breusch SJ, Lukoschek M, Mau H, Ewerbeck V, Thomsen M. A ten- to 15-year follow-up of the Cementlesse Spotorno stem. J Bone Joint Surg Br 2003;85-B:209–14. 3. Grübl A, Chiari C, Giurea A, Gruber M, Kaider A, Marker M, Zehetgruber H, Gottsauner-Wolf F. Cementlesse total hip arthroplasty with the rectangular titanium Zweymüller stem. J Bone Joint Surg Am 2006;88:2210–5. 4. Garcia-Cimbrelo E, Cruz-Pardos A, Madero R, Ortega-Andreu M. Total hip arthroplasty with use of the Cementlesse Zweymüller Alloclassic system: A ten to thirteen-year follow-up study. J Bone Joint Surg Am 2003;85:296–303. 5. Huo MH, Parvizi J, Bal BS, Mont MA. What’s new in total hip arthroplasty. J Bone Joint Surg Am 2008;90:2043–55. 6. Kirschner S, Witzleb WC, Krummenauer F, Mettelsiefen J, Günther KP. Early results of a prospective randomized controlled trial comparing a standard approach against two minimal invasive approaches in total hip arthroplasty. (manuscript in review). 7. Lewinnek GE, Lewis JL, Tarr R, Compere CL, Zimmerman JR. Dislocations after total hip-replacement arthroplasties. J Bone Joint Surg Am 1978;60:217–20.
Klaus-Peter Günther et al. 8. Min BW, Song KS, Bae KC, Cho CH, Kang CH, Kim SY. The effect of stem alignment on results of total hip arthroplasty with a cementless tapered-wedge femoral component. J Arthroplasty 2008;23(3):418–23. 9. Mallory TH, Lombardi AV, Leith JR, Fujita H, Hartman JF, Capps SG, Kefauver CA, Adams JB, Vorys GC. Minimal 10-year results of a tapered cementless femoral component in total hip arthroplasty. J Arthroplasty 2001;16(8 Suppl 1): 49–54. 10. Reikerås O, Gunderson RB. Long-term results of HA coated threaded versus HA coated hemispheric press fit cups: 287 hips followed for 11 to 16 years. Arch Orthop Trauma Surg 2006;126(8):503–8. 11. Engh CA, Hopper RHJ, Engh CAJ. Long-term porous-coated cup survivorship using spikes, screws, and press-fitting for initial fixation. J Arthroplasty 2004;19(7 Suppl 2):54–60. 12. Gabbar OA, Rajan RA, Londhe S, Hyde ID. Ten-to twelveyear follow-up of the furiong hydroxyapatite-coated femoral stem and threaded acetabular cup in patients younger than 65 years. J Arthroplasty 2008;23(3):413–7. 13. Reigstad O, Siewers P, Røkkum M, Espehaug B. Excellent long-term survival of an uncemented press-fit stem and screw cup in young patients: follow-up of 75 hips for 15–18 years. Acta Orthop 2008;79(2):194–202. 14. Zweymüller KA, Steindl M, Schwarzinger U. Good stability and minimal osteolysis with a biconical threaded cup at 10 years. Clin Orthop Relat Res 2007;463:128–37. 15. Mäkela KT, Eskelinen A, Pulkkinen P, Paavolainen P, Remes V. Total hip arthroplasty for primary osteoarthritis in patients fifty-five year of age or older. An analysis of the finnish arthroplasy registry. J Bone Joint Surg Am 2008;90: 2160–70.
How to Treat a Meniscal Lesion? Olivier Charrois and The GREC group
The role of menisci is essential to the biomechanics of the knee joint. They act as mechanical links which allow better load distribution between the cartilaginous surfaces of the femur and the tibia, absorb stress peaks and also contribute to the stability of the joint. Being so important to the function of the joint, they are prone to traumatic injuries and degeneration which can both occur with or without the coexistence of ligamentous lesions. Previously, when a meniscal lesion was diagnosed, a meniscectomy was considered to be the solution for many years. In spite of a decline in the morbidity thanks to the evolution of surgical practice and especially to the development of arthroscopic techniques, the effects of this very common procedure on the joint biomechanics have not changed and the development of the osteoarthritis is not infrequent [9]. It is time that the association of a meniscal lesion with routine meniscectomy is abandoned and that alternative methods of treatment such as conservative treatment, repair and grafting be considered.
Biomechanics of the Menisci and the Sequelae of Meniscectomies The menisci improve the congruence of the knee joint adjusting the spherical surfaces of the femoral condyles to the tibial facets, the medial of which is slightly concave and the lateral convex in shape. This has two consequences for the biomechanics of the joint which are better load distribution and passive joint stability. As 60% of load-transmitting forces are carried by the menisci, their resection alters this transmission and results in the emergence of stress peaks which cause damage to the articular cartilage.
Olivier Charrois () Clinique Arago, 95 Boulevard Arago, 75014 Paris, France e-mail:
[email protected]
The importance of these peaks increases with the degree of meniscal resection [1]. The meniscectomy also facilitates the antero-posterior translation of the tibia, particularly when the cruciate ligaments have been injured [1, 24]. These proved and well-known roles of the menisci have led for a long time to a conclusion that there was a simple geometrical relation between the amount of the meniscus removed and the consequences of this procedure. Two important remarks should be made here in order to better explain the importance of each of the characteristics of a meniscectomy and to provide information which could help to understand the dynamic function of the menisci. 1. The first comment concerns the meniscal anatomy. A meniscus is composed of longitudinal fibres attached to a peripheral rim which is more resistant to exerted forces. While the development of bi-podal posture was accompanied by disappearance of circular menisci, this ancient form is still reflected in their functional arrangement by internal architecture of the fibres. If this meniscal circle is completely interrupted by a radial tear or during a meniscectomy, the functional outcome is the same as for a total meniscectomy in spite of the little amount of removed meniscal tissue. On the contrary, a meniscus which has been horizontally torn retains its function despite the persistent pain that is often caused by this lesion. 2. The second remark concerns the complexity of meniscal kinematics during joint movement. While the medial compartment is rather static and transfers less force owing to the architecture of the lower limb, the lateral compartment is more dynamic and its meniscus follows the femoral condyle as it moves acting as an elastic band. This capability to follow the complex movements of the tibial and femoral surfaces and to conform to these conditions depends on firm anchorage of the distal parts of the meniscus, the horns, and on the ability to avoid extrusion thanks to retaining shape and position with the aid of the intermeniscal and the menisco-femoral ligaments. The mere fact that the meniscus is located well in its place does not suffice. If it is either detached from its anchorage points or
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torn or cut radially to its capsular margin, it loses the capability to transfer the load and to stabilize the joint. The consequences of a meniscectomy are not related simply to the degree of the meniscal resection but rather to the disruption of the normal knee biomechanics. Clinical results confirm these considerations as the onset of osteoarthritis of the knee is commonly observed, apart from early complications. This happens even more frequently when the lateral meniscus is concerned [8]. Ten years after the surgery 22 and 42% of patients who had undergone a medial or lateral meniscectomy respectively showed radiological signs of developed osteoarthritis [9].
Meniscal Repair Although meniscal repair is not yet routinely performed, at least in France (125,000 meniscectomies versus almost 3,000 meniscal repairs annually), it is not a recent innovation. The first reported meniscal repair dates back to 1883 [2] and the first arthroscopic repair was performed in 1969 by Ikeuchi.
Principles of Meniscal Repair The biomechanical background of meniscal repair was investigated only after the first repairs had already been carried out. ● Thanks to the research into the meniscal vascularity [4] it was possible to assess the feasibility of the procedure and its restrictions. Meniscal tissue is well-vascularized during foetal life and early childhood, but this diminishes with time. In the adult the white zone of the meniscus is nourished by imbibition and blood supply to the meniscal body extends only to the limit of the red and white zones. Therefore, it seems that the zone situated between this point and the capsular margin is able to cicatrize. ● Due to the horizontal orientation of the meniscal fibres the solidity of a repair is provided when the suture or other device is directed vertically rather than horizontally in order to hold the fibres together. ● For these reasons, the correct placement of the repair device and its mechanical characteristics influence the resistance of the repaired meniscus to distracting forces with the threshold varying from 30 to over 100 N for vertical non-resorbable sutures [20]. Apart from that, there are two other two other parameters which are more difficult to assess but should be considered. These are
the resistance to shearing forces which becomes even more important in the case of a mobile meniscus (as with the lateral one) and the harmlessness of the repair devices which can potentially cause significant increases in transmitted forces leading to cartilaginous injury. ● The last mechanical principle to be taken into account when deciding upon the repair technique concerns the evolution of the fixation strength in comparison with that of the newly-cicatrising tissue. While the strength of most resorbable sutures decreases rapidly with time [3], this is not compensated fast enough by the increasing resistance of the repair zone [11]. Having considered the above-mentioned principles it is possible to define the following rules of meniscal repairs: ● A repair should only be planned for tears situated within the vascularized area (red–red or red–white zones) which need first to be rasped in order to dispose of the fibrous tissues that could impede vascularization and, as its consequence, prevent scar tissue formation. ● Horizontal fibres of the meniscus must be comprised in the repair. ● The site of the repair must not only resist distracting forces but also conform to shearing forces. ● Repair devices must not harm the cartilage. ● Resorbable sutures must retain their mechanical properties for a sufficient period of time to allow the newly formed scar tissue to mature. Apart from this set of rules, it doesn’t seem that the choice of surgical technique, whether it is all-inside, inside-out or outside-in, nor the approach used for the surgery have a significant influence on the mechanical properties of the repair and they need to be chosen according to the localisation of the lesion, its type and the surgeon’s experience.
Results The results of meniscal repairs were analysed during the 2003 symposium of the French Arthroscopic Society (SFA) with 278 repairs investigated [7]. This multi-centre project comprised a retrospective study of 203 repairs aimed to estimate the failure rate and mid-term outcome (average follow-up 45 months, 1–19 years) and a prospective study of 75 repairs dating back at least 6 months and aimed to assess the morbidity and the cicatrization process (arthro-CT scan). The rate of intra-operative surgical complications (meniscal or chondral injuries, failure to secure the tear, implant
How to Treat a Meniscal Lesion?
damage or loss) was 8% and was associated with simple sutures in 60% of cases. A temporary or permanent nerve lesion was found in 5 cases (4 medial sural nerve and 1 peroneal nerve lesions) and occurred always when a contraincision was carried out which was therefore insufficient means of nerve protection. No damage to the nerves was done during the all-inside procedures. The rate of secondary meniscectomies was important and reached 23% in the retrospective study which included repairs performed with various techniques on knees in which some of existing ACL tears were left alone (these rates were 24 and 11% for the medial and lateral meniscus respectively). All these failures occurred during the first 2 years after surgery. According to the classification system of Henning, cicatrization was complete in 39% of cases, partial in 34% and none in 27% of repairs. An investigation into horizontal healing of the tear revealed that the detached area diminished by more than 50% in over 75% of cases. It led to a conclusion that even in case of partial cicatrization this diminution of the tear restores meniscal stability sufficiently to prevent an eventual meniscectomy. A delay of the surgery by more than 12 weeks was described as a negative factor. The failure rate was not affected neither by the surgical approach nor by the repair device used during the procedure. The results of repairs performed in the stable knees were comparable to those carried out in the ACL-reconstructed knees and were better for the lateral meniscus repairs. The rate of scar tissue formation in the red–red zone (73%) was comparable with that of the red–white junction (72%) which confirmed its ability to heal. The extent of the initial tear was a negative prognostic factor, just like the extent of a meniscectomy. If the significative number of the cases included in this study had allowed a statistical analysis, we would have probably thought that the moderate results were related to old techniques which were later abandoned, to the fact that the ACL was not always reconstructed in the unstable knees and to the surgical experience which was still insufficient. These conclusions were confirmed by a more recent prospective study [18] of 53 all-inside meniscal repairs performed on stable and ACL-reconstructed knees as the rate of secondary meniscectomies did not exceed 5.7% during at least 24 months after the surgery. Apart from that, the study demonstrated that the meniscal volume decreased by more or less 9% after the formation of the scar tissue. This change could be possibly attributed to rasping, suture tension or meniscal retraction related to the cicatrising tissue. The capability to protect the cartilage in spite of the reduced volume remains yet to be investigated.
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Meniscal Replacement The development of surgical practice in the field of meniscal tears remained far from the international trends for a long time. Then, the French Orthopaedic Surgeons, alerted by their mediocre long-term results and short-term complications likely to follow meniscectomies, first developed the concept of meniscal-sparing contemplating meniscal repair and abstention. Faced with young suffering patients who had undergone a meniscectomy and/or when the condition of previously operated joints had already been deteriorating towards osteoarthritis, the French orthopaedic surgeons were undecided for a long time. In spite of the fact that the meniscal transplantation had been advocated in this situation by Carl Wirth and Dieter Kohn [13] since the eighties and despite the surgical technique which had been initially developed in Europe thanks to the impetus of René and Peter Verdonk [23] and then in the United States where it is still used, the first meniscal transplantation in France was carried out only in 2002 and the grafts are hardly accessible. The goal of meniscal grafting is to relieve pain in the compartment where the meniscectomy has been performed and to protect it against the biomechanical sequelae of meniscal resection. In our experience, meniscal transplantations were carried out to combat the consequences of previous meniscectomies and up to now they have not been recommended for primary prevention. In this situation the meniscus could be replaced with an allograft or a regeneration scaffold.
Allografts Different types of grafts (patellar or quadriceps tendon, vascularized ligament pedicle flaps) were suggested before they were abandoned in favour of the meniscal grafts. The removal of the graft is carried out during a multiorgan removal. Some of the conservation techniques like lyophilization or irradiation to ensure viral destruction were abandoned because of the deterioration of meniscal matrix which altered its biomechanical characteristics and therefore could potentially increase the risk of rupture [25]. The debate, which is still open, has focussed on the conditions which influence graft cellularity and on its role in the longterm evolution of the meniscus and the joint. Fresh allografts [22] raise important logistic problems with their removal, transport, storage and long-term preservation. This is why the French Meniscal Transplantation Group so strongly supported the cryo-preservation of the graft with a cellular protecting substance (dimethylsulfoxide, DMSO).
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The graft is chosen according to the measurements of the original meniscus. However, it is still unclear which method should be used to ensure the best match of the size of the graft with the tibial plateau in order to avoid the biomechanical consequences of graft extrusion, which are not uncommon. The graft implantation can be carried out by an arthrotomy with a possible de-insertion of a collateral ligament [23] or arthroscopically, which is technically demanding but realizable for both menisci. A combined approach can also be considered. The graft is sutured to the joint capsule as during a meniscal tear repair and its horns are either fixed using special devices or secured with the technique of bone blocks, which theoretically improves the stability of the graft and facilitates its cellular colonisation. Clinical studies confirm the capability of the graft to cicatrize to the joint capsule and show that the cellular colonisation of the graft is facilitated by the selection of a viable graft [22]. There is also an agreement over the straightforward improvement in the functional capacity of the patient after the surgery [23]. Nevertheless, none of these studies proved that the meniscal transplantation could alter the course of cartilaginous lesions and eventually osteoarthritis. Moreover, the number of factors needed to be taken into account (age, initial condition of the cartilage, mechanical axe of the knee, associated meniscectomy) does not improve the indications for this technique. In our opinion, these grafts should be at present reserved for young patients (aged 50 years or less) suffering from severe pain after a meniscectomy, whose knees are correctly aligned, stable or ACL-reconstructed and which are not yet too damaged (medial joint line narrowing less than 50% on the Rosenberg view, grade 1 or 2 during the arthroscopic evaluation). The French Meniscal Transplantation Group has also launched the first prospective study to clarify these criteria.
Scaffolds The limited allograft availability, the risk of viral transmission and the need for meniscal patches to replace only part of a meniscus have led to the development of synthetic meniscal substitutes. This doesn’t mean a meniscal prosthesis, but rather a porous scaffold which would induce its cellular colonisation. The first scaffold produced, the CMI (Centerpulse) [19] consisted of bovine collagen matrix. The multi-centre studies which have been conducted in the USA and in Europe [5] have already proved the feasibility of their arthroscopic implantation, their capability to relieve the post-meniscectomy pain and their colonisation by fibrous, chondral or synovial tissue. However the original architecture
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of the meniscus was not restored. As for the allografts, their long-term capability to protect the cartilage has not been demonstrated. More recently, another substitute made of resorbable polyurethane, the Actift (Orteq) has been introduced. The utility of this implant, which is mechanically more resistant, is currently evaluated.
The Influence of Associated Lesions on the Treatment of Meniscal Tear The menisci and the anterior cruciate ligament constitute the main elements responsible for the antero-posterior stability of the knee joint. Therefore, they are often injured simultaneously in cases of serious trauma to this joint. In a retrospective study of 156 cases, Gadeyne et al. [10] noticed the co-existence of an ACL injury with lesions of the medial meniscus, of the lateral meniscus and of both menisci in 25.6, 21.8 and 9% of cases respectively. As the co-existence of a meniscal lesion influences the indications for the ACL reconstruction, its treatment cannot be considered independently of the ligamentous condition.
Indication for ACL Reconstruction in Cases of Associated Ligamentous and Meniscal Trauma When the indications for the ACL reconstruction are debatable because of the lack of functional instability, low-functional demands and age, the co-existence of a meniscal lesion is by itself a drawback to be taken into account. The short-term functional result of a meniscectomy on an unstable knee is worse than on a stable knee [14] and arthritic deterioration is much more frequent [15]. The ACL reconstruction is then justified but the necessity of an associated meniscectomy remains a negative factor for the stabilization [6] and the long-term evolution of the joint [12, 16]. Owing to these facts, preserving as much of the meniscus as is possbile is of vital importance. The stability of the knee is the key prognostic factor when a decision about a meniscal repair is to be made. Indeed, apart from Sommerlath and Hamberg [21] who noticed only 11% of failures of meniscal repairs in unstable knees, all other authors seem to agree about the important failure rate of repairs without joint stabilization. A 2003 study of the French Arthroscopy Society symposium [7] investigated 145 meniscal repairs in initially unstable knees. Only 14 of these knees were not stabilized. The secondary meniscectomy rate in this sub-group was the double of the one of the ACL-reconstructed knees. The overall rate of secondary
How to Treat a Meniscal Lesion?
meniscectomies in the ACL-reconstructed knees was comparable to the rate of repairs carried out in stable knees. As joint stability is crucial to meniscal healing, one might put into question the necessity of carrying out a meniscal repair during the ACL reconstruction. There are only few studies which concern this possibility. Pierre et al. [17] studied the evolution of 95 meniscal lesions considered as stable (tears of size below 20 mm and non-luxable when pulled with an arthroscopic probe) which were left in place without a repair during the ACL reconstruction surgery. None of the 35 lateral meniscal lesions required a secondary meniscectomy unlike 17% of the 60 medial lesions. The main prognostic element was the size of the lesion. This study confirms greater ability to heal of the lateral meniscus after ACL reconstruction and also the fact that the apparent stability of a lesion is not enough to justify the abstention from a meniscal repair. These authors propose to repair neither lateral nor medial meniscal lesions which don’t exceed 10 mm. This opinion, justified by their results, can however be questioned with two arguments: 1. First, we didn’t noticed any particular morbidity when the hybrid devices were used to ease the meniscal repair which was made simultaneously with the ACL reconstruction and without a counter-incision. 2. On the other hand, the 2003 symposium study [7] proved that the functional result of a meniscal repair and the residual pain relief were correlated with the quality of anatomical healing. This is why we recommend repair of every peripheral detachment of the medial meniscus and all unstable tears of the lateral meniscus in addition to the ACL reconstruction.
Secondary Meniscal Lesions in Unstable Knees The occurrence of a meniscal lesion is part of a natural history of chronic instability of the knee and its isolated treatment with a meniscectomy aggravates the evolution of the joint [12, 16]. A clinical and radiological assessment of the joint condition is essential to determine if the meniscal lesion is isolated, if there exists a ligamentous deficiency causing other disturbances than an isolated anterior instability and verify the condition of the cartilaginous surfaces. If the meniscal lesion is isolated, the indications are the same as those for regular traumatic lesions: ACL reconstruction and meniscal sparing. When there are signs of global osteoarthritic changes, which are generally associated with large degenerative meniscal lesions, the choice of the suitable treatment becomes more complicated. If the chondral degradation is limited (joint line narrowing below 50% in extension and schuss radiographs, chondropathy not
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stripping the subchondral bone), it is worthwhile to consider a reconstructive surgery which could consist of the ACL reconstruction, an osteotomy when the chondropathy is medial and occurs in a genu varum and possibly a meniscal replacement as these meniscal lesions are rarely repairable. When the osteoarthritis has been already documented, neither ligamentous nor meniscal surgery (partial resection, grafting, implanting a meniscal substitute) seem to be able to alter the evolution of the disease.
Occurence of a Meniscal Lesion in ACL-Reconstructed Knees When a meniscal lesion occurs in an ACL-reconstructed knee, the efficiency of the ligamentoplasty must be put into doubt. An objective assessment of joint laxity (Telos or KT100) is essential in order to decide whether the meniscal lesion resulted from an additional trauma and therefore the indications for its treatment would be the same as for a stable knee, or it is the consequence of a residual laxity. In the last case, a new procedure must be considered, especially if the meniscal lesion can be repaired.
Conclusion The long-term results of meniscectomies have confirmed the biomechanical role of the menisci as well as some predictable consequences of their resection. As regards meniscal lesions, the use of a meniscectomy is often logical as it is, thanks to arthroscopic surgery, a relatively simple procedure with good short and mid-term results in the vast majority of cases. Nevertheless, it is frequently followed by osteoarthritis in the long run which should not be disregarded. We think that it should only be proposed when no alternatives are available. ● Many meniscal lesions may heal by cicatrization. Meniscal repairs support this process of restoration and also restore meniscal stability. These repairs concern primarily vertical lesions located within the vascularized zone (red–red or red–white area). The operation should be carried out within the first 3 months after injury. Arthroscopic techniques may be a great aid but one must bear in mind that the repair needs to be solid and that the tear edges must be first rasped to dispose of the fibrous tissue. If an ACL tear co-exists, this ligament must be reconstructed to allow the meniscus to cicatrize. ● If a meniscal tear is irreparable, abstention should be taken into account. Many lesions are or can become asymptomatic and, if the tear is stable (e.g. a horizontal
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cleavage one), the meniscus remains stable. Rare complaints of the patient need to be weighed against the risk of long-term osteoarthritis development. ● If a meniscal lesion is neither reparable nor relieved with time or conservative treatment, it is logical to consider a meniscectomy. It is important to spare as much of the meniscal tissue as possible as well as not to do any damage to meniscal horn nor disrupt the peripheral continuity as these are the key structures responsible for the biomechanical characteristics of the meniscus. ● In case of young patients complaining of significant pain after a meniscectomy who may sometimes present early osteoarthritic changes a meniscal transplantation may be proposed as long as the knee is correctly aligned (or realigned) and stable (or after the ACL reconstruction). It has been proved that meniscal substitution is an effective means to relieve pain and to enhance the function of the joint. The position of each of the possible substitutes (allografts and scaffolds), clear indications for their use and their capability to protect the cartilage have not yet been established.
Acknowledgements The author would like to thank Philippe Beaufils (Versailles, France) who taught him the fundamental part of what has been communicated here and who filled him with passion to understand the rest.
References 1. Ahmed AM. The load-bearing role of the knee menisci. In: VC Mow, SP Arnoczky, and DW Jackson (eds.), Knee meniscus: basic and clinical foundations, pp. 59–73. New York: Raven Press; 1992. 2. Annandale TH. An operation for displaced semilunar cartilage. Brit Med JK. 1885;1:779–81. 3. Arnoczky SP, Lavagnino M. Tensile fixation strengths of absorbable meniscal repair devices as a function of hydrolysis time. An in vitro experimental study. Am J Sports Med. 2001;29:118–23. 4. Arnoczky SP, Warren RF. Microvasculature of the human meniscus. Am J Sports Med. 1982;10:90–5. 5. Beaufils P, Moyen B, Charrois O and The European CMI Group. Reconstruction du ménisque médial par le CMI: résultats préliminaires de l’étude européenne. Rev Chir Orthop Reparatrice Appar Mot. 2002;88(suppl 6):S44–5.
O. Charrois et al. 6. Bercovy M, Weber E. Evaluation of laxity, rigidity and compliance of the normal and pathological knee. Application to survival curves of ligamentoplasties. Rev Chir Orthop Reparatrice Appar Mot. 1995;81(2):114–27. 7. Cassard X, Verdonk R, Almqvist KF, Nourrissat G, Thoreux P, Kerdilès N, Charrois O, Katabi M, Kelberine F, Candoni P, Aït Si Selmi T, Hulet C, Billot N, Beaufils P, Bamberg A, Pujol N, Gihr D, Accadbled F. Meniscal repair. Rev Chir Orthop Reparatrice Appar Mot. 2003;90(suppl 80):3S49–75. 8. Charrois O, Ayral X, Beaufils P. Rapid chondrolysis following lateral meniscectomy the knee following lateral meniscectomy. Rev Chir Orthop Reparatrice Appar Mot. 1998; 84(1):88–92. 9. Chatain F, Robinson AH, Adeleine P, Chambat P, Neyret P. The natural history of the knee following arthroscopic meniscectomy. Knee Surg Sports Traumatol Arthrosc. 2001; 9:15–8. 10. Gadeyne S, Besse JL, Galand-Desme S, Lerat JL, Moyen B. Analysis of meniscal lesions accompanying anterior cruciate ligament tears: a retrospective analysis of 156 patients. Rev Chir Orthop Reparatrice Appar Mot.2002;92(5):448–54. 11. Koukoubis TD, Glisson RR, Feagin JA, Jr, Seaber AV, Schenkman D, Korompilias AV, Stahl DL. Meniscal fixation with an absorbable staple. An experimental study in dogs. Knee Surg Sports Traumatol Arthrosc. 1997;5(1):22–30. 12. McConville OR, Kipnis JM, Richmond JC, Rockett SE, Michaud MJ. The effect of meniscal status on knee stability and function after anterior cruciate ligament reconstruction. Arthroscopy. 1993;9(4):431–39. 13. Milachowski KA, Weismeier K, Wirth CJ, Kohn D. Meniscus transplantation and anterior cruciate ligament replacement– results 2–4 years postoperative. Sportverletz Sportschaden. 1990;4(2):73–8. 14. Neyret P, Donell ST, Dejour D, Dejour H. Partial meniscectomy and anterior cruciate ligament rupture in soccer players. A study with a minimum 20-year followup. Am J Sports Med 1993;21(3):455–60. 15. Neyret P, Walch G, Dejour H. Intramural internal meniscectomy using the Trillat technic. Long-term results of 258 operations. Rev Chir Orthop Reparatrice Appar Mot. 1988; 74(7):637–46. 16. O’Brien et al. Degenerative arthritis of the knee following anterior cruciate ligament injury: a multicentric, long term follow-up study. Am J Sports Med. 1989;17:716–25. 17. Pierre A, Hulet C, Locker B, Schiltz D, Delbarre JC, Vielpeau C. Outcome of 95 stable meniscal tears left in place after reconstruction of the anterior cruciate ligament. Rev Chir Orthop Reparatrice Appar Mot. 2001.87(7):661–8. 18. Pujol N, Panarella L, Selmi TA, Neyret P, Fithian D, Beaufils P. Meniscal healing after meniscal repair: a CT arthrography assessment. Am J Sports Med. 2008;36(8):1489–95. 19. Rodkey WG, Steadman JR, Li ST. A clinical study of collagen meniscus implant to restore the injured meniscus. Clin Orthop. 1999;367S:281–92. 20. Seil R, Rupp S, Jurecka C, Georg T, Kohn D. Réparation Méniscale par fixations biodégradables: étude biomécanique comparative. Rev Chir Orthop Reparatrice Appar Mot. 2003;89:35–43.
How to Treat a Meniscal Lesion? 21. Sommerlath K, Hamberg P. Healed meniscal tears in unstable knees. A long-term followup of seven years. Am J Sports Med.1989;17(2):161–3. 22. Verdonk PC, Demurie A, Almqvist KF, Veys EM, Verbruggen G, Verdonk R. Transplantation of viable meniscal allograft. Surgical technique. J Bone Joint Surg Am. 2006;88(suppl 1): 109–18.
211 23. Verdonk R. Meniscal transplantation. Acta Orthop Belg 2002;68:118–27. 24. Walker PS, Erkman MJ. The role of the menisci in force transmission across the knee. Clin Orthop. 1975;109:184–92. 25. Wirth CJ, Peters G, Milachowski KA, Weismeier KG, Kohn D. Long-term results of meniscal allograft transplantation. Am J Sports Med. 2002;30(2):174–81.
Soft-Tissue Balance in Total Knee Arthroplasty David E. Beverland
Dictionary definitions of balance include “a state where things are of equal weight or force” and “to be in a position where you will stand without falling to either side”. Modern total condylar knee arthroplasty began in the latter half of the 1970s and at that time the patient population was elderly and quite happy to use a stick to stop themselves from falling to either side. Since then patient selection has expanded to include many patients who want to continue their involvement in sports like golf and doubles tennis but increasingly patients also want to able to ski and even be involved in contact sports. The difference in soft-tissue balance required to enable an elderly patient to walk with a stick or cane is very different to that of a patient who wants to be involved in contact sports. At present neither our surgical abilities nor our implant designs are advanced enough to allow us to feel happy about our total knee arthroplasty (TKA) patients playing football! Probably the person most associated with establishing the initial success of TKA is the late John Insall. With respect to achieving soft-tissue balance he popularised the use of spacer blocks and the concept of balanced and equal flexion and extension gaps [1]. He also advocated the excision of both cruciate ligaments. This was the philosophy of knee replacement to which I was introduced and to date I have not seen any good reason to change. Although I excise both cruciates I do believe that where possible we should retain soft-tissues and not substitute for them. I defend my present practice of cruciate excision with the theory that they function as a single unit and that unless both are present there is no proven benefit in keeping one. There have been bicruciate-retaining versions of TKA such as the LCS [2] but they have not been widely used, are surgically difficult to insert and to my knowledge there are no published results that demonstrate any benefits as compared with more conventional designs.
David E. Beverland Outcomes Unit, Musgrave Park Hospital, Belfast, BT9 7JB, UK e-mail:
[email protected]
Biomechanics of Total Knee Arthroplasty The biomechanics of total knee replacement are complex. The normal knee has a sloping joint surface such that the articular surface of the tibia has a variable varus slope relative to its mechanical axis and also a variable posterior slope. The medial tibio-femoral articulation behaves much like a ball-and-socket joint with relatively little A-P movement and the lateral femoral condyle rolls back on the tibia with flexion, this movement being controlled by the cruciate complex. This form of femoro-tibial movement creates the ideal load pattern for the patello-femoral joint. It is also now clear that the normal knee is not is not balanced in flexion but is tighter on the medial side [3]. Also not all normal knees have a neutral mechanical axis (co-linear alignment of hip, knee and ankle centres). As surgeons we approach this highly complex joint by trying, often unsuccessfully, to create a neutral mechanical axis and to make a new joint surface at right angles to the mechanical axis. We excise one or more cruciates and then insert a tibio-femoral articulation that creates paradoxical movement and a less than ideal climate for the patello-femoral joint. Clinically the results are remarkably good but perhaps not ideal for the high demand patient. Given the limitations of contemporary TKA design the surgeon needs to ensure that any further compromise to the joint is minimised. I feel that the collateral ligaments namely the superficial medial collateral and the lateral collateral ligament (LCL) should be preserved and not released irrespective of deformity. Traditional teaching has been to “release” these ligaments to balance the knee in the coronal plane. In severe deformity these releases are often extensive and in a varus knee can include the superficial MCL (medial collateral ligament) the pes anserinus tendons and semi-membranosus. In the valgus knee it can include the IT (ilio-tibial) band, elevation of the lateral collateral, popliteus and the lateral head of gastrocnemius from the lateral femoral condyle and even excision of
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the fibular head or elongation of biceps femoris. It is my opinion that none of the above structures should be released even in the presence of severe deformity. Furthermore it is my hypothesis that the superficial MCL and the LCL are not involved in the arthritic process, that they do not shorten and that they therefore do not contribute to the fixed deformity in either varus or valgus knees. Undoubtedly in the type II valgus knees the posterior part of the superficial MCL can elongate but the anterior portion is unaffected. Consequently in the primary valgus knee the flexion gap maintains its normal tension medially at least until surgery begins! Thus in all primary knees my soft-tissue management is very conservative. Apart from excising the cruciates the only other structure that I cut as opposed to release is the affected part of the posterior capsule and this I do infrequently except in the valgus knee.
Aims of Total Knee Arthroplasty In biomechanical terms the aims of TKA are correction of deformity, restoration of normal alignment and soft-tissue balance combined with sound component fixation. Figure 1 summarises the deformities that we see. Patellofemoral sub-luxation: In TKA this deformity usually occurs as a result of lateral facet patello-femoral osteoarthritis (PFOA). This frequently occurs in combination with tibio-femoral degenerative change but can also occur in isolation. There is debate about how isolated PFOA should be managed surgically. It has been my practice to manage the older patient with total knee replacement without patellar resurfacing [4]. The majority of these knees have a Sperner 4 deformity of the patella [5] with patellar maltracking or subluxation. It is essential that at the end of the procedure
Deformity Sagittal Plane
Coronal Plane
TibioFemoral
Valgus
Varus
Patellofemoral
PF subluxation
TibioFemoral
Fixed flexion
Recurvatum
Fig. 1 Summary of deformities in the sagittal and coronal planes
the patella tracks well. This means that the abnormal lateral facet has to be removed. I call this “patella contouring” and this is illustrated in Fig. 2. Once the patella has been contoured in this way the patella almost always tracks well and it is rare to have to do any further patellar release. I never resurface the patella. When performing a total knee replacement for isolated PFOA the tibio-femoral joint is normal and therefore the knee is balanced to begin with. Therefore in such cases when the proximal tibial and distal femoral bone cuts have been made the extension gap should be balanced. In the past, when it was not, it suggested to me that the arbitrary valgus angle of 5° that I had used for the distal femoral cut had not restored the correct mechanical axis for that knee. It was in this clinical situation that I first started to re-cut the distal femur at a different angle, either more than or less than 5°, in order to balance the soft-tissues as opposed to “releasing” soft-tissues to balance the bone cuts. This is made possible by routinely performing a “pre-cut” or conservative cut on the distal femur as discussed later. When necessary the definitive distal femoral cut can be made at a different angle in order to balance the extension gap. I feel that this restores the appropriate mechanical axis for that individual lower limb. If you like “restoring a functional, but not necessarily a neutral, mechanical axis”.
Genu Recurvatum This is not a common problem in primary knee arthroplasty and I will not discuss it.
Fixed Flexion and Restoration of Joint-Line Fixed flexion is a common deformity that is frequently associated with a varus or valgus deformity and restoration of joint-line is important in optimising soft-tissue balance. The reason for discussing them together is because I feel that errors in joint-line are frequently made in patients with fixed flexion. It is important to remember that each bone cut has its own joint line. Thus the proximal tibial cut, the anterior and posterior femoral cuts and the distal femoral cut all have individual joint lines. One of the commonest errors is to raise the joint line on the tibia. This is particularly a problem in association with fixed flexion because if the tibial joint line is raised this makes the knee even more tight in extension. There are five common causes.
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Fig. 2 Contouring the patella. (a) Evert the patella using a towel clip. (b) Cut the lateral facet using a saw – this cut needs to be aggressive. (c) Once the osteotomy has been performed the bone fragment is excised using sharp dissection – X-ray inset of
Sperner 4 on pre-operative skyline view. (d) The finished appearance with post-operative skyline view X-ray inset in the same case demonstrating central tracking of the patella
1. Making the A-P femoral cuts too anterior: In this situation too much bone is removed from the posterior femoral condyles which makes the flexion gap larger. As a result a thicker polythene insert has to be used to restore the correct tension in the flexion gap thus raising the tibial joint line. 2. Using an under-sized femoral component: Most knee systems reference off the anterior femoral cortex to avoid notching. Therefore if the femoral component is too small again too much bone is removed from the posterior femoral condyles which as before means a thicker polythene insert being used to restore flexion gap tension. In both 1 and 2 not only does this raise the joint line on the tibia but over- resection of the posterior femoral condyles also alters the posterior femoral joint-line and decreases the posterior condylar offset. In posterior cruciate-retaining knees this has been shown to result in a loss of flexion [6, 7] although this does not appear to be the case in cruciate-sacrificing designs [7, 8].
3. Release of either the superficial MCL or the LCL creates laxity in flexion and therefore an increased flexion gap. This has to be compensated for by using a thicker polythene thus raising the tibial joint-line. This is particularly common in knees with fixed flexion and either varus or valgus deformities. 4. Making the flexion gap too tight by using too thick a polythene also raises the tibial joint line. 5. Under-resection of the tibia: In most knee systems the minimal thickness of the tibial tray and insert is ³10 mm. This therefore dictates the minimal tibial resection required to avoid raising the tibial joint line.
Soft-Tissue Balance in the Varus Knee with or without Fixed Flexion I use a standard mid-line incision which is 20 cm long when flexed to 90° and 15 cm in extension. I use a modified
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Insall-type arthrotomy [9] which passes proximally along the medial edge of the quadriceps tendon and over the top of the patella and then distally along the medial edge of the patellar ligament. My exposure of the proximal tibia is minimal even in the presence of severe varus deformity – one scalpel blade depth below joint line as far back as the midcoronal plane. I release the infra-patellar bursa and excise the fat pad in the region of the antero-lateral corner of the tibia. This is followed by a notchplasty using a narrow osteotome which exposes the cruciates after which by using sharp dissection I release both cruciates from their femoral attachment. I then dislocate the tibia anteriorly using a bone lever and place a second lever over the lateral edge of the tibia. The lateral meniscus and cruciates are then excised thus exposing the proximal tibia. Often in the presence of significant varus deformity there is an apparent external rotation deformity of the tibia. This is caused by an anteromedial osteophyte. On occasion this osteophyte is quite large and is most easily removed using a saw. Otherwise bone nibblers suffice with clearance of osteophyte at this stage being carried back as far as the mid-coronal plane of the tibia. The proximal tibial resection jig is then applied to the tibia. I place the rod distally at the ankle midway between the two malleoli so as to avoid cutting the tibia in valgus. At times I will err in favour of a varus cut but not by more than 1° (10 mm of medial or lateral displacement of the jig at the ankle changes the angle of the tibial cut by approximately 1°). I adjust the slope of the tibial cut to try and match the native slope on lateral tibial condyle. I always aim to remove at least 11 mm of bone from the lateral tibial plateau and I confirm this by using a caliper to measure the resected bone allowing 1.5 mm for the depth of the saw blade. In the presence of severe deformity this will leave a defect on the medial tibial condyle which will be discussed below. Caution must be used in every case with the saw blade to avoid damage to the anterior fibres of the superficial MCL on the medial side and to the popliteus in the postero-lateral corner. The commonest time to inadvertently damage the superficial MCL is during tibial resection. This often only involves the most anterior fibres of the MCL which results in medial laxity in flexion and will require a thicker insert and thus raise the joint line on the tibia. Also in surgical techniques, such as the LCS, where femoral rotation and thus the A-P femoral bone cuts are set off the mechanical axis of the tibia the resultant external rotation of the femur means that the femoral component is internally rotated. Surgeons are often unaware of this complication because the intact posterior fibres of the superficial MCL prevent laxity in extension.
D.E. Beverland
Having resected the proximal tibia, external rotation of the foot tends to bring its postero-medial corner forward where with sharp dissection the fibres of the deep MCL are released from the tibia. This is only required when there are osteophytes to remove from this area. In many cases of severe varus (>20°) there is a large slightly mobile osteophyte in this area that has to be carefully excised using sharp dissection. I now proceed to the anterior and posterior (AP) femoral cuts. I use the LCS which sets femoral rotation off the tibial axis. In severe varus I often do preliminary A-P cuts by cutting on top of the saw capture rather than through it which makes the cuts conservative by 5 mm. Either a conservative or definitive posterior femoral cut allows easy access to the posterior aspect of the knee when all osteophytes can be removed from the posterior femoral condyles as well as meniscal remains, loose bodies and any residual PCL (posterior cruciate ligament) attachment to the femur. At this stage in the operation all osteophytes have been removed from the tibia and the posterior aspect of the femur and the flexion gap can now be measured using a spacer block. The next step is a “pre-cut” or conservative cut on the distal femur. This cut takes off 5 mm less bone than the amount predicted to restore the distal femoral joint line. My pre-cut is always in 5° of valgus relative to the anatomical axis. Having done this cut any remaining osteophytes are removed from the medial and lateral sides of the femoral condyle and it also provides a good opportunity to remove osteophytes from the patella. An appropriately sized spacer block is then used to firstly assess the dimension of the extension gap and secondly its collateral balance. The latter is assessed by applying a gentle varus and then valgus stress to the extension gap with the spacer block in place and the knee in full extension. The extension gap is correct when, with the spacer block in situ, the weight of the leg completely closes the extension gap so that the flat surfaces of the spacer block, distal femur and proximal tibia are in full contact. This indicates full extension. Then with gentle varus and then valgus stress the gap opens 1–2 mm on both sides. This indicates that the tension in the posterior capsule and the two collaterals are equal – this is a “balanced gap”. There are a number of possible scenarios. 1. The extension gap is balanced and is 5 mm less than the flexion gap – solution – re-cut to remove 5 mm more distal femur thus producing balanced and equal flexion and extension gaps. 2. The extension gap is snug medially but slack laterally – solution – according to my hypothesis this suggests that the initial 5° cut is in too much valgus for this knee and
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between the medial femoral and tibial condyles. Then with a sucker the postero-medial capsule can be palpated to confirm that it is tight before cutting it under direct vision. This has the effect of both correcting the fixed flexion deformity as well as the varus deformity as shown in Fig. 3. Again this achieves the aims of balanced and equal flexion and extension gaps without raising the joint line on the distal femur. Release of the postero-medial capsule in the varus knee is only required in knees with fixed flexion of >20° and even then not always.
Tibial Defect in a Varus Knee Fig. 3 Effect of cutting a tight postero-medial capsule. As well as correcting the fixed flexion deformity it also corrects the varus deformity. NB knee is in extension
At this stage the final cuts can be made and the components inserted. In the situation of a tibial defect as shown in Fig. 4 careful inspection normally reveals that the defect is crescentshaped with an anterior and posterior horn. This crescentshaped area of bone is very sclerotic and strong and therefore the area of unsupported bone on the medial side of the white line, as shown in Fig. 4, is small. As a result I use a standard cementless tibial component without wedges, without a longer stem and without bone graft.
Soft-Tissue Balance in the Valgus Knee with or without Fixed Flexion
Fig. 4 Varus knee with a significant medial tibial defect demonstrating that the true area of unsupported surface is small
therefore depending on the discrepancy I re-cut in 3 or 4°. This does not raise the joint line but takes more bone off the tighter medial side and thus achieves the aims of balanced and equal flexion and extension gaps. 3. The extension gap is snug laterally and slack medially which is less common in a varus knee – solution – same scenario as number 2 except that the re-cut is in 6 or 7°. 4. With the spacer block in place and the knee fully extended when the extension gap is stressed into varus and valgus the gap opens both medially and laterally but more so laterally. This indicates that the posterior capsule is tight on the medial side – solution – the spacer block is removed the knee is kept in extension and the posterior capsule is put under tension by using a laminar spreader placed
I use a medial approach for all valgus knees irrespective of deformity. The tibial preparation tends to be more straightforward than in the varus knee. Any tibial defects tend to be smaller and are usually contained in that the cortical rim is intact. The depth of tibial resection from the normal medial side should normally be less than 10 mm. This is because of the normal inherent varus tibial slope which means less bone is removed from the medial side when the tibia is cut in neutral relative to the mechanical axis. As in the varus knee having done the A-P femoral cuts all osteophytes are cleared from the posterior femoral condyles. Again I use a 5° distal femoral pre-cut after which the extension gap is assessed in exactly the same way as for the varus knee. However unlike the varus knee posterior capsule release is commonly required. In the valgus knee when the extension gap is assessed with the spacer block often the medial laxity is greater than can be corrected by just performing a re-cut in 6 or 7° and this indicates the need to cut the postero-lateral capsule. As before the knee must be extended and then the postero-lateral capsule is put under tension using laminar spreaders positioned laterally between the lateral femoral and
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a neutral mechanical axis. This philosophy does go against perceived wisdom which states firmly that a knee that is not neutrally aligned has an increased risk of early failure [10]. Although there is now some evidence that that knees left in more than 3° of varus or valgus relative to the mechanical axis do not necessarily have a higher failure rate [11]. Doing an initial “pre-cut” of 5° on the distal femur allows the definitive cut to be both measured in terms of the amount of bone that needs to be removed to achieve full extension and also adjusted in angle so as to balance the collateral ligaments. The technique also depends on the careful removal of osteophytes and when required release of either the postero-medial or postero-lateral capsule. The former is rarely required in the varus knee but the latter is frequently required in the valgus knee.
Fig. 5 Valgus knee with tight postero-lateral capsule demonstrating the effect of cutting this structure. Not only does it correct fixed flexion it also corrects the valgus deformity. NB the knee is in extension
tibial condyles. In this position the popliteus tendon is clearly visible, as illustrated by the yellow band in Fig. 5 and is also clearly not tight. When using the sucker it is easy to palpate the tight region of the postero-lateral capsule just lateral to the popliteus. When this is cut using a small blade on a long handle it is normal to see the lateral side of the joint open up. As with the varus knee this corrects both the fixed flexion and the valgus deformity as shown in Fig. 5. In the type II valgus knee where the MCL has become stretched caution is required. In this situation the knee should not be fully balanced in extension but with the spacer block in place the extension gap should stay closed medially. In other words there should be no gapping medially unless a valgus stress is applied. Type II valgus knees tend to occur in low demand elderly female patients and because the knee is stable in flexion they do not complain of instability.
Summary My philosophy of soft-tissue balance is based on the assumption that the medial and LCLs do not contract and therefore should not be released irrespective of deformity. I also feel that we should be trying to restore pre-morbid alignment and not necessarily be always focussed on the restoration of
References 1. Insall JN. Technique of total knee replacement. Instr Course Lect 1981;30:324. 2. Hamelynck K. LCS Mobile Bearing Total Knee Arthroplasty. Springer, Berlin 2002:96–100. 3. Tokuhara Y, Kadoya Y, Nakagawa S, Kobayashi A, Takaoka K. The flexion gap in normal knees. An MRI study. J Bone Joint Surg Br 2004;86(8):1133–1136. 4. Thompson NW, Ruiz AL, Breslin E, Beverland DE. Total knee arthroplasty without patellar resurfacing in isolated patellofemoral osteoarthritis. J Arthroplasty 2001;16(5):607–612. 5. Sperner G, Wantschek P, Benedetto KP, Glotzer W. Spatergebnisse bei Patellafrakturen. Akt Traumatol 1990;20:24. 6. Bellemans J, Banks S, Victor J, Vandenneucker H, Moemans A. Fluoroscopic analysis of the kinematics of deep flexion in total knee arthroplasty. Influence of posterior condylar offset. J Bone Joint Surg Br 2002;84(1):50–53. 7. Arabori M, Matsui N, Kuroda R, Mizuno K, Doita M, Kurosaka M, Yoshiya S. Posterior condylar offset and flexion in posterior cruciate-retaining and posterior stabilized TKA. J Orthop Sci 2008;13(1):46–50. 8. Hanratty BM, Thompson NW, Wilson RK, Beverland DE. The influence of posterior condylar offset on knee flexion after total knee replacement using a cruciate-sacrificing mobilebearing implant. J Bone Joint Surg Br 2007;89(7):915–918. 9. Insall J. A midline approach to the knee. J Bone Joint Surg 1971;53-A(8):1584–1589. 10. Ritter MA, Faris PM, Keating EM, Meding JB. Postoperative alignment of total knee replacement. Its effect on survival. Clin Orthop Relat Res 1994;299:153–156. 11. Mark W Pagnano MW, Trousdale RT, Berry DJ, Parratte S. The mechanical axis may be the wrong target in computerassisted TKA. AAOS Podium No:203, 2008, March 06, Room 3014–3018.
Revision Total Knee Arthroplasty with Bone Loss Josef Hochreiter and Karl Knahr
Introduction It is anticipated that in the near future far more patients will seek help for knee osteoarthritis and that total knee replacements (TKR) will increase as a consequence of age, epidemic proportions of obesity and a reduced willingness to accept physical incapacity. Consequently, also the number of revision TKRs (RTKR) will increase [1, 2].
the individual patient. Several classifications have been proposed, the Anderson Orthopaedic Research Institute (AORI) classification described by Engh being the most frequently used, with type I, II and III defects for the femur and tibia separately [4]. After examination of the soft tissue and ligaments, a classification system permits the surgeon to properly plan the surgery (type of bone graft, implant design), and to analyse the clinical results after RTKR. Because the defects are often underestimated pre-operatively, the final classification is made after debridement (Fig. 1).
Classification Mal-alignment and instability are common indications for RTKR, although aseptic loosening, osteolysis and infection are reported to be the three most frequent reasons for the loosening of a knee prosthesis. Other factors include extensor mechanism dysfunction or loss of function [3]. The surgical options in RTKR will depend on the underlying cause, which must be understood prior to surgery to avoid a poor outcome. In the majority of cases the reason is quite obvious to the clinician but sometimes it proves to be very subtle. Patient history, physical examination, (dynamic) X-rays, synovial fluid analysis, CT for rotatory alignment, or radionucleotide scans are necessary to make the proper diagnosis. A careful functional assessment of the patient’s level of activity and his/her expectations should also be performed and referred pain should be excluded. The use of a classification system for bone defects is helpful in determining the optimal therapeutic option for
Restoration of the Joint Line Re-establishing a correct joint-line position is recognized as one of the most important factors in achieving normal ligament balancing and normal knee kinematics. Failure of Total Knee Replacement is always accompanied by major bone loss and pathologic changes in ligaments. This is the reason why elevation of the joint-line occurs predominantly in revisions. We know from the literature that joint-line elevation can be seen in nearly 80% of the revisions, but only in 1% of the primaries [5]. Diagnosis of joint-line elevation is easy to recognize by comparing the pre- and post-operative height from tibial tubercle to tibial plateau in lateral X-rays and in measuring the position of the patella. Mal-position of the joint-line is connected with different clinical conditions such as anterior knee pain, mid-flexion instability and reduction of flexion mobility.
Anterior Knee Pain Josef Hochreiter () Department of Orthopaedic Surgery, St. Vincent’s Hospital, Linz, Austria e-mail:
[email protected]
Join-line elevation in relation to the tibia is followed by patella baja which is the reason for impingement with the polythene and tibial tray in flexion [6].
G. Bentley (ed.), European Instructional Lectures. European Instructional Course Lectures 9, DOI: 10.1007/978-3-642-00966-2_22, © 2009 EFORT
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Fig. 1 Anderson Orthopaedic Research Institute Classification (AORI)
Mid-Flexion Instability Despite sufficient stability in extension and flexion there is certain instability in mid-flexion when the joint-line is elevated. The patient complains of pain and insecurity when climbing stairs and walking downhill [7].
Fig. 2 Multi-directional/uni-directional movement and wear
Reduction of Flexion Mobility
Treatment Options for Bone Loss
One important reason for joint-line elevation in revision is the down-sizing of the femur as a result of bone loss. A smaller femoral implant and posterior offset lead to a reduction of flexion mobility [8]. Improving the surgical technique of revisions is the most important factor to avoid joint-line elevation. The principles in the reconstruction of the knee joint are the restoration of the tibia as well as the sizing and positioning of the femur in accordance with flexion and extension stability.
Because the joint-line has to be restored in revision TKA to enable a balanced and stable knee, it is crucial to manage the bone loss. AORI Type I defects may be filled with cement, morsellized bone graft or metal augments. AORI Type II defects <5 mm may also be filled with cement. For defects between 5 and 10 mm, metal augments should be used. Defects over 10 mm can be restored with structural bulk allografts or with metal augments. AORI Type III defects can be reconstructed with metal augments, structural bulk allografts, tantalum cones or custom prosthesis [10].
Mobile-Bearing Revisions Mobile-bearing knees were designed to reduce polyethylene wear. Femoro-tibial contact areas were increased in order to reduce contact stresses. It has been proved that the principle of uni-directional and multi-directional movement of the metallic implant over the mobile insert is a leading factor to reduce polyethylene wear (Fig. 2) [9]. Mobile bearings provide a significant advantage in the performance of revision knee arthroplasties. The advantages provided by using a rotating platform include wear reduction in torque (and loosening) forces on the proximal tibia, and a significant reduction in stress on a constrained polyethylene post.
Cement Filling For smaller AORI Type I defects cement can be used alone (Fig. 1a, b) or in combination with screws. Ritter [11] treated 57 tibial defects in primary TKAs with cement and screws. With an average filling of 9 mm, no component loosening could be seen within a minimum of 3 years. Dorr et al. [12] recommended that the cement column filling a tibial deficit should not exceed 5 mm.
Morsellized Bone Grafting and Impaction Grafting Good results of morsellized bone grafting in total hip arthroplasty and the ability of the graft to incorporate and remodel
Revision Total Knee Arthroplasty with Bone Loss
has led to the use of this technique in revision TKA. Autogenous or allograft morsellized bone can fill smaller defects (AORI Type I). Larger defects have to be contained with wire mesh and the bone has to be impacted. Benjamin et al. [13] was able to show good radiographic incorporation at a 2-year follow-up. With a histological evaluation, Whiteside and Bicalho [14] demonstrated that the grafts re-vascularised and re-modelled. Lotke et al. [15] treated 48 patients with impaction grafting. In 11 patients stainless steel mesh was additionally used. At follow-up after 3.8 years there were no mechanical failures and there was good radiographic incorporation of the graft. However, there was a 5% incidence of infections.
Modular Metal Augmentation AORI Type II and larger uncontained defects can be treated with modular metal augments. The first use of wedges in the treatment of bone deficiencies was reported by Brand et al. [16] in 1989. A large variety of augments including hemi-wedges, full wedges and spacers are available for the femoral and tibial components and these modular augments are available in most revision systems (Fig. 3). Due to the variety of augments in most cases the jointline can be restored using this method (Fig. 4). In order to fit these wedges into the bone defect precise cuts have to be made. In smaller bone defects this can lead to additional bone loss.
a
Fig. 4 (a) Intra-operative Bone loss (AORI Type II) and (b) post-operative X-ray
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a
b
Fig. 3 Wedges and sleeves
In order to decrease the load acting upon the wedges and therefore enhance the stability, the revision components are normally implanted using straight or offset stems. Brand et al. [16] and Patel et al. [17] demonstrated 25% non-progressive radiolucencies without clinical correlation at 3.5 and 7 years respectively. Although long-term results are not yet available, mid-term results are satisfactory. Patel et al. [17] treated 102 patients with an AORI Type II defect using metal wedges and stems. At a 7-year follow-up (range 5–11 years) he demonstrated a survival rate of 92%.
Structural Allograft Bulk or structural allografts should only be used for large bone defects AORI Type II or III. The allograft can be used
b
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to reconstruct femoral or tibial defects. Mostly femoral heads are used to remodel the lost bone. In cases where the entire distal femur or proximal tibia is missing the allograft has to be united with good structural host bone using a step cut, and the union point has to be by-passed with a cemented stem. Backstein et al. [18] treated 68 patients with over 10 mm femoral and between 20 and 40 mm tibial defects using structural allografts. At a 5.4-year follow-up he described 13 graft-related complications: 1 graft non-union, 3 aseptic loosenings, 3 peri-prosthetic fractures, 2 instabilities and 4 infections (6.5%). Clatworthy et al. [19] performed 52 revision TKAs using grafts. He reported a 5-year success rate of 92%, which dropped to 72% at 10 years and an infection rate of 8%. Parks and Engh [20] performed a histological analysis of 9 bulk allografts that were used in revision TKA after an average 41 month. No grafts collapsed, but new bone only grew over dead bone in the periphery and there were no signs of revascularisation. Dorr et al. [12] treated 24 knees with tibial defects with bone grafts. At a 3–6-year follow-up he demonstrated 22 unions and 2 non-unions of which one collapsed. He recommended a bone graft for defects of the tibial plateau involving more than 50% of the bone support.
Trabecular Metal Cones In cases of large bone defects tantalum cones can be used. When processed into trabecular porous metal it demonstrates a high strength and low stiffness. Trabecular metal cones are manufactured in various standard forms to fill metaphyseal defects of the femur and tibia. The rough surface of the metal has a high friction coefficient against the bone, thus providing primary stability in a press-fit fixation. The bone-metal interface is not cemented and allows bone ingrowth into the porous surface which creates a secondary stability. The implant is then cemented onto the tantalum plateau. Additionally a stemmed revision system has to be used to bridge the defect and to stabilise the prosthesis. Radnay and Scuderi [10] implanted 10 tibial and 2 femoral cones in AORI Type II and III defects. At a 10-month follow-up good radiographic incorporation with no evidence of bone resorption or progressive radiolucent lines could be seen. Although the first results are promising we have to wait for long-term follow-ups.
Custom Megaprosthesis In AORI Type III defects with major metaphyseal bone loss custom tumour megaprosthesis can be used to restore the
Josef Hochreiter and Karl Knahr
joint-line. Bruns et al. [21] used MUTAR megaprosthesis with a conical fluted stem to bridge bone defects in 25 patients treated for bone tumours. At 2.5-year follow-up he had a 87% survival rate. There was no radiological evidence of loosening. Stem stress-shielding was seen in 11 patients. Kawai et al. [22] treated 55 patients with a malignant tumour of the distal part of the femur using the Lane-Burstein prosthesis with a 85, 67 and 48% survival rate at 3, 5 and 10 years. Springer et al. [23] used the modular segmental kinematic rotating-hinge prosthesis to treat 25 patients with nonneoplastic bone loss. At 5-year follow-up he had an increase of the Knee Society score from 45.4 pre-operatively to 75.5 post-operatively The most common complication was deep infection (5 patients).
Conclusion In revision total knee surgery the joint-line has to be reconstructed in order to create a stable and balanced knee. Upon removal of the implant, care must be taken to preserve as much host bone as possible. The extent of bone loss is assessed pre- and intra-operatively so that the surgeon can choose the ideal technique to fill the defect. The AORI classification system is the most frequently used to quantify bone loss. In most cases AORI Type I defects can be treated with cement filling alone or in combination with screws. Morsellized auto- or allografts can also be used to fill these contained defects. Larger defects can be treated by impacting the morsellized graft and by containing it with wire mesh. AORI Type II and smaller Type III defects can be managed in most cases by using metal augments and stemmed implants. There is a large variety of these augments including hemi-wedges, full wedges and spacers, which are available in most revision systems. In case of larger metaphyseal defects structural bulk allografts, tantalum cones and megaprosthesis have to be considered as salvage alternatives.
References 1. Kurtz S, Ong K, Lau E, et al. “Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030”, J. Bone Joint Surg. Am. (2007), 89: 780–785 2. Vessely M B, Whaley A L, Harmsen W S, et al. “The Chitranjan Ranawat Award: Long term survivorship and failure modes of 1000 cemented condylar total knee arthroplasties”, Clin. Orthop. Relat. Res. (2006), 452: 28–34 3. Sharkey P F, Hozack W J, Rothman R H, Shastri S, Jacoby S M. “Why are total knee arthroplasties failing today”, Clin. Orthop. Relat. Res. (2002), 404: 7–14
Revision Total Knee Arthroplasty with Bone Loss 4. Engh G A, Ammeen D J. “Classification and preoperative radiographic evaluation: Knee”, Orthop. Clin. North Am. (1998), 29 (2): 205–217 5. Partington P F, Sawhney J, Rorabeck C H, Barrack R L, Moore J. “Joint line restoration after revision total knee arthroplasty”, Clin. Orthop. Relat. Res. (1999), 367: 167–175 6. Figgie H E, Goldberg V M, Heiple K G, Moller H S, Gordon N H. “The influence of tibial-patellofemoral location on function of the knee in patients with the posterior stabilized condylar knee prosthesis”, J. Bone Joint Surg. Am. (1986), 68 (7): 1035–1040 7. Martin J W, Whitside L A. “The influence of joint line position on knee stability after condylar knee arthroplasty”, Clin. Orthop. Relat. Res. (1990), 259: 146–156 8. Yoshii I, Whiteside L A, White S E. “Influence of prosthetic joint line position on knee kinematics and patellar position”, J. Arthroplasty (1991), 6: 169–177 9. McEwen H M, Fisher J, Goldsmith A A, Auger D D, Hardaker C, Stone M H. “Wear of fixed bearing and rotating platform mobile bearing knees subjected to high levels of internal and external tibial rotation”, J. Mater. Sci. Mater. Med. (2001), 12(10–12): 1049–1052. 10. Radnay C S, Scuderi G R. “Management of bone loss: Augments, cones, offset stems”, Clin. Orthop. Relat. Res. (2006), 446: 83–92 11. Ritter M A. “Screw and cement fixation of large defects in total knee arthroplasty”, J. Arthroplasty (1986), 1: 125–129 12. Dorr L D, Ranawat C S, Sculco T A., et al. “Bone graft for tibial defects in total knee arthroplasty”, Clin. Orthop. Relat. Res. (1986), 205: 153–165 13. Benjamin J, Engh G, Parsley B, et al. “Morselized bone grafting of defects in revision total knee arthroplasty”, Clin. Orthop. Relat. Res. (2001), 392: 62–67
223 14. Whiteside L, Bicalho P S. “Radiologic and histological analysis of morselized allograft in revision total knee replacement”, Clin. Orthop. Relat. Res. (1998), 357: 149–156 15. Lotke P A, Carolan G F, Puri N. “Impaction grafting for bone defects in revision total knee arthroplasty”, Clin. Orthop. Relat. Res. (2006), 446: 99–103 16. Brand M G, Daley R J, Ewald F C, et al. “Tibial tray augmentation with modular metal wedges for tibial bone stock deficiency”, Clin. Orthop. Relat. Res. (1989), 248: 71–79 17. Patel J V, Masonis J L, Guerin J, et al. “The fate of augments to treat type-2 bone defects in revision knee arthroplasty”, J. Bone Joint Surg. Br. (2004), 86: 195–199 18. Backstein D, Safir O, Gross A. “Management of bone loss: Structural grafts in revision total knee arthroplasty”, Clin. Orthop. Relat. Res. (2006), 446: 104–112 19. Clatworthy M G, Ballance J, Brick G W, et al. “The use of structural allograft for uncontained defects in revision total knee arthroplasty. A minimum 5 year review”, J. Bone Joint Surg. Am. (2001), 83: 404–411 20. Parks N L, Engh G A. “The Ranawat Award. Histology of nine structural bone grafts used in total knee arthroplasty”, Clin. Orthop. Relat. Res. (1997), 345: 17–23 21. Bruns J, Delling G, Gruber H, et al. “Cementless fixation of megaprostheses using a conical fluted stem in the treatment of bone tumours”, J. Bone Joint Surg. Br. (2007), 89: 1084–1087 22. Kawai A, Muschler G F, Lane J M, et al. “Prosthetic knee replacement after resection of a malignant tumor of the distal part of the femur. Medium to long-term results”, J. Bone Joint Surg. Am. (1998), 80: 636–647 23. Springer B D, Sim F H, Hanssen A D, et al. “The modular segmental kinematic rotating hinge for nonneoplastic limb salvage.” Clin. Orthop. Relat. Res. (2004), 421: 181–187
Ankle Arthritis X. Crevoisier
Definition Ankle arthritis (Greek arthron: joint, -itis: inflammation) strictly means inflammation of the ankle joint. This definition allows usage of “ankle arthritis” as a purely descriptive term for an ankle condition independently from its aetiology.
Epidemiology and Aetiology There are limited data documenting the precise incidence of ankle arthritis. It has been reported, however, that 15–20% of the population in Europe and North America suffers from some form of arthritis, and that approximately 10% of all cases of arthritis involve the ankle joint [1–5]. Unlike arthritis of the hand, spine, hip and knee, primary ankle arthritis is rare [6]. In 70–80% of cases, ankle arthritis is caused by trauma and/or abnormal biomechanics, including fractures of the ankle, osteochondral damage, and chronic instability resulting from ligamentous injuries [7–9]. Another important aetiology for ankle arthritis is rheumatoid arthritis in 10–15% of cases [10, 11]. Other causes include deformities of the lower limbs, infection, metabolic disturbances, neurologic diseases and idiopathic conditions.
Pathophysiology Several factors contribute to the complex pathogenesis of ankle arthritis. This pathogenesis includes several paradoxes and is poorly understood. The ankle carries loads of
X. Crevoisier Centre Hospitalier Universitaire Vaudois (CHUV), Site Hôpital Orthopédique, Pierre-Decker 4, 1011 Lausanne, Switzerland e-mail:
[email protected]
up to five times the body weight during level walking [12] and these loads increase while running or performing more demanding physical activities. The other lower limb joints are subjected to similar loads during ambulation [13]. Furthermore, the ankle is subjected to more weight-bearing force per square centimetre than any other joint in the body [8]. Finally, the ankle is the most commonly-injured human joint [8]. Yet, the incidence of symptomatic ankle arthritis compared to that of the hip or the knee appears to be much lower. All these considerations suggest that the ankle is associated with unique anatomic, biomechanical and metabolic properties which may explain its resilience to symptomatic degeneration. Articular Cartilage. One of these special properties is certainly the cartilage thickness and its compressive modulus. The ankle has the thinnest cartilage of the lower limb joints and this cartilage is also quite uniform in thickness [14]. It has been shown that a thin cartilage has a high compressive modulus [14]. A thin cartilage with high compressive modulus acts to equalize the stresses across the joint [15]. Furthermore, a mathematical model has shown that as pressure through the ankle joint increases, the load-bearing area changes from two localized areas to a much larger region [16]. In other terms, under loading, the joints becomes more congruent, which may help to dissipate force. Another advantage of these changes in congruity may be a better cartilage lubrication and nutrition [16]. Contact area, articular congruence and stability. Adequate stability is required to preserve the articular congruence and the largest contact area while loading the ankle. It has been shown that medial structures are the primary stabilizers of the ankle [17–19]. Neither lateral displacement of the lateral malleolus nor mortise widening were shown to have significant impact on ankle articular contact area. Conversely, sectioning the deltoid ligament was shown to decrease the contact area by up to 30%. Trauma of the ankle joint more frequently affects the lateral than medial stabilizers and this may be a further explanation for its resilience to arthritis even in case of lateral insufficiency.
G. Bentley (ed.), European Instructional Lectures. European Instructional Course Lectures 9, DOI: 10.1007/978-3-642-00966-2_23, © 2009 EFORT
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Ankle arthritis will result from pathologic conditions that disturb these special anatomic, biomechanical and metabolic properties of the ankle. Trauma. Ankle fractures are the first cause of post-traumatic ankle arthritis [5]. The most cited study focussing on the development of ankle arthritis after rotational ankle fractures is that performed by Lindsjo in 1985 [7]. The average incidence of post-traumatic arthritis was 14% in this study. It was reported that, using the Weber classification, arthritis occurred in 4% of type A fractures, in 12% of type B fractures and in 33% of type C fractures. The quality of the initial reduction and fixation was reported to be an important determinant but the severity of the injury itself was also thought to have strong predictive value for outcome. The relative importance of these factors was not established. A further determinant of outcome is the presence or not of a posterior fragment. A fragment larger than 20% of the tibial articular surface was shown to be associated with post-traumatic arthritis in 34% of cases [20, 21]. Tibial plafond and talus fractures are less common than rotational fractures of the ankle and, unlike the latter, they are frequently caused by high energy trauma. The consequence of this is the risk of avascular necrosis of the bone and a higher initial articular damage than in rotational fractures. Thus, the prognosis depends not only upon the adequacy of the reduction and fixation but also upon the osteochondral vitality [22, 23]. Chronic lateral ankle laxity caused by lateral ligament injuries has been shown to cause unbalanced loading of the medial joint space and to possibly result in medial compartment osteoarthritis [24, 25] and to account for 15% of post-traumatic ankle arthritis [5]. Rheumatoid arthritis. The ankle is less commonly affected by rheumatoid arthritis than the hindfoot and the forefoot joints The ankle joint is involved in a late stage of rheumatoid arthritis and is usually affected only in the patients with severe disease [26]. The pathophysiology of rheumatoid arthritis of the ankle includes synovitis leading to cartilage erosion and destruction of the stabilizers. Another aspect of pathophysiology in the rheumatoid ankle is the abnormal biomechanics caused by hindfoot deformities with typical lateralization of the forces acting through the ankle joint [27, 28]. Abnormal hindfoot biomechanics. Mal-alignment of the hindfoot may also cause abnormal force distribution across the ankle joint (Fig. 1). An in vitro study simulating flatfoot deformity by sectioning the arch supporting structures demonstrated lateral shift of the peak pressure and 35% reduction of the articular contact area when axial load was applied to the ankle [29]. The authors concluded that this abnormal biomechanical behaviour associated with acquired flatfoot
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Fig. 1 Abnormal hindfoot alignment causes pathological force distribution across the ankle joint. This a-p weight-bearing radiograph of the ankle shows lateral joint space narrowing, lateral tilt and translation of the talus, and fatigue fracture of the fibula as consequences of longstanding hindfoot valgus mal-alignment
deformity may be responsible for long-term degenerative changes in the ankle and hindfoot. Conversely, pes cavus deformity was found to be associated with chronic lateral instability of the ankle and subsequent medial ankle arthritis [30].
Clinical Presentation and Functional Limitation Symptomatology and clinical examination. As mentioned above, despite its relatively high prevalence, ankle arthritis is less frequently symptomatic than arthritis of the hip or that of the knee. Typical clinical presentation includes swelling, stiffness, and pain in the anterior tibio-talar area. Pain increases during uphill walking, due to difficulties of extending the ankle during ambulation. Varus or valgus deformity is often present (Fig. 2) and careful clinical and radiological examination is mandatory (Fig. 3) to establish if the deformity has intra- or extra-articular aetiology, or both. Assessing the exact deformity pattern is very important for the choice of treatment. A further step of clinical examination is to assess the active and passive function of the neighbouring joints as well as the foot alignment.
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Fig. 2 Clinical appearance of ankle arthritis frequently includes swelling and mal-alignment. In this case varus mal-alignment is present
Gait analysis. There are few studies reporting results of gait analysis in ankle osteoarthritis. Shih et al. [31] evaluated twenty patients with ankle arthritis and reported diminished ankle plantarflexion and dorsiflexion torques; velocity, stride length, and cadence were decreased in arthritic patients, which is consistent with the temporal-distance parameters described by Khazzam et al. Amongst 34 ankle arthritis patients [32]; the arthritic limbs had shorter singlelimb-stance and longer double-stance during free and fast walking speeds; the magnitude of vertical forces during push-off were reduced in arthritic ankles. Stauffer et al. [12] reported that arthritic patients had reduced motion and altered their gait to reduce forces acting across the ankle joint. Zerahn and Kofoed [33] reported decreased velocity, range of motion and increased foot contact duration in arthritic patients. Khazzam et al. [32] showed altered kinematic data in all planes for tibial, hindfoot and forefoot motion. Quality of life. A recent study conducted by Glazebrook et al. [2] demonstrated that patients with end-stage ankle arthritis had, severe pain, diminished health-related quality
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Fig. 3 Weight-bearing a-p radiograph of the ankle seen in Fig. 1. The intra-articular origin of the varus mal-alignment is demonstrated with significant narrowing of the medial joint space. Deltoïd ligament shortening and lateral ligament insufficiency can also be suspected based on this radiograph and should be confirmed clinically. If TAR is intended in this case these factors are important for the pre-operative planning
of life, limited physical function, and diminished physical ability to fulfil occupational duties that are at least as severe as that in patients with end-stage hip arthrosis. Moreover, ankle arthritis patients were shown to experience greater emotional and mental distress than did those with end-stage hip arthrosis.
Radiological Presentation Osteoarthritis. Basic radiological examination includes weight-bearing a-p and lateral X-rays of the ankle. Classic osteoarthritis signs include joint space narrowing, subchondral sclerosis, subchondral cysts and osteophytes. Specific signs of ankle osteoarthritis are flattening of the talar tome and forward translation of the talus (Fig. 4). While examining the X-rays, special attention should be given to the alignment of the ankle in the frontal plane (Fig. 3). If extra-articular
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Fig. 4 Lateral weight-bearing radiograph of an arthritic ankle. In post-traumatic arthritis, anterior translation of the talus, narrowing of the anterior joint space, and anterior tibio-talar flattening are frequently encountered
mal-alignment is suspected standing a-p views of the lower limbs will bring more information. Rheumatoid arthritis. Joint space narrowing is also associated with rheumatoid arthritis of the ankle but, unlike osteoarthritis, no subchondral sclerosis and no osteophytes are present.
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response at 9 months and 1 year. The duration of this response was varied and patient factors affecting the response remain unclear. In our experience, the efficacy of this treatment is inconstant in duration and amount of pain reduction but belongs certainly to the alternatives for patients who will/can not be operated. Intra-articular hyaluronic acid injection has also been shown to be efficient in Kellgren-Lawrence grades I and II [36] and even grade III [37] arthritis of the ankle with clinical effects lasting for 6 months or more [36] but the need for further investigation with larger trials and longer follow-up was recognized [37]. Footwear and braces. Major principles of footwear modification and braces are to simultaneously reduce motion of the ankle joint and improve forward progression of the tibia during ambulation. Ankle-foot orthoses may be used to reduce ankle motion. Nevertheless, it has been demonstrated that rigid ankle-foot orthoses are associated with abnormal forefoot biomechanics and that articulated ankle-foot braces are as efficient as rigid orthoses in limiting coronal hindfoot motion and simultaneously allow more physiological gait and kinetics [38]. Applying a rocker-bottom sole and a shock absorbing heel allows forward rotational translation of the tibia without sagittal motion of the ankle and, therefore, improves the gait pattern in cases of painful ankle arthritis. Lifestyle. Modifying professional activities (if possible!), and sports activities also belong to the therapeutic strategy for ankle arthritis. In case of obesity weight loss helps not only to reduce the constraints on the diseased ankle but also improves the efficacy of both conservative and surgical treatment options [39].
Conservative Treatment There is a paucity of studies focussing on or comparing conservative treatment options for symptomatic ankle arthritis and a recent update has concluded that the role and effectiveness for conservative treatment needs to be further determined [34]. Medication. As for other painful joint conditions nonsteroidal anti-inflammatory drugs are often the first step of conservative treatment but their long-term use may be associated with complications. Intra-articular corticosteroid is often used to decrease inflammation and pain [8]. There is only one recent publication [35] (level 2 of clinical evidence) reporting the use of intra-articular corticosteroid injection at the ankle. The authors reported improvement following corticosteroid injection up to 6 months post-injection. The magnitude of the response at 2 months was found to predict a sustained
Surgical Treatment Total ankle replacement (TAR) and ankle arthrodesis are the major surgical treatment options for ankle arthritis. Arthroscopic debridement, articular distraction using external fixation devices, and supramalleolar and/or hindfoot corrective osteotomies have also been reported and will be briefly discussed. Arthrodesis. Since its first description by Albert in 1879 [40] arthrodesis has been historically the most commonlyapplied operative treatment for ankle arthritis. Ankle arthrodesis may be used for end-stage ankle arthritis but also for symptomatic and conservative treatment resistant ankle arthritis at any stage. Previous infections, large osteochondral defects, osteonecrosis of the talus and/or of the distal tibia, rheumatoid arthritis, metabolic arthropathies, failed
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total ankle replacement all are also indications for ankle arthrodesis. Numerous techniques of fixation have been described and have evolved through the time [8]. They include: cast fixation alone, compressive external fixation as developed by Charnley [41], and internal fixation with screws or plates. Ankle arthrodesis can be achieved by open procedure or arthroscopically. When compared with internal fixation, external compressive fixation has the disadvantage of a voluminous external device, of a higher non-union rate (21 vs. 5%) and of the increased infection rate (15 vs. 0%), mostly related to pin tracts [42]. Nevertheless, external compressive fixation is still used in cases of bad softtissue condition, recent infection (Fig. 5) and poor bone quality. The antero-lateral approach (Fig. 6) is most commonly used for open procedure and fixation is usually achieved using crossed screws (Figs. 7 and 8) [43]. Studies comparing screw and plate fixation have shown a higher rate of fusion with screws [43–46]. Less soft-tissue stripping and better compression at the fusion site may account for the better fusion rate [8]. Furthermore, in vitro assessment of
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Fig. 6 Intra-operative view of an ankle arthrodesis. The anterolateral approach with distal peroneal osteotomy allows easy visualization of the ankle joint and permits good control of the fixation position, especially in the sagittal and coronal planes
Fig. 7 Intra-operative view of ankle fusion with crossed screws. The ankle has been positioned in neutral dorsiflexion, slight valgus and external rotation
Fig. 5 Radiographs of an ankle arthrodesis performed for septic arthritis. External compressive fixation as described by Charnley is still used for ankle arthrodesis in case of bad soft tissues condition or recent articular infection
screw fixation has shown that crossed-screw fixation creates better primary stability than parallel-screw fixation [47]. When compared with open procedures, arthroscopic ankle fusion has been shown to be associated with reduced morbidity and hospitalization time, and fusion rate up to 97% [48]. Nevertheless, arthroscopic ankle arthrodesis is a difficult technique that is not to be used in case of significant mal-alignment [48]. After ankle arthrodesis the total mobility of the foot relative to the lower leg decreases by 70% in the sagittal plane [49]. Ankle immobility is partially compensated by increased sagittal motion in the hindfoot and midfoot (Figs. 9 and 10) and by increased coronal motion of the hindfoot [50, 51]. In order to facilitate this compensatory motion, the ankle should be fused in neutral dorsiflexion (Figs. 7 and 8), in slight (5–10°) external rotation and in
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Fig. 8 Ap (a) and lateral (b) weight-bearing radiographs showing bone union 4 months after ankle arthrodesis with compressive crossed screws
Fig. 9 Lateral functional weight-bearing radiographs in maximal flexion (a) and maximal extension (b) of a fused ankle. After ankle arthrodesis immobility is partially compensated by increased motion in the hindfoot and midfoot joints but this creates high constraints on these joints which potentially leads to secondary arthritis
5° of hindfoot valgus [49, 50]. This position and the absence arthritis of the sub-talar joint are major determinant of postoperative function and long-term outcome [50, 52]. Furthermore, footwear modification by adding a rocker-bottom sole allows almost normal ambulation after ankle arthrodesis has been performed [53]. One of the most frequently reported complication following ankle arthrodesis is non-union. Nevertheless, in recent series reporting the use of internal fixation with screws, the non-union rate did not exceed 10% [50, 52, 54, 55]. Risk factors for non-union include infection, smoking, poor vascular condition, general status after high energy trauma, aseptic osteonecrosis of the talus, pre-existing sub-talar joint arthrodesis, poor patient compliance and inadequate surgical
technique [54]. In smokers the risk for non-union is four times higher than in non-smokers. Infection is another important potential complication. Infection rates ranging from 4 to 19% have been reported [43, 50]. In terms of outcome, despite a high short- and mid-term patient satisfaction more critical long-term studies have uniformly demonstrated arthritis and restricted articular motion of the neighbour hindfoot joints, functional deficit and a significant alteration of the quality of life [56, 57]. Furthermore, 60% of patients with pre-existing sub-talar or mid-tarsal arthritis are expected to worsen these degenerative changes after ankle fusion [52, 58]. To our knowledge, ankle arthrodesis has not been shown to have negative influence on the knee.
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Fig. 10 Clinical function of the foot after ankle arthrodesis. The need for ankle fixation in neutral dorsiflexion is emphasized. Thus, plantarflexion (a) is much easier compensated than dorsal extension (b)
Total ankle replacement (TAR). The first total ankle arthroplasty was performed in 1970 using the concept of an inverted hip prosthesis [59]. This technique, however, had to be abandoned soon because of a high failure rate. Specific ankle implants were then designed. These first generation ankle prostheses were of two types: constrained or unconstrained [59]. The results were also poor with rates of implant loosening seen at up to 90% at 10 years. Early loosening was mainly attributed to the over- or under-constraint, and to the cemented fixation [59–61]. In the 1980s, semi-constrained second generation ankle prostheses were designed [5]. Initially they included two components and necessitated syndesmosis fusion. Most of the current models are now three-component mobile-bearing prostheses (Fig. 11). They have the potential to minimize bone resection (Figs. 11 and 12), maintain congruency, and respect the original anatomy of the ankle joint surfaces. Economical bone resection is thought to create better conditions in case
Fig. 12 Intra-operative view of a TAR procedure showing economical osseous resection associated with second generation implants
Fig. 11 Weight-bearing a-p radiograph of the ankle after TAR. Most of the current models are now three-component uncemented mobile-bearing prostheses that maintain congruency, respect the original anatomy of the ankle, and require minimal bone resection
of implant failure requiring conversion of the replacement to a fusion. All current ankle prostheses rely on bone ingrowth for implant fixation [5]. Uncemented fixation has the advantages of a minimal bone resection, and the absence of exothermic reaction. In vitro assessment of TAR has shown a better preservation of foot and ankle kinematics than after ankle arthrodesis [62]. Compared to ankle arthrodesis, in vivo assessment of TAR has shown better kinematics of the foot (Figs. 13 and 14), even if TAR does not restore normal movement or walking speed [63–65]. Nevertheless, gait improvement and pain significant pain reduction has been observed. Pain reduction is thought to be more determinant than articular motion for the normalization of gait [33].
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Fig. 13 Clinical function of the foot in maximal flexion (a) and extension (b) after total replacement of the left ankle. Even if TAR doesn’t restore physiologic motion, as illustrated in (b) where both ankles can be seen, it allows better kinematics than ankle fusion does
The current follow-up time of second generation prostheses is still too short to demonstrate that TAR is associated with less secondary degenerative changes of the neighbour hindfoot joints than ankle arthrodesis. Nevertheless, short and mid-term results are encouraging. Patient satisfaction rate is 60–90% and survival rate of the implants is 80–90% at 10 years [63, 64, 66, 67]. Complications associated with TAR include malleolar fractures in 6–10% of cases, skin necrosis in 2–14% of cases, aseptic loosening in 2–14% of cases, recurrent pain and stiffness in 3–5% of cases and infections in 4–5% of cases [63, 64, 67]. Skin necrosis, malleolar fractures, pain, and stiffness can usually be treated without implant removal. Major complications, however, frequently require conversion of the TAR to a fusion. Fortunately, the 80–90% union rate of ankle arthrodesis after failed ankle arthroplasty has
Fig. 14 Lateral radiographs of a prosthetic ankle showing maximal flexion (a) and extension (b). These figures can be compared with Figs. 9a and b. Partial preservation of ankle motion in TAR is associated with less compensatory motion in the hindfoot and midfoot joints
been shown to be almost equivalent to that of primary fusion [68, 69]. Total ankle replacement vs. arthrodesis: decision making. A recent systematic review of the literature concluded that intermediate outcome of TAR appears to be similar to that of ankle arthrodesis [70]. Nevertheless, the authors underlined the heterogeneity among existing studies and also concluded that their work exposed the major lack of objective, prospective, and controlled data on either procedure. Careful patient selection is probably a very important predictive factor. To be successful, TAR requires correct lower limb and hindfoot alignment, and adequate ligaments balancing. In case of hindfoot mal-alignment arthrodesis will be the solution of choice, unless corrective osteotomies are performed prior to TAR [71]. TAR is more appropriated for patients with low functional demand.
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Young age of the patient has not been demonstrated to have negative prognostic value for TAR [63, 66, 67]. In young patients presenting bilateral ankle arthritis or ankle arthritis associated to sub-talar or Chopart joint arthritis TAR will be preferred to fusion. In the following conditions ankle fusion will be preferred: recent or recurrent infection, severe osteopenia, osteonecrosis, poor skin quality, poor vascular condition. Articular distraction. Progressive articular distraction of the ankle in daily 1 mm increments using an external fixation devices has been described in 1999 by Van Roermund and Lafeber [72] The same group of physicians reported that In 73% of the patients, significant clinical benefit from joint distraction of severe OA ankles was maintained for at least 7 years [73] but that there was a need for further research to determine predictive factors of patient response to this treatment. Supra-malleolar or/and hindfoot corrective osteotomies. Few clinical studies reported the efficacy of peri-articular corrective osteotomies for ankle arthritis [74–76]. One reason for performing these procedures is to offer young patients a surgical alternative to major procedures in case of ankle arthritis. Another aim of corrective osteotomies is to provide favourable conditions for future TAR. Most of the studies to date are too small to allow firm conclusion about efficacy of these techniques. Nevertheless, there is one homogenous series of 25 patients that reported low tibial osteotomy to be indicated for varus-type osteoarthritis of stage 2 or stage 3a [74]. Arthroscopic ankle debridement. The role of arthroscopy in the management of patients with ankle arthritis cannot be ascertained from the current literature. A recent 5-year survival analysis revealed that over 50% of patients with osteoarthritic changes had major surgery or repeat arthroscopy at 5-year follow-up [77].
Conclusion and Perspectives The aetiology and epidemiology of ankle arthritis are well known. Trauma and its consequences has been identified as the major cause of ankle arthritis. Nevertheless, since the ankle is the most frequently–injured joint of the human body the relatively low prevalence of ankle arthritis still remains a partial mystery. Assessing the efficacy of the numerous treatment options for ankle arthritis is still a huge challenge and requires improvement in biomechanical understanding of the ankle, objective prospective evaluation, and development of ankle-specific outcome tools.
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References 1. Lawrence RC, Helmick CG, Arnett FC, Deyo RA, Felson DT, Giannini EH, Heyse SP, Hirsch R, Hochberg MC, Hunder GG, Liang MH, Pillemer SR, Steen VD, Wolfe F. Estimates of the prevalence of arthritis and selected musculoskeletal disorders in the United States. Arthritis Rheum 1998;41–5:778–99. 2. Glazebrook M, Daniels T, Younger A, Foote CJ, Penner M, Wing K, Lau J, Leighton R, Dunbar M. Comparison of health-related quality of life between patients with end-stage ankle and hip arthrosis. J Bone Joint Surg Am 2008;90–3: 499–505. 3. Hunsche E, Chancellor JV, Bruce N. The burden of arthritis and nonsteroidal anti-inflammatory treatment. A European literature review. Pharmacoeconomics 2001;19 Suppl 1:1–15. 4. Wang PP, Elsbett-Koeppen R, Geng G, Badley EM. Arthritis prevalence and place of birth: findings from the 1994 Canadian National Population Health Survey. Am J Epidemiol 2000; 152–5:442–5. 5. Saltzman 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. 6. Cushnaghan J, Dieppe P. Study of 500 patients with limb joint osteoarthritis. I. Analysis by age, sex, and distribution of symptomatic joint sites. Ann Rheum Dis 1991;50–1:8–13. 7. Lindsjo U. Operative treatment of ankle fracture-dislocations. A follow-up study of 306/321 consecutive cases. Clin Orthop 1985;199:28–38. 8. Thomas RH, Daniels TR. Ankle arthritis. J Bone Joint Surg Am 2003;85-A-5:923–36. 9. Valderrabano V, Horisberger M, Russell I, Dougall H, Hintermann B. Etiology of ankle osteoarthritis. Clin Orthop Relat Res Epub 2008/10/03. 10. Toolan BC, Hansen ST, Jr. Surgery of the rheumatoid foot and ankle. Curr Opin Rheumatol 1998;10–2:116–9. 11. Michelson J, Easley M, Wigley FM, Hellmann D. Foot and ankle problems in rheumatoid arthritis. Foot Ankle Int 1994;15–11:608–13. 12. Stauffer RN, Chao EY, Brewster RC. Force and motion analysis of the normal, diseased, and prosthetic ankle joint. Clin Orthop 1977–127:189–96. 13. Unsworth A. Tribology of human and artificial joints. Proc Inst Mech Eng [H] 1991;205–3:163–72. 14. Shepherd DE, Seedhom BB. Thickness of human articular cartilage in joints of the lower limb. Ann Rheum Dis 1999; 58–1:27–34. 15. Simon WH, Friedenberg S, Richardson S. Joint congruence. A correlation of joint congruence and thickness of articular cartilage in dogs. J Bone Joint Surg Am 1973;55–8:1614–20. 16. Wynarsky GT, Greenwald AS. Mathematical model of the human ankle joint. J Biomech 1983;16–4:241–51. 17. Curtis MJ, Michelson JD, Urquhart MW, Byank RP, Jinnah RH. Tibiotalar contact and fibular malunion in ankle fractures. A cadaver study. Acta Orthop Scand 1992;63–3:326–9.
236 18. Clarke HJ, Michelson JD, Cox QG, Jinnah RH. Tibio-talar stability in bimalleolar ankle fractures: a dynamic in vitro contact area study. Foot Ankle 1991;11–4:222–7. 19. Pereira DS, Koval KJ, Resnick RB, Sheskier SC, Kummer F, Zuckerman JD. Tibiotalar contact area and pressure distribution: the effect of mortise widening and syndesmosis fixation. Foot Ankle Int 1996;17–5:269–74. 20. Cedell CA. Supination-outward rotation injuries of the ankle. A clinical and roentgenological study with special reference to the operative treatment. Acta Orthop Scand 1967;Suppl 110:3+. 21. McDaniel WJ, Wilson FC. Trimalleolar fractures of the ankle. An end result study. Clin Orthop Relat Res 1977;122: 37–45. 22. Daniels TR, Smith JW. Talar neck fractures. Foot Ankle 1993;14–4:225–34. 23. Marsh JL, Buckwalter J, Gelberman R, Dirschl D, Olson S, Brown T, Llinias A. Articular fractures: does an anatomic reduction really change the result? J Bone Joint Surg Am 2002;84-A-7:1259–71. 24. Harrington KD. Degenerative arthritis of the ankle secondary to long-standing lateral ligament instability. J Bone Joint Surg Am 1979;61–3:354–61. 25. McBride DJ, Ramamurthy C. Chronic ankle instability: management of chronic lateral ligamentous dysfunction and the varus tibiotalar joint. Foot Ankle Clin 2006;11–3:607–23. 26. Belt EA, Kaarela K, Maenpaa H, Kauppi MJ, Lehtinen JT, Lehto MU. Relationship of ankle joint involvement with subtalar destruction in patients with rheumatoid arthritis. A 20year follow-up study. Joint Bone Spine 2001;68–2:154–7. 27. Jaakkola JI, Mann RA. A review of rheumatoid arthritis affecting the foot and ankle. Foot Ankle Int 2004;25–12:866–74. 28. Michelson J, Easley M, Wigley FM, Hellmann D. Foot and ankle problems in rheumatoid arthritis. Foot Ankle Int 1994; 15–11:608–13. 29. Friedman MA, Draganich LF, Toolan B, Brage ME. The effects of adult acquired flatfoot deformity on tibiotalar joint contact characteristics. Foot Ankle Int 2001;22–3:241–6. 30. Fortin PT, Guettler J, Manoli A, 2nd. Idiopathic cavovarus and lateral ankle instability: recognition and treatment implications relating to ankle arthritis. Foot Ankle Int 2002;23–11:1031–7. 31. Shih LY, Wu JJ, Lo WH. Changes in gait and maximum ankle torque in patients with ankle arthritis. Foot Ankle 1993;14–2:97–103. 32. Khazzam M, Long JT, Marks RM, Harris GF. Preoperative gait characterization of patients with ankle arthrosis. Gait Posture 2006;24–1:85–93. 33. Zerahn B, Kofoed H. Bone mineral density, gait analysis, and patient satisfaction, before and after ankle arthroplasty. Foot Ankle Int 2004;25–4:208–14. 34. Martin RL, Stewart GW, Conti SF. Posttraumatic ankle arthritis: an update on conservative and surgical management. J Orthop Sports Phys Ther 2007;37–5:253–9. 35. Ward ST, Williams PL, Purkayastha S. Intra-articular corticosteroid injections in the foot and ankle: a prospective 1-year follow-up investigation. J Foot Ankle Surg 2008;47–2: 138–44.
X. Crevoisier 36. Sun SF, Chou YJ, Hsu CW, Hwang CW, Hsu PT, Wang JL, Hsu YW, Chou MC. Efficacy of intra-articular hyaluronic acid in patients with osteoarthritis of the ankle: a prospective study. Osteoarthr Cartil 2006;14–9:867–74. 37. Karatosun V, Unver B, Ozden A, Ozay Z, Gunal I. Intraarticular hyaluronic acid compared to exercise therapy in osteoarthritis of the ankle. A prospective randomized trial with long-term follow-up. Clin Exp Rheumatol 2008;26–2:288–94. 38. Kitaoka HB, Crevoisier XM, Harbst K, Hansen D, Kotajarvi B, Kaufman K. The effect of custom-made braces for the ankle and hindfoot on ankle and foot kinematics and ground reaction forces. Arch Phys Med Rehabil 2006;87–1:130–5. 39. O’Reilly S, Doherty M. Lifestyle changes in the management of osteoarthritis. Best Pract Res Clin Rheumatol 2001;15–4: 559–68. 40. Albert E. Zur resektion des Kniegelenkes. Wien Med Presse 1879;20:705–8. 41. Charnley J. Compression arthrodesis of the ankle and shoulder. J Bone Joint Surg Br 1951;33B-2:180–91. 42. Moeckel BH, Patterson BM, Inglis AE, Sculco TP. Ankle arthrodesis. A comparison of internal and external fixation. Clin Orthop 1991–268:78–83. 43. Holt ES, Hansen ST, Mayo KA, Sangeorzan BJ. Ankle arthrodesis using internal screw fixation. Clin Orthop 1991–268: 21–8. 44. Chen YJ, Huang TJ, Shih HN, Hsu KY, Hsu RW. Ankle arthrodesis with cross screw fixation. Good results in 36/40 cases followed 3–7 years. Acta Orthop Scand 1996;67–5:473–8. 45. Maurer RC, Cimino WR, Cox CV, Satow GK. Transarticular cross-screw fixation. A technique of ankle arthrodesis. Clin Orthop 1991;268:56–64. 46. Morgan CD, Henke JA, Bailey RW, Kaufer H. Long-term results of tibiotalar arthrodesis. J Bone Joint Surg Am 1985; 67–4:546–50. 47. Friedman RL, Glisson RR, Nunley JA, 2nd. A biomechanical comparative analysis of two techniques for tibiotalar arthrodesis. Foot Ankle Int 1994;15–6:301–5. 48. Ferkel RD, Hewitt M. Long-term results of arthroscopic ankle arthrodesis. Foot Ankle Int 2005;26–4:275–80. 49. Abdo RV, Wasilewski SA. Ankle arthrodesis: a long-term study. Foot Ankle 1992;13–6:307–12. 50. Bertrand M, Charissoux JL, Mabit C, Arnaud JP. [Tibio-talar arthrodesis: long term influence on the foot]. Rev Chir Orthop Reparatrice Appar Mot 2001;87–7:677–84. 51. Wu WL, Su FC, Cheng YM, Huang PJ, Chou YL, Chou CK. Gait analysis after ankle arthrodesis. Gait Posture 2000; 11–1:54–61. 52. Ben Amor H, Kallel S, Karray S, Saadaoui F, Zouari M, Litaiem T, Douik M. [Consequences of tibiotalar arthrodesis on the foot. A retrospective study of 36 cases with 8.5 years of followup]. Acta Orthop Belg 1999;65–1:48–56. 53. Trouillier H, Hansel L, Schaff P, Rosemeyer B, Refior HJ. Long-term results after ankle arthrodesis: clinical, radiological, gait analytical aspects. Foot Ankle Int 2002;23–12: 1081–90. 54. Cooper PS. Complications of ankle and tibiotalocalcaneal arthrodesis. Clin Orthop 2001;391:33–44.
Ankle Arthritis 55. Takakura Y, Tanaka Y, Sugimoto K, Akiyama K, Tamai S. Long-term results of arthrodesis for osteoarthritis of the ankle. Clin Orthop 1999–361:178–85. 56. Coester LM, Saltzman CL, Leupold J, Pontarelli W. Longterm results following ankle arthrodesis for post-traumatic arthritis. J Bone Joint Surg Am 2001;83-A-2:219–28. 57. Fuchs S, Sandmann C, Skwara A, Chylarecki C. Quality of life 20 years after arthrodesis of the ankle. a study of adjacent joints. J Bone Joint Surg Br 2003;85–7:994–8. 58. Conti RJ, Walter JH, Jr. Effects of ankle arthrodesis on the subtalar and midtarsal joints. J Foot Surg 1990;29–4:334–6. 59. Henne TD, Anderson JG. Total ankle arthroplasty: a historical perspective. Foot Ankle Clin 2002;7–4:695–702. 60. Saltzman CL. Perspective on total ankle replacement. Foot Ankle Clin 2000;5–4:761–75. 61. Neufeld SK, Lee TH. Total ankle arthroplasty: indications, results, and biomechanical rationale. Am J Orthop 2000; 29–8:593–602. 62. Valderrabano V, Hintermann B, Nigg BM, Stefanyshyn D, Stergiou P. Kinematic changes after fusion and total replacement of the ankle: part 1: Range of motion. Foot Ankle Int 2003;24–12:881–7. 63. Buechel FF, Sr., Buechel FF, Jr., Pappas MJ. 10-year evaluation of cementless Buechel-Pappas meniscal bearing total ankle replacement. Foot Ankle Int 2003;24–6:462–72. 64. Anderson T, Montgomery F, Carlsson A. Uncemented STAR total ankle prostheses. 3 to 8-year follow-up of fifty-one consecutive ankles. J Bone Joint Surg Am 2003;85-A-7: 1321–9. 65. Piriou P, Culpan P, Mullins M, Cardon JN, Pozzi D, Judet T. Ankle replacement versus arthrodesis: a comparative gait analysis study. Foot Ankle Int 2008;29–1:3–9. 66. Kofoed H, Lundberg-Jensen A. Ankle arthroplasty in patients younger and older than 50 years: a prospective series with long-term follow-up. Foot Ankle Int 1999;20–8: 501–6.
237 67. Wood PL, Deakin S. Total ankle replacement. The results in 200 ankles. J Bone Joint Surg Br 2003;85–3:334–41. 68. Kitaoka HB, Romness DW. Arthrodesis for failed ankle arthroplasty. J Arthroplasty 1992;7–3:277–84. 69. Carlsson A, Markusson P, Sundberg M. Radiostereometric analysis of the double-coated STAR total ankle prosthesis: a 3–5 year follow-up of 5 cases with rheumatoid arthritis and 5 cases with osteoarthrosis. Acta Orthop 2005;76–4: 573–9. 70. Haddad SL, Coetzee JC, Estok R, Fahrbach K, Banel D, Nalysnyk L. Intermediate and long-term outcomes of total ankle arthroplasty and ankle arthrodesis. A systematic review of the literature. J Bone Joint Surg Am 2007;89–9:1899–905. 71. Clare MP, Sanders RW. Preoperative considerations in ankle replacement surgery. Foot Ankle Clin 2002;7–4:709–20. 72. van Roermund PM, Lafeber FP. Joint distraction as treatment for ankle osteoarthritis. Instr Course Lect 1999;48: 249–54. 73. Ploegmakers JJ, van Roermund PM, van Melkebeek J, Lammens J, Bijlsma JW, Lafeber FP, Marijnissen AC. Prolonged clinical benefit from joint distraction in the treatment of ankle osteoarthritis. Osteoarthr Cartil 2005;13–7: 582–8. 74. Tanaka Y, Takakura Y, Hayashi K, Taniguchi A, Kumai T, Sugimoto K. Low tibial osteotomy for varus-type osteoarthritis of the ankle. J Bone Joint Surg Br 2006;88–7:909–13. 75. Takakura Y, Tanaka Y, Kumai T, Tamai S. Low tibial osteotomy for osteoarthritis of the ankle. Results of a new operation in 18 patients. J Bone Joint Surg Br 1995;77–1:50–4. 76. Hintermann B, Knupp M, Barg A. [Osteotomies of the distal tibia and hindfoot for ankle realignment]. Orthopade 2008; 37–3:212–8, 20–3. 77. Hassouna H, Kumar S, Bendall S. Arthroscopic ankle debridement: 5-year survival analysis. Acta Orthop Belg 2007; 73–6:737–40.
Hallux Rigidus: Arthroplasty or Not? S. Giannini, F. Vannini, R. Bevoni, and D. Francesconi
Introduction Hallux rigidus (HR) is characterized by restriction of motion at first metatarsophalangeal joint (MPTJ) [1]. The gradual onset of pain and limitation of dorsi-flexion at the MPTJ is characteristic of the disease process, although often there may be a normal range of plantar-flexion [2]. The great toe is either fixed in plantar-flexion or limited in dorsiflexion because of the proliferation of bone around the articular surface of the head of the first metatarsal, particularly on the dorsal aspect. The severity of the degenerative changes is markedly dependent on the duration of symptomatology [2]. The pain and limited motion associated with arthritis of hallux metatarsophalangeal (HMP) joint produces a syndrome of functional disability that may include progressive loss of the propulsion function of the foot, “transfer” lesser metatarsalgia and gait alteration [3]. HR has been reported to affect one in forty-five individuals who are more than 50 years of age [4]. After hallux valgus, it is the most common affliction of the great toe and the most common form of degenerative joint disease in the foot [5]. There is no single cause for HR. Trauma, organic disorders, previous surgery are to be considered common causes which favour the onset of HR [6, 7]. Furthermore, anatomic abnormality of the first ray, especially in bilateral occurrence in the absence of other synovial joint involvement such as first ray elevation, has been identified as a predisposing factor [5]. However all these causes result in a pathologic process of isolated arthritis of the first MTP joint that leads to the formation of osteophytes and a thinning of the articular space [2]. Conservative management of symptomatic HR depends on a patient’s symptoms and the magnitude of the degen-
erative process. Use of NSAID’s, a stiff insole to reduce excursion of the MTP joint, orthoses providing rigidity to the forepart of the shoe can be effective in early first-grade disease [8]. Typically grade II and III HR require surgical treatment [8] and different techniques such as Cheilectomy [9–11], dorsal wedge osteotomy [12], tendon arthroplasty [13], capsular interposition arthroplasty [14, 15], Keller’s arthroplasty [16], and even arthroscopic procedures [17] have been proposed over time. A radiographic classification of HR has been developed by Regnauld [18] and a treatment algorithm has been previously proposed in order to choose the appropriate treatment accordingly [19–22]. With grade III HR salvage procedures include arthrodesis [23–26], excisional arthroplasty [27], soft-tissue interpositional arthroplasty [13–15] or prosthetic replacement [28–30]. Arthrodesis can be a satisfactory operation. The functional excellence and durability of the results obtained are impressive, although sacrifice of joint movement is an obvious drawback of the technique [23]. The value of prosthetic implants instead is still a theme for debate. The advantages of the procedure include preservation of the motion and a wide variety of implants have been proposed over time [31–35]. Nevertheless high risk of failure of the implant and serious complications have been reported [30, 36–41]. The aim of this study is to review the literature in order to investigate the validity of the treatments currently proposed for end-stage HR.
Arthrodesis S. Giannini (*) Via Pupilli 1, 40136 Bologna, Italy e-mail:
[email protected]
For patients who have severe arthritis of the first MPTJ, arthrodesis is still considered the gold standard particularly in younger and more active patients [42].
G. Bentley (ed.), European Instructional Lectures. European Instructional Course Lectures 9, DOI: 10.1007/978-3-642-00966-2_24, © 2009 EFORT
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Fusion ideally requires a set angle of 15° dorsi-flexion and 5–10° of valgus [22]. Many techniques are available for first MTP joint arthrodesis and fixation such as wires, screws, plates. Specificallydeveloped reamers have been described [43–45]. Fusion rates between 90 and 100% have been reported [43–48]. Wulker et al. [26] reported that results of first MPTJ atrhrodesis were good and excellent in approximately 80%. Fitzgerald and Wilkinson [23] in a review of the literature reported that the predictability and consistency of the result of arthrodesis with good results occurred in approximately 90% of cases. DeFrino et al. [36] studied 10 feet in 9 patients with severe HR. Arthrodesis of the first MTP joint was assessed with the AOFAS hallux score, by radiography and by dynamic pedobarography. After 34 months on average, all pre-operative tests were repeated and gait analysed. Their patients showed subjectively a significant clinical improvement. The mean AOFAS score improved from 38 to 90 and the pedobarographic analysis demonstrated restoration of weight-bearing on the first ray with greater maximum force carried by the toe pad at toe-off. However, kinematic data indicated a significantly shorter step length with some loss of ankle plantar-lexion at toe-off on the fused side. The kinematic data indicated a reduction in both ankle torque and ankle power at push-off. Nonetheless, there was effective pain relief and a high level of patient satisfaction. Goucher et al. [41] prospectively evaluated 50 patients who underwent first MTP arthrodesis using dome-shaped reamers to prepare the joint and a dorsal plate with a single compression screw for fixation (Level IV evidence). A 96% satisfaction rate, 92% union rate, and significant increase in AOFAS scores were achieved at an average follow-up of 16 months. The revision rate was 4%. Thirteen patients had single-grade radiographic progression of arthritic change at the interphalangeal joint. Flavin and Stephens [49] prospectively followed 12 patients who underwent first MTP arthrodesis using dorsal plate fixation with an average follow-up of 18 months (Level IV evidence). All patients showed radiographic signs of union at 6 weeks and there was a significant increase in AOFAS hallux and SF-36 scores. No complications were reported in this small series. Arthrodesis will provide predictable results with pain relief, but it is not free from complications [2]. In 1984, Beauchamp et al. [6] reported seven wound infections and five failed fusions in a report of 34 fusions of the first joint and non-union rates up to 13% of the patients have been described elsewhere [26].
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Futhermore fusion sacrifices motion which may lead to patient dissatisfaction and some limitation in shoe wear and activity [50, 51].
Arthroplasty Theoretically, arthroplasty should not only provide pain relief, but also restore motion and maintain joint stability. Many different designs and solutions have been proposed over time [31–35]. Different categories such as: silastic implants, hemi-arthroplasty, total metallic or ceramic implants and interposition arthroplasty have been described.
Silastic Implants Due to the initial success of silastic joint replacement in the hand, these implants were adapted for use in the MTP joint. Silastic implants designed as a dynamic spacer able to maintain joint space and motion have been used widely in the past, generally with reported good outcomes, but unfortunately silicone particulate synovitis was common [31, 32, 38]. Swanson et al. reported the results of the procedure in 105 patients, predominately with rheumatoid arthritis, with a mean follow-up of 2.5 years with satisfactory radiographic results in 84 (Level IV evidence) [31]. Cracchiolo et al. [28] prospectively followed 86 patients with rheumatoid arthritis or RH for a mean duration of 5.8 years (Level IV evidence). Eighty-three percent of patients reported subjective satisfaction with an average range of motion of 42°. Radiographically, however, osteophyte formation was noted in 23 patients and 12 of these had nearly 50% articular space encroachment. Radiographic cysts were identified in 35% of patients and eight implants fractured. Furthermore several authors reported data suggesting mechanical failure of the implants leading to siliconeinduced synovitis and osteolysis [37–41]. Grandberry et al. [37] in a 90 patient study using a silicone prosthesis, observed that, although clinical results were encouraging, in most of the cases there were alarming rates of fracture and deformation of the implant. These findings increased with the duration of implantation. To address this, new systems were designed for insertion with titanium grommets to reduce the stress applied to the silastic and to increase survival of the arthroplasty. Sebold and Cracchiolo [34] reported on 47 patients with rheumatoid arthritis or HR who joints were replaced with this new design at an average follow-up of 51 months (Level IV evidence).
Hallux Rigidus: Arthroplasty or Not?
In this series, 30 patients were subjectively completely satisfied. No implant fractured, although the arthroplasties developed peri-prosthetic radiolucencies in 5 patients, and the implants subsided in 15. The authors contrasted their results with a similar group of 41 patients who had received hinged implants. Thirty of these arthroplasties had radiolucencies and 2 implants fractured. The authors concluded that the use of titanium grommets protected the silicone prosthesis and improved longevity of the arthroplasty. Nevertheless the potential effects of silicone debris leading to foreign-body reaction, synovitis and bone erosion in the hallux still are cause of concern. In addition, the systemic effects of silicone microfragments invading the lymphoreticular system are still unknown and silastic implants are almost abandoned [39, 52].
Hemi-Arthroplasty Metatarsal Hemi-Arthroplasty Townley and Taranow [3] performed a large retrospective review of 279 patients treated with a metallic hemiarthroplasty of the proximal phalanx after minimal metatarsal head resection, with follow-up ranging from 8 months to 33 years (Level IV evidence). Pre-operative diagnoses included HR, rheumatoid arthritis and hallux valgus associated with osteoarthritis. The authors reported good or excellent results in 95% of patients. Only 2 patients with a diagnosis of HR were dissatisfied with their result. One patient had a post-operative infection while the other received an oversized implant. The remaining failures occurred in 8 patients with hallux valgus and 3 with rheumatoid arthritis. There was only one case of clinical or radiographic evidence of loosening which occurred in a patient with rheumatoid arthritis and poor bone quality. Botto-van Bemden and SanGiovanni [53] reported on the early follow-up results of 24 first metatarsal head re-surfacing procedures that were performed with use of the hemicontoured articular prosthesis (HemiCAP; Arthrosurface, Franklin, MA) for the treatment of advanced HR. Concomitant osseous and soft-tissue procedures were included for the correction of deformity and improvement of dorsi-flexion motion. After an average follow-up of 12 months, the average AOFAS score improved from 54.7 pre-operatively to 70 post-operatively, the average visual analogue pain score improved from 6.4 to 3.5, and average dorsi-flexion increased from 20.2 to 51°. While the authors considered this prosthesis to be a reliable alternative for the treatment of
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advanced HR, the device was recommended primarily for the treatment of arthritis pain and not for the restoration of motion.
Phalangeal Arthroplasty Metallic implants have been available for arthroplasties of the great toe for many years [38, 54]. Brage and Ball [55] while supporting fusion, note the value of a metallic hemi-arthroplasty, in its ability to allow restoration of alignment and maintenance of motion, length and strength in the great toe, which they consider to be fundamental in attaining a good clinical result. In a 10 patient (13 toes) study at 66 months follow-up, Konkel and Menger [35] evaluated the results of a titanium (Swanson) hemi-great toe implant. All the titanium prosthesis had subsided to varying degrees with lucencies around the implant. The rate of subsidence was most rapid during the first 2 years. One implant (8 years after insertion) was removed because of pain and stiffness that occurred after a hyperextension injury with fracture that the patient sustained while running. One patient had “transfer” metatarsalgia involving the second metatarsal. Four great toes in three patients with the greatest subsidence had mild great toe clawing and no visible great toe push-off during normal walking. One patient developed fullthickness ulcerations One patient developed a scar contracture with hyperextension of the great toe. At last follow-up, 37–105 months post-operatively, pain was absent in six toes, mild and occasional in five toes, moderate and daily in one toe and severe with vigorous activity in one toe. The outcome from a clinical trial of 23 cobalt-chrome hemi-arthroplasty implants in 19 patients has been recently evaluated by Sorbie and Saunders [56]. The patients’ ages ranged from males 41 to 61 (average age, 51.6) years and females 35 to 70 (average age, 54) years. The implant used was made of quality wrought cobalt, chromium-28 and molybdenum-6 alloy as specified in ASTM-F1537 (American Society for Testing Materials, Philadelphia, PA). The implant was aimed to be positioned in the proximal phalanx after a minimal amount of subchondral bone resection. The follow-up time from the day of surgery averaged 68 (range, 34–72) months. At follow-up a statistically significant improvement was found in all the cases. No complications were described in the paper with the exception of 2 patients dissatisfied of the range of motion gained.
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Total Metallic or Ceramic Implants Recent improvements in the biomaterials and understanding of biomechanics of the first MTP joint have revived the concept of total joint replacement. With the success of cobaltchrome alloy and polyethylene in hip and knee arthroplasties, some systems for great toe replacement have been introduced [33]. In MTP joint arthroplasty, these are designed as two-component, semi-constrained or non-constrained articulations. Papagelopoulos et al. [33] reported their experience with 93 primary implants (79 patients) of the first MTP joint using cemented metal and polyethylene components and silicone implants. The mean age of their patients was 56 (19–75) years. The average duration of follow-up evaluation in 75 patients who were alive and without re-operation was 12 (2–7) years. At 10 years, implant survival was 82% in patients 57 years of age or younger, and 90% in patients older than 57 years. The authors concluded that the overall probability that an implant would be in situ was 82% at 15 years after arthroplasty. Survivorship was higher in patients who were older than 58 years. Koenig and Horwitz [57] reported a 5-year study of 61 total joint arthroplasties using the Biomet total toe system. Of the 61 cases, 49 had a diagnosis of HR and 12 had a diagnosis of hallux valgus. Ten involved revision of failed silastic elastomer implant arthroplasty. The patients’ age ranged from 29 to 72 (mean of 54.5) years. All patients had end-stage arthrosis. They reported overall excellent results in 51 of 61 (83%) with 10 having various levels of compromised results. Pulavarti et al. [58] reviewed the intermediate results of 32 patients (36 replacements) with a minimum follow-up of 36 months. The Bio-Action great toe implant (OsteoMed, Addison, TX) a non-constrained, two-component total joint replacement system with a phalangeal component, was chosen.At the latest follow-up, there was significant improvement in the degree of pain, functional abilities, and footwear requirements as compared with pre-operative status. Twenty-five of 32 patients (79%) returned to normal or an occasionally affected lifestyle after the operation. Twenty-six of 32 of patients (81%) wore conventional footwear, and 3 of 32 patients (9%) wore footwear with inserts. No patient had significant “transfer” metatarsalgia. Twenty-eight of 32 patients (88%) had improvement in function. Three patients who continued to have pain after the operation rated the result as poor. Two of these three patients had revision surgery. One patient had removal of the implant and excision arthroplasty, and the other patient had arthrodesis of the joint 30 months after the primary
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replacement. There was no obvious cause for the poor results in all the three cases. Failures due to foreign-body granulomatous infiltration associated with metallic wear debris with peri-implant osteolysis leading to aseptic loosening and failure of titanium single-stem hallux implants were described by Ghalambor et al. [59].
Interposition Artrhroplasty Since the first description by Keller [60] in 1904, resection arthroplasty of the proximal part of the proximal phalanx has been an easy and commonly-performed operation. The patient, however, loses the big toe as a functional digit. Contracture of soft-tissues may produce an ugly, displaced, uncontrollable, cosmetically unattractive, great toe. Reducing the amount of resected bone risks continued pain and poor function. Interpositional arthroplasty, in which a biologic substance is utilized as an interpositional spacer in the first MTP joint, was developed as an alternative for the treatment of advanced HR [55]. Barca [13] placed the rolled plantaris tendon at the base of the first phalanx in 12 cases. He claimed that after 21 months, there was improved motion and reduced pain. Hamilton and Hubbard [14] felt that capsular interposition arthroplasty could give predictable pain relief in carefully selected individuals with severe (Grade III) HR. They used minimal resection of the phalanx, and interposed the dorsal capsule and the extensor hallucis brevis tendon in the space created. However, approximately 30% of the patients undergoing the procedure experienced some degree of post-operative, transfer metatarsalgia and required an orthosis for sports. A study by Lau and Daniels [42] was a retrospective comparison of cheilectomy with a capsular interpositional arthroplasty technique involving the use of an EHB tendon graft, on 11 cases (5 females and 6 males). Reported complications included asymptomatic callouses (3/11, 27.3%), post-operative weakness of the great toe (8/11, 72.7%) and metatarsalgia (3/11, 27.3%). In addition, one patient suffered a stress fracture of the second metatarsal, which was treated non-operatively, and one patient was awaiting arthrodesis. Mroczek and Miller [61] used a modest metatarsal cheilectomy with an oblique resection of the phalanx base preserving the flexor hallucis brevis attachment combined with interposition arthroplasty of the dorsal joint capsule. They claimed that such a modification produced a satisfactory outcome while maintaining plantar -flexion power and the length of the toe.
Hallux Rigidus: Arthroplasty or Not?
In twenty-two feet with grade-3 HR (18 feet in elderly patients or in patients with low functional demands, three feet in young patients who refused arthrodesis, and one foot in a professional soccer player), an arthroplasty with a biore-absorbable poly(DL-lactic acid) spacer was performed. The implant is inserted after minimal resection of the metatarsal head and reaming of the medullary canal. One foot had a localized infection at the MPTJ with sinus formation. The implant did not require revision, but the infection resulted in ankylosis in an acceptable position. Sufficient ROM and good pain reduction was provided by the procedure in the remaining cases [22]. Miller and Maffulli [62] recommend interposition arthroplasty using the ipsilateral gracilis tendon for patients who did not want an arthrodesis. Kennedy et al. [63] report on 18 patients (21 feet) with severe joint cartilage loss, who had interpositional arthroplasty at an average age of 56 years and at a mean time of 38 months follow-up. All had relief of pain. The mean increase of range of motion was 37° and follow-up AOFAS mean was 78.4. They had a 6% complication rate. Berlet et al. [64] used a minimally-invasive soft tissue arthroplasty, inserting human acellular regenerative tissue matrix as a spacer. The sesamoid articulation also was resurfaced. They described preliminary (mean, 10.1 months) results in 8 patients with an average age of 50.2 years. The pre-operation AOFAS score averaged 66.7 and 89.6 at follow-up. No complications were reported, there was no incidence of first metatarsal shortening, hallux hammer-toe deformities, or transfer metatarsalgia, Finally, at a mean length of follow-up of 10.1 months, there were no reported failures, suggesting early durability of the procedure.
Discussion The objectives of operative treatment of HR are relief of pain and restoration of as much function of the joint as possible giving special consideration to preservation of length and alignment of the great toe. The ideal surgical procedure for the management of HR remains a controversial subject. The consistently favourable results reported in many Level II and IV studies constitute fair evidence (Grade B recommendation) to support the use of arthrodesis for the treatment of advanced-stage HR [48, 49, 51]. In order to further investigate the general impression that the results after first MTPJ replacement are inferior to those after MTPJ arthrodesis, Gibson and Thomson [65] proposed
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a controlled randomized trial to compare the clinical outcomes of arthrodesis with total joint arthroplasty since no comparative prospective randomized studies were available. In 63 patients (77 feet) affected by first MTPJ osteoarthritis, arthrodesis was compared to first MTP joint prosthesis. The toe replacement chosen (BIOMET-Merck Ltd., Warsaw, IN) was an unconstrained joint. The metatarsal prosthesis was manufactured from cobalt chrome with a titanium plasma-spray coating (0.18–0.25 µm). In contrast, the phalangeal component was cast from pure titanium with a grit blasted surface and UHMW polyethylene (ArCom®) insert. All of the arthrodeses united, while six of the patients who received arthroplasty required revision within 2 years. In the remaining patients there was no difference at 2 years in the level of satisfaction in respect to pain relief between patients of the two groups, but more patients in the arthrodesis group preferred both their functional result and the appearance of their toe after arthrodesis. Nevertheless at 24 months, one patient (3%) after arthrodesis and 12 (40%) after arthroplasty (not including the six revisions) would not have undergone the same surgery again. The authors concluded that the 82% improvement at 2 years after arthrodesis exceeded that after successful arthroplasty (45%), and arthrodesis had a lower complication rate and cost less. In a level III study, Raikin et al. [66] investigated the results of a series of patients with osteoarthritis of the first MPTJ treated with either a metallic hemi-arthroplasty or an arthrodesis between 1999 and 2005. Eight of the feet in which the hemiprosthesis had survived had evidence of plantar cutout of the prosthetic stem on the final follow-up radiographs. At the time of final follow-up (at a mean of 79.4 months), the satisfaction ratings in the hemi-arthroplasty group were good or excellent for 12 feet, fair for 2 and poor or a failure for 7. The mean pain score was 2.4 of 10. All 27 of the arthrodeses achieved fusion, and no revisions were required. At the time of final follow-up (at a mean of 30 months), the satisfaction ratings in this group were good or excellent for 22 feet, fair for 4 and poor for 1. The mean pain score was 0.7 out of 10. Two patients required hardware removal, which was performed as an office procedure with the use of local anesthesia. The AOFAS-HMI and visual analogue pain scores and satisfaction were significantly better in the arthrodesis group. The conclusion was that Arthrodesis is more predictable than a metallic hemi-arthroplasty for alleviating symptoms and restoring function in patients with severe osteoarthritis of the first MPTJ. Given these unfavourable results in multiple studies with different implants confirmed by prospective comparative studies by Gibson and Thomson [65] and by Raikin et al. [66], hemi-arthroplasty cannot be recommended at
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this time for the management of HR. The results of Gibson’s prospective, randomized trial constitute a Grade B recommendation of arthrodesis as a predictable surgery able to eliminate painful motion and to maintain stability of the first ray with limited incidence of “transfer” metatarsalgia instead of arthroplasty. However, intrinsic stiffness connected with arthrodesis can lead to patient dissatisfaction. In addition, gait patterns can be altered, with a decreased step length and some loss of ankle plantar-flexion at toe-off on the fused side and these disadvantages should lead to search for new solutions [36]. Still controversial is also the role of interposition arthroplasty. The relatively high incidence of complications and the lower post-operative AOFAS score observed in the Lau and Daniel study [42] may lend support to the Roukis et al. [67] theory asserting that many of the capsular interpositional arthroplasty techniques are merely modifications of the original Keller procedure and, hence, are associated with the same complications. Encouraging results were otherwise reported with interposition arthoplasties with minimal bony resection of the metatarsal head. Among these good results was reported the use of a human acellular dermal regenerative tissue matrix or Poly-D-L-lactic-acyd as a spacer aimed to induce the formation of a fibrous tissue at the joint space that can maintain the stability and length of the toe [22, 64]. The same philosophy of minimal bone resection in order to preserve MTP joint function, is shared by the hemi-contoured articular prosthesis HemiCAP Arthrosurface, with encouraging results. Small numbers and short follow-up interval are limitations of this studiey [53]. Larger, prospective randomized studies directly comparing the various soft-tissue interpositional spacer materials or Arthrosurface may assist in determining the optimal spacer for performing interpositional arthroplasty. Further research about biomimetic materials and autologous cells may be an interesting topic of research aimed to obtain in the future reabsorbable implants or spacers able to stimulate formation of a regenerative tissue as close as possible to the native joint.
Reference 1. Shereff, M. J. and Baumhauer, J. F.: Hallux rigidus and osteoarthrosis of the first metatarsophalangeal joint. J. Bone Joint Surg. Am. 80:898–908, 1998. 2. Mann, R. A., Coughlin, M. J., and DuVries, H. L.: Hallux rigidus: A review of the literature and a method of treatment. Clin. Orthop. 57–63, 1979.
S. Giannini et al. 3. Townley, C. O. and Taranow, W. S.: A metallic hemiarthroplasty resurfacing prosthesis for the hallux metatarsophalangeal joint. Foot Ankle Int. 15:575–580, 1994. 4. Gould, N.: Hallux rigidus: Cheilotomy or implant? Foot Ankle. 1:315–320, 1981. 5. Horton, G. A., Park, Y. W., and Myerson, M. S.: Role of metatarsus primus elevatus in the pathogenesis of hallux rigidus. Foot Ankle Int. 20(12):777–780, 1999. 6. Beauchamp, C. G., Kirby, T., Rudge, S. R., Worthington, B. S., and Nelson, J.: Fusion of the first metatarsophalangeal joint in forefoot arthroplasty. Clin. Orthop. 249–253, 1984. 7. McMaster, M. J.: The pathogenesis of hallux rigidus. J. Bone Joint Surg. Br. 60:82–87, 1978. 8. Coughlin, M. J.: Arthritides. In Coughlin, M. J. and Mann, R. A. (eds), Surgery of the foot and ankle, Seventh ed., pp. 560–650. St. Louis, Mosby, 1999. 9. Feldman, R. S., Hutter, J., Lapow, L., and Pour, B.: Cheilectomy and hallux rigidus. J. Foot Surg. 22:170–174, 1983. 10. Mackay, D. C., Blyth, M., and Rymaszewski, L. A.: The role of cheilectomy in the treatment of hallux rigidus. J. Foot Ankle Surg. 36:337–340, 1997. 11. Heller, W. A. and Brage, M. E.: The effects of cheilectomy on dorsiflexion of the first metatarsophalangeal joint. Foot Ankle Int. 18:803–808, 1997. 12. Blyth, M. J., Mackay, D. C., and Kinninmonth, A. W.: Dorsal wedge osteotomy in the treatment of hallux rigidus. J. Foot Ankle Surg. 37:8–10, 1998. 13. Barca, F.: Tendon arthroplasty of the first metatarsophalangeal joint in hallux rigidus: Preliminary communication. Foot Ankle Int. 18:222–228, 1997. 14. Hamilton, W. G. and Hubbard, C. E.: Hallux rigidus. Excisional arthroplasty. Foot Ankle Clin. 5:663–671, 2000. 15. Hamilton, W. G., O’Malley, M. J., Thompson, F. M., and Kovatis, P. E.: Roger Mann Award 1995. Capsular interposition arthroplasty for severe hallux rigidus. Foot Ankle Int. 18:68–70, 1997. 16. Wrighton, J. D.: A ten-year review of Keller’s operation. Review of Keller’s operation at the Princess Elizabeth Orthopaedic Hospital, Exeter. Clin. Orthop. 89:207–214, 1972. 17. van Dijk, C. N., Veenstra, K. M., and Nuesch, B. C.: Arthroscopic surgery of the metatarsophalangeal first joint. Arthroscopy. 14:851–855, 1998. 18. Regnauld, B. (ed): Disorders of the great toe. In: The foot, pp. 269–349. Berlin, Springer, 1986. 19. Feltham, G. T., Hanks, S. E., and Marcus, R. E.: Age-based outcomes of cheilectomy for the treatment of hallux rigidus. Foot Ankle Int. 22:192–197, 2001. 20. Mann, R. A. and Clanton, T. O.: Hallux rigidus: Treatment by cheilectomy. J. Bone Joint Surg. Am. 70:400–406, 1988. 21. Trantalis, J. J.: The role of cheilectomy in the treatment of hallux rigidus. J. Foot Ankle Surg. 37:171, 1998. 22. Giannini, S., Ceccarelli, F., Faldini, C., Bevoni, R., Grandi, G., and Vannini, F.: What’s new in surgical options for hallux rigidus? J. Bone Joint Surg. Am. 86-A (Suppl 2):72–83, 2004. 23. Fitzgerald, J. A. and Wilkinson, J. M.: Arthrodesis of the metatarsophalangeal joint of the great toe. Clin. Orthop. 70–77, 1981.
Hallux Rigidus: Arthroplasty or Not? 24. Lipscomb, P. R.: Arthrodesis of the first metatarsophalangeal joint for severe bunions and hallux rigidus. Clin. Orthop. 48–54, 1979. 25. Trnka, H. J.: Arthrodesis procedures for salvage of the hallux metatarsophalangeal joint. Foot Ankle Clin. 5:673–686, ix, 2000. 26. Wulker, N.: [Arthrodesis of the metatarsophalangeal joint of the large toe]. Orthopade. 25:187–193, 1996. 27. Shapiro, F. and Heller, L.: The Mitchell distal metatarsal osteotomy in the treatment of hallux valgus. Clin. Orthop. 225–231, 1975. 28. Cracchiolo, A., III, Weltmer, J. B., Jr., Lian, G., Dalseth, T., and Dorey, F.: Arthroplasty of the first metatarsophalangeal joint with a double-stem silicone implant. Results in patients who have degenerative joint disease failure of previous operations, or rheumatoid arthritis. J. Bone Joint Surg. Am. 74:552–563, 1992. 29. Jarde, O., Wable, E., Havet, E., de Lestang, M., and Vives, P.: [Interpositioned metallic prosthesis for hallux rigidus: Review of 42 cases with a metatarsophalangeal prosthesis]. Rev. Chir. Orthop. Reparatrice Appar. Mot. 87:67–72, 2001. 30. Shankar, N. S.: Silastic single-stem implants in the treatment of hallux rigidus. Foot Ankle Int. 16:487–491, 1995. 31. Swanson, A. B., Lumsden, R. M., and Swanson, G. D.: Silicone implant arthroplasty of the great toe: A review of single stem and flexible hinge implants. Clin. Orthop. 142:30–43, 1979. 32. Swanson, A. B.: Implant arthroplasty for the great toe. Clin. Orthop. 85:75–81, 1972. 33. Papagelopoulos, P. J., Kitaoka, H. B., and Ilstrup, D. M.: Survivorship analysis of implant arthroplasty for the first metatarsophalangeal joint. Clin. Orthop. 302:164–172, 1994. 34. Sebold, E. J. and Cracchiolo, A. 3rd: Use of titanium grommets in silicone implant arthroplasty of the hallux metatarsophalangeal joint. Foot Ankle Int. 17(3):145–151, 1996. 35. Konkel, K. F. and Menger, A. G.: Mid-term results of titanium hemi-great toe implants. Foot Ankle Int. 27(11):922– 929, 2006. 36. DeFrino, P. F., Brodsky, J. W., Pollo, F. E., Crenshaw, S. J., and Beischer, A. D.: First metatarsophalangeal arthrodesis: A clinical, pedobarographic and gait analysis study. Foot Ankle Int. 23:496–502, 2002. 37. Granberry, W. M., Noble, P. C., Bishop, J. O., and Tullos, H. S.: Use of a hinged silicone prosthesis for replacement arthroplasty of the first metatarsophalangeal joint. J. Bone Joint Surg. Am. 73:1453–1459, 1991. 38. Gordon, M. and Bullough, P. G.: Synovial and osseous inflammation in failed silicone-rubber prostheses. J. Bone Joint Surg. Am. 64:574–580, 1982. 39. Shereff, M. J. and Jahss, M. H.: Complications of silastic implant arthroplasty in the hallux. Foot Ankle. 1:95–101, 1980. 40. Johnson, K. A. and Buck, P. G.: Total replacement arthroplasty of the first metatarsophalangeal joint. Foot Ankle. 1:307–314, 1981. 41. Lemon, R. A., Engber, W. D., and McBeath, A. A.: A complication of Silastic hemiarthroplasty in bunion surgery. Foot Ankle. 4:262–266, 1984.
245 42. Lau, J. T. and Daniels, T. R.: Outcomes following cheilectomy and interpositional arthroplasty in hallux rigidus. Foot Ankle Int. 22:462–470, 2001. 43. Coughlin, M. J. and Shurnas, P. S.: Hallux rigidus: Demographics, etiology, and radiographic assessment. Foot Ankle Int. 24(10):731–743, 2003. 44. Goucher, N. R. and Coughlin, M. J.: Hallux metatarsophalangeal joint arthrodesis using dome-shaped reamers and dorsal plate fixation: A prospective study. Foot Ankle Int. 27(11):869–876, 2006. 45. Phillips, J. E. and Hooper, G.: A simple technique for arthrodesis of the first metatarsophalangeal joint. J. Bone Joint Surg. 68-B:774–775, 1996. 46. Southgate, J. J. and Urry, S. R.: Hallux rigidus: The longterm results of dorsal wedge osteotomy and arthrodesis in adults. J. Foot Ankle Surg. 36:136–140, 1997. 47. Thomson, C. E., Westland, E., Maguire, D., and Gibson, J. N. A.: Evaluation of in-shoe plantar pressures and patient satisfaction following first metatarsophalangeal joint arthrodesis. J. Bone Joint Surg.82-B (Suppl III ):218, 2000. 48. Mann, R. A. and Thompson, F. M.: Arthrodesis of the first metatarsophalangeal joint for hallux valgus in rheumatoid arthritis. J. Bone Joint Surg. Am. 66:687–692, 1984. 49. Flavin, R. and Stephens, M. M.: Arthrodesis of the first metatarsophalangeal joint using a dorsal titanium contoured plate. Foot Ankle Int. 25(11):783–787, 2004. 50. Fadel, G., Abboud, R., and Rowley, D.: Implant arthroplasty of the hallux metatarsophalangeal joint. The Foot. 12:1–9, 2002. 51. Fitzgerald, J.: A review of long-term results of arthrodesis of the first metatarsophalangeal joint. J. Bone Joint Surg. 51-B:488–493, 1969. 52. Shiel, W. C. Jr. and Jason, M.: Granulomatous inguinal lymphadenopathy after bilateral metatarsophalangeal joint silicone arthroplasty. Foot Ankle. 6(5):216–218, 1986. 53. Botto-van Bemden, A. L. and SanGiovanni, T. P.: A new technique for the surgical management of advanced hallux rigidus with or without deformity. A poster presented on Specialty Day at the Annual Meeting of the American Academy of Orthopaedic Surgeons. 2007 Feb 17; San Diego, CA; pp. 218. 54. Leavitt, K. M., Nirenberg, M. S., Wood, B., and Yong, R. M.: Titanium hemigreat toe implant: A preliminary study of its efficacy. J. Foot Surg. 30:289–293, 1991. 55. Brage, M. E. and Ball, S. T.: Surgical options for salvage of end-stage hallux rigidus. Foot Ankle Clin. 7:49–73, 2002. 56. Sorbie, C. and Saunders, G. A.: Hemiarthroplasty in the treatment of hallux rigidus. Foot Ankle Int. 29(3):273–281, 2008. 57. Koenig, R. D. and Horwitz, L. R.: The biomet total toe system utilizing the Koenig score: A five-year review. J. Foot Ankle Surg. 35:23–26, 1996. 58. Pulavarti, R. S., McVie, J. L., and Tulloch, C. J.: First metatarsophalangeal joint replacement using the bio-action great toe implant: Intermediate results. Foot Ankle Int. 26(12):1033–1037, 2005. 59. Ghalambor, N., Cho, D. R., Goldring, S. R., Nihal, A., and Trepman, E.: Microscopic metallic wear and tissue response in failed titanium hallux metatarsophalangeal implants: Two cases. Foot Ankle Int. 23(2):158–162, 2002.
246 60. Keller, W. L.: The surgical treatment of bunions and hallux valgus. NY. Med. J. 80:741–742, 1904. 61. Mroczek, K. J. and Miller, S. D.: The modified oblique Keller procedure: A technique for dorsal approach interposition arthroplasty sparing the flexor tendons. Foot Ankle Int. 24:521–522, 2003. 62. Miller, D. and Maffulli, N.: Free gracilis interposition arthroplasty for severe hallux rigidus. Bull. Hosp. Joint Dis. 62:121–124, 2005. 63. Kennedy, J. G., Chow, F. Y., Dines, J., Gardner, M., and Bohne, W. H.: Outcomes after interpositional arthroplasty for treatment of hallux rigidus. Clin. Orthop. Rel. Res. 445:210–215, 2006. 64. Berlet, G. C., Hyer, C. F., Lee, T. H., Philbin, T. M., Hartman, J. F., and Wright, M. L.: Interpositional arthroplasty of the
S. Giannini et al. first MTP joint using a regenerative tissue matrix for the treatment of advanced hallux rigidus. Foot Ankle Int. 29(1): 10–21, 2008. 65. Gibson, A. and Thomson, C. E.: Arthrodesis or total replacement arthroplasty for hallux rigidus. Foot Ankle Int. 26(9):680–690, 2005. 66. Raikin, S. M., Ahmad, J., Pour, A. E., and Abidi, N.: Comparison of arthrodesis and metallic hemiarthroplasty of the hallux metatarsophalangeal joint. J. Bone Joint Surg. Am. 89(9):1979– 1985, 2007. 67. Roukis, T. S., Landsman, A. S., Ringstrom, J. B., and Kirschner, P.: Wuenschel MDistally based capsule-periosteum interpositional arthroplasty for hallux rigidus. Indications, operative technique, and short-term follow-up. J. Am. Podiatr. Med. Assoc. 93(5):349–366, 2003.